Gene amplification in esophageal adenocarcinomas and Barrett's with high-grade dysplasia.
作者： Mark D. Iannettoni , Mark B. Orringer , Matthew Schipper , Lin Lin , Charles T. Miller
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摘要: Purpose: The purpose of this study was to determine the frequency and overall contribution specific gene amplification events in formation Barrett’s adenocarcinomas. relationship clinical-pathological variables its potential usefulness as a marker for early cancer detection were also examined. Experimental Design: We used quantitative PCR Southern blot analysis screen 87 cases adenocarcinoma presence or absence 13 distinct events. Gene then examined correlation with other clinical (survival, stage, nodal involvement, tumor invasion, smoking history, gender). Additionally, 22 specimens high-grade dysplasia (HGD) amplification. Results: One more present 50 (57%) ERBB2 amplified 19 (21.8%), CCNE1 11 (12.6%), GATA4 9 (10.3%), KRAS EGFR 7 (8.0%), CCND1 6 (6.8%), HNF3 α 5 (5.7%), PIK 3 CA C-MYC 4 (4.6%), DYRK2 2 (2.3%), AIB1 , AKT1 IGF1R 0 (0%) tumors. found correlate negatively survival ( P amplicon positively correlated Increased copy number (1 22), GATA (2 CCNE 1 CCND 22) genes observed one adenocarcinomas HGD. Conclusions: high esophageal HGD indicates important role these development. results underscore possible approaches chemotherapeutic strategies (ErbB2 cyclin D1) targeted against products.
aacrjournals.org参考文章(43)
Barbara J. McKenna, Henry D. Appelman, Dysplasia of the gut: the diagnosis is harder than it seems. Journal of Clinical Gastroenterology. ,vol. 34, pp. 111- 116 ,(2002) , 10.1097/00004836-200202000-00002
Stuart Jon Spechler, Raj K. Goyal, Barrett's esophagus : pathophysiology, diagnosis, and management Elsevier. ,(1985)
R.H. Hardwick, D. Alderson, R.J. Morgan, P.V. Newcomb, Amplification of cyclin D1 and MDM-2 in oesophageal carcinoma Ejso. ,vol. 25, pp. 364- 367 ,(1999) , 10.1053/EJSO.1999.0658
Mark B. Orringer, Susan L. Dagenais, Lin Lin, Charles T. Miller, David G. Beer, Thomas W. Glover, Sanjeev Aggarwal, Theodore K. Lin, Jorge I. Contreras, Amplification and Overexpression of the Dual-Specificity Tyrosine-(Y)-Phosphorylation Regulated Kinase 2 (DYRK2) Gene in Esophageal and Lung Adenocarcinomas Cancer Research. ,vol. 63, pp. 4136- 4143 ,(2003)
Mark B. Orringer, Samir M. Hanash, Rork D. Kuick, Michael S. Prescott, Sang Y. Chun, Puja Singh, Lin Lin, David G. Beer, Thomas W. Glover, Zhouqin Zhu, Identification and Characterization of a 19q12 Amplicon in Esophageal Adenocarcinomas Reveals Cyclin E as the Best Candidate Gene for this Amplicon Cancer Research. ,vol. 60, pp. 7021- 7027 ,(2000)
Soji Ozawa, Masaki Kitajima, Yuko Kitagawa, Nobuyoshi Shimizu, Nobutoshi Ando, Masakazu Ueda, Further evidence for prognostic significance of epidermal growth factor receptor gene amplification in patients with esophageal squamous cell carcinoma. Clinical Cancer Research. ,vol. 2, pp. 909- 914 ,(1996)
Michael J. Edwards, Dennis R. Gable, Alex B. Lentsch, J. David Richardson, The rationale for esophagectomy as the optimal therapy for Barrett's esophagus with high-grade dysplasia. Annals of Surgery. ,vol. 223, pp. 585- 591 ,(1996) , 10.1097/00000658-199605000-00014
I. Gantz, Y. Konda, Y.-K. Yang, D.E. Miller, H.A. Dierick, T. Yamada, Molecular cloning of a novel receptor (CMKLR1) with homology to the chemotactic factor receptors Cytogenetic and Genome Research. ,vol. 74, pp. 286- 290 ,(1996) , 10.1159/000134436
Axel K Walch, Horst F Zitzelsberger, Jochen Bruch, Gisela Keller, Daniela Angermeier, Michaela M Aubele, James Mueller, Hubert Stein, Herbert Braselmann, Jörg R Siewert, Heinz Höfler, Martin Werner, None, Chromosomal imbalances in Barrett's adenocarcinoma and the metaplasia-dysplasia-carcinoma sequence. American Journal of Pathology. ,vol. 156, pp. 555- 566 ,(2000) , 10.1016/S0002-9440(10)64760-8
Diane L. Persons, Wendy S. Croughan, Kristen A. Borelli, Rachel Cherian, Interphase Cytogenetics of Esophageal Adenocarcinoma and Precursor Lesions Cancer Genetics and Cytogenetics. ,vol. 106, pp. 11- 17 ,(1998) , 10.1016/S0165-4608(98)00036-3