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Titolo:
Genomic instability: potential contributions to tumour and normal tissue response, and second tumours, after radiotherapy
Autore:
Hendry, JH;
Indirizzi:
Christie Hosp NHS Trust, Paterson Inst Canc Res, CRC, Expt Radiat Oncol Grp, Manchester M20 4BX, Lancs, England Christie Hosp NHS Trust Manchester Lancs England M20 4BX , Lancs, England
Titolo Testata:
RADIOTHERAPY AND ONCOLOGY
fascicolo: 2, volume: 59, anno: 2001,
pagine: 117 - 126
SICI:
0167-8140(200105)59:2<117:GIPCTT>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
BREAST-CANCER PATIENTS; NIJMEGEN BREAKAGE SYNDROME; CELL NEVUS SYNDROME; IRRADIATED MAMMALIAN-CELLS; ATAXIA-TELANGIECTASIA GENE; NONPOLYPOSIS COLON-CANCER; DOSE-RATE IRRADIATION; DOUBLE-STRAND BREAKS; LETHAL MUTATIONS; IONIZING-RADIATION;
Keywords:
genomic instability; radiotherapy; tumour response; normal tissue response; carcinogenesis; residual injury;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
120
Recensione:
Indirizzi per estratti:
Indirizzo: Hendry, JH Christie Hosp NHS Trust, Paterson Inst Canc Res, CRC, Expt Radiat Oncol Grp, Manchester M20 4BX, Lancs, England Christie Hosp NHS Trust Manchester Lancs England M20 4BX gland
Citazione:
J.H. Hendry, "Genomic instability: potential contributions to tumour and normal tissue response, and second tumours, after radiotherapy", RADIOTH ONC, 59(2), 2001, pp. 117-126

Abstract

Purpose: Induced genomic instability generally refers to a type of damage which is transmissible down cell generations, and which results in a persistently enhanced frequency of de novo mutations, chromosomal abnormalities or lethality in a significant fraction of the descendant cell population. The potential contribution of induced genomic instability to tumour and normal tissue response, and second tumours, after radiotherapy, is explored. Results: The phenomenon of spontaneous genomic instability is well known in some rare genetic diseases (e.g. Gorlin's syndrome),and there is evidencein such cases that it can lead to a greater propensity for carcinogenesis (with shortened latency) which is enhanced after irradiation. It is unclearwhat role induced genomic instability plays in the response of normal individuals, but persistent chromosomal instability has been detected in vivo in lymphocytes and keratinocytes from irradiated normal individuals. Such induced genomic instability might play some role in tumour response in a subset of tumours with specific defects in damage response genes, but again itscontribution to radiocurability in the majority of cancer patients is unclear. In normal tissues, genomic instability induced in wild-type cells leading to delayed cell death might contribute to more severe or prolonged early reactions as a consequence of increased cell loss, a longer time requiredfor recovery, and greater residual injury. In tumours, induced genomic instability reflected in delayed reductions in clonogenic capacity might contribute to the radiosensitivity of primary tumours, and also to a lower incidence, longer latency and slower growth rate of recurrences and metastases. Conclusions: The evidence which is reviewed shows that there is little information at present to support these propositions, but what exists is consistent with their expectations. Also, it is not yet clear to what extent mutations associated with genomic instability, particularly gene polymorphisms, or other low penetrant gene mutations, contribute to the recognized spectrum of normal tissue radiosensitivity amongst cancer patients, or in the general population. Tests for such genetic modifications may help in the search for more accurate prognostic markers of response, which hopefully could be used in addition to other strategies to further improve the outcome for cancer patients,given radiotherapy. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/09/20 alle ore 07:32:46