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Titolo:
SV40 and cell cycle perturbations in malignant mesothelioma
Autore:
Testa, JR; Giordano, A;
Indirizzi:
Fox Chase Canc Ctr, Human Genet Program, Philadelphia, PA 19111 USA Fox Chase Canc Ctr Philadelphia PA USA 19111 , Philadelphia, PA 19111 USA Thomas Jefferson Univ, Jefferson Med Coll, Dept Pathol Anat & Cell Biol, Philadelphia, PA 19107 USA Thomas Jefferson Univ Philadelphia PA USA 19107 hiladelphia, PA 19107 USA
Titolo Testata:
SEMINARS IN CANCER BIOLOGY
fascicolo: 1, volume: 11, anno: 2001,
pagine: 31 - 38
SICI:
1044-579X(200102)11:1<31:SACCPI>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
LARGE-T-ANTIGEN; LARGE TUMOR-ANTIGEN; RETINOBLASTOMA SUSCEPTIBILITY GENE; HUMAN PLEURAL MESOTHELIOMA; 40-LIKE DNA-SEQUENCES; PRB2/P130 INTERACTION; SUPPRESSOR P53; LUNG-CANCER; SIMIAN-VIRUS-40; FAMILY;
Keywords:
SV40; cell cycle deregulation; tumor suppressor gene products pRb, p53, p14(ARF), p16(INK4a);
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
65
Recensione:
Indirizzi per estratti:
Indirizzo: Testa, JR Fox Chase Canc Ctr, Human Genet Program, 7701 Burholme Ave, Philadelphia, PA 19111 USA Fox Chase Canc Ctr 7701 Burholme Ave Philadelphia PAUSA 19111 A
Citazione:
J.R. Testa e A. Giordano, "SV40 and cell cycle perturbations in malignant mesothelioma", SEM CANC B, 11(1), 2001, pp. 31-38

Abstract

Although epidemiological findings have established that exposure to asbestos fibers is the major cause of malignant mesothelioma (MM) recent studies have implicated simian virus 40 (SV40) in the etiology of some of these tumors. Cytogenetic and molecular genetic evidence suggests that multiple somatic genetic events are required for tumorigenic conversion of a mesothelialcell. As with many other types of cancer; in MM critical oncogenic events exert their action via perturbations of the cell cycle. Interactions between the retinoblastoma (Rb)family of proteins and oncoproteins encoded by SV40 lead to cell cycle alterations. Likewise, inhibition of the p53 tumor suppressor by SV40 can inactivate a crucial cell cycle checkpoint, thereby permitting cells to undergo mitosis regardless of the presence of DNA damage. Many MMs exhibit loss and/or inactivation of the tumor suppressors p16(INK4a) and p14(ARF), components of the pRb and p53 cell cycle regulatory pathways, respectively. Recent investigations have demonstrated that SV40 large Tantigen, isolated from frozen biopsies of human MM specimens, binds to andinactivates various tumor suppressor gene products such as pRb and p53. Inthis review we discuss how SV40-oncosuppressor interactions can lead to functional alterations of the pRb- and p53-dependent cell cycle regulatory pathways and thereby contribute to neoplastic transformation of human mesothelial cells.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 11:56:39