期刊
CURRENT OPINION IN ONCOLOGY
卷 19, 期 5, 页码 452-457出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/CCO.0b013e3281eb8ea7
关键词
Akt/mammalian target of rapamycin; angiogenesis; Kaposi's sarcoma; Kaposi's sarcoma herpesvirus; viral cyclin
类别
资金
- NCI NIH HHS [R01 CA109232-02, R01 CA163217, U01 CA121947, R01 CA109232-03, R01 CA109232-04, R01 CA109232-05, R01 CA109232-03S1, R01 CA109232-01, U01-CA 121947, R01 CA109232] Funding Source: Medline
- NIDCR NIH HHS [R01 DE018304, R01 DE018304-03, R01 DE018304-02, R01 DE018304-01] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA163217, U01CA121947, R01CA109232] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH [R01DE018304] Funding Source: NIH RePORTER
Purpose of review To summarize major recent findings on the biology of human herpesvirus-8, i.e. Kaposi's sarcoma-associated herpesvirus, and the implications of these findings for Kaposi's sarcoma treatment. Recent findings Although reduced in incidence in developed countries since the introduction of highly active antiretroviral therapy, Kaposi's sarcoma incidence is still markedly increased in HIV-infected patients in resource-rich areas of the world and is a major complication among HIV-infected individuals in sub-Saharan Africa. The Akt/mammalian target of rapamycin pathway has emerged as a major driving force in Kaposi's sarcoma. In addition, the roles of p53, the Kaposi's sarcoma-associated herpesvirus viral cyclin and nuclear factor-KB in the development and progression of Kaposi's sarcoma are being further clarified, and therapeutic agents are being developed that may target these pathogenetic mechanisms. New Kaposi's sarcoma treatments should be considered that target the molecular interface between virus and host. Summary The growing knowledge of Kaposi's sarcoma biology provides multiple opportunities for rational targeted therapies. Further research is needed to better understand the mechanisms by which Kaposi's sarcoma develops and to develop therapeutic strategies that prevent resistance to treatment.
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