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Anti-Cancer Effect of Dipyridamole

Editor:

This is about the anti-cancer effect of dipyridamole. It 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 ClarkÕs 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 followup 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. It 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. OÕMeara 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 OÕMearaÕs students. In any event Michaels had a report in The Lancet in the October 17, 1964 issue (pp. 832-5) with the title ÒCancer Incidence and MortalityÓ 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 Ð 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 OÕMeara 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.

Wayne Martin
25 Orchard Drive
Fairhope, Alabama 36532 USA
334-928-3975
Fax 334-928-0150



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