Some<unk> es, especially gliomas (25%), as well as adenocarcinomas of the pancreas and lung, are associated with hypercoagulability (the tendency to form blood clots) for reasons that are incompletely understood, but may be related to factors secreted by the tumors, in particular a circulating pool of cell-derived tissue factor-containing microvesicles. Some adenocarcinomas secrete mucin that can interact with selectin found on platelets, thereby causing small clots to form. Moreover, most malignant tumors overexpress and secrete heparanase, an enzyme that degrade heparan sulfate and endogenous heparin, and thus contribute to the hypercoagulable state in cancer patients. Potential Mechanisms of Cancer-Related Hypercoagulability: Cancer-associated thrombosis can result from: (1) stasis, i.e., direct pressure on blood vessels by the tumor mass, poor performance status, and bed rest following surgical procedures; (2) iatrogenic, due to treatment with antineoplastic medications; and (3) secretion of heparanase from malignant tumors that results in degradation of endogenous heparin. Nasser NJ, Fox J, Agbarya A. Cancers (Basel). 2020 Feb 29;12(3):566. https://doi.org/10.3390/cancers12030566 In patients with<unk> -associated hypercoagulable states, the blood may spontaneously form clots in the portal vessels (portal vein thrombosis), the deep veins of the limbs (deep vein thrombosis), or the superficial veins (superficial vein thrombosis) anywhere on the body. These clots present as visibly swollen blood vessels (thrombophlebitis), especially the veins, or as intermittent pain in the affected areas.
Trousseau sign of malignancy
Koebner phenomenon
Skin tag
Fat pad sign
Janeway lesion
Cameron lesions
Tree-in-bud sign
Bankart lesion