Background

Cancer growth requires physical contact between platelets and tumour cells. This extracellular supply of growth factors is essential for cell growth. All dividing cells have receptors for platelets. Blocking them inhibits cell growth and prevents metastasis and drug resistance. Heparins and even non-anticoagulant highly sulfated relatives can effectively block these receptors, offering a well-tolerated and cost-effective treatment that may reduce cancer drug doses and minimise side effects.

Methods

Heparins can prevent cancer-associated thrombosis in tumour patients and slow down tumour progression. High platelet counts cause more rapid tumour growth. These observations are related. All primary cell cultures from tumours and normal tissues require a supplement, usually foetal bovine serum, to thrive. This supplement contains growth factors necessary for cell division. These are not synthesised in cancer cells but in megakaryocytes in the bone marrow and are transported in our circulation in platelets and released from platelets during serum production. Receptors for growth factors enable cells to take up these. A mechanism must therefore exist in vivo which allows cells to acquire these factors.

Results

All cells in the cell cycle, malignant and benign, possess platelet receptors. After docking to these receptors, platelets fuse with the cell membrane and release their contents into the cytoplasm. Proliferating cells now receive growth factors and the molecular machinery for making the same.

The anticoagulant effect of heparins and their blockade of the platelet receptor are independent of each other. Blocking the physical contact between cells and platelets inhibits cell growth. This is the mode of action of the heparins on tumour growth. Remarkably, not only is cell proliferation thereby blocked competitively but it also prevents metastasis. Such adjuvant treatment also prevents resistance to anticancer drugs.

Conclusion

Modified non-anticoagulant heparins and highly sulfated heparans, devoid of anticoagulatory activities, also effectively block these receptors. In contrast, fondaparinux does not affect the platelet binding to cells. Platelets thus assume a new, hitherto little-appreciated role in regulating cell growth.

The dosage of anticancer drugs can be reduced through such adjuvant treatment. Adverse side effects will become rarer, and metastases and chemoresistance will be a thing of the past.

Offenlegung Interessenkonflikt:

Der Autor verneint Interessenkonflikte. Er ist CVO (Chief Visionary Officer) des kleinen Unternehmens Cell Receptor GmbH, und dessen Muttergesellschaft, welche gegründet wurden, um eine klinische Studie zum vorstehenden Thema zu ermöglichen und wundert sich darüber, dass einfache und effektive Verfahren zur Verbesserung onkologischer Ergebnisse nicht die ihnen gebührende Beachtung finden.