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J Investig Dermatol Symp Proc. 2003 Jun;8(1):72-5.
Molecular mechanisms of chemotherapy-induced hair loss.

Botchkarev VA.

Department of Dermatology, Boston University School of Medicine, Boston, MA 02118, USA. vladbotu.edu

Hair loss (alopecia) is a much-feared side-effect of many chemotherapy protocols and is one of the most psychological devastating aspects of cancer therapy. So far, no satisfactory strategy for suppressing chemotherapy-induced alopecia is at hand. During the last decade, some progress in understanding molecular mechanisms of chemotherapy-induced hair loss has been achieved using rodent models. However, the pathobiology of the response of human hair follicle to chemotherapy remains largely unknown. Here, we review molecular mechanisms that control apoptosis in the hair follicle induced by chemotherapy and delineate the basic strategy for pharmacological inhibition of this devastating side-effect of cancer treatment. We focus on the roles of p53 and its target genes that are essential in mediating responses of hair follicle cells. We assume that local pharmacological inhibition of p53 activity may serve as an effective treatment to prevent chemotherapy-induced hair loss. Sufficient pharmacological inhibition of chemotherapy-induced hair loss may require a combination of inhibitors to block complementary or redundant pathways of apoptosis in hair follicles.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12894998&dopt=Abstract [PubMed - in process]
















DHEA is a natural hormone, and it is produced in our body by the adrenal glands. DHEA has been suggested to provide numerous potential benefits. DHEA (or dehydroepiandrosterone) is converted into androgens (male hormones) or estrogens (female hormones) in the cells.





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