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The Causes And Treatments Of Basal Cell Carcinoma

971 words - 4 pages

Basal-Cell Carcinoma (BCC) is a common human skin malignancy with rare occurrence of local advancements or malignancies(1,2,3). BCC accounted for approximately 80% the 2 million cases of nonmelanoma skin cancer cases diagnosed in 2006 (1). The risk of disease metastasis is very low and ranges from 0.0028 5o 0.55 percent and the survival rate is anywhere from 8months to 3.6 years from initial tumor metastasis (2). Extensive studies in the last couple decades have identified the Hedgehog pathway to be the main player in the development of these types of tumors (2,3). Hedgehog pathway starts with the binding of the Hedgehog ligand to the 12-pass transmembrane receptors, PTCH 1/2, located in the cell cilium (1,2,3). This receptor binding activates the Hedgehog pathway by further activating the smoothened protein receptor (Smo), that inturn leads to activation of glioma-associated protein (Gli). Gli proteins are zinc finger transcription factors that regulate expression of genes involved in cell cycle regulation, angiogenesis and anti-apoptotic pathways. Although these genes are essential during embryogenesis, dysregulation of these genes can have devastating effects in adulthood. Thus, suppression of the Hedgehog pathway keeps a check on the aberrant expression of these oncogenes. Of the three types of aberrant Hedgehog activation pathways, the ligand-independent constitutive activation caused by mutations in either the negative regulators or the smoothened receptor, lead to BCC tumor development (2). Thus, understanding the role of Hedgehog pathway in regulating BCC will yield a better understanding of the molecular mechanisms involved in BCC tumerogenesis and development of effective-targeted treatment options.

Like many other skin malignancies, BCC is sporadic and the rate of BCC is affected by increased exposure to UV radiation, the family history, immunosuppression, hereditary syndromes such as Gorlin syndrome, Rombo Syndrome, etc (1). Gorlin’s syndrome patients have been shown to have a variety of types of germline mutation in the PTCH gene leading to abberant Hedgehog pathway. Genetic analyses have shown some of the sporadic BCC cases to have mutations in the PTCH gene as well, indicating a crucial role for the Hegdehog pathway in BCC tumerogenesis (1,2,3). Translation of these bench-side research findings to therapeutic development has resulted in development of various treatment options for BCC. BCC is generally treated with local approaches including surgical excision, radiotherapy, and photodynamic therapy. But, in rare cases of local invasive (advanced) BCC or the malignant (terminal) BCC where surgical excision or radiotherapy is not an option, chemotherapeutic agent, Cisplatin-based regimens have been used with variable efficiency (1,2). Identification of the first naturally occurring steroidal alkaloid inhibitor of Smo in Hedgehog pathway, Cyclopamine, instigated researchers to develop selective Smo inhibitors that can be used for...

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