结直肠癌分子发病机制的新见解。
New insights into the molecular pathogenesis of colorectal cancer.
作者信息
Hung Kenneth E, Chung Daniel C
机构信息
Gastrointestinal Unit, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, 50 Blossom Street, Boston, MA 02114, USA.
出版信息
Drug Discov Today Dis Mech. 2006 Winter;3(4):439. doi: 10.1016/j.ddmec.2006.10.005.
Although there have been tremendous advances in the management of colorectal cancer (CRC), there is still a need for improved therapeutic approaches. On a molecular genetic level, CRC is one of the best-understood solid malignancies, and these insights can serve as a foundation for the design of novel targeted therapies. We present new genetic and epigenetic pathways that highlight the heterogeneous mechanisms in CRC pathogenesis, including the roles of the MYH DNA repair gene and of aberrant DNA hypermethylation and imprinting. We then describe some of the successful targeted therapies that inhibit COX2, EGFR, and VEGF as well as potential new targets that have been revealed by studies of molecular genetics.
尽管在结直肠癌（CRC）的治疗方面已经取得了巨大进展，但仍需要改进治疗方法。在分子遗传学层面，CRC是理解最为透彻的实体恶性肿瘤之一，这些认知可为新型靶向治疗的设计奠定基础。我们展示了新的遗传和表观遗传途径，这些途径突出了结直肠癌发病机制中的异质性机制，包括MYH DNA修复基因以及异常DNA高甲基化和印记的作用。然后，我们描述了一些成功的靶向治疗方法，这些方法可抑制COX2、EGFR和VEGF，以及分子遗传学研究揭示的潜在新靶点。
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