Abstract
Nonmelanoma skin cancer (NMSC) is the most prevalent cancer in light-skinned populations, and includes mainly Basal Cell Carcinomas (BCC), representing around 75% of NMSC and Squamous Cell Carcinomas (SCC). The incidence of these tumors is continuously growing. It was found that the overall number of procedures for NMSC in US rose by 76%, from 1,158,298 in 1992 to 2,048,517 in 2006. Although mortality from NMSC tends to be very low, clearly the morbidity related to these skin cancers is very high. Treatment options for NMSC include both surgical and nonsurgical interventions. Surgery was considered the gold standard therapy, however, advancements in the knowledge of pathogenic mechanisms of NMSCs led to the identification of key targets for drug intervention and to the consequent development of several targeted therapies. These represent the future in treatment of these common forms of cancer ensuring a high cure rate, preservation of the maximal amount of normal surrounding tissue and optimal cosmetic outcome. Here, we will review recent advancements in NMSC targeted therapies focusing on BCC and SCC.
Highlights
In the USA, there are more new cases of skin cancer each year compared with the combined incidence of cancers of breast, prostate, lung, and colon cancers, with more than 1.5 million skinCancers 2011, 3 cancers diagnosed yearly in the United States
Overexpression of COX-2 has been revealed in various neoplasms ranging from colorectal cancer to breast cancer, as well as skin cancer [1,2]
Normal skin has minimal levels of COX-2 and PGE-2, with levels of COX-2 increasing in correlation with the severity of skin tumors from premalignant actinic keratosis to squamous cell carcinoma [2,3]
Summary
In the USA, there are more new cases of skin cancer each year compared with the combined incidence of cancers of breast, prostate, lung, and colon cancers, with more than 1.5 million skinCancers 2011, 3 cancers diagnosed yearly in the United States. GDC- 0449 has antitumor activity in a mouse model of medulloblastoma and in xenograft models of primary human tumor cells, including colorectal cancer and pancreatic carcinoma, in which its effects correlate with blockade of the hedgehog pathway [27,28,29]. The effects of EGFR on apoptosis and cell cycle arrest result, at least in part, from its activation of phosphatidyl inositol-3-kinase (PI3K)/Akt signaling [47,49].
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