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Titolo:
The role of tumor suppressor gene therapy for anticancer treatment
Autore:
Putzer, BM;
Indirizzi:
Univ Essen Gesamthsch Klinikum, Inst Mol Biol Tumorforsch, IMB, D-45122 Essen, Germany Univ Essen Gesamthsch Klinikum Essen Germany D-45122 5122 Essen, Germany
Titolo Testata:
TUMORDIAGNOSTIK & THERAPIE
fascicolo: 1, volume: 21, anno: 2000,
pagine: 1 - 7
SICI:
0722-219X(200002)21:1<1:TROTSG>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
ADENOVIRUS-MEDIATED TRANSFER; CYCLIN-DEPENDENT KINASES; SQUAMOUS-CELL CARCINOMA; HUMAN GLIOMA-CELLS; P53 GENE; IN-VIVO; LUNG-CANCER; RECOMBINANT ADENOVIRUS; RETINOBLASTOMA PROTEIN; COMBINATION THERAPY;
Keywords:
tumor suppressor genes; neoplasia; gene therapy; adenovirus vectors;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
72
Recensione:
Indirizzi per estratti:
Indirizzo: Putzer, BM Univ Essen Gesamthsch Klinikum, Inst Mol Biol Tumorforsch, IMB,Hufelandstr 55, D-45122 Essen, Germany Univ Essen Gesamthsch Klinikum Hufelandstr 55 Essen Germany D-45122
Citazione:
B.M. Putzer, "The role of tumor suppressor gene therapy for anticancer treatment", TUMORDIAGN, 21(1), 2000, pp. 1-7

Abstract

Gene therapy using wild-type tumor suppressor genes which are frequently mutated in human cancers has the potential to provide cancer treatment basedon cell growth retardation and induction of apoptosis in cancer cells. Over the past few years, significant insight has been gained regarding the functions of tumor suppressors and how they participate in the complex biochemical pathways governing the negative regulation of cell growth and tumor development. Tumor cells have typically acquired damage to genes that directly regulate their cell cycle. Mutations within the RB-pathway (D-cyclins/CDKs/CDKIs/RB/E2F) are the most frequent abnormalities identified in human cancers. Beside inactivation of the tumor suppressor protein p53, alterations in the RE-pathway frequently affect the retinoblastoma protein (RB) and thecyclin-dependent kinase inhibitors (CDKIs) p16(INK4a) and p21(WAF1). Thesealterations are responsible for the enhanced proliferative capacity and resistance of the cells to commonly used therapies such as radio- and chemotherapy. Although all cancers contain multiple abnormalities apart from the RB-pathway controlling various aspects of cellular proliferation, correctionof a single specific molecular alteration by reintroduction of wild-type tumor suppressor function, in some cases is sufficient to induce tumor cell death by apoptosis. However, it is beyond the capabilities of currently available methods for in vivo gene transfer to restore normal gene function inevery cancer cell. Therefore, mechanisms by which a toxic transgene expressed in transduced cells can alter growth of non-transduced cells, by a so called bystander effect is essentially important for successful gene replacement strategies. This review summarizes current preclinical and clinical efforts on gene replacement approaches with adenoviral gene delivery systems,discusses limitations of therapy and highlights the prospects for future clinical investigations.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/08/20 alle ore 22:32:34