Antioncogene p53 e risposta apoptotica: Nuove ipotesi sulle basi molecolari della resistenza dei tumori alla radioterapia

Translated title of the contribution: The antioncogene p53 and radiation induced apoptosis: Recent hypotheses on the molecular bases of radioresistance

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Recent experimental data indicate that in normal or neoplastic cells, DNA damage induced by ionizing radiation may work as a signal to trigger apoptosis. a characteristic suicide program inherent to multicellular organisms. The morphological signatures of apoptosis are cell shrinkage, nuclear condensation and genomic fragmentation down to the size of individual nucleosome units (apoptotic bodies). A number of genes have been identified as involved regulators of apoptosis. The tumor suppressor gene p53 has emerged as a main modulator and inducer of apoptosis. Cells containing wild-type p53 function undergo G1 arrest following DNA damage by ionizing radiations. DNA repair processes are, then, activated before the damaged genome can be replicated, with resultant genetic instability. If DNA repair fails, the wild p53 gene may trigger apoptosis and the cell with persisting DNA damage, dies. Cells with loss of functional p53 gene by either gene mutation or deletion appear unable to undergo radiation-induced apoptosis. This evidence may underlie the increased likelihood for p53 deficient cells to develop oncogenetic processes after irradiation exposure. According to p53-triggering apoptosis patterns, cancer cells with a normal p53 gene might be more sensitive to radiotherapy and less proliferating than tumor cells with p53 deficient function. If these data are confirmed, tumors harboring p53 gene mutation might be managed best with particularly aggressive or experimental treatment protocols Conversely, a higher therapeutic index between malignant and normal cells might be obtained in tumors with fast activation of p53 dependent apoptotic response. Before any definitive conclusions are drawn, further knowledge of the different genes which are known to be involved in the regulation of apoptosis, is warranted.

Original languageItalian
Pages (from-to)298-302
Number of pages5
JournalRadiologia Medica
Volume92
Issue number3
Publication statusPublished - Sep 1996

Fingerprint

Tumor Suppressor Genes
Radiation
Apoptosis
p53 Genes
DNA Damage
Ionizing Radiation
DNA Repair
Neoplasms
Genes
Nucleosomes
Sequence Deletion
Clinical Protocols
Suicide
Radiotherapy
Genome
Mutation

ASJC Scopus subject areas

  • Radiology Nuclear Medicine and imaging

Cite this

@article{6557f50ee015494f98bc4d778c2b9c1c,
title = "Antioncogene p53 e risposta apoptotica: Nuove ipotesi sulle basi molecolari della resistenza dei tumori alla radioterapia",
abstract = "Recent experimental data indicate that in normal or neoplastic cells, DNA damage induced by ionizing radiation may work as a signal to trigger apoptosis. a characteristic suicide program inherent to multicellular organisms. The morphological signatures of apoptosis are cell shrinkage, nuclear condensation and genomic fragmentation down to the size of individual nucleosome units (apoptotic bodies). A number of genes have been identified as involved regulators of apoptosis. The tumor suppressor gene p53 has emerged as a main modulator and inducer of apoptosis. Cells containing wild-type p53 function undergo G1 arrest following DNA damage by ionizing radiations. DNA repair processes are, then, activated before the damaged genome can be replicated, with resultant genetic instability. If DNA repair fails, the wild p53 gene may trigger apoptosis and the cell with persisting DNA damage, dies. Cells with loss of functional p53 gene by either gene mutation or deletion appear unable to undergo radiation-induced apoptosis. This evidence may underlie the increased likelihood for p53 deficient cells to develop oncogenetic processes after irradiation exposure. According to p53-triggering apoptosis patterns, cancer cells with a normal p53 gene might be more sensitive to radiotherapy and less proliferating than tumor cells with p53 deficient function. If these data are confirmed, tumors harboring p53 gene mutation might be managed best with particularly aggressive or experimental treatment protocols Conversely, a higher therapeutic index between malignant and normal cells might be obtained in tumors with fast activation of p53 dependent apoptotic response. Before any definitive conclusions are drawn, further knowledge of the different genes which are known to be involved in the regulation of apoptosis, is warranted.",
keywords = "Apoptosis, Radiotherapy, Tumor suppressor gene p53",
author = "Renzo Corv{\`o}",
year = "1996",
month = "9",
language = "Italian",
volume = "92",
pages = "298--302",
journal = "Radiologia Medica",
issn = "0033-8362",
publisher = "Springer-Verlag Italia s.r.l.",
number = "3",

}

TY - JOUR

T1 - Antioncogene p53 e risposta apoptotica

T2 - Nuove ipotesi sulle basi molecolari della resistenza dei tumori alla radioterapia

AU - Corvò, Renzo

PY - 1996/9

Y1 - 1996/9

N2 - Recent experimental data indicate that in normal or neoplastic cells, DNA damage induced by ionizing radiation may work as a signal to trigger apoptosis. a characteristic suicide program inherent to multicellular organisms. The morphological signatures of apoptosis are cell shrinkage, nuclear condensation and genomic fragmentation down to the size of individual nucleosome units (apoptotic bodies). A number of genes have been identified as involved regulators of apoptosis. The tumor suppressor gene p53 has emerged as a main modulator and inducer of apoptosis. Cells containing wild-type p53 function undergo G1 arrest following DNA damage by ionizing radiations. DNA repair processes are, then, activated before the damaged genome can be replicated, with resultant genetic instability. If DNA repair fails, the wild p53 gene may trigger apoptosis and the cell with persisting DNA damage, dies. Cells with loss of functional p53 gene by either gene mutation or deletion appear unable to undergo radiation-induced apoptosis. This evidence may underlie the increased likelihood for p53 deficient cells to develop oncogenetic processes after irradiation exposure. According to p53-triggering apoptosis patterns, cancer cells with a normal p53 gene might be more sensitive to radiotherapy and less proliferating than tumor cells with p53 deficient function. If these data are confirmed, tumors harboring p53 gene mutation might be managed best with particularly aggressive or experimental treatment protocols Conversely, a higher therapeutic index between malignant and normal cells might be obtained in tumors with fast activation of p53 dependent apoptotic response. Before any definitive conclusions are drawn, further knowledge of the different genes which are known to be involved in the regulation of apoptosis, is warranted.

AB - Recent experimental data indicate that in normal or neoplastic cells, DNA damage induced by ionizing radiation may work as a signal to trigger apoptosis. a characteristic suicide program inherent to multicellular organisms. The morphological signatures of apoptosis are cell shrinkage, nuclear condensation and genomic fragmentation down to the size of individual nucleosome units (apoptotic bodies). A number of genes have been identified as involved regulators of apoptosis. The tumor suppressor gene p53 has emerged as a main modulator and inducer of apoptosis. Cells containing wild-type p53 function undergo G1 arrest following DNA damage by ionizing radiations. DNA repair processes are, then, activated before the damaged genome can be replicated, with resultant genetic instability. If DNA repair fails, the wild p53 gene may trigger apoptosis and the cell with persisting DNA damage, dies. Cells with loss of functional p53 gene by either gene mutation or deletion appear unable to undergo radiation-induced apoptosis. This evidence may underlie the increased likelihood for p53 deficient cells to develop oncogenetic processes after irradiation exposure. According to p53-triggering apoptosis patterns, cancer cells with a normal p53 gene might be more sensitive to radiotherapy and less proliferating than tumor cells with p53 deficient function. If these data are confirmed, tumors harboring p53 gene mutation might be managed best with particularly aggressive or experimental treatment protocols Conversely, a higher therapeutic index between malignant and normal cells might be obtained in tumors with fast activation of p53 dependent apoptotic response. Before any definitive conclusions are drawn, further knowledge of the different genes which are known to be involved in the regulation of apoptosis, is warranted.

KW - Apoptosis

KW - Radiotherapy

KW - Tumor suppressor gene p53

UR - http://www.scopus.com/inward/record.url?scp=0030237484&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030237484&partnerID=8YFLogxK

M3 - Articolo

C2 - 8975319

AN - SCOPUS:0030237484

VL - 92

SP - 298

EP - 302

JO - Radiologia Medica

JF - Radiologia Medica

SN - 0033-8362

IS - 3

ER -