Pancreatic cancer survivors?

Discussion in 'Health and medical' started by Mr Ducky, Jan 26, 2004.

  1. Mr Ducky

    Mr Ducky Guest

    Is there anyone here who has achieved long term (several years) survival of metastatic pancreatic
    cancer, or who personally knows someone who has? How about cancer of the small intestine?

    If so, please describe the treatment. I'm interested in both conventional and alternative
    treatments.

    I'd also like to know if anyone here has personal experience with the Dr. Gonzalez treatment (again,
    you or someone you know). I've already read many articles on the web, so please don't post a copy of
    dr-gonzalez.com or quackwatch.

    Thank you.
     
    Tags:


  2. J

    J Guest

    Mr Ducky wrote:

    > Is there anyone here who has achieved long term (several years) survival of metastatic pancreatic
    > cancer, or who personally knows someone who has? How about cancer of the small intestine?

    http://www.pancan.org/Patient/Inspiration/inspirStories.html Surgery and sometimes chemo. (some
    stories aren't updated) If you or a loved one has pancreatic cancer, please come over (post only to)
    news:alt.support.cancer (no crossposts please) Thank you. J
     
  3. [email protected] (Mr Ducky) wrote in
    news:[email protected]:

    > Is there anyone here who has achieved long term (several years) survival of metastatic pancreatic
    > cancer, or who personally knows someone who has? How about cancer of the small intestine?
    >
    > If so, please describe the treatment. I'm interested in both conventional and alternative
    > treatments.
    >
    > I'd also like to know if anyone here has personal experience with the Dr. Gonzalez treatment
    > (again, you or someone you know). I've already read many articles on the web, so please don't post
    > a copy of dr-gonzalez.com or quackwatch.
    >
    > Thank you.

    Duck,

    You can get a lot of good pancreatic cancer answer on the ACOR mail list for that subject. On each
    of the lists the are many people with experience it that type. http://www.acor.org/mailing.html?l=p

    Why would anyone want personal experince with the Gonzales treatment? Cancer tries in many ways to
    destroy your dignity, but you don't have to throw it away on snake oil.

    Frank
     
  4. "Mr Ducky" <[email protected]> wrote in message
    news:[email protected]...
    > Is there anyone here who has achieved long term (several years) survival of metastatic pancreatic
    > cancer, or who personally knows someone who has? How about cancer of the small intestine?
    >
    > If so, please describe the treatment. I'm interested in both conventional and alternative
    > treatments.
    >
    > I'd also like to know if anyone here has personal experience with the Dr. Gonzalez treatment
    > (again, you or someone you know). I've already read many articles on the web, so please don't post
    > a copy of dr-gonzalez.com or quackwatch.
    >
    > Thank you.

    Well are you just looking for someone to tell you the truth or just what you want to hear?
    Pancreatic cancer responds very poorly to conventional medical treatment and not at all to all known
    alternatives. MIKE
     
  5. Orac

    Orac Guest

    In article <[email protected]>,
    "Mike Radcliffe" <[email protected]> wrote:

    > "Mr Ducky" <[email protected]> wrote in message
    > news:[email protected]...
    > > Is there anyone here who has achieved long term (several years) survival of metastatic
    > > pancreatic cancer, or who personally knows someone who has? How about cancer of the small
    > > intestine?
    > >
    > > If so, please describe the treatment. I'm interested in both conventional and alternative
    > > treatments.
    > >
    > > I'd also like to know if anyone here has personal experience with the Dr. Gonzalez treatment
    > > (again, you or someone you know). I've already read many articles on the web, so please don't
    > > post a copy of dr-gonzalez.com or quackwatch.
    > >
    > > Thank you.
    >
    > Well are you just looking for someone to tell you the truth or just what you want to hear?
    > Pancreatic cancer responds very poorly to conventional medical treatment and not at all to all
    > known alternatives.

    Correct. And the five year survival for all comers with pancreatic cancer is less than 1%. For those
    whose tumor can be successfully resected with negative surgical margins, at best it's around 20%.

    --
    Orac |"A statement of fact cannot be insolent."
    |
    |"If you cannot listen to the answers, why do you inconvenience me with questions?"
     
  6. Ducky,

    Mr Ducky wrote:

    > Is there anyone here who has achieved long term (several years) survival of metastatic pancreatic
    > cancer, or who personally knows someone who has?

    Rompin' Ronnie Hawkins, the Canadian (born in the U.S.A.) country singer has apparently had good
    success with his treatment over the past year and a half or so. You might want to check out his
    website (try Google). Also, the following information was offered in an ACOR discussion group
    (esophageal cancer) I am a member of. Might be worth a look:

    The complete segment can be accessed by going to www.abclocal.go.com/kgo finding the
    Dr. Edell link. The information was originally reported by www.ivanhoe.com/newsalert/. Dr. David
    Agus at Cedars-Sinai was the doctor who reported the research information to Ivanhoe.

    Best wishes and good luck, Hans

    > How about cancer of the small intestine?
    >
    > If so, please describe the treatment. I'm interested in both conventional and alternative
    > treatments.
    >
    > I'd also like to know if anyone here has personal experience with the Dr. Gonzalez treatment
    > (again, you or someone you know). I've already read many articles on the web, so please don't post
    > a copy of dr-gonzalez.com or quackwatch.
    >
    > Thank you.
     
  7. J

    J Guest

    ballstoyourpartner wrote:

    > Mr Ducky wrote:
    >
    > > Is there anyone here who has achieved long term (several years) survival of metastatic
    > > pancreatic cancer, or who personally knows someone who has?
    >
    > Rompin' Ronnie Hawkins, the Canadian (born in the U.S.A.) country singer has apparently had good
    > success with his treatment over the past year and a half or so. You might want to check out his
    > website (try Google).

    Here's the "spin" I was able to find..

    http://www.epinions.com/content_73529200260/show_~allcom August 21/02 Just wanted to let you know,
    it was reported in the weekend paper that Ronnie Hawkins came through the surgery fine last week.
    They think they got all of the tumour and he is presently recovering in Toronto General Hospital

    http://www.cannabisclub.ca/CP_042603.html Hawkins says pot & whisky cured him Source: Canadian
    Press, 04/26/03
    - Less than a year after he was diagnosed with pancreatic cancer and operated on, apparently
    unsuccessfully, Ronnie Hawkins announced he is cancer-free, due to unconventional treatments,
    which included "whisky and pot," The Toronto Sun reported yesterday. "I'd have to go into hours to
    tell you about all the Indian recipes and the stuff that' was sent to me," Hawkins told The Sun,
    "I don't know which one cured me, but it might have been a combination of all of it. Personally, I
    think it was the whisky and the pot," he said. The Hawkins family planned to release the news
    yesterday. "It was very serious, it disappeared, it's gone, and nobody knows how to explain it,"
    said Hawkins, who chose not to undergo chemotherapy in the wake of surgery.

    http://www.rocktober.com/blogarchive/2002_08_25_blogarchive.html Ronnie Hawkins Has Tumor Removed
    Ronnie Hawkins of The Band, has been diagnosed with cancer and underwent surgery Aug. 13 to remove
    part of a tumor that was found to be cancerous. Doctors said there was no sign the cancer had
    spread, and no immediate plans for Hawkins to undergo chemotherapy. Hawkins left the hospital on
    Aug. 19 and has been resting at home since.

    http://www.eastnorthumberland.com/news/news2003/newsFebruary2003/Hawk02262003.html

    Over the past year Hawkins has had three major operations to treat a non-cancerous pancreatic
    tumour. But he's recovered sufficiently that he plans to start rehearsing this week to prepare for a
    return to the stage sometime in March. "I don't want to set a date because I've got to take my time
    on getting ready," Hawkins said.

    http://www.canoe.ca/JamConcertsE2K/hawkins_ronnie_032703-sun.html Thursday, March 27, 2003 OTTAWA --
    Heart surgery and a cancer scare haven't stopped Ronnie Hawkins, who thrilled more than 400 fans at
    Barrymore's Music Hall on Thursday night in his first set since his health was found to be in
    serious jeopardy last year. []

    And apparently one of the 3 surgeries was a heart bypass on or around July 3/02 No mention of small
    intestine involvement, if that was part of the OP's inquiry/situation. So heart bypass, probably an
    exploratory (ERCP?) (or partial tumour removal) and removal of the rest ???

    > <snipped>
    >
    > > How about cancer of the small intestine?
    > >

    <snipped>

    J
     
  8. Mark

    Mark Guest

    Orac <[email protected]> wrote in message news:<[email protected]>...
    > In article <[email protected]>,
    > "Mike Radcliffe" <[email protected]> wrote:
    >
    > > "Mr Ducky" <[email protected]> wrote in message
    > > news:[email protected]...
    > > > Is there anyone here who has achieved long term (several years) survival of metastatic
    > > > pancreatic cancer, or who personally knows someone who has? How about cancer of the small
    > > > intestine?
    > > >
    > > > If so, please describe the treatment. I'm interested in both conventional and alternative
    > > > treatments.
    > > >
    > > > I'd also like to know if anyone here has personal experience with the Dr. Gonzalez treatment
    > > > (again, you or someone you know). I've already read many articles on the web, so please don't
    > > > post a copy of dr-gonzalez.com or quackwatch.
    > > >
    > > > Thank you.
    > >
    > > Well are you just looking for someone to tell you the truth or just what you want to hear?
    > > Pancreatic cancer responds very poorly to conventional medical treatment and not at all to all
    > > known alternatives.
    >
    > Correct. And the five year survival for all comers with pancreatic cancer is less than 1%. For
    > those whose tumor can be successfully resected with negative surgical margins, at best it's
    > around 20%.

    I wouldn't want your job, Orac. At least when my patients develop a malignancy (the most recent --
    mediastinal neuroblastoma in a 10 month old) the prognosis is a lot better.

    Bless you guys. I couldn't do it.

    Mark, MD
     
  9. Orac

    Orac Guest

    In article <[email protected]>,
    [email protected] (Mark) wrote:

    > Orac <[email protected]> wrote in message news:<[email protected]>...
    > > In article <[email protected]>,
    > > "Mike Radcliffe" <[email protected]> wrote:

    > > > Well are you just looking for someone to tell you the truth or just what you want to hear?
    > > > Pancreatic cancer responds very poorly to conventional medical treatment and not at all to all
    > > > known alternatives.
    > >
    > > Correct. And the five year survival for all comers with pancreatic cancer is less than 1%. For
    > > those whose tumor can be successfully resected with negative surgical margins, at best it's
    > > around 20%.
    >
    >
    > I wouldn't want your job, Orac. At least when my patients develop a malignancy (the most recent --
    > mediastinal neuroblastoma in a 10 month old) the prognosis is a lot better.

    Actually, I think I have more trouble dealing with kids with cancer. More of them survive than
    adults, but it would tear me apart to deal with the ones who don't. On the other hand, pediatric
    cancers are one of the success stories of modern oncology, which I frequently point out to the
    "alternative" medicine zealots who, in their hatred of conventional medicine, make the incorrect
    claim that conventional medicine never cures cancer. Thirty or forty years ago, most such cancers
    were a death sentence. Now, depending on the tumor, long term survival rates can be higher than 80%.

    > Bless you guys. I couldn't do it.

    I wish I could take credit for it. Actually, I don't deal with pancreatic cancer much anymore. One
    of the problems with being in an academic setting is that you get pidgeon-holed into your specialty
    and it's very hard to branch out. We have two surgeons who do essentially all the pancreatic cancer
    at the institution. I haven't done any in a few years now.

    On the other hand even while not doing the pancreas stuff, we still get some sad cases--usually when
    on call. The saddest case I've seen lately was a 31 year old woman with a bowel obstruction that
    turned out to be carcinomatosis from an unknown (but probably GI) primary. She has two small
    children. She's starting chemotherapy, but that's pretty unlikely to keep her going long.

    --
    Orac |"A statement of fact cannot be insolent."
    |
    |"If you cannot listen to the answers, why do you inconvenience me with questions?"
     
  10. ballstoyourpartner wrote:

    > Ducky,
    >
    > Mr Ducky wrote:
    >
    > > Is there anyone here who has achieved long term (several years) survival of metastatic
    > > pancreatic cancer, or who personally knows someone who has?
    >
    > Rompin' Ronnie Hawkins, the Canadian (born in the U.S.A.) country singer has apparently had good
    > success with his treatment over the past year and a half or so. You might want to check out his
    > website (try Google). Also, the following information was offered in an ACOR discussion group
    > (esophageal cancer) I am a member of. Might be worth a look: The complete segment can be accessed
    > by going to www.abclocal.go.com/kgo finding the
    > Dr. Edell link. The information was originally reported by www.ivanhoe.com/newsalert/. Dr. David
    > Agus at Cedars-Sinai was the doctor who reported the research information to Ivanhoe.

    Sorry to have been less-than-clear on that second part, the articles cited are in respect of a new
    drug called 2C4.

    Balls

    >
    >
    > Best wishes and good luck, Hans
    >
    > > How about cancer of the small intestine?
    > >
    > > If so, please describe the treatment. I'm interested in both conventional and alternative
    > > treatments.
    > >
    > > I'd also like to know if anyone here has personal experience with the Dr. Gonzalez treatment
    > > (again, you or someone you know). I've already read many articles on the web, so please don't
    > > post a copy of dr-gonzalez.com or quackwatch.
    > >
    > > Thank you.
     
  11. Roger

    Roger Guest

    "Orac" <[email protected]> wrote in message
    news:eek:[email protected]...
    > In article <[email protected]>,
    > "Mike Radcliffe" <[email protected]> wrote:
    >
    > > "Mr Ducky" <[email protected]> wrote in message
    > > news:[email protected]...
    > > > Is there anyone here who has achieved long term (several years) survival of metastatic
    > > > pancreatic cancer, or who personally knows someone who has? How about cancer of the small
    > > > intestine?
    > > >
    > > > If so, please describe the treatment. I'm interested in both conventional and alternative
    > > > treatments.
    > > >
    > > > I'd also like to know if anyone here has personal experience with the Dr. Gonzalez treatment
    > > > (again, you or someone you know). I've already read many articles on the web, so please don't
    > > > post a copy of dr-gonzalez.com or quackwatch.
    > > >
    > > > Thank you.
    > >
    > > Well are you just looking for someone to tell you the truth or just what
    you
    > > want to hear? Pancreatic cancer responds very poorly to conventional medical
    treatment
    > > and not at all to all known alternatives.
    >
    > Correct. And the five year survival for all comers with pancreatic cancer is less than 1%. For
    > those whose tumor can be successfully resected with negative surgical margins, at best it's
    > around 20%.

    There was a relatively famous African-American actor that died about a month ago of panc cancer who
    had it for four years according to the news article I read. He was one of the main characters in the
    movie, Shaft (I think that was the movie). Don't know the details on his case but it just goes to
    show some people do live awhile with it.

    It would seem if a panc cancer patient kept his/her blood sugar (and insulin) levels low (such as by
    eating a mostly protein-based diet), took high doses of statin drugs (along with co-enzyme Q10 for
    protection from the high doses of statin drugs), took EPA fatty acids (to reduce arachidonic acid
    levels and AA metabolites) along with chemo, survival times might get a lot more impressive.

    Losing weight as fast as possible through exercise (to deprive the cancer cells of saturated fatty
    acids from body fat used for membranes of new cells) would also seem to lengthen survival. And
    taking anti-angiogenic substances such as NSAIDs would seem to help too.

    Roger

    >
    > --
    > Orac |"A statement of fact cannot be insolent."
    > |
    > |"If you cannot listen to the answers, why do you inconvenience me with questions?"
     
  12. Orac

    Orac Guest

    In article <[email protected]>,
    "Roger" <[email protected]> wrote:

    > "Orac" <[email protected]> wrote in message news:eek:[email protected]...
    > > In article <[email protected]>,
    > > "Mike Radcliffe" <[email protected]> wrote:
    > >
    > > > "Mr Ducky" <[email protected]> wrote in message
    > > > news:[email protected]...
    > > > > Is there anyone here who has achieved long term (several years) survival of metastatic
    > > > > pancreatic cancer, or who personally knows someone who has? How about cancer of the small
    > > > > intestine?
    > > > >
    > > > > If so, please describe the treatment. I'm interested in both conventional and alternative
    > > > > treatments.
    > > > >
    > > > > I'd also like to know if anyone here has personal experience with the Dr. Gonzalez treatment
    > > > > (again, you or someone you know). I've already read many articles on the web, so please
    > > > > don't post a copy of dr-gonzalez.com or quackwatch.
    > > > >
    > > > > Thank you.
    > > >
    > > > Well are you just looking for someone to tell you the truth or just what
    > you
    > > > want to hear? Pancreatic cancer responds very poorly to conventional medical
    > treatment
    > > > and not at all to all known alternatives.
    > >
    > > Correct. And the five year survival for all comers with pancreatic cancer is less than 1%. For
    > > those whose tumor can be successfully resected with negative surgical margins, at best it's
    > > around 20%.
    >
    > There was a relatively famous African-American actor that died about a month ago of panc cancer
    > who had it for four years according to the news article I read. He was one of the main characters
    > in the movie, Shaft (I think that was the movie). Don't know the details on his case but it just
    > goes to show some people do live awhile with it.

    Yes, but it's very uncommon. The median survival for unresectable pancreatic cancer is on the order
    of 6-12 months, and the median survival after a successful resection with negative margins is less
    than two years.

    > It would seem if a panc cancer patient kept his/her blood sugar (and insulin) levels low (such as
    > by eating a mostly protein-based diet),

    There is no scientific evidence I am aware of for this, or that any diet-based manipulations have
    an effect on pancreatic cancer survival. However, I'm always willing to look at evidence someone
    else shows me.

    >took high doses of statin drugs (along with co-enzyme Q10 for protection from the high doses of
    >statin drugs),

    There is no scientific evidence I am aware of for this.

    >took EPA fatty acids (to reduce arachidonic acid levels and AA metabolites) along with chemo,
    >survival times might get a lot more impressive.

    There is no scientific evidence I am aware of for this.

    > Losing weight as fast as possible through exercise (to deprive the cancer cells of saturated fatty
    > acids from body fat used for membranes of new cells) would also seem to lengthen survival.

    Nope. This has been an argument going back and forth for decades, and the bottom line is that there
    is no good evidence that losing weight will prolong survival. Indeed, frequently the cancer makes
    its victims lose weight uncontrollably (the cancer cachexia syndrome).

    >And taking anti-angiogenic substances such as NSAIDs would seem to help too.

    Antiangiogenic drugs may have a role, but the jury is still out and trials are ongoing. NSAIDs do
    not appear to have much of a role in treatment, although they may be preventative.

    I think you may be confusing things that are meant to be preventative with those that can actually
    treat pancreatic cancer. For instance, there is evidence that a number of dietary manipulations
    *might* decrease its incidence. However, once the cancer is there, there is no dietary manipulation
    known that will prolong survival.

    --
    Orac |"A statement of fact cannot be insolent."
    |
    |"If you cannot listen to the answers, why do you inconvenience me with questions?"
     
  13. Roger

    Roger Guest

    "Orac" <[email protected]> wrote

    > "Roger" <[email protected]> wrote:
    >
    > > "Orac" <[email protected]> wrote
    > >
    > > > "Mike Radcliffe" wrote:
    > > >
    > > > > Pancreatic cancer responds very poorly to conventional medical
    > > treatment
    > > > > and not at all to all known alternatives.
    > > >
    > > > Correct. And the five year survival for all comers with pancreatic cancer is less than 1%. For
    > > > those whose tumor can be successfully resected with negative surgical margins, at best it's
    > > > around 20%.
    > >
    > > There was a relatively famous African-American actor that died about a
    month
    > > ago of panc cancer who had it for four years according to the news
    article I
    > > read. He was one of the main characters in the movie, Shaft (I think
    that
    > > was the movie). Don't know the details on his case but it just goes to
    show
    > > some people do live awhile with it.
    >
    > Yes, but it's very uncommon. The median survival for unresectable pancreatic cancer is on the
    > order of 6-12 months, and the median survival after a successful resection with negative margins
    > is less than two years.

    Perhaps with people taking some of the measures I suggest, the median survival would be
    significantly longer. I believe the evidence from valid scientific sources (such as can be found at
    Pubmed) backs this notion up (some of which I will present in this post).

    >
    >
    > > It would seem if a panc cancer patient kept his/her blood sugar (and insulin) levels low (such
    > > as by eating a mostly protein-based diet),
    >
    > There is no scientific evidence I am aware of for this, or that any diet-based manipulations have
    > an effect on pancreatic cancer survival. However, I'm always willing to look at evidence someone
    > else shows me.

    It stands to reason that if cancer cells use sugar for their main energy source (rather than fat)
    and sugar is a much less efficient source of energy (thus requiring the cancer cells to need a lot
    more of it), by cutting off their supply of sugar, tumor growth will slow and perhaps stop.

    Here's a study (found at Pubmed) that shows that insulin is a growth factor of panc cancer cells.
    I'll just include part of the abstract (go to Pubmed to see all of it)

    ------- start -------- Pancreas. 2000 Oct;21(3):310-20.

    Physiological concentrations of insulin augment pancreatic cancer cell proliferation and glucose
    utilization by activating MAP kinase, PI3 kinase and enhancing GLUT-1 expression.

    Department of Biomedical Sciences, Creighton University, School of Medicine, Omaha, Nebraska
    68178, USA.

    Insulin, but not somatostatin and glucagon, induced pancreatic cancer cell growth in a concentration-
    and time-dependent manner. At concentrations within the range of those in the intrapancreatic
    vasculature, insulin (10(-10)-10(-8) mol/L) markedly increased [3H]-thymidine incorporation. Insulin
    significantly enhanced glucose utilization of pancreatic cancer cells before it enhanced cell
    proliferation. ---- end -----

    Thus insulin and glucose are needed for panc cancer cell proliferation. Reducing both would seem to
    reduce proliferation.

    > >took high doses of statin drugs (along with co-enzyme Q10 for protection from
    the
    > > high doses of statin drugs),
    >
    > There is no scientific evidence I am aware of for this.

    Cancer cells rely on some of the downstream products from the HMG-CoA enzyme which statins block.
    Cancer cells need cholesterol, geranylgeranyl pyrophosphate and farnesyl pyrophosphate - all of
    which are downstream products of the HMG-CoA enzyme. Co Q10 is also a downstream product which is
    why it should be taken with statins (Co Q10 does not increase cancer cell proliferation).

    Here's one of many studies at Pubmed about statins and panc cancer cell proliferation. I'll post the
    whole study.

    ---start ----

    Gastroenterology. 2002 Feb;122(2):308-17.

    3-hydroxy-3-methylglutaryl-coenzyme a reductase inhibitors reduce human pancreatic cancer cell
    invasion and metastasis.

    Department of Tumor Biochemistry, Osaka Medical Center for Cancer and Cardiovascular Diseases,
    Osaka, Japan.

    BACKGROUND & AIMS: Inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase blocks
    the mevalonate metabolic pathway, which is necessary for the isoprenylation of a number of small
    guanosine triphosphatases. We examined the effects of HMG-CoA reductase inhibitors, fluvastatin and
    lovastatin, on human pancreatic cancer cell invasion in vitro and experimental liver metastasis in
    vivo. METHODS: Cell invasion was studied in a modified Boyden chamber assay. The translocation of
    RhoA was assessed by immunoblotting. Experimental liver metastases were induced in nude mice by
    intrasplenic inoculation of ASPC-1 human pancreatic cancer cells. RESULTS: Fluvastatin and
    lovastatin inhibited the in vitro cancer cell invasion induced by epidermal growth factor (EGF) in a
    manner sensitive to C3 transferase, a specific inhibitor of Rho. Treatment of ASPC-1 cells with
    fluvastatin markedly attenuated the EGF-induced translocation of RhoA from the cytosol to the
    membrane fraction and caused cell rounding. The effects of fluvastatin could be reversed by the
    addition of all-trans-geranylgeraniol. Administration of fluvastatin to nude mice reduced both
    metastatic tumor formation in the liver and the growth of established liver metastases at doses
    recommended for the treatment of hypercholesterolemia in humans. CONCLUSIONS: HMG-CoA reductase
    inhibitors can be antimetastatic agents with the potential for useful clinical applications.

    ---- end -----

    >
    >
    > >took EPA fatty acids (to reduce arachidonic acid levels and AA metabolites) along with chemo,
    > >survival times might
    get a
    > > lot more impressive.
    >
    > There is no scientific evidence I am aware of for this.

    Here's a study from Pubmed.

    ----- start ----- Br J Cancer. 1996 Nov;74(9):1375-83.

    Cell cycle arrest and induction of apoptosis in pancreatic cancer cells exposed to eicosapentaenoic
    acid in vitro.

    Lai PB, Ross JA, Fearon KC, Anderson JD, Carter DC.

    Lister Research Laboratories, Department of Surgery, University of Edinburgh, Royal Infirmary, UK.

    Eicosapentaenoic acid (EPA) has been shown to have an inhibitory effect on the growth of several
    pancreatic cancer cell lines in vitro. This study investigates the mechanism of growth inhibition
    and cytotoxicity of EPA on the pancreatic cancer cell line MIA PaCa-2. Cells were analysed for cell
    count, viability, cell cycle distribution and ultrastructural changes. There was a time- and dose-
    dependent decrease in cell count and viability in cultures of pancreatic cancer cells supplemented
    with EPA. Flow cytometric DNA analysis of MIA PaCa-2 cells incubated with EPA demonstrated the
    presence of sub G1 populations corresponding to the presence of apoptotic cells and the blockade of
    cell cycle progression in S-phase and G2/M-phase. The presence of apoptosis in EPA-supplemented
    cultures was further confirmed by DNA fragmentation and ultrastructural changes associated with
    apoptosis. Therefore, we conclude that EPA mediates its effect on the pancreatic cancer cell line
    MIA PaCa-2, at least in part, via cell cycle arrest and the induction of apoptosis.

    ------ end ------

    EPA also is good because it competes with arachidonic acid (AA) so that high levels of EPA mean less
    AA is used by the cancer cells. AA aids cancer cells because the Cox 2 and Lox enzymes transform AA
    into substances (such as 5-HETE, 5-LOX and 12-LOX) which promote panc cancer cell proliferation.

    Here's an abstract from Pubmed that discusses this:

    ---- start -----

    Pancreatology. 2001;1(4):291-9. Related Articles, Links

    Cyclooxygenases and lipoxygenases as potential targets for treatment of pancreatic cancer.

    Department of Biomedical Sciences, Creighton University School of Medicine, 2500 California Plaza,
    Omaha, NE 68178, USA.

    Pancreatic adenocarcinoma is characterized by poor prognosis, late diagnosis and lack of response
    to conventional therapies. The incidence of this disease shows no sign of declining in the Western
    world. Thus, new targets need to be identified for pancreatic cancer treatment. In particular, new
    chemotherapeutic agents would be extremely beneficial for control of unresectable cancer and
    metastatic lesions as well as for prevention of this deadly disease. Mounting evidence suggests
    that both lipoxygenases (LOXs) and cyclooxygenases (COXs), the key enzymes for arachidonic acid
    metabolism, have a profound influence on the development and progression of several human cancers.
    Recent evidence suggests that both COX and LOX pathways are important in pancreatic cancer.
    Results from immunocytochemical, RT-PCR, and Western blotting studies have shown that COX,
    specifically COX-2, is upregulated in human pancreatic cancer cell lines as well as human
    pancreatic cancer tissues compared with normal ductal cells and normal pancreas specimens. Agents
    that block COX enzymes significantly inhibit pancreatic cancer growth both in vitro and in vivo,
    in parallel with induction of apoptosis. Expression of both 5-LOX and 12-LOX is also seen in
    pancreatic cancer, although compared to the expression of COX this has not been extensively
    investigated. Chemical inhibitors or antisense oligonucleotides that block either 5-LOX or 12-LOX
    cause marked inhibition of pancreatic cancer cell proliferation. On the other hand, LOX
    metabolites stimulate growth of the tumor cells and reverse LOX-inhibitor-induced growth
    inhibition, suggesting the specific role of LOX in regulating pancreatic cancer cell
    proliferation. Although questions still need to be answered, such as the underlying mechanisms for
    COX and LOX-induced growth inhibition, both COX and LOX pathways are potential targets for
    pancreatic cancer treatment and chemoprevention. COX and LOX enzyme inhibitors are available and
    have been shown to be relatively safe in the treatment of other diseases.

    ------ end -------

    The above abstract also shows why non-steroidal anti-inflammatory drugs (NSAIDS) are cancer
    fighters. Most of the NSAIDS lower cox 2 levels so that the products of cox 2 which increase
    proliferation are also lowered. Some of them also lower lox enzymes as well (go to Pubmed to see
    which ones do). Here's a 2003 study about some new ones that lower both cox 2 and lox and apparently
    are safer:

    ---- start ----

    Eur J Med Chem. 2003 Jul-Aug;38(7-8):645-59.

    Dual inhibition of cyclooxygenase-2 (COX-2) and 5-lipoxygenase (5-LOX) as a new strategy to provide
    safer non-steroidal anti-inflammatory drugs.

    Lab. de Chimie Moleculaire Structurale, Facultes Universitaires N.-D. de la Paix, Rue de Bruxelles
    61, B-5000, Namur, Belgium

    Dual COX/5-LOX (cyclooxygenase/5-lipoxygenase) inhibitors constitute a valuable alternative to
    classical non-steroidal anti-inflammatory drugs (NSAIDs) and selective COX-2 inhibitors for the
    treatment of inflammatory diseases. Indeed, these latter present diverse side effects, which are
    reduced or absent in dual-acting agents. In this review, COX and 5-LOX pathways are first described
    in order to highlight the therapeutic interest of designing such compounds. Various structural
    families of dual inhibitors are illustrated.

    ----- end ------

    > > Losing weight as fast as possible through exercise (to deprive the
    cancer
    > > cells of saturated fatty acids from body fat used for membranes of new cells) would also seem to
    > > lengthen survival.
    >
    > Nope. This has been an argument going back and forth for decades, and the bottom line is that
    > there is no good evidence that losing weight will prolong survival. Indeed, frequently the cancer
    > makes its victims lose weight uncontrollably (the cancer cachexia syndrome).

    The cancer is making the patient lose weight because the cancer is using the body fat as a source of
    fatty acids that it needs for cell (and other interior) membranes for new cells. If the patient
    didn't have much body fat to give to the tumor, the tumor is limited on how much it can grow because
    without fatty acids, it can't build cell membranes (and other membranes inside the cell).

    This also makes the cancer cells use the fatty acids that are supplemented in the diet so that if
    EPA is taken in by the patient and that is the only source of fatty acid, new cancer cells will have
    to use that as a source of fatty acids.

    >
    >
    > >And taking anti-angiogenic substances such as NSAIDs would seem to help too.
    >
    > Antiangiogenic drugs may have a role, but the jury is still out and trials are ongoing. NSAIDs do
    > not appear to have much of a role in treatment, although they may be preventative.

    I addressed above why NSAIDs should be taken by cancer patients (to lower cox 2 and lox enzyme
    levels). There was a study presented last year at the big cancer conference in Florida that showed
    good success in cancer patients taking Celebrex.

    And here's a study at Pubmed that shows cox 2 inhibitors and statin drugs work synergistically in
    stopping cancer cells (colon cancer cells in this case).

    ---- start ----

    Oncol Rep. 2002 Jul-Aug;9(4):879-85.

    Synergistic interaction between highly specific cyclooxygenase-2 inhibitor, MF-tricyclic and
    lovastatin in murine colorectal cancer cell lines.

    Department of Immunology, Centre of Biostructure Research, The Medical University of Warsaw, Poland.

    Statins, anti-hypercholesterolemic agents, have previously been reported to induce apoptosis and
    exert antitumor activity when combined with other antitumor agents. The potential of lovastatin in
    combination with highly specific COX-2 inhibitor (MF-tricyclic) to induce anti-proliferative
    activity against tumour cells was evaluated using the combination index (CI) method. Murine
    colorectal cancer (colon-26, CMT-93), melanoma (B16F10) and human bladder carcinoma cells (T24) were
    tested. Exposure of colon-26 and CMT-93 cells resulted in synergistic interactions in both cell
    lines with CI<1 for 20-80% inhibition of cell growth in both cell lines. This synergy was not
    observed in the B16F10 melanoma and T24 bladder carcinoma cells. MF-tricyclic (40 microg/ml),
    augmented lovastatin-induced apoptosis up to
    2.5-fold in colon-26 cancer cells. Combination of a specific COX-2 inhibitor, MF-tricyclic, may
    increase antiproliferative effects of lovastatin in colon cancer cells and this effect was due to
    an augmented apoptosis.

    > I think you may be confusing things that are meant to be preventative with those that can actually
    > treat pancreatic cancer.

    Everything I posted is about treating existing panc cancer and the abstracts I have posted here show
    why these ideas are for existing cancer.

    > For instance, there is evidence that a number of dietary manipulations *might* decrease its
    > incidence.

    The evidence is overwhelming that being overweight is a cause of it and that's probably related to
    the high levels of insulin in overweight people. Smoking also causes it but I don't know why (other
    than cigarette smoke being a mutagen and may be absorbed in high levels by the pancreas).

    > However, once the cancer is there, there is no dietary manipulation known that will prolong
    > survival.

    My guess is few of any of these things have been tried much in controlled studies despite there
    being overwhelming scientific evidence indicating they should, at the minimum, slow cancer growth
    significantly. Why they are not standard practice is a subject for another day.

    If all the things I suggest are tried (along with chemo since some of them are synergistic with
    existing chemo for panc cancer), perhaps the cancer stops growing or even regresses.

    For those reading this and want to do their own searches at Pubmed (which I highly recommend),
    here's the link to it:

    http://www.ncbi.nlm.nih.gov/PubMed/

    Roger

    >
    > --
    > Orac |"A statement of fact cannot be insolent."
    > |
    > |"If you cannot listen to the answers, why do you inconvenience me with questions?"
     
  14. Orac

    Orac Guest

    In article <[email protected]>,
    "Roger" <[email protected]> wrote:

    > "Orac" <[email protected]> wrote
    >
    > > "Roger" <[email protected]> wrote:
    > >
    > > > "Orac" <[email protected]> wrote
    > > >
    > > > > "Mike Radcliffe" wrote:
    > > > >
    > > > > > Pancreatic cancer responds very poorly to conventional medical
    > > > treatment
    > > > > > and not at all to all known alternatives.
    > > > >
    > > > > Correct. And the five year survival for all comers with pancreatic cancer is less than 1%.
    > > > > For those whose tumor can be successfully resected with negative surgical margins, at best
    > > > > it's around 20%.
    > > >
    > > > There was a relatively famous African-American actor that died about a
    > month
    > > > ago of panc cancer who had it for four years according to the news
    > article I
    > > > read. He was one of the main characters in the movie, Shaft (I think
    > that
    > > > was the movie). Don't know the details on his case but it just goes to
    > show
    > > > some people do live awhile with it.
    > >
    > > Yes, but it's very uncommon. The median survival for unresectable pancreatic cancer is on the
    > > order of 6-12 months, and the median survival after a successful resection with negative margins
    > > is less than two years.
    >
    > Perhaps with people taking some of the measures I suggest, the median survival would be
    > significantly longer.

    Perhaps, but, your studies notwithstanding, it is very much a question for study.

    >I believe the evidence from valid scientific sources (such as can be found at Pubmed) backs this
    >notion up (some of which I will present in this post).

    Perhaps. But it is a long stretch from the kinds of studies you've cited to actual
    clinical evidence.

    > > > It would seem if a panc cancer patient kept his/her blood sugar (and insulin) levels low (such
    > > > as by eating a mostly protein-based diet),
    > >
    > > There is no scientific evidence I am aware of for this, or that any diet-based manipulations
    > > have an effect on pancreatic cancer survival. However, I'm always willing to look at evidence
    > > someone else shows me.
    >
    > It stands to reason that if cancer cells use sugar for their main energy source (rather than fat)
    > and sugar is a much less efficient source of energy (thus requiring the cancer cells to need a lot
    > more of it), by cutting off their supply of sugar, tumor growth will slow and perhaps stop.

    It "stands to reason," but may well be wrong. Cancer cells are much more avid at taking up glucose,
    and another possible (perhaps equally possible) result would be the increased starvation of normal
    cells, rather than the starvation of cancer cells. (Indeed, the entire basis of the PET scan is how
    much more avidly cancer cells take up glucose than normal cells.) It is known that dietary energy
    restriction can decrease carcinogenesis. It is not know whether dietary energy restriction can
    decrease tumor growth enough to prolong survival, nor is it known whether the deleterious effects of
    dietery energy restriction (worsening of cancer cachexia) would outweigh potential beneficial
    effects (possibility of slowing down tumor growth).

    > Here's a study (found at Pubmed) that shows that insulin is a growth factor of panc cancer cells.
    > I'll just include part of the abstract (go to Pubmed to see all of it)
    >
    > ------- start -------- Pancreas. 2000 Oct;21(3):310-20.
    >
    > Physiological concentrations of insulin augment pancreatic cancer cell proliferation and glucose
    > utilization by activating MAP kinase, PI3 kinase and enhancing GLUT-1 expression.
    >
    > Department of Biomedical Sciences, Creighton University, School of Medicine, Omaha, Nebraska
    > 68178, USA.
    >
    > Insulin, but not somatostatin and glucagon, induced pancreatic cancer cell growth in a concentration-
    > and time-dependent manner. At concentrations within the range of those in the intrapancreatic
    > vasculature, insulin (10(-10)-10(-8) mol/L) markedly increased [3H]-thymidine incorporation.
    > Insulin significantly enhanced glucose utilization of pancreatic cancer cells before it enhanced
    > cell proliferation. ---- end -----
    >
    > Thus insulin and glucose are needed for panc cancer cell proliferation. Reducing both would seem
    > to reduce proliferation.

    This is an in vitro cell culture study. The in vivo situation is much more complex. Also, insulin is
    a growth factor for many different cell types, not just pancreatic cancer cells.

    > > >took high doses of statin drugs (along with co-enzyme Q10 for protection from
    > the
    > > > high doses of statin drugs),
    > >
    > > There is no scientific evidence I am aware of for this.
    >
    > Cancer cells rely on some of the downstream products from the HMG-CoA enzyme which statins block.
    > Cancer cells need cholesterol, geranylgeranyl pyrophosphate and farnesyl pyrophosphate - all of
    > which are downstream products of the HMG-CoA enzyme. Co Q10 is also a downstream product which is
    > why it should be taken with statins (Co Q10 does not increase cancer cell proliferation).
    >
    > Here's one of many studies at Pubmed about statins and panc cancer cell proliferation. I'll post
    > the whole study.
    >
    > ---start ----
    >
    > Gastroenterology. 2002 Feb;122(2):308-17.
    >
    > 3-hydroxy-3-methylglutaryl-coenzyme a reductase inhibitors reduce human pancreatic cancer cell
    > invasion and metastasis.
    >
    > Department of Tumor Biochemistry, Osaka Medical Center for Cancer and Cardiovascular Diseases,
    > Osaka, Japan.
    >
    > BACKGROUND & AIMS: Inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase blocks
    > the mevalonate metabolic pathway, which is necessary for the isoprenylation of a number of small
    > guanosine triphosphatases. We examined the effects of HMG-CoA reductase inhibitors, fluvastatin
    > and lovastatin, on human pancreatic cancer cell invasion in vitro and experimental liver
    > metastasis in vivo. METHODS: Cell invasion was studied in a modified Boyden chamber assay. The
    > translocation of RhoA was assessed by immunoblotting. Experimental liver metastases were induced
    > in nude mice by intrasplenic inoculation of ASPC-1 human pancreatic cancer cells. RESULTS:
    > Fluvastatin and lovastatin inhibited the in vitro cancer cell invasion induced by epidermal growth
    > factor (EGF) in a manner sensitive to C3 transferase, a specific inhibitor of Rho. Treatment of
    > ASPC-1 cells with fluvastatin markedly attenuated the EGF-induced translocation of RhoA from the
    > cytosol to the membrane fraction and caused cell rounding. The effects of fluvastatin could be
    > reversed by the addition of all-trans-geranylgeraniol. Administration of fluvastatin to nude mice
    > reduced both metastatic tumor formation in the liver and the growth of established liver
    > metastases at doses recommended for the treatment of hypercholesterolemia in humans. CONCLUSIONS:
    > HMG-CoA reductase inhibitors can be antimetastatic agents with the potential for useful clinical
    > applications.
    >
    > ---- end -----

    Interesting abstract, but it's a mouse study. I tried to download the entire article, but
    unfortunately my university doesn't have an online subscription to this particular journal. It may
    be worth pursuing in a clinical study, but I am as yet unaware of any. To show the perils in
    extrapolating these sorts of studies to humans, I would only point out the example of antiangiogenic
    therapy, like angiostatin or endostatin. As you recall, in 1998, these were reported to show amazing
    results in mice. Judah Folkman made the cover of Time Magazine. Unfortunately, subsequent clinical
    trials have been disappointing, with results in humans much less impressive.

    Through all the hype, Judah Folkman was quite realistic about his discovery. His famous quote: "If
    you have a cancer and you are a mouse, we can take good care of you. Going from mice to people is a
    big jump, with lots of failures."

    That about sums it up. Certainly I hope some of these things pan out. However, the history of cancer
    research tells me that that most of them probably will not. They are probably worth investigating.

    > > >took EPA fatty acids (to reduce arachidonic acid levels and AA metabolites) along with chemo,
    > > >survival times might
    > get a
    > > > lot more impressive.
    > >
    > > There is no scientific evidence I am aware of for this.
    >
    > Here's a study from Pubmed.
    >
    > ----- start ----- Br J Cancer. 1996 Nov;74(9):1375-83.
    >
    > Cell cycle arrest and induction of apoptosis in pancreatic cancer cells exposed to
    > eicosapentaenoic acid in vitro.
    >
    > Lai PB, Ross JA, Fearon KC, Anderson JD, Carter DC.
    >
    > Lister Research Laboratories, Department of Surgery, University of Edinburgh, Royal Infirmary, UK.
    >
    > Eicosapentaenoic acid (EPA) has been shown to have an inhibitory effect on the growth of several
    > pancreatic cancer cell lines in vitro. This study investigates the mechanism of growth inhibition
    > and cytotoxicity of EPA on the pancreatic cancer cell line MIA PaCa-2. Cells were analysed for
    > cell count, viability, cell cycle distribution and ultrastructural changes. There was a time- and
    > dose-dependent decrease in cell count and viability in cultures of pancreatic cancer cells
    > supplemented with EPA. Flow cytometric DNA analysis of MIA PaCa-2 cells incubated with EPA
    > demonstrated the presence of sub G1 populations corresponding to the presence of apoptotic cells
    > and the blockade of cell cycle progression in S-phase and G2/M-phase. The presence of apoptosis in
    > EPA-supplemented cultures was further confirmed by DNA fragmentation and ultrastructural changes
    > associated with apoptosis. Therefore, we conclude that EPA mediates its effect on the pancreatic
    > cancer cell line MIA PaCa-2, at least in part, via cell cycle arrest and the induction of
    > apoptosis.
    >
    > ------ end ------

    More cell culture data. What about in vivo data?

    > EPA also is good because it competes with arachidonic acid (AA) so that high levels of EPA mean
    > less AA is used by the cancer cells. AA aids cancer cells because the Cox 2 and Lox enzymes
    > transform AA into substances (such as 5-HETE, 5-LOX and 12-LOX) which promote panc cancer cell
    > proliferation.

    Maybe.

    > Here's an abstract from Pubmed that discusses this:
    >
    > ---- start -----
    >
    > Pancreatology. 2001;1(4):291-9. Related Articles, Links
    >
    > Cyclooxygenases and lipoxygenases as potential targets for treatment of pancreatic cancer.
    >
    > Department of Biomedical Sciences, Creighton University School of Medicine, 2500 California Plaza,
    > Omaha, NE 68178, USA.
    >
    > Pancreatic adenocarcinoma is characterized by poor prognosis, late diagnosis and lack of response
    > to conventional therapies. The incidence of this disease shows no sign of declining in the Western
    > world. Thus, new targets need to be identified for pancreatic cancer treatment. In particular, new
    > chemotherapeutic agents would be extremely beneficial for control of unresectable cancer and
    > metastatic lesions as well as for prevention of this deadly disease. Mounting evidence suggests
    > that both lipoxygenases (LOXs) and cyclooxygenases (COXs), the key enzymes for arachidonic acid
    > metabolism, have a profound influence on the development and progression of several human cancers.
    > Recent evidence suggests that both COX and LOX pathways are important in pancreatic cancer.
    > Results from immunocytochemical, RT-PCR, and Western blotting studies have shown that COX,
    > specifically COX-2, is upregulated in human pancreatic cancer cell lines as well as human
    > pancreatic cancer tissues compared with normal ductal cells and normal pancreas specimens. Agents
    > that block COX enzymes significantly inhibit pancreatic cancer growth both in vitro and in vivo,
    > in parallel with induction of apoptosis. Expression of both 5-LOX and 12-LOX is also seen in
    > pancreatic cancer, although compared to the expression of COX this has not been extensively
    > investigated. Chemical inhibitors or antisense oligonucleotides that block either 5-LOX or 12-LOX
    > cause marked inhibition of pancreatic cancer cell proliferation. On the other hand, LOX
    > metabolites stimulate growth of the tumor cells and reverse LOX-inhibitor-induced growth
    > inhibition, suggesting the specific role of LOX in regulating pancreatic cancer cell
    > proliferation. Although questions still need to be answered, such as the underlying mechanisms for
    > COX and LOX-induced growth inhibition, both COX and LOX pathways are potential targets for
    > pancreatic cancer treatment and chemoprevention. COX and LOX enzyme inhibitors are available and
    > have been shown to be relatively safe in the treatment of other diseases.
    >
    > ------ end -------

    COX-2 inhibitors tend to be antiangiogenic, you know.

    However, all of this is in cell culture and animal data. I am as yet unaware of any convincing
    clinical data that it works. It may well be promising; however, that remains to be tested.

    > The above abstract also shows why non-steroidal anti-inflammatory drugs (NSAIDS) are cancer
    > fighters. Most of the NSAIDS lower cox 2 levels so that the products of cox 2 which increase
    > proliferation are also lowered. Some of them also lower lox enzymes as well (go to Pubmed to see
    > which ones do). Here's a 2003 study about some new ones that lower both cox 2 and lox and
    > apparently are safer:
    >
    > ---- start ----
    >
    > Eur J Med Chem. 2003 Jul-Aug;38(7-8):645-59.
    >
    > Dual inhibition of cyclooxygenase-2 (COX-2) and 5-lipoxygenase (5-LOX) as a new strategy to
    > provide safer non-steroidal anti-inflammatory drugs.
    >
    > Lab. de Chimie Moleculaire Structurale, Facultes Universitaires N.-D. de la Paix, Rue de Bruxelles
    > 61, B-5000, Namur, Belgium
    >
    > Dual COX/5-LOX (cyclooxygenase/5-lipoxygenase) inhibitors constitute a valuable alternative to
    > classical non-steroidal anti-inflammatory drugs (NSAIDs) and selective COX-2 inhibitors for the
    > treatment of inflammatory diseases. Indeed, these latter present diverse side effects, which are
    > reduced or absent in dual-acting agents. In this review, COX and 5-LOX pathways are first
    > described in order to highlight the therapeutic interest of designing such compounds. Various
    > structural families of dual inhibitors are illustrated.
    >
    > ----- end ------

    COX inhibitors are a very hot area of research right now, but their exact role in cancer therapy has
    yet to be determined. Certainly there is evidence that they can prevent colorectal cancer, but it
    remains to be seen if the number of cancers prevented is worth the potential complications.

    > > > Losing weight as fast as possible through exercise (to deprive the
    > cancer
    > > > cells of saturated fatty acids from body fat used for membranes of new cells) would also seem
    > > > to lengthen survival.
    > >
    > > Nope. This has been an argument going back and forth for decades, and the bottom line is that
    > > there is no good evidence that losing weight will prolong survival. Indeed, frequently the
    > > cancer makes its victims lose weight uncontrollably (the cancer cachexia syndrome).
    >
    > The cancer is making the patient lose weight because the cancer is using the body fat as a source
    > of fatty acids that it needs for cell (and other interior) membranes for new cells.

    Too simplistic, I'm afraid, same as the glucose argument. This argument seems to hold in the
    carcinogenesis phase. It may not hold once the cancer is established.

    >If the patient didn't have much body fat to give to the tumor, the tumor is limited on how much it
    >can grow because without fatty acids, it can't build cell membranes (and other membranes inside
    >the cell).
    >
    > This also makes the cancer cells use the fatty acids that are supplemented in the diet so that if
    > EPA is taken in by the patient and that is the only source of fatty acid, new cancer cells will
    > have to use that as a source of fatty acids.

    Would it were that simple! Cancer and cancer cachexia are much more complex than that. For example,
    some cancers cause cancer cachexia; some don't. Feeding the patient will not overcome the cancer
    cachexia. Indeed, that was the dominant concept in the 1970's, and 1980's. Unfortunately, the
    concept that overfeeding cancer patients could treat cachexia was well-disproven in many clinical
    trials in the late 1970's through the early 1990's, and it did not appear that feeding the patient
    accelerated tumor growth. Unfortunately, the converse does not appear to be true. Not feeding a
    patient (glucose or fat) does not appear to slow down the growth of an established cancer, although,
    as I mentioned before, there is a fair amount of evidence that dietary energy restriction can
    inhibit carcinogenesis.

    It is possible, even likely, that limiting food intake will decrease the risk of cancer. Numerous
    studies suggest that this might be true for some cancers. However, once cancer is growing, no
    manipulation of diet has yet been shown in humans to be effective in treating it.

    [Snip]

    > > However, once the cancer is there, there is no dietary manipulation known that will prolong
    > > survival.
    >
    > My guess is few of any of these things have been tried much in controlled studies despite there
    > being overwhelming scientific evidence indicating they should, at the minimum, slow cancer growth
    > significantly.

    No, there is some evidence that they *might* slow cancer growth significantly in vivo.
    "Overwhelming" is overselling it a bit. And it would appear things are moving in the direction of
    testing them in humans.

    >Why they are not standard practice is a subject for another day.
    >
    > If all the things I suggest are tried (along with chemo since some of them are synergistic with
    > existing chemo for panc cancer), perhaps the cancer stops growing or even regresses.

    Possibly, but there is a reason for my tendency to pessimism. Many strategies that appeared
    extremely effective in mice have failed to work nearly as well in humans. Immunotherapy,
    antiangiogenic therapy, etc., for example. That does not mean that we should stop investigating
    these areas. It simply means that none of them alone will be the magic bullet.

    Remember Folkman's words, for they are wise: "If you have a cancer and you are a mouse, we can take
    good care of you. Going from mice to people is a big jump, with lots of failures."

    [Snip]

    --
    Orac |"A statement of fact cannot be insolent."
    |
    |"If you cannot listen to the answers, why do you inconvenience me with questions?"
     
  15. J

    J Guest

    Roger wrote:

    > <snipped>
    >
    > And here's a study at Pubmed that shows cox 2 inhibitors and statin drugs work synergistically in
    > stopping cancer cells (colon cancer cells in this case).

    http://www.cancerpage.com/news/article.asp?id=6173

    Rofecoxib No Aid to Chemotherapy in Metastatic Colorectal Cancer

    By David Douglas

    NEW YORK Jul 30, 2003 (Reuters Health) - Addition of the cyclooxygenase (COX)-2 inhibitor rofecoxib
    to chemotherapy in patients with metastatic colon cancer increases toxicity without improving
    efficacy, researchers report in the 20th of July issue of the International Journal of Cancer.

    Nevertheless, lead investigator Dr. Carlos R. Becerra told Reuters Health that "COX-2 inhibitors
    hold great promise in the treatment of patients with metastatic solid malignancies such as colon and
    lung cancer."

    "Currently clinical studies are ongoing or have been completed exploring the use of COX-2 inhibitors
    either as single agents or in association with chemotherapy for these and other malignancies."

    In particular, Dr. Becerra of the University of Texas Southwestern Medical Center, Dallas, and
    colleagues conducted a phase II study of supplementary rofecoxib therapy in 10 patients with
    metastatic colorectal cancer. All tumors exhibited "moderate" COX-2 overexpression.

    The subjects were treated with 5-fluorouracil and leucovorin along with rofecoxib at doses of up to
    50 mg daily.

    Among side effects were gastrointestinal bleeding in 4 patients, stomatitis in 3, diarrhea in 2
    and thrombocytopenia in another. Furthermore, there were no partial or complete responses in any
    of the subjects.

    Thus, "unfortunately," Dr. Becerra concluded, "the results did not meet our expectations and the
    study had to be terminated early secondary to increased toxicity and lack of efficacy of the
    regimen studied."

    SOURCE:

    International Journal of Cancer 2003;105:868-872. <snipped> J
     
  16. Roger

    Roger Guest

    "Orac" <[email protected]> wrote
    >
    > "Roger" <[email protected]> wrote:
    >
    > > "Orac" <[email protected]> wrote
    > >
    > > > "Roger" <[email protected]> wrote:
    > > >
    > > > > "Orac" <[email protected]> wrote
    > > > >
    > > > > > "Mike Radcliffe" wrote:
    > > > > >
    > > > > > > Pancreatic cancer responds very poorly to conventional medical
    > > > > treatment
    > > > > > > and not at all to all known alternatives.
    > > > > >
    > > > > > Correct. And the five year survival for all comers with pancreatic cancer is less than 1%.
    > > > > > For those whose tumor can be successfully resected with negative surgical margins, at best
    > > > > > it's around 20%.
    > > > >
    > > > > There was a relatively famous African-American actor that died about
    a
    > > month
    > > > > ago of panc cancer who had it for four years according to the news
    > > article I
    > > > > read. He was one of the main characters in the movie, Shaft (I
    think
    > > that
    > > > > was the movie). Don't know the details on his case but it just goes
    to
    > > show
    > > > > some people do live awhile with it.
    > > >
    > > > Yes, but it's very uncommon. The median survival for unresectable pancreatic cancer is on the
    > > > order of 6-12 months, and the median survival after a successful resection with negative
    > > > margins is less
    than
    > > > two years.
    > >
    > > Perhaps with people taking some of the measures I suggest, the median survival would be
    > > significantly longer.
    >
    > Perhaps, but, your studies notwithstanding, it is very much a question for study.

    My understanding of conventional cancer treatment is a lot of oncologists are unaware of how
    statins, cox 2 inhibitors, lowering glucose and insulin, and certain fats fight cancer. And the
    chances of there being any big clinical study like what would be done when a drug is trying to get
    approved is pretty small since there's little economic incentive for any big company to put out the
    money. None of these things are patentable that are unique (for example, there are several statins
    on the market). So unless the US govt or another govt funds the studies, the studies won't be done.
    And thus all the numerous studies (and that's an understatement) on Pubmed about the effectiveness
    of statins and cox 2 inhibitors and particular fats will be ignored.

    Thus a cancer patient can decide to look at the evidence and decide to do some thinking and act on
    all the evidence instead of letting others do the thinking (or nonthinking) for them. It's similar
    to smoking and lung cancer.

    They've never done studies on humans proving smoking causes lung cancer but they've done studies
    with animals and on cell cultures and looked at epidemiological data and come to the reasonable and
    proper conclusion that smoking causes lung cancer. Similarly one can go do Pubmed and find at least
    a hundred studies on the effectiveness of what I've outlined. Some of the studies are in vitro, some
    are in vivo, and some are with human patients. Because lots of oncologists are unaware of all the
    evidence is not a good reason for patients to make use of that evidence.

    >
    >
    > >I believe the evidence from valid scientific sources (such as can be found at Pubmed) backs this
    > >notion up (some of which I will present in this post).
    >
    > Perhaps. But it is a long stretch from the kinds of studies you've cited to actual clinical
    > evidence.

    There is some clinical evidence, not a lot for the reasons I stated above. But people have to do
    some thinking for themselves by looking at what the evidence shows.

    >
    >
    > > > > It would seem if a panc cancer patient kept his/her blood sugar (and insulin) levels low
    > > > > (such as by eating a mostly protein-based diet),
    > > >
    > > > There is no scientific evidence I am aware of for this, or that any diet-based manipulations
    > > > have an effect on pancreatic cancer survival. However, I'm always willing to look at evidence
    > > > someone else shows me.
    > >
    > > It stands to reason that if cancer cells use sugar for their main energy source (rather than
    > > fat) and sugar is a much less efficient source of
    energy
    > > (thus requiring the cancer cells to need a lot more of it), by cutting
    off
    > > their supply of sugar, tumor growth will slow and perhaps stop.
    >
    > It "stands to reason," but may well be wrong.

    Nothing's 100% guaranteed. Everything's a percentage. If logic and reason and evidence supports
    something, I'll go with it.

    > Cancer cells are much more avid at taking up glucose,

    Which is a reason to keep blood glucose levels low.

    > and another possible (perhaps equally possible) result would be the increased starvation of normal
    > cells, rather than the starvation of cancer cells.

    I'm just saying keep blood glucose levels from getting high.

    > (Indeed, the entire basis of the PET scan is how much more avidly cancer cells take up glucose
    > than normal cells.) It is known that dietary energy restriction can decrease carcinogenesis. It is
    > not know whether dietary energy restriction can decrease tumor growth enough to prolong survival,
    > nor is it known whether the deleterious effects of dietery energy restriction (worsening of cancer
    > cachexia) would outweigh potential beneficial effects (possibility of slowing down tumor growth).

    I'm not recommending restriction of energy. I'm recommending keeping blood glucose (and thus insulin
    levels) from getting high.

    >
    >
    > > Here's a study (found at Pubmed) that shows that insulin is a growth
    factor
    > > of panc cancer cells. I'll just include part of the abstract (go to
    Pubmed
    > > to see all of it)
    > >
    > > ------- start -------- Pancreas. 2000 Oct;21(3):310-20.
    > >
    > > Physiological concentrations of insulin augment pancreatic cancer cell proliferation and glucose
    > > utilization by activating MAP kinase, PI3
    kinase
    > > and enhancing GLUT-1 expression.
    > >
    > > Department of Biomedical Sciences, Creighton University, School of
    Medicine,
    > > Omaha, Nebraska 68178, USA.
    > >
    > > Insulin, but not somatostatin and glucagon, induced pancreatic cancer
    cell
    > > growth in a concentration- and time-dependent manner. At concentrations within the range of
    > > those in the intrapancreatic vasculature, insulin (10(-10)-10(-8) mol/L) markedly increased [3H]-
    > > thymidine incorporation. Insulin significantly enhanced glucose utilization of pancreatic cancer
    > > cells before it enhanced cell proliferation. ---- end -----
    > >
    > > Thus insulin and glucose are needed for panc cancer cell proliferation. Reducing both would seem
    > > to reduce proliferation.
    >
    > This is an in vitro cell culture study. The in vivo situation is much more complex. Also, insulin
    > is a growth factor for many different cell types, not just pancreatic cancer cells.

    Though the in vivo situation is always complex, I'm going to believe it's also a growth factor for
    panc cancer cells inside animals (including humans) since at the cellular level, I see no reason why
    it would be different.

    In addition, abstracts can be found at Pubmed where insulin was found to be a growth promoter in
    vivo. I'll just the give the title of one here that showed this and the crucial part:

    --- start --- Int J Pancreatol. 1998 Dec;24(3):169-80.

    Gastrointestinal hormones as potential adjuvant treatment of exocrine pancreatic adenocarcinoma.

    Department of Surgery, Baylor College of Medicine, Houston, TX, USA.

    METHODS: Eighty-eight articles were identified from a Medline search using the terms pancreatic
    adenocarcinoma and the individual names of gastrointestinal hormones. RESULTS: In general,
    somatostatin, vasoactive intestinal polypeptide, pancreatic polypeptide, and pancreastatin inhibit
    pancreatic adenocarcinoma growth. Cholecystokinin, secretin, bombesin, gastrin, EGF, TGF-alpha,
    insulin, and IGF-1 have a growth-promoting effect.

    ----- end ----

    So the evidence is pretty clear that insulin is a growth promoter of panc cancer in humans.

    >
    >
    > > > >took high doses of statin drugs (along with co-enzyme Q10 for protection
    from
    > > the
    > > > > high doses of statin drugs),
    > > >
    > > > There is no scientific evidence I am aware of for this.
    > >
    > > Cancer cells rely on some of the downstream products from the HMG-CoA
    enzyme
    > > which statins block. Cancer cells need cholesterol, geranylgeranyl pyrophosphate and farnesyl
    > > pyrophosphate - all of which are downstream products of the HMG-CoA enzyme. Co Q10 is also a
    > > downstream product
    which
    > > is why it should be taken with statins (Co Q10 does not increase cancer
    cell
    > > proliferation).
    > >
    > > Here's one of many studies at Pubmed about statins and panc cancer cell proliferation. I'll post
    > > the whole study.
    > >
    > > ---start ----
    > >
    > > Gastroenterology. 2002 Feb;122(2):308-17.
    > >
    > > 3-hydroxy-3-methylglutaryl-coenzyme a reductase inhibitors reduce human pancreatic cancer cell
    > > invasion and metastasis.
    > >
    > > Department of Tumor Biochemistry, Osaka Medical Center for Cancer and Cardiovascular Diseases,
    > > Osaka, Japan.
    > >
    > > BACKGROUND & AIMS: Inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase
    > > blocks the mevalonate metabolic pathway, which is necessary for the isoprenylation of a number
    > > of small guanosine triphosphatases. We examined the effects of HMG-CoA reductase
    inhibitors,
    > > fluvastatin and lovastatin, on human pancreatic cancer cell invasion in vitro and experimental
    > > liver metastasis in vivo. METHODS: Cell invasion
    was
    > > studied in a modified Boyden chamber assay. The translocation of RhoA
    was
    > > assessed by immunoblotting. Experimental liver metastases were induced
    in
    > > nude mice by intrasplenic inoculation of ASPC-1 human pancreatic cancer cells. RESULTS:
    > > Fluvastatin and lovastatin inhibited the in vitro cancer cell invasion induced by epidermal
    > > growth factor (EGF) in a manner
    sensitive
    > > to C3 transferase, a specific inhibitor of Rho. Treatment of ASPC-1
    cells
    > > with fluvastatin markedly attenuated the EGF-induced translocation of
    RhoA
    > > from the cytosol to the membrane fraction and caused cell rounding. The effects of fluvastatin
    > > could be reversed by the addition of all-trans-geranylgeraniol. Administration of fluvastatin to
    > > nude mice reduced both metastatic tumor formation in the liver and the growth of established
    > > liver metastases at doses recommended for the treatment of hypercholesterolemia in humans.
    > > CONCLUSIONS: HMG-CoA reductase
    inhibitors
    > > can be antimetastatic agents with the potential for useful clinical applications.
    > >
    > > ---- end -----
    >
    > Interesting abstract, but it's a mouse study. I tried to download the entire article, but
    > unfortunately my university doesn't have an online subscription to this particular journal. It may
    > be worth pursuing in a clinical study, but I am as yet unaware of any.

    There have been two clinical trials that I have read but both were badly designed IMO. They gave the
    patients the drug for 7 days out of 28 days. Thus for close to 75% of the time, the production of
    the downstream products of HMG-CoA were at normal levels. In addition since they were clinical
    trials, many of the patients received doses much lower than what in vitro studies had shown were
    effective. Despite this, there were patients that responded.

    But if I'm a cancer patient, I'm not going to wait until the perfect study is done because it isn't
    going to be done because there are multiple statin drugs on the market and probably some of them are
    not patentable so there's not the economic incentive for the perfect studies to be done.

    So a patient should get the papers of the clinical trials done with it for a guide (by going to
    Pubmed, finding the studies and then going to a university that would have those papers). Using
    those papers as a guide, take a statin at a level tolerable (and affordable) and also take CoQ10 to
    reduce toxicity.

    > To show the perils in extrapolating these sorts of studies to humans, I would only point out the
    > example of antiangiogenic therapy, like angiostatin or endostatin. As you recall, in 1998, these
    > were reported to show amazing results in mice. Judah Folkman made the cover of Time Magazine.
    > Unfortunately, subsequent clinical trials have been disappointing, with results in humans much
    > less impressive.

    I forget where I read this but I have heard that actually, all and all, they are getting decent
    results with one or both of them and it's just going to take time to finish the trials and figure
    out the best doses, etc. Getting any new drug on the market takes almost forever so this isn't
    surprising. I think someday they will be used in cancer therapy.

    >
    > Through all the hype, Judah Folkman was quite realistic about his discovery. His famous quote: "If
    > you have a cancer and you are a mouse, we can take good care of you. Going from mice to people is
    > a big jump, with lots of failures."
    >
    > That about sums it up. Certainly I hope some of these things pan out. However, the history of
    > cancer research tells me that that most of them probably will not. They are probably worth
    > investigating.

    Well as I said, if cancer patients wait for the perfect studies to be performed with statins,
    they'll be dead (if not from cancer, from old age!). The data is overwhelming in vitro and in vivo
    that they work and the reasons they work are well known (to those doing studies with them).

    If I am a panc cancer patient, I'm going to take them because I realize that existing chemo alone
    won't do anything. Each person can decide on their own if they want to ignore all the evidence in
    support of statins effectiveness and wait for the perfect study that will never be performed, or
    they can look at the abundance of studies out there and do some thinking and ask the right questions
    and then take some action. It's a personal decision.

    >
    >
    > > > >took EPA fatty acids (to reduce arachidonic acid levels and AA metabolites) along with chemo,
    > > > >survival times
    might
    > > get a
    > > > > lot more impressive.
    > > >
    > > > There is no scientific evidence I am aware of for this.
    > >
    > > Here's a study from Pubmed.
    > >
    > > ----- start ----- Br J Cancer. 1996 Nov;74(9):1375-83.
    > >
    > > Cell cycle arrest and induction of apoptosis in pancreatic cancer cells exposed to
    > > eicosapentaenoic acid in vitro.
    > >
    > > Lai PB, Ross JA, Fearon KC, Anderson JD, Carter DC.
    > >
    > > Lister Research Laboratories, Department of Surgery, University of Edinburgh, Royal
    > > Infirmary, UK.
    > >
    > > Eicosapentaenoic acid (EPA) has been shown to have an inhibitory effect
    on
    > > the growth of several pancreatic cancer cell lines in vitro. This study investigates the
    > > mechanism of growth inhibition and cytotoxicity of EPA
    on
    > > the pancreatic cancer cell line MIA PaCa-2. Cells were analysed for cell count, viability, cell
    > > cycle distribution and ultrastructural changes.
    There
    > > was a time- and dose-dependent decrease in cell count and viability in cultures of pancreatic
    > > cancer cells supplemented with EPA. Flow
    cytometric
    > > DNA analysis of MIA PaCa-2 cells incubated with EPA demonstrated the presence of sub G1
    > > populations corresponding to the presence of
    apoptotic
    > > cells and the blockade of cell cycle progression in S-phase and
    G2/M-phase.
    > > The presence of apoptosis in EPA-supplemented cultures was further
    confirmed
    > > by DNA fragmentation and ultrastructural changes associated with
    apoptosis.
    > > Therefore, we conclude that EPA mediates its effect on the pancreatic
    cancer
    > > cell line MIA PaCa-2, at least in part, via cell cycle arrest and the induction of apoptosis.
    > >
    > > ------ end ------
    >
    > More cell culture data. What about in vivo data?

    There's plenty of it out there. Do a search on Pubmed and you'll find it. And with regard to panc
    cancer, EPA is also anti-cachexia according to some Pubmed studies.

    > > EPA also is good because it competes with arachidonic acid (AA) so that
    high
    > > levels of EPA mean less AA is used by the cancer cells. AA aids cancer cells because the Cox 2
    > > and Lox enzymes transform AA into substances
    (such
    > > as 5-HETE, 5-LOX and 12-LOX) which promote panc cancer cell
    proliferation.
    >
    > Maybe.

    There's tons of studies, in vitro and in vivo, at Pubmed showing the AA metabolites are cancer
    promoters.

    >
    > > Here's an abstract from Pubmed that discusses this:
    > >
    > > ---- start -----
    > >
    > > Pancreatology. 2001;1(4):291-9. Related Articles, Links
    > >
    > > Cyclooxygenases and lipoxygenases as potential targets for treatment of pancreatic cancer.
    > >
    > > Department of Biomedical Sciences, Creighton University School of
    Medicine,
    > > 2500 California Plaza, Omaha, NE 68178, USA.
    > >
    > > Pancreatic adenocarcinoma is characterized by poor prognosis, late
    diagnosis
    > > and lack of response to conventional therapies. The incidence of this disease shows no sign of
    > > declining in the Western world. Thus, new
    targets
    > > need to be identified for pancreatic cancer treatment. In particular,
    new
    > > chemotherapeutic agents would be extremely beneficial for control of unresectable cancer and
    > > metastatic lesions as well as for prevention of
    this
    > > deadly disease. Mounting evidence suggests that both lipoxygenases
    (LOXs)
    > > and cyclooxygenases (COXs), the key enzymes for arachidonic acid
    metabolism,
    > > have a profound influence on the development and progression of several human cancers. Recent
    > > evidence suggests that both COX and LOX pathways
    are
    > > important in pancreatic cancer. Results from immunocytochemical, RT-PCR,
    and
    > > Western blotting studies have shown that COX, specifically COX-2, is upregulated in human
    > > pancreatic cancer cell lines as well as human pancreatic cancer tissues compared with normal
    > > ductal cells and normal pancreas specimens. Agents that block COX enzymes significantly inhibit
    > > pancreatic cancer growth both in vitro and in vivo, in parallel with induction of apoptosis.
    > > Expression of both 5-LOX and 12-LOX is also seen
    in
    > > pancreatic cancer, although compared to the expression of COX this has
    not
    > > been extensively investigated. Chemical inhibitors or antisense oligonucleotides that block
    > > either 5-LOX or 12-LOX cause marked
    inhibition
    > > of pancreatic cancer cell proliferation. On the other hand, LOX
    metabolites
    > > stimulate growth of the tumor cells and reverse LOX-inhibitor-induced
    growth
    > > inhibition, suggesting the specific role of LOX in regulating pancreatic cancer cell
    > > proliferation. Although questions still need to be answered, such as the underlying mechanisms
    > > for COX and LOX-induced growth
    inhibition,
    > > both COX and LOX pathways are potential targets for pancreatic cancer treatment and
    > > chemoprevention. COX and LOX enzyme inhibitors are
    available
    > > and have been shown to be relatively safe in the treatment of other diseases.
    > >
    > > ------ end -------
    >
    > COX-2 inhibitors tend to be antiangiogenic, you know.

    That's exactly my point. The cox 2 enzyme makes a lot of cancer promoting substances including
    angiogenic substances. So does the lox enzymes.

    >
    > However, all of this is in cell culture and animal data. I am as yet unaware of any convincing
    > clinical data that it works. It may well be promising; however, that remains to be tested.

    The data presented for Celebrex, a selective cox 2 inhibitor, at the big Florida cancer
    conference (sponsored by Journal of Clin Oncology I think) was pretty convincing that it was
    working in human patients.

    >
    >
    > > The above abstract also shows why non-steroidal anti-inflammatory drugs (NSAIDS) are cancer
    > > fighters. Most of the NSAIDS lower cox 2 levels so
    that
    > > the products of cox 2 which increase proliferation are also lowered.
    Some
    > > of them also lower lox enzymes as well (go to Pubmed to see which ones
    do).
    > > Here's a 2003 study about some new ones that lower both cox 2 and lox
    and
    > > apparently are safer:
    > >
    > > ---- start ----
    > >
    > > Eur J Med Chem. 2003 Jul-Aug;38(7-8):645-59.
    > >
    > > Dual inhibition of cyclooxygenase-2 (COX-2) and 5-lipoxygenase (5-LOX)
    as a
    > > new strategy to provide safer non-steroidal anti-inflammatory drugs.
    > >
    > > Lab. de Chimie Moleculaire Structurale, Facultes Universitaires N.-D. de
    la
    > > Paix, Rue de Bruxelles 61, B-5000, Namur, Belgium
    > >
    > > Dual COX/5-LOX (cyclooxygenase/5-lipoxygenase) inhibitors constitute a valuable alternative to
    > > classical non-steroidal anti-inflammatory drugs (NSAIDs) and selective COX-2 inhibitors for the
    > > treatment of
    inflammatory
    > > diseases. Indeed, these latter present diverse side effects, which are reduced or absent in dual-
    > > acting agents. In this review, COX and 5-LOX pathways are first described in order to highlight
    > > the therapeutic
    interest
    > > of designing such compounds. Various structural families of dual
    inhibitors
    > > are illustrated.
    > >
    > > ----- end ------
    >
    > COX inhibitors are a very hot area of research right now, but their exact role in cancer therapy
    > has yet to be determined. Certainly there is evidence that they can prevent colorectal cancer, but
    > it remains to be seen if the number of cancers prevented is worth the potential complications.

    Well I'm talking about using it in people with panc cancer. Patients with such a disease don't have
    the time to wait for the perfect studies to be performed. They have to go to Pubmed, look at all the
    studies, ask some questions, and take some intelligent action. Having the internet now makes this
    possible now. Having a medical university close by is also nice because then whole papers can be
    read and not just abstracts.

    >
    >
    > > > > Losing weight as fast as possible through exercise (to deprive the
    > > cancer
    > > > > cells of saturated fatty acids from body fat used for membranes of
    new
    > > > > cells) would also seem to lengthen survival.
    > > >
    > > > Nope. This has been an argument going back and forth for decades, and the bottom line is that
    > > > there is no good evidence that losing weight will prolong survival. Indeed, frequently the
    > > > cancer makes its victims lose weight uncontrollably (the cancer cachexia syndrome).
    > >
    > > The cancer is making the patient lose weight because the cancer is using
    the
    > > body fat as a source of fatty acids that it needs for cell (and other interior) membranes for
    > > new cells.
    >
    > Too simplistic, I'm afraid, same as the glucose argument. This argument seems to hold in the
    > carcinogenesis phase. It may not hold once the cancer is established.

    From what I've read, this is what is happening. The cancer cells produce substances to get fat from
    the body. If the tumors are not big, then a reduction in body fat through exercise would reduce the
    pool of fatty acids available to the tumors and thus slow growth.

    In addition, losing weight would reduce blood levels of insulin, a panc cancer growth promoter.

    > >If the patient didn't have much body fat to give to the tumor, the tumor is limited on how much
    > >it can grow
    because
    > > without fatty acids, it can't build cell membranes (and other membranes inside the cell).
    > >
    > > This also makes the cancer cells use the fatty acids that are
    supplemented
    > > in the diet so that if EPA is taken in by the patient and that is the
    only
    > > source of fatty acid, new cancer cells will have to use that as a source
    of
    > > fatty acids.
    >
    > Would it were that simple! Cancer and cancer cachexia are much more complex than that. For
    > example, some cancers cause cancer cachexia; some don't. Feeding the patient will not overcome the
    > cancer cachexia.

    EPA is an anti-cachexia agent. But the cancer cells have only two places to get fatty acids - the
    body or the diet. And if there isn't much on the body, then it limits how fast it can grow. Not
    saying it's going to cure the person, but I don't see how it wouldn't slow growth down. And if fat
    levels are low, the cancer cells will gladly take the EPA given thru diet.

    > Indeed, that was the dominant concept in the 1970's, and 1980's. Unfortunately, the concept that
    > overfeeding cancer patients could treat cachexia was well-disproven in many clinical trials in the
    > late 1970's through the early 1990's, and it did not appear that feeding the patient accelerated
    > tumor growth. Unfortunately, the converse does not appear to be true. Not feeding a patient
    > (glucose or fat) does not appear to slow down the growth of an established cancer, although, as I
    > mentioned before, there is a fair amount of evidence that dietary energy restriction can inhibit
    > carcinogenesis.

    I'm not recommending starving or overfeeding the patient.

    >
    > It is possible, even likely, that limiting food intake will decrease the risk of cancer. Numerous
    > studies suggest that this might be true for some cancers. However, once cancer is growing, no
    > manipulation of diet has yet been shown in humans to be effective in treating it.

    Well there's plenty of in vivo and in vitro studies that show certain fats slow down and maybe even
    make the tumor regress (I'd have to search for studies on that but I believe I've seen studies where
    the tumor regressed in vivo).

    Once again, if panc cancer patients wait for the studies on humans you think should be performed
    before they take action, they'll be dead because for economic reasons those studies will NEVER be
    performed. So panc cancer patients should look at all the studies, ask some questions, and then use
    all those studies (and there's tons of them).

    >
    > [Snip]
    >
    > > > However, once the cancer is there, there is no dietary manipulation known that will prolong
    > > > survival.
    > >
    > > My guess is few of any of these things have been tried much in
    controlled
    > > studies despite there being overwhelming scientific evidence indicating
    they
    > > should, at the minimum, slow cancer growth significantly.
    >
    > No, there is some evidence that they *might* slow cancer growth significantly in vivo.

    If you go to Pubmed and do some searching, you'll see there's no "might" about it. Like I said,
    there's tons of in vivo and in vitro studies showing without a doubt that they are slowing or
    stopping or reversing cancer growth. But with rare exception (such as the Celebrex study), you will
    never see human studies because few of these things are uniquely patentable.

    > "Overwhelming" is overselling it a bit.

    Spend some time at Pubmed and you'll see the evidence is overwhelming.

    > And it would appear things are moving in the direction of testing them in humans.

    The private sector tests only things that are under patent for a long time. That leaves the
    government and I don't think they do any studies with human patients testing different substances.
    Thus as I said, the data that's out there (and fortunately there's lots of it) is pretty much all a
    panc cancer patient is going to get on these substances.

    Then they have to do some research, do some intelligent thinking, ask some questions and then take
    intelligent action.

    >
    >
    > >Why they are not standard practice is a subject for another day.
    > >
    > > If all the things I suggest are tried (along with chemo since some of
    them
    > > are synergistic with existing chemo for panc cancer), perhaps the cancer stops growing or even
    > > regresses.
    >
    > Possibly, but there is a reason for my tendency to pessimism. Many strategies that appeared
    > extremely effective in mice have failed to work nearly as well in humans. Immunotherapy,
    > antiangiogenic therapy, etc., for example. That does not mean that we should stop investigating
    > these areas. It simply means that none of them alone will be the magic bullet.

    They won't be but in combination they may be very effective. But for the reasons I've stated, you'll
    never find this out in a Pubmed study (with rare exceptions). It seems the conventional cancer
    treatment is the one looking for the magic bullet. They're trying to produce the magic pill that's
    going to stop cancer. That's pretty unrealistic for some cancers IMO. But using several strategies
    simultaneously makes a lot more sense to me. And fortunately some of the things I've recommended
    make panc cancer chemo even more effective.

    >
    > Remember Folkman's words, for they are wise: "If you have a cancer and you are a mouse, we can
    > take good care of you. Going from mice to people is a big jump, with lots of failures."

    Panc cancer patients who think the pharmaceutical industry is going to invent some magic pill that's
    going to stop panc cancer are not being realistic. Using Pubmed, they now can take an active role in
    their treatment (which is synergistic with conventional treatment). Doing that they might have a
    chance since they can find out about things they won't hear from their doctor (for various reasons -
    none because of bad intentions by the doctor - mostly because they don't know about any of this
    stuff). The power of having Pubmed is pretty revolutionary for all cancer patients. They might as
    well use it.

    One other thing I didn't mention that I should that has shown overwhelming and very powerful
    anticancer action (including in a human study that can be found at Pubmed) at achievable blood
    levels in humans is a substance in green tea called EGCG which stands for epigallocatechin gallate.
    Go to Pubmed to see all the studies on it:

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=PubMed

    Roger

    >
    >
    >
    >
    >
    > [Snip]
    >
    > --
    > Orac |"A statement of fact cannot be insolent."
    > |
    > |"If you cannot listen to the answers, why do you inconvenience me with questions?"
     
  17. Mr Ducky

    Mr Ducky Guest

    Frank Gingrich <[email protected]> wrote in message news:<[email protected]>...
    > Why would anyone want personal experince with the Gonzales treatment? Cancer tries in many ways to
    > destroy your dignity, but you don't have to throw it away on snake oil.

    It certainly is peculiar, but while few cancer treatments seem very dignified, this one at least has
    some evidence of efficacy. Do you have some personal experience with the treatment, or are you
    dismissing it simply because it seems so strange?

    This page has information about a small trial study of the treatment:

    http://www.dr-gonzalez.com/pilot_study_abstract_txt.htm

    "From January 1993 to April 1996 in the authors' private practice, 10 patients with inoperable, biopsy-
    proven pancreatic adenocarcinoma were entered into the trial. After one patient dropped out, an 11th
    patient was added to the study (however, all 11 are considered in the data tabulation). Patients
    followed the treatment at home, under the supervision of the authors.

    As of 12 January 1999, of 11 patients entered into the study, 9 (81%) survived one year, 5 (45%)
    survived two years, and at this time, 4 have survived three years. Two patients are alive and doing
    well: one at three years and the other at four years. These results are far above the 25% survival
    at one year and 10% survival at two years for all stages of pancreatic adenocarcinoma reported in
    the National Cancer Data Base from 1995."
     
  18. Steph

    Steph Guest

    "Mr Ducky" <[email protected]> wrote in message
    news:[email protected]...
    > Frank Gingrich <[email protected]> wrote in message
    news:<[email protected]>...
    > > Why would anyone want personal experince with the Gonzales treatment? Cancer tries in many ways
    > > to destroy your dignity, but you don't have to throw it away on snake oil.
    >
    > It certainly is peculiar, but while few cancer treatments seem very dignified, this one at least
    > has some evidence of efficacy. Do you have some personal experience with the treatment, or are you
    > dismissing it simply because it seems so strange?
    >
    > This page has information about a small trial study of the treatment:
    >
    > http://www.dr-gonzalez.com/pilot_study_abstract_txt.htm
    >

    Why don't you understand the deficiencies of this "study"?
     
  19. Mr Ducky

    Mr Ducky Guest

    "Roger" <[email protected]> wrote in message news:<[email protected]>...
    > "Orac" <[email protected]> wrote
    > > Perhaps, but, your studies notwithstanding, it is very much a question for study.
    >
    > My understanding of conventional cancer treatment is a lot of oncologists are unaware of how
    > statins, cox 2 inhibitors, lowering glucose and insulin, and certain fats fight cancer. And the
    > chances of there being any big clinical study like what would be done when a drug is trying to get
    > approved is pretty small since there's little economic incentive for any big company to put out
    > the money. None of these things are patentable that are unique (for example, there are several
    > statins on the market). So unless the US govt or another govt funds the studies, the studies won't
    > be done. And thus all the numerous studies (and that's an understatement) on Pubmed about the
    > effectiveness of statins and cox 2 inhibitors and particular fats will be ignored.
    >
    > Thus a cancer patient can decide to look at the evidence and decide to do some thinking and act on
    > all the evidence instead of letting others do the thinking (or nonthinking) for them. It's similar
    > to smoking and lung cancer.

    This is an interesting discussion. Orac, do you think that there is some truth to what Roger is
    saying concerning non-patentable treatments? If not, would you say that the treatments he is
    proposing are not actually promising, or that they are being aggressively pursued?

    Roger, what is your background? Are you or someone you know pursing these treatments?

    Thanks
     
  20. Jack

    Jack Guest

    I get furious reading some of these studies because so many "bounce" participants out early due to
    severe side effects. Worse still, because they haven't "completed" the study, no reference is made
    to them or the side effects they suffered. I thought studies were devised to TELL US side effects,
    not HIDE them from us.

    By the way, I've found EXCELLENT, current information on break-through pancreatic cancer treatments
    and protocols as well as interviews (video, audio, and transcripts) with some of the leading doc's
    and researchers treating PC. You can find them at http://www.robertsreview.com.

    Jack

    "Steph" <[email protected]> wrote in message news:<J_XXb.521794$X%[email protected]>...
    > "Mr Ducky" <[email protected]> wrote in message
    > news:[email protected]...
    > > Frank Gingrich <[email protected]> wrote in message
    > news:<[email protected]>...
    > > > Why would anyone want personal experince with the Gonzales treatment? Cancer tries in many
    > > > ways to destroy your dignity, but you don't have to throw it away on snake oil.
    > >
    > > It certainly is peculiar, but while few cancer treatments seem very dignified, this one at least
    > > has some evidence of efficacy. Do you have some personal experience with the treatment, or are
    > > you dismissing it simply because it seems so strange?
    > >
    > > This page has information about a small trial study of the treatment:
    > >
    > > http://www.dr-gonzalez.com/pilot_study_abstract_txt.htm
    > >
    >
    >
    > Why don't you understand the deficiencies of this "study"?
     
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