"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?"