A defect in thromboxane A2 synthesis may be a factor predisposing to cancer.
A failure of thromboxane (TX) A2 synthesis may be a factor in cancer. Such a loss could explain the susceptibility to mutation, the excess prostaglandin production, the glycolytic mode of metabolism and the deranged calcium pumping characteristic of cancers. Ionising radiation and phorbols both have actions similar to inhibitors of TXA2 synthesis whereas colchicine and oxygen have actions consistent with stimulation of TXA2 synthesis. The concept accounts logically for hitherto unexplained features of cancer and suggests new strategies for the prevention and treatment of cancer.
D000818:Animals; D004247:DNA / Q000235:genetics / Q000378:metabolism; D006801:Humans; D009154:Mutation; D009369:Neoplasms / Q000209:etiology / Q000378:metabolism* / Q000628:therapy; D011453:Prostaglandins / Q000096:biosynthesis; D011565:Psoriasis / Q000150:complications; D011832:Radiation Injuries / Q000150:complications; D013928:Thromboxane A2 / Q000096:biosynthesis* / Q000378:metabolism / Q000528:radiation effects; D013931:Thromboxanes / Q000096:biosynthesis*; D014466:Ultraviolet Rays; D014983:Xeroderma Pigmentosum / Q000150:complications
D011453:Prostaglandins; D013931:Thromboxanes; D013928:Thromboxane A2; D004247:DNA