title: Correlation of AIB1 overexpression with advanced clinical stage of human colorectal carcinoma.
abstract: AIB1, a member of the steroid receptor coactivator 1 family, has been cloned on 20q12 and is a candidate oncogene in human breast cancer. It is commonly amplified and overexpressed in several types of human cancers. In this study, we examined the expression of AIB1, as related to clinicopathologic features, in 85 human colorectal cancers (CRCs). The status of the number of AIB1 copies, p53 expression, and DNA ploidy was also analyzed. The overexpression of AIB1 was detected in 35% of CRCs. Amplification of AIB1 was observed in 10% of CRCs. In addition, the overexpression of AIB1 was observed more frequently in CRCs in later clinical stages (T3 N1 M0/T3 N0 2M1), compared with that in T3 N0 M0 stage (P < .05). These results suggest that overexpression of AIB1 might provide a selective advantage for the developmental growth and/or progression of subsets of CRCs. In addition, a significant correlation (P < .05) of overexpression of AIB1 with p53 overexpression as well as with aneuploid DNA content was observed in these CRCs. The overexpression of p53 was also correlated significantly with CRC DNA ploidy (P < .05). Furthermore, there was a substantial population of CRCs showing overexpression of both AIB1 and p53 protein and all had aneuploid DNA content; most of these were in the later clinical stage. These findings suggest a possible convergence of AIB1 with a pathway involving p53, which might induce chromosomal instability and affect the clinical phenotype of a subset of CRCs.
authors.affiliation: Cancer Center, Sun Yat-Sen University, Guangzhou 510275, China.
authors.forename: Dan
authors.initials: D
authors.lastname: Xie
authors.forename: Jonathan S T
authors.initials: JS
authors.lastname: Sham
authors.forename: Wei-Fen
authors.initials: WF
authors.lastname: Zeng
authors.forename: Han-Liang
authors.initials: HL
authors.lastname: Lin
authors.forename: Jiong
authors.initials: J
authors.lastname: Bi
authors.forename: Li-Hong
authors.initials: LH
authors.lastname: Che
authors.forename: Liang
authors.initials: L
authors.lastname: Hu
authors.forename: Yi-Xin
authors.initials: YX
authors.lastname: Zeng
authors.forename: Xin-Yuan
authors.initials: XY
authors.lastname: Guan
mesh_terms: D000123:Acetyltransferases / Q000378:metabolism*; D000230:Adenocarcinoma / Q000235:genetics / Q000378:metabolism* / Q000556:secondary; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000782:Aneuploidy; D002467:Cell Nucleus / Q000378:metabolism / Q000473:pathology; D015179:Colorectal Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D004273:DNA, Neoplasm / Q000032:analysis; D005260:Female; D005434:Flow Cytometry; D005784:Gene Amplification; D051548:Histone Acetyltransferases; D006801:Humans; D007124:Immunoenzyme Techniques; D017404:In Situ Hybridization, Fluorescence; D008198:Lymph Nodes / Q000378:metabolism / Q000473:pathology; D008207:Lymphatic Metastasis / Q000473:pathology; D008297:Male; D008875:Middle Aged; D056921:Nuclear Receptor Coactivator 3; D015513:Oncogene Proteins / Q000378:metabolism*; D040081:Protein Array Analysis; D015534:Trans-Activators / Q000378:metabolism*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: D004273:DNA, Neoplasm; D015513:Oncogene Proteins; D015534:Trans-Activators; D016159:Tumor Suppressor Protein p53; D000123:Acetyltransferases; D051548:Histone Acetyltransferases; C538866:NCOA3 protein, human; D056921:Nuclear Receptor Coactivator 3