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Anti-Cancer Effect of Dipyridamole
This is about the anti-cancer effect of dipyridamole. Dipyridamole is a harmless
widely-used drug in treating patients who have survived an episode of
thrombotic stroke or coronary thrombosis, that has a vast potential of being a
harmless anti-cancer drug.
First let us look at the report in the
Lancet
in the March 23, 1985 issue, p. 693, by E.H. Rhodes et al. of St. Hileir and
Kingman Hospital in Surrey, England. These doctors for the past 11 years had
been maintaining melanoma patients with Clark's level IV and III disease on
dipyridamole, 300 mg a day. Thirty of these patients were maintained on this
dose of dipyridamole. Of them, 26 had level IV disease and four had level III
disease. At five years, the survival of the level IV patients was 74%. The
five-year survival for the total of the 30 of level IV and III disease was 77%.
None of the level III patients died. Reference was given that the expected
five-year survival for level IV melanoma is 32%. In the case of melanoma, 100%
of deaths are caused by distant metastases. Reference was given that when
metastases in many forms of solid malignant tumors are formed from the vascular
network, the tumor cells moving in the blood circulation, at the beginning of
metastasis formation, are attached to the vascular endothelium. Reference is
also given that dipyridamole tends to prevent this attachment of cancer cells
flowing in the blood circulation to the endothelium and thus tends to prevent
the formation of metastases.
Dipyridamole, like aspirin, inhibits platelet adhesion, and thus tends to
prevent the vascular thrombosis of heart attacks and strokes. In the
Lancet
in the December 12, 1987 issue (pp. 1,371-4) was the report of the European
Stroke Prevention Study. The introduction to this report reviewed the indicated
lack of benefit in treating with aspirin, patients who had survived a small
stroke, a TIA, a temporary ischemic attack. In this trial, dipyridamole 300 mg
a day was added to treatment with aspirin and the results were outstanding.
Over a two-year period, stroke deaths were decreased by 50%, deaths from
myocardial infarction decreased by 38% and deaths from cancer by 25%.
The numbers of patients involved were small, however here is another indication
of an anti-cancer effect of dipyridamole.
I have had a long exchange with Dr. Betty Rhodes who has been in retirement for
about eight years. She treated melanoma with dipyridamole because she is a
dermatologist and that is the kind of cancer that she treated. She has been
disappointed that there has been no follow-up on this most hopeful indication
that she has demonstrated of dipyridamole in treating melanoma. She feels that
dipyridamole may be just as effective in treating many other forms of solid
malignant tumors.
The above-indicated anti-cancer effect of dipyridamole may be due only to its
prevention of metastases, however Eva Bestida et al. of the University of
Barcelona had a report in
Cancer Research
in the September 1985 issue (pp. 4,048-4,062) on the inhibition of certain
human cancer cell growths by dipyridamole. Dipyridamole caused an inhibition of greater
than 80% of adinosine, thymidine and uridine. These are substances needed by
cancer cells to prosper. This may indicate an anti-cancer effect of
dipyridamole other than in the prevention of metastases.
In 1958, Professor R.A.Q. O'Meara of Trinity College, Dublin Ireland, had a
report on Coagulation and Cancer in the
Irish Journal of Medical Science
, vol. 394, pp. 474-9. I met with him briefly in 1965. At that time he felt
that with both the primary tumor or a metastasis, clotting factors are given
off by cancer cells and then cancer cells tend to become coated with fibrin. He
felt that our cancer cell-killing immunocytes can kill cancer cells more
effectively if they can make contact with cancer cells. He felt that this
fibrin coat on cancer cells acts as a protective barrier to prevent them from
being killed by immune attack.
I think that L. Michaels may have been one of O'Meara's students. In any event
Michaels had a report in the
Lancet
in the October 17, 1964 issue (pp. 832-5) with the title 'Cancer Incidence and
Mortality in patients having Anticoagulant Therapy'. In that time frame nearly
every patient who had survived a heart attack or a thrombotic stroke was
maintained for year after year on warfarin. The concept was that warfarin would
prevent the formation of the red or fibrin thrombus. Michaels did a study of
such patients to the extent of over 1,500 patient years. There was among them
only one death — that of a primary lung cancer when in this group eight
cancer deaths had been expected.
Warfarin will tend to prevent the red or fibrin part of a blood clot.
Dipyridamole, by preventing the formation of the white or platelet thrombus,
will also be preventing the formation of a fibrin thrombus.
The tendency of cancer cells to give off clotting factors puts cancer patients
at a far greater risk of death from vascular thrombosis. They are greatly more
at risk of death from a heart attack or stroke.
In 1958 at the time of the first O'Meara report, there was very little thought
being given to the role of platelets in heart attacks and thrombotic strokes.
Beginning in 1945, the standard treatment for survivors of heart attacks or
thrombotic strokes was to anticoagulate with warfarin or similar
anticoagulating drugs. By 1970 the practice had almost completely come to an
end. It was decided that anticoagulant treatment was not increasing survival.
By then it was understood that in the vascular tree, there will never be the
formation of a red or fibrin thrombus without there first being a white or
platelet thrombus. The discovery of the factors in the arachidonic acid cascade
and of the platelet aggregation substance thromboxane A2 was the basis for the
Nobel Award for Medicine in 1982. It then followed that a platelet thrombus
with no fibrin thrombus could be enough of an occlusion to cause a thrombotic
stroke or a heart attack.
With this understanding, along with the knowledge that aspirin will tend to
reduce the aggregation of platelets, the entire medical establishment replaced
warfarin with aspirin in treating heart attacks and thrombotic strokes.
Since that time there have been three trials in England in using aspirin in the
prevention of a heart attack and two in the USA. Of these five trials only one,
the Physicians Health Study in the USA showed any benefit at all. This one
trial that did show some benefit in the prevention of a heart attack used
Bufferin and Bufferin contains aspirin and magnesium.
There are many reasons to believe that dipyridamole at 300 mg a day will be far
more effective in the prevention of heart attacks and strokes than aspirin.
Moreover dipyridamole has none of the harmful side effects of aspirin.
As of March 1999, there is now a new light thrown on the harm of platelet
aggregation, this time with respect to cancer. In
Cancer Research
March 1999, pp. 1295-3000, B. Nieswandt et al. of the University of Regensburg,
Germany had a report on platelet aggregation and cancer. Using three different
tumor cell lines in mice, it was demonstrated that tumor cells can activate
platelet aggregation and that platelet aggregates deactivates cytotoxic NK
cells, preventing NK cells from killing cancer cells.
This is to suggest that dipyridamole is a harmless drug. The generic form of it
costs less than one dollar a day for treatment. It has in one small trial been
demonstrated that it is effective against melanoma. There is every reason to
feel that it may be effective against a broad spectrum of cancers.
If it were granted that all cancer patients are at a greater risk of heart
attacks and strokes, it is hoped that many doctors will treat cancer patients
with dipyridamole for this reason. However if they do so, it will soon be found
that dipyridamole will be having a marked anti-cancer effect.
Last updated 10 September 2002
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