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Titolo:
Reduced COX-2 protein in colorectal cancer with defective mismatch repair
Autore:
Karnes, WE; Shattuck-Brandt, R; Burgart, LJ; DuBois, RN; Tester, DJ; Cunningham, JM; Kim, CY; McDonnell, SK; Schaid, DJ; Thibodeau, SN;
Indirizzi:
Mayo Clin & Mayo Fdn, Dept Lab Med & Pathol, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn Rochester MN USA 55905 thol, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn, Dept Internal Med, Rochester, MN 55905 USA Mayo Clin& Mayo Fdn Rochester MN USA 55905 Med, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn, Dept Hlth Sci Res, Rochester, MN 55905 USA Mayo Clin& Mayo Fdn Rochester MN USA 55905 Res, Rochester, MN 55905 USA Vanderbilte,niv, Sch Med, Div Gastroenterol, Dept Cell Biol & Med, Nashvill Vanderbilt Univ Nashville TN USA 37232 ol, Dept Cell Biol & Med, Nashvill
Titolo Testata:
CANCER RESEARCH
fascicolo: 23, volume: 58, anno: 1998,
pagine: 5473 - 5477
SICI:
0008-5472(199812)58:23<5473:RCPICC>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROSTAGLANDIN-ENDOPEROXIDE SYNTHASE-2; NONSTEROIDAL ANTIINFLAMMATORY DRUGS; FAMILIAL ADENOMATOUS POLYPOSIS; INTESTINAL EPITHELIAL-CELLS; HUMAN COLON-CANCER; MICROSATELLITE INSTABILITY; FACTOR-BETA; TRANSCRIPTIONAL REGULATION; CYCLOOXYGENASE-2 LEVELS; ASPIRIN USE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
57
Recensione:
Indirizzi per estratti:
Indirizzo: Thibodeau, SN Mayo5905n & Mayo Fdn, Dept Lab Med & Pathol, 200 1st St SW, Rochester, MN 5 Mayo Clin & Mayo Fdn 200 1st St SW Rochester MN USA 55905 5
Citazione:
W.E. Karnes et al., "Reduced COX-2 protein in colorectal cancer with defective mismatch repair", CANCER RES, 58(23), 1998, pp. 5473-5477

Abstract

Most colorectal adenomas and carcinomas arise in the setting of chromosomal instability characterized by progressive loss of heterozygosity, In contrast, approximately 15-20% of colorectal neoplasms arise through a distinct genetic pathway characterized by microsatellite instability (MSI) associated with frequent loss of expression of one of the DNA mismatch repair enzymes, most often hMLH1 or hMSH2. These distinct genetic pathways are reflectedby differences in tumor histopathology, distribution in the colon, prognosis, and dwell time required for progression from adenoma to carcinoma. To determine whether these two groups of tumors differ in their expression of cyclooxygenase-2 (COX-2), a putative chemopreventative target, immunostaining for this protein was performed in colorectal cancers categorized by the presence (n = 41) and absence (n = 66) of defective mismatch repair. Defective mismatch repair was defined by the presence of tumor microsatellite instability (MSI-H, greater than or equal to 40% of markers demonstrating instability) and by the absence of protein expression for either hMLH1 or hMSH2. Overall, our results showed that low or absent COX-2 staining was significantly more common among tumors with defective mismatch repair (P = 0.001), Other features predictive of Low COX-2 staining included marked tumor infiltrating lymphocytosis, and solid/cribiform or signet ring histological patterns. These observations indicate that colorectal cancers with molecular and phenotypic characteristics of defective DNA mismatch repair express Lowerlevels of COX-2, The clinical implications of this biological distinction remain unknown but should be considered when assessing the efficacy of COX-2 inhibitors for chemoprevention in patients whose tumors may arise in the setting of defective DNA mismatch repair.

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Documento generato il 30/10/20 alle ore 09:46:03