Multivariate analysis of immunohistochemical evaluation of protein expression in pancreatic ductal adenocarcinoma reveals prognostic significance for persistent Smad4 expression only

[1]  M. Marinus,et al.  DNA Mismatch Repair , 2012, EcoSal Plus.

[2]  A. Benson,et al.  The influence of total nodes examined, number of positive nodes, and lymph node ratio on survival after surgical resection and adjuvant chemoradiation for pancreatic cancer: a secondary analysis of RTOG 9704. , 2011, International journal of radiation oncology, biology, physics.

[3]  Douglas B. Evans,et al.  Overexpression of receptor tyrosine kinase Axl promotes tumor cell invasion and survival in pancreatic ductal adenocarcinoma , 2011, Cancer.

[4]  C. Iacobuzio-Donahue,et al.  Prognostic significance of tumorigenic cells with mesenchymal features in pancreatic adenocarcinoma. , 2010, Journal of the National Cancer Institute.

[5]  J. Cameron,et al.  Adjuvant Chemoradiation for Pancreatic Adenocarcinoma: The Johns Hopkins Hospital—Mayo Clinic Collaborative Study , 2010, Annals of Surgical Oncology.

[6]  D. Semeraro,et al.  Lymph Node Ratio Versus Number of Affected Lymph Nodes as Predictors of Survival for Resected Pancreatic Adenocarcinoma , 2010, World Journal of Surgery.

[7]  C. Bassi,et al.  Resectable Pancreatic Cancer: Who Really Benefits From Resection? , 2009, Annals of Surgical Oncology.

[8]  Giovanni Parmigiani,et al.  SMAD4 Gene Mutations Are Associated with Poor Prognosis in Pancreatic Cancer , 2009, Clinical Cancer Research.

[9]  A. Jemal,et al.  Cancer Statistics, 2009 , 2009, CA: a cancer journal for clinicians.

[10]  C. Lepage,et al.  Management and prognosis of pancreatic cancer over a 30-year period , 2009, British Journal of Cancer.

[11]  T. Keck,et al.  The Lymph Node Ratio is the Strongest Prognostic Factor after Resection of Pancreatic Cancer , 2009, Journal of Gastrointestinal Surgery.

[12]  G. Feldmann,et al.  The Axl receptor tyrosine kinase confers an adverse prognostic influence in pancreatic cancer and represents a new therapeutic target , 2009, Cancer biology & therapy.

[13]  Sunil Krishnan,et al.  Long-Term Survival After Multidisciplinary Management of Resected Pancreatic Adenocarcinoma , 2009, Annals of Surgical Oncology.

[14]  Laura H. Tang,et al.  Pancreatic Adenocarcinoma: The Actual 5-Year Survivors , 2008, Journal of Gastrointestinal Surgery.

[15]  J. Donohue,et al.  Long-Term Survival After Pancreatoduodenectomy for Pancreatic Adenocarcinoma: Is Cure Possible? , 2008, Annals of surgery.

[16]  M. Choti,et al.  Prognostic relevance of lymph node ratio following pancreaticoduodenectomy for pancreatic cancer. , 2007, Surgery.

[17]  G. Offerhaus,et al.  Early onset gastric cancer: on the road to unraveling gastric carcinogenesis. , 2007, Current molecular medicine.

[18]  H. Friess,et al.  Molecular characterisation of pancreatic ductal adenocarcinoma in patients under 40 , 2006, Journal of Clinical Pathology.

[19]  T. Kunkel,et al.  DNA mismatch repair. , 2005, Annual review of biochemistry.

[20]  S. Thibodeau,et al.  Defective DNA Mismatch Repair in Long-Term (≥3 Years) Survivors with Pancreatic Cancer , 2005, Pancreatology.

[21]  R. Schmid,et al.  Pancreatic cancer: basic and clinical aspects. , 2005, Gastroenterology.

[22]  J. Cameron,et al.  Multicomponent Analysis of the Pancreatic Adenocarcinoma Progression Model Using a Pancreatic Intraepithelial Neoplasia Tissue Microarray , 2003, Modern Pathology.

[23]  M. Yashiro,et al.  Prognostic value of microsatellite instability in resectable pancreatic cancer. , 2002, Clinical cancer research : an official journal of the American Association for Cancer Research.

[24]  C. Rosty,et al.  Molecular pathogenesis of pancreatic cancer. , 2002, Hematology/oncology clinics of North America.

[25]  A. Lindblom,et al.  © 1999 Cancer Research Campaign Article no. bjoc.1998.0314 Microsatellite instability and mismatch repair gene inactivation in sporadic pancreatic and colon tumours , 2022 .

[26]  R. Hruban,et al.  Pancreatic adenocarcinomas with DNA replication errors (RER+) are associated with wild-type K-ras and characteristic histopathology. Poor differentiation, a syncytial growth pattern, and pushing borders suggest RER+. , 1998, The American journal of pathology.

[27]  Scott E. Kern,et al.  DPC4, A Candidate Tumor Suppressor Gene at Human Chromosome 18q21.1 , 1996, Science.

[28]  L. Tanoue.  Cancer Statistics, 2009 , 2010 .

[29]  T. Takada,et al.  Influence of resection margins and treatment on survival in patients with pancreatic cancer: meta-analysis of randomized controlled trials. , 2008, Archives of surgery.

[30]  A. Sparks,et al.  Immunohistochemical labeling for Dpc4 mirrors genetic status in pancreatic adenocarcinomas: A new marker of DPC4 inactivation , 2000 .

[31]  S. Rivkees.  Basic and Clinical Aspects , 1997 .

[32]  Ryan J. Huxtable,et al.  Basic and clinical aspects , 1996 .