The molecular programme of tumour reversion: the steps beyond malignant transformation

被引：141

作者：

Telerman, Adam ^{[1
]}

Amson, Robert ^{[1
]}

机构：

[1] Ecole Normale Super, UMR 8113, LBPA, F-94235 Cachan, France

来源：

NATURE REVIEWS CANCER | 2009年 / 9卷 / 03期

关键词：

ACUTE PROMYELOCYTIC LEUKEMIA; HISTAMINE-RELEASING-FACTOR; DIFFERENTIALLY EXPRESSED CDNAS; FAMILIAL ALZHEIMERS-DISEASE; EMBRYONAL CARCINOMA-CELLS; TRANS RETINOIC ACID; INHIBITOR P21 GENE; WILD-TYPE; MUTANT PRESENILIN-1; BETA-CATENIN;

D O I：

10.1038/nrc2589

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

How cells become malignant has preoccupied scientists for over a century. However, the converse question is also valid: are tumour cells capable of reverting from their malignant state? Askanazy's studies in 1907 indicated that teratoma cells could differentiate into normal somatic tissues and current evidence indicates that some tumour cells have acquired the molecular circuitry that results in the negation of chromosomal instability, translocations, oncogene activation and loss of tumour suppressor genes. Studying these extremely rare events of tumour reversion and deciphering these pathways, which involve SIAH1, presenilin 1, TSAP6 and translationally controlled tumour protein (TCTP), could lead to new avenues in cancer treatment.

引用

页码：206 / 215

页数：10

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