通过癌基因失活实现癌症康复。

Rehabilitation of cancer through oncogene inactivation.

作者信息

Shachaf Catherine M, Felsher Dean W

机构信息

Division of Oncology, Departments of Medicine and Pathology, Stanford University, 269 Campus Drive, Stanford, CA 94305-5151, USA.

出版信息

Trends Mol Med. 2005 Jul;11(7):316-21. doi: 10.1016/j.molmed.2005.05.003.

DOI:10.1016/j.molmed.2005.05.003

PMID:15955741

Abstract

The inactivation of the MYC oncogene alone can reverse tumorigenesis. Upon MYC inactivation, tumors stereotypically reverse, undergoing proliferative arrest, cellular differentiation and/or apoptosis. The precise consequences of MYC inactivation appear to depend upon both genetic and epigenetic parameters. In some types of cancer following MYC inactivation, tumor cells become well differentiated and biologically and histologically normal, inducing sustained tumor regression. However, in some cases, these normal-appearing cells are actually dormant tumor cells and upon MYC reactivation they rapidly recover their tumorigenic properties. Future therapies to treat cancer will need to address the possibility that tumor cells can camouflage a normal phenotype following treatment, resting in a dormant, latently cancerous state.

摘要

仅MYC癌基因的失活就能逆转肿瘤发生。MYC失活后，肿瘤通常会发生逆转，经历增殖停滞、细胞分化和/或凋亡。MYC失活的确切后果似乎取决于遗传和表观遗传参数。在某些类型的癌症中，MYC失活后，肿瘤细胞会分化良好，生物学和组织学上均恢复正常，从而导致肿瘤持续消退。然而，在某些情况下，这些看似正常的细胞实际上是休眠的肿瘤细胞，MYC重新激活后，它们会迅速恢复其致瘤特性。未来治疗癌症的疗法将需要考虑到肿瘤细胞在治疗后可能伪装成正常表型，处于休眠、潜在癌变状态的可能性。