Hair follicles and their role in skin cancer


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Hair follicles as a source of cancer cells

The hair follicles have unique regenerative properties that can have significant benefit for the skin. However, sometimes these very properties become detrimental to the skin health. A number of links have been discovered between stem cells and neoplasia. Stem cells have the ability to renew themselves, while cancer is regarded as powered with “out-of-control” self renewal. This indicates toward high probability of common mechanisms for achieving these processes. Because stem cells persist and divide lifelong, they are more prone to accumulate the requisite number of mutations to cause overt neoplasia as compared to progenitor cells. Hair follicles retain at least two stem cell populations. Keratinocyte stem cells are located in the bulge region while melanocyte stem cells are retained in the hair follicle outer root sheath.

Maintenance of epidermis depends on a population of multi-potential stem cells; they are able to generate all of the differentiated epidermal lineages. Different kinds of skin cancers are believed to have started as disorders of adult epidermal stem cells--that serve as the ultimate source of cells for both of these tissues. Also, because of their long-term exposure to environmental mutagens, epidermal stem cells are likely to accumulate multiple mutations and undergo abnormal clonal expansion.

Basal cell carcinomas

The most common type of cancer suffered by the Caucasians is cell carcinomas that arise from the basal layer of the epidermis. There are compelling data that suggest uncontrolled activation of the Hedgehog (Hh) signalling pathway in the pathogenesis of BCCs and several other types of tumors. Hh signaling activity in hair follicle epithelium is restricted to periods of active growth and is limited by the transient expression of SHH. However, this pathway is constitutively active in BCCs, due to mutations in genes called PTC or SMO. Transgenic human-skin models confirm that the activation of the Hh pathway is an early event in tumor formation.

The etiology of human BCCs suggests that tumors share several common characteristics with immature hair follicles, including similar histology, ultrastructure, and patterns of keratin gene expression. Morphological observations have suggested that many BCCs directly originate from the follicular outer root sheath, and possibly directly from the bulge, stem cell associated, region. Biochemically, BCCs express cytokeratin profiles found in normal follicular outer root sheath cells. The normal expression of Ptch in developing hair follicle and the presence of Ptch mutations in both hereditary and sporadic BCCs suggest that BCC development recapitulates the hair growth cycle. The presence of nuclear ?-catenin, a key mediator of hair follicle growth, has recently been shown to correlate with increased proliferation of tumor cells in BCCs. All these evidences together suggest that some BCCs arise from a common cell type within the hair follicle and it is possible that BCCs, including those not directly derived from hair follicles, keep many of the properties and mechanisms used by hair follicles for BCC growth and survival.

Other cancers

There are also several other more rare cancer presentations directly derived from hair follicles including trichilemmomas, trichoepitheliomas, trichoblastomas, keratoacanthomas, proliferating trichilemmal tumors, and pilomatricomas. The recent findings tell us that both sporadic trichilemmomas and BCCs contain mutations of the same genes. This makes compelling evidence that these cancers share a common tumorgenic mechanism and are closely linked to the hair follicle.

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