A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns

Author:

Notta Faiyaz,Chan-Seng-Yue Michelle,Lemire Mathieu,Li Yilong,Wilson Gavin W.,Connor Ashton A.,Denroche Robert E.,Liang Sheng-Ben,Brown Andrew M. K.,Kim Jaeseung C.,Wang Tao,Simpson Jared T.,Beck Timothy,Borgida Ayelet,Buchner Nicholas,Chadwick Dianne,Hafezi-Bakhtiari Sara,Dick John E.,Heisler Lawrence,Hollingsworth Michael A.,Ibrahimov Emin,Jang Gun Ho,Johns Jeremy,Jorgensen Lars G. T.,Law Calvin,Ludkovski Olga,Lungu Ilinca,Ng Karen,Pasternack Danielle,Petersen Gloria M.,Shlush Liran I.,Timms Lee,Tsao Ming-Sound,Wilson Julie M.,Yung Christina K.,Zogopoulos George,Bartlett John M. S.,Alexandrov Ludmil B.,Real Francisco X.,Cleary Sean P.,Roehrl Michael H.,McPherson John D.,Stein Lincoln D.,Hudson Thomas J.,Campbell Peter J.,Gallinger Steven

Publisher

Springer Science and Business Media LLC

Subject

Multidisciplinary

Reference30 articles.

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2. Moskaluk, C. A., Hruban, R. H. & Kern, S. E. p16 and K-RAS gene mutations in the intraductal precursors of human pancreatic adenocarcinoma. Cancer Res. 57, 2140–2143 (1997)

3. Wilentz, R. E. et al. Inactivation of the p16 (INK4A) tumor-suppressor gene in pancreatic duct lesions: loss of intranuclear expression. Cancer Res. 58, 4740–4744 (1998)

4. Wilentz, R. E. et al. Loss of expression of Dpc4 in pancreatic intraepithelial neoplasia: evidence that DPC4 inactivation occurs late in neoplastic progression. Cancer Res. 60, 2002–2006 (2000)

5. Lüttges, J. et al. Allelic loss is often the first hit in the biallelic inactivation of the p53 and DPC4 genes during pancreatic carcinogenesis. Am. J. Pathol. 158, 1677–1683 (2001)

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