The membrane cluster hypothesis of mitogenesis and carcinogenesis.
This paper modifies and extends an earlier one on the same subject. It explains why external (but not internal) surface molecules of plasma membrane clusters may be rapidly scattered by any external challenging bioelectrical field. Temporary clusters from challenges may induce mitosis in cells near wounds and in epithelial stem cells. Weak challenges of much longer duration may initiate carcinogenesis by permanent clusters. Basic intracellular ligand/receptors or oncogene products in sufficient concentration at the membrane inner lipid layer may form permanent clusters rapidly. Additive increase of inner surface clusters by initiating agents is equated to promotion; accelerated cluster growth to progression. As a malignant cell grows, its cluster population increases until its membrane becomes permeable enough to stimulate mitosis. A progression mechanism is suggested that is consistent with the known properties of ras p21 proteins. The effect of long term exposure to power transmission line fields on mitosis and carcinogenesis is discussed. An approach to anticancer therapy is suggested, using a hypothesis-based mechanism for the anti-cancer activity of retinoic acid.
Beech
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JA
D000818:Animals; D016588:Anticarcinogenic Agents / Q000494:pharmacology / Q000627:therapeutic use; D002455:Cell Division; D002462:Cell Membrane / Q000502:physiology*; D002471:Cell Transformation, Neoplastic; D006801:Humans; D008051:Lipid Bilayers; D008563:Membrane Lipids / Q000502:physiology*; D008954:Models, Biological; D009369:Neoplasms / Q000188:drug therapy / Q000517:prevention & control; D010743:Phospholipids / Q000502:physiology; D014212:Tretinoin / Q000494:pharmacology / Q000627:therapeutic use
D016588:Anticarcinogenic Agents; D008051:Lipid Bilayers; D008563:Membrane Lipids; D010743:Phospholipids; D014212:Tretinoin