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Titolo:
Cyclin D1 and p16 alterations in advanced premalignant lesions of the upper aerodigestive tract: Role in response to chemoprevention and cancer development
Autore:
Papadimitrakopoulou, VA; Izzo, J; Mao, L; Keck, J; Hamilton, D; Shin, DM; El-Naggar, A; den Hollander, P; Liu, D; Hittelman, WN; Hong, WK;
Indirizzi:
Univ Texas, MD Anderson Canc Ctr, Dept Thorac Head & Neck Med Oncol, Houston, TX 77030 USA Univ Texas Houston TX USA 77030 d & Neck Med Oncol, Houston, TX 77030 USA Univ Texas, MD Anderson Canc Ctr, Dept Expt Therapeut, Houston, TX 77030 USA Univ Texas Houston TX USA 77030 ept Expt Therapeut, Houston, TX 77030 USA Univ Texas, MD Anderson Canc Ctr, Dept Pathol, Houston, TX 77030 USA Univ Texas Houston TX USA 77030 c Ctr, Dept Pathol, Houston, TX 77030 USA Univ Texas, MD Anderson Canc Ctr, Dept Biostat, Houston, TX 77030 USA UnivTexas Houston TX USA 77030 Ctr, Dept Biostat, Houston, TX 77030 USA
Titolo Testata:
CLINICAL CANCER RESEARCH
fascicolo: 10, volume: 7, anno: 2001,
pagine: 3127 - 3134
SICI:
1078-0432(200110)7:10<3127:CDAPAI>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
SQUAMOUS-CELL CARCINOMA; BRONCHIAL EPITHELIAL-CELLS; PRIMARY TUMORS; RETINOIC ACID; PROTEIN EXPRESSION; GENE AMPLIFICATION; ORAL LEUKOPLAKIA; PROGNOSTIC VALUE; NECK-CANCER; EARLY EVENT;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Papadimitrakopoulou, VA Univ Texas, MD Anderson Canc Ctr, Dept Thorac Head& Neck Med Oncol, 1500 Holcombe Blvd,Box 432, Houston, TX 77030 USA Univ Texas 1500 Holcombe Blvd,Box 432 Houston TX USA 77030
Citazione:
V.A. Papadimitrakopoulou et al., "Cyclin D1 and p16 alterations in advanced premalignant lesions of the upper aerodigestive tract: Role in response to chemoprevention and cancer development", CLIN CANC R, 7(10), 2001, pp. 3127-3134

Abstract

Purpose: To better understand the role of G(1)-S transition regulator abnormalities in the pathogenesis of advanced premalignant lesions of the upperaerodigestive tract and the biological effects of chemoprevention, we studied biopsies obtained sequentially from participants in a prospective trialusing 13-cis retinoic acid, IFN-alpha, and alpha -tocopherol for 12 months. Experimental design: Cyclin DI and p16 expression were analyzed by immunohistochemistry, loss of heterozygosity by polymerse chain reacting amplification, and then electrophoretic separation of the products, methylation of the p16 promoter by methylation-specific polymerase chain reacting, and cyclin DI gene amplification by fluorescence in situ hybridization. Results: Baseline dysregulation of cyclin DI expression was found in 50% (14 of 28) and was reversed in 6 of 14 cases, whereas p 16 expression was lost in 46 % (13 of 28) and regained in 2 of 13 cases. Loss of heterozygosityat 9p21 occurred in 68% and p16(INK4a), promoter methylation occurred in 75% of cases, with increasing frequency from mild to severe dysplasia. Cyclin DI gene amplification was identified in two cases. Cyclin DI protein dysregulation at last follow-up alone and in combination with p16 loss was associated with histological progression and cancer development (P < 0.01). Conclusions: Additional study of these alterations in a larger sample and exploration of the upstream signaling partners of these cell cycle regulators in vivo is warranted to identify cancer risk profiles that would be meaningful targets for chemopreventive intervention.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 09:44:08