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Chemotherapy-induced Hair loss
Cell Stress Chaperones. 2008;13:8
Prevention of chemotherapy-induced Hair loss.....
Jimenez JJ,.et al
edited for hair loss
Alopecia (hair loss) is experienced by thousands of cancer patients every year. Substantial-to-severe hairloss is induced by anthracyclines, taxanes, alkylating compounds, etc. Currently, no treatment appears to be generally effective in reliably preventing hair loss due to chemotherapy. We observed in experiments using different rodent models that localized administration of heat or subcutaneous/intradermal injection of geldanamycin or 17-(allylamino)-17-demethoxygeldanamycin induced a stress protein response in hair follicles and effectively prevented hair loss from adriamycin,.....
Alopecia (hair loss) is arguably the most feared side effect of cancer chemotherapy. Despite substantial efforts, no reliable and generally effective preventative treatment has become available. Scalp tourniquets and cooling devices have been utilized for decades to restrict blood flow to the scalp during chemotherapy treatment. Although such treatments were found to be successful in reducing alopecia in connection with certain chemotherapy regimens, they were difficult to standardize and not generally useful over the wide range of pharmacological regimens used in the clinic. Although more recent studies utilizing improved hypothermia devices reported increased reliability, certain antineoplastic drug combinations, notably combinations comprising a taxane could not be protected against. Among the many pharmacological approaches for alopecia prevention that were investigated, vitamin D3 appeared to be the most promising protective compound because it was effective against several different antineoplastic agents in preclinical experiments. However, a clinical trial was ultimately unsuccessful.All cells possess protective mechanisms that increase their resistance to various adverse conditions. Perhaps best known is the ubiquitous stress protein (Hsp) response that involves the enhanced expression of classical stress proteins such as Hsp90, Hsp70, and Hsp25, and of certain other proteins such as P-glycoprotein, in response to physical or chemical stresses. Elevated levels of Hsps are known to result in increased stress tolerance. The spectrum of toxicants an activated stress protein response can mitigate against is broad. As shown by previous studies, elevated levels of the cohort of Hsps or of individual Hsps are also protective against cytotoxicity from many antineoplastic agents used in the clinic. Table 1 summarizes selected studies relating to the reduction or prevention of toxicity from adriamycin, cyclophosphamide, taxol, and etoposide. Because the stress protein response is an intracellular protective mechanism, it should be possible to locally activate a stress protein response in noncancerous tissues without affecting the cytotoxic effects of an antineoplastic agent in cancerous tissues. We hypothesized that localized activation of a stress protein response in the hair follicles of a patient’s scalp (and eyebrows) would prevent chemotherapy-induced hair loss and that this protective effect could be achieved without reduction of tumor therapy efficacy......
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