ArticleJAMA oncology2018
Association of Alterations in Main Driver Genes With Outcomes of Patients With Resected Pancreatic Ductal Adenocarcinoma.
Article in JAMA oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 160 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
160 citing papers in PubMed, 266 citations in OpenAlex.
- A Phase II Trial of Niraparib in Patients with Advanced Pancreatic Cancer Harboring Pathogenic Variants in ATM, BRCA1, BRCA2, PALB2, and CHEK2.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Trial
- Multicenter randomized controlled trial of neoadjuvant chemoradiotherapy alone or in combination with pembrolizumab in patients with resectable or borderline resectable pancreatic adenocarcinoma.Journal for immunotherapy of cancer · 2023Trial
- Driver mutation profiling by next-generation sequencing predicts survival and recurrence after curative-intent resection for pancreatic ductal adenocarcinoma: a genomic cohort study.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- High SMAD4 Expression is Associated with Improved Clinical Outcomes in Patients with Resectable Pancreatic Cancer: An Analysis of NRG Oncology/RTOG 9704.International journal of radiation oncology, biology, physics · 2026Article
- ARNTL2 promotes metastatic phenotypes through SERPINE1 transcription in KRAS G12D pancreatic cancer.iScience · 2026Article
- Genotype-Informed Whole-Animal Kinome Screening Reveals Shared Kinase Vulnerabilities Across Driver Contexts in PDAC.Cancer science · 2026Article
- Unexpected Long-Term Survival in Resected Pancreatic Ductal Adenocarcinoma Harboring KRAS G12R with an Ultra-Low-VAF SMAD4 Mutation: A Case Report and Mini-Review.Reports (MDPI) · 2026Article
- Local Recurrence After Pancreatic Cancer Resection: A Multidisciplinary Review of Risk Factors and Potential Causes, Diagnostic Innovations, Emerging Therapeutic Frontiers, and Prevention Strategies.Current treatment options in oncology · 2026Review
- The AUTACE That Degrades KRAS and Engages CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Prognostic Significance of Portal Vein Tumor Thrombus in Pancreatic Ductal Adenocarcinoma Treated With Chemoradiotherapy.Annals of gastroenterological surgery · 2026Article
- Inference of upstream-mutation and metabolomic-signature causality identifies prognostic biomarkers and therapeutic targets in pancreatic cancer.Nature communications · 2026Article
- Olverembatinib, a novel BCR-ABL tyrosine kinase inhibitor, exhibits anti-tumor activity and synergizes with gemcitabine in pancreatic ductal adenocarcinoma.NPJ precision oncology · 2026Article
- Crosstalk between KRAS and miRNAs in pancreatic cancer: Opportunities for its diagnosis, prognosis and therapeutic intervention (Review).International journal of oncology · 2026Review
- Article
- Prognostic Implications of Codon-SpecificJCO precision oncology · 2026Article
- Pancreatic cancer: molecular pathogenesis and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Nimotuzumab Plus Gemcitabine-based Adjuvant Chemotherapy for Resectable Pancreatic Cancer: A Retrospective Observational Study.Pancreas · 2026Observational
- Key Considerations for TargetingDrug design, development and therapy · 2026Review
- Article
- Nomogram based on preoperative contrast-enhanced CT predicts early liver metastasis in pancreatic ductal adenocarcinoma.Quantitative imaging in medicine and surgery · 2025Article
100 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
43 authors at 7 institutions in 1 country.
Funding
Abstract
importanceAlthough patients with resected pancreatic adenocarcinoma are at high risk for disease recurrence, few biomarkers are available to inform patient outcomes.
objectiveTo evaluate the alterations of the 4 main driver genes in pancreatic adenocarcinoma and patient outcomes after cancer resection. DESIGN, SETTING, AND
participantsThis study analyzed protein expression and DNA alterations for the KRAS, CDKN2A, SMAD4, and TP53 genes by immunohistochemistry and next-generation sequencing in formalin-fixed, paraffin-embedded tumors in 356 patients with resected pancreatic adenocarcinoma who were treated at the Dana-Farber/Brigham and Women's Cancer Center (October 26, 2002, to May 21, 2012), University of Rochester Medical Center (March 1, 2006, to November 1, 2013), or Stanford Cancer Institute (September 26, 1995, to May 22, 2013). Associations of driver gene alterations with disease-free survival (DFS) and overall survival (OS) were evaluated using Cox proportional hazards regression with estimation of hazard ratios (HRs) and 95% CIs and adjustment for age, sex, tumor characteristics, institution, and perioperative treatment. Data were collected September 9, 2012, to June 28, 2016, and analyzed December 17, 2016, to March 14, 2017. MAIN OUTCOMES AND MEASURES: The DFS and OS among patients with resected pancreatic adenocarcinoma.
resultsOf the 356 patients studied, 191 (53.7%) were men and 165 (46.3%) were women, with a median (interquartile range [IQR]) age of 67 (59.0-73.5) years. Patients with KRAS mutant tumors had worse DFS (median [IQR], 12.3 [6.7 -27.2] months) and OS (20.3 [11.3-38.3] months) compared with patients with KRAS wild-type tumors (DFS, 16.2 [8.9-30.5] months; OS, 38.6 [16.6-63.1] months) and had 5-year OS of 13.0% vs 30.2%. Particularly poor outcomes were identified in patients with KRAS G12D-mutant tumors, who had a median (IQR) OS of 15.3 (9.8-32.7) months. Patients whose tumors lacked CDKN2A expression had worse DFS (median, 11.5 [IQR, 6.2-24.5] months) and OS (19.7 [10.9-37.1] months) compared with patients who had intact CDKN2A (DFS, 14.8 [8.2-30.5] months; OS, 24.6 [14.1-44.6] months). The molecular status of SMAD4 was not associated with DFS or OS, whereas TP53 status was associated only with shorter DFS (HR, 1.33; 95% CI, 1.02-1.75; P = .04). Patients had worse DFS and OS if they had a greater number of altered driver genes. Compared with patients with 0 to 2 altered genes, those with 4 altered genes had worse DFS (HR, 1.79 [95% CI, 1.24-2.59; P = .002]) and OS (HR, 1.38 [95% CI, 0.98-1.94; P = .06]). Five-year OS was 18.4% for patients with 0 to 2 gene alterations, 14.1% for those with 3 alterations, and 8.2% for those with 4 alterations. CONCLUSIONS AND RELEVANCE: Patient outcomes are associated with alterations of the 4 main driver genes in resected pancreatic adenocarcinoma.
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