Pancreatic cancer survivors?



M

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.
 
F

Frank Gingrich

Guest
[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
 
M

Mike Radcliffe

Guest
"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
 
O

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?"
 
B

Ballstoyourpart

Guest
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.
 
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
 
M

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
 
O

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?"
 
B

Ballstoyourpart

Guest
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.
 
R

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?"
 
O

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?"
 
R

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?"
 
O

Orac

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

> "Orac" <[email protected]> wrote
>
> > "Roger" <[email protected]> wrote:
> >
> > > "Orac" <[email protected]om> 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?"
 
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
 
R

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?"
 
M

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."
 
S

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"?
 
M

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
 
J

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"?