KRAS, TP53, CDKN2A, SMAD4, BRCA1, and BRCA2 Mutations in Pancreatic Cancer
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Title
KRAS, TP53, CDKN2A, SMAD4, BRCA1, and BRCA2 Mutations in Pancreatic Cancer
Authors
Keywords
-
Journal
Cancers
Volume 9, Issue 12, Pages 42
Publisher
MDPI AG
Online
2017-04-28
DOI
10.3390/cancers9050042
References
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Related references
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- BRCA1 and BRCA2 mutations sensitize to chemotherapy in patient-derived pancreatic cancer xenografts
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- (2014) Steffen Ormanns et al. BMC CANCER
- Projecting Cancer Incidence and Deaths to 2030: The Unexpected Burden of Thyroid, Liver, and Pancreas Cancers in the United States
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- Identification of common variants in BRCA2 and MAP2K4 for susceptibility to sporadic pancreatic cancer
- (2013) L. Huang et al. CARCINOGENESIS
- KRAS mutation status is not predictive for objective response to anti-EGFR treatment with erlotinib in patients with advanced pancreatic cancer
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- SMAD4 Genetic Alterations Predict a Worse Prognosis in Patients With Pancreatic Ductal Adenocarcinoma
- (2012) Puneet Singh et al. PANCREAS
- The Predictive Role of p16 Deletion, p53 Deletion, and Polysomy 9 and 17 in Pancreatic Ductal Adenocarcinoma
- (2012) Yanli Luo et al. PATHOLOGY & ONCOLOGY RESEARCH
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- Impact of KRAS Mutations on Clinical Outcomes in Pancreatic Cancer Patients Treated with First-line Gemcitabine-Based Chemotherapy
- (2011) S. T. Kim et al. MOLECULAR CANCER THERAPEUTICS
- Elevated Transcript Levels From the MDM2 P1 Promoter and Low p53 Transcript Levels Are Associated With Poor Prognosis in Human Pancreatic Ductal Adenocarcinoma
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- Polymorphisms of p16, p27, p73, and MDM2 Modulate Response and Survival of Pancreatic Cancer Patients Treated with Preoperative Chemoradiation
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