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Titolo:
Epigenetic lesions causing genetic lesions in human cancer: promoter hypermethylation of DNA repair genes
Autore:
Esteller, M;
Indirizzi:
John Hopkins Oncol Ctr, Div Canc Biol, Baltimore, MD 21231 USA John Hopkins Oncol Ctr Baltimore MD USA 21231 ol, Baltimore, MD 21231 USA
Titolo Testata:
EUROPEAN JOURNAL OF CANCER
fascicolo: 18, volume: 36, anno: 2000,
pagine: 2294 - 2300
SICI:
0959-8049(200012)36:18<2294:ELCGLI>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
SPORADIC BREAST-CANCER; TUMOR-SUPPRESSOR GENES; O-6-METHYLGUANINE-DNA METHYLTRANSFERASE; MICROSATELLITE INSTABILITY; COLORECTAL-CARCINOMA; MOLECULAR-DETECTION; HUMAN NEOPLASIA; LUNG-CANCER; METHYLATION; BRCA1;
Keywords:
DNA methylation; tumour suppressor genes; DNA repair genes; hMLH1; MGMT; epigenetics;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Esteller, M John Hopkins Oncol Ctr, Div Canc Biol, Room 530,5th Floor,1650Orleans St,Baltimore, MD 21231 USA John Hopkins Oncol Ctr Room 530,5th Floor,1650 Orleans St Baltimore MD USA 21231
Citazione:
M. Esteller, "Epigenetic lesions causing genetic lesions in human cancer: promoter hypermethylation of DNA repair genes", EUR J CANC, 36(18), 2000, pp. 2294-2300

Abstract

The existence of genetic alterations affecting genes involved in cellular proliferation and death, such as TP53 and K-ras, is one of the most common features of tumour cells. Recently, gene inactivation by promoter hypermethylation has been demonstrated. Methylation is the main epigenetic modification in mammals and abnormal methylation of the CpG islands located in the promoter region of the genes leads to transcriptional silencing. Examples include the p16(INK4a), p15(INK4B), p14(ARF), Von Hippel-Lindau (VHL), the oestrogen and progesterone receptors, E-cadherin, death associated protein (DAP) kinase and the first tumour suppressor gene described, retinoblastoma (Rb) gene. In most cases, methylation involves loss of expression, absence of a coding mutation and restoration of transcription by the use of demethylating agents. However, is there a linkage between genetic and epigenetic alterations? Our results show one side of this puzzle demonstrating that epigenetic lesions drive genetic lesions in cancer. Four specific epigenetic lesions, promoter hypermethylation of the DNA mismatch repair gene hMLH1, theDNA alkyl-repair gene O(6)-methylguanine-DNA methyltransferase (MGMT), thedetoxifier glutathione S-transferase P1 (GSTP1) and the familial breast cancer gene BRCA1 may lead to four specific genetic lesions, microsatellite instability, G to A transitions, steroid-related adducts and double-strand breaks in DNA. This is probably only the beginning of an extensive list of epigenetic events that change and make the genetic environment of the transformed cell unstable. (C) 2000 Elsevier Science Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 12/07/20 alle ore 09:39:18