Cited by 264Pancreatic and Hepatic Oncology ResearchCancer Genomics and DiagnosticsCholangiocarcinoma and Gallbladder Cancer Studies

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Association of Alterations in Main Driver Genes With Outcomes of Patients With Resected Pancreatic Ductal Adenocarcinoma

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Qian, Zhi Rong, Rubinson, Douglas A., Nowak, Jonathan A., Morales-Oyarvide, Vicente, Dunne, Richard F., Kozak, Margaret M., Welch, Marisa W., Brais, Lauren K., Da Silva, Annacarolina, Li, Tingting, Li, Wanwan, Masuda, Atsuhiro, Yang, Juhong, Shi, Yan, Gu, Mancang, Masugi, Yohei, Bui, Justin, Zellers, Caitlin L., Yuan, Chen, Babic, Ana, Khalaf, Natalia, Aguirre, Andrew, Ng, Kimmie, Miksad, Rebecca A., Bullock, Andrea J., Chang, Daniel T., Tseng, Jennifer F., Clancy, Thomas E., Linehan, David C., Findeis-Hosey, Jennifer J., Doyle, Leona A., Thorner, Aaron R., Ducar, Matthew, Wollison, Bruce, Laing, Angelica, Hahn, William C., Meyerson, Matthew, Fuchs, Charles S., Ogino, Shuji, Hornick, Jason L., Hezel, Aram F., Koong, Albert C., Wolpin, Brian M.·2018·JAMA Oncology

DOI 10.1001/jamaoncol.2017.3420PMC PMC5844844

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Abstract

IMPORTANCE: Although patients with resected pancreatic adenocarcinoma are at high risk for disease recurrence, few biomarkers are available to inform patient outcomes. OBJECTIVE: To evaluate the alterations of the 4 main driver genes in pancreatic adenocarcinoma and patient outcomes after cancer resection. DESIGN, SETTING, AND PARTICIPANTS: This 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. RESULTS: Of 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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Bisht, S., & Feldmann, G. (2018) · Oncology Research and Treatment · doi:10.1159/000493437 · Cited by 14
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Hong, J. Y., Cho, H. J., Kim, S. T., Park, Y. S., Shin, S. H., Han, I. W., Lee, J., Heo, J. S., & Park, J. O. (2021) · Therapeutic Advances in Medical Oncology · doi:10.1177/17588359211038478 · Cited by 14
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Hinzpeter, R., Kulanthaivelu, R., Kohan, A. A., Avery, L. M., Pham, N., Ortega, C., Metser, U., Haider, M. A., & Veit‐Haibach, P. (2022) · Cancers · doi:10.3390/cancers14246224 · Cited by 13
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“First, we investigated four major gene alterations (KRAS, TP53, SMAD4, and CDKN2A), which were reported to be associated with the postoperative prognosis of PDAC in previous reports.(10,11) Second, we investigated the immune and fibrotic environments of the tumor, which may influence the prognosis of PDAC.”
BackgroundMethodSelf-citation
Endocrine-exocrine signaling drives obesity-associated pancreatic ductal adenocarcinomaPreprint
Chung, K. M., Singh, J., Lawres, L., Dorans, K. J., Garcia, C. C., Burkhardt, D. B., Robbins, R., Bhutkar, A. J., CARDONE, R. L., Zhao, X., et al. (2019) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/663583 · Cited by 14
Self-citation
Iron-Dependent Cell Death: A New Treatment Approach against Pancreatic Ductal Adenocarcinoma
Lopez-Blazquez, C., Lacalle-González, C., Sanz-Criado, L., Otieno, M. O., García‐Foncillas, J., & Martínez‐Useros, J. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241914979 · Cited by 15
“PDAC has a characteristic mutational proﬁle, where mutations in the genes KRAS , cyclin-dependent kinase inhibitor 2A ( CDKN2A ), tumor protein p53 ( TP53 ) and SMAD family member 4 ( SMAD4 ) stand out [6,7].”
Background
Concurrent targeting of GSK3 and MEK as a therapeutic strategy to treat pancreatic ductal adenocarcinoma
Fukuda, J., Kosuge, S., Satoh, Y., Sekiya, S., Yamamura, R., Ooshio, T., Hirata, T., Sato, R., Hatanaka, K. C., Mitsuhashi, T., et al. (2024) · Cancer Science · doi:10.1111/cas.16100 · Cited by 13
“23 In fact, patients with all four mu - tations have the worst prognosis among all the PDAC patients, 24,25 highlighting the importance of developing a corresponding animal model carrying this ‘ 4-hit ’ genotype to cause endogenous tumors.”
Background
Single-cell and bulk RNA sequencing identifies T cell marker genes score to predict the prognosis of pancreatic ductal adenocarcinoma
Zheng, H., Li, Y., Zhao, Y., & Jiang, A. (2023) · Scientific Reports · doi:10.1038/s41598-023-30972-7 · Cited by 12
Pancreatic ductal adenocarcinoma cells reshape the immune microenvironment: Molecular mechanisms and therapeutic targets
Zhao, Y., Qin, C., Chen, L., Li, Z., Zhao, B., Li, T., Zhang, X., & Wang, W. (2024) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2024.189183 · Cited by 14
Self-citation
Advances in Novel Targeted Therapies for Pancreatic Adenocarcinoma
Hoang, T. A., & Tsang, E. S. (2025) · Journal of Gastrointestinal Cancer · doi:10.1007/s12029-024-01149-w · Cited by 15
Impact of Driver Mutations on the Evolution of Isolated Metachronous Lung Metastasis of Pancreatic Ductal adenocarcinoma
Vitellius, C., Griveaux, O., Morvant, B., Pedrono, E., Venara, A., Ingster, O., Baize, N., Dincuff, E., Rousselet, M., Guardiola, P., et al. (2020) · Molecular Diagnosis & Therapy · doi:10.1007/s40291-020-00472-9 · Cited by 11
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“Several other common gene mutations included TP53, SMAD4, and CDKN2A, each of which was mutated in >50% of different but mostly overlapping patients [49,50].”
Background
Role of neoadjuvant therapy for nonmetastatic pancreatic cancer: Current evidence and future perspectives
Cassese, G., Han, H., Yoon, Y., Lee, J. S., Lee, B., Cubisino, A., Panaro, F., & TROISI, R. I. (2023) · World Journal of Gastrointestinal Oncology · doi:10.4251/wjgo.v15.i6.911 · Cited by 11
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“[32,46,47,58].”
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“Furthermore, prior studies show that KRAS mutations are associated with poor clinical outcomes, but we were unable to detect this relationship as only two patients were KRAS wild-type in our cohort [52,53].”
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Li, X., Hou, W., Xiao, C., Yang, H., Zhao, C., & Cao, D. (2024) · Cellular Oncology · doi:10.1007/s13402-024-00970-6 · Cited by 10
“The development of intratumoral and inter-tumoral heterogeneity is a hallmark of malignant TME progression [23, 24].”
Precision immune regulation in KRAS-mutated cancers: the final piece of the puzzle?
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A Novel Ferroptosis-Related Gene Signature Predicts Recurrence in Patients With Pancreatic Ductal Adenocarcinoma
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“However, few biomarkers and models considering genetic and genomic features of PDAC patients have been identified as postoperative predictors of recurrence in PDAC (Qian et al., 2018).”
BackgroundSelf-citation
Integrated genomic analysis to identify druggable targets for pancreatic cancer
Mugiyanto, E., Adikusuma, W., Irham, L. M., Huang, W., Chang, W., & Kuo, C.-N. (2022) · Frontiers in Oncology · doi:10.3389/fonc.2022.989077 · Cited by 12
“Genes including KRAS, TP53, and SMAD4 had also been reported from previous studies (57, 58).”
Result
Disparities in Pancreatic Cancer Outcomes in the Disaggregated Asian American Population
Kooragayala, K., Lou, J., Dibato, J. E., & Hong, Y. K. (2023) · Annals of Surgical Oncology · doi:10.1245/s10434-023-14454-8 · Cited by 10
TP53 missense mutation reveals gain-of-function properties in small-sized KRAS transformed pancreatic ductal adenocarcinoma
Zhou, Y., Jin, J., Ji, Y., Zhang, J., Fu, N., Chen, M., Wang, J., Qin, K., Jiang, Y., Cheng, D., et al. (2023) · Journal of Translational Medicine · doi:10.1186/s12967-023-04742-y · Cited by 11
“Although TP53 missense mutation induced potential early metastases, TP53 truncating mutation was reported to more negatively correlated with patients’ survival than TP53 mis-sense mutation, [24, 25] so we then evaluated whether this was due to tumor’s sensitivity to chemotherapy.”
Background
Influence of KRAS mutations, persistent organic pollutants, and trace elements on survival from pancreatic ductal adenocarcinoma
Porta, M. S., Pumarega, J. A., Amaral, A. F. S., Genkinger, J. M., Camargo, J., Mucci, L. A., Alguacil, J., Gasull, M., Zhang, X., Morales, E., et al. (2020) · Environmental Research · doi:10.1016/j.envres.2020.109781 · Cited by 10
“70 when adjusting only for age, sex, and stage, which is similar to findings from other studies (Rachakonda et al., 2013; Qian et al., 2018).”
BackgroundResultSelf-citation
Predictors of Long-Term Survival in Pancreatic Ductal Adenocarcinoma after Pancreatectomy: TP53 and SMAD4 Mutation Scoring in Combination with CA19-9
Ono, M., Ono, Y., Nakamura, T., Tsuchikawa, T., Kuraya, T., Kuwabara, S., Nakanishi, Y., Asano, T., Matsui, A., Tanaka, K., et al. (2022) · Annals of Surgical Oncology · doi:10.1245/s10434-022-11630-0 · Cited by 10
“, KRAS G12D) is associated with poor prognosis.(13,14) A genome-wide study also demonstrated that rare mutations such as those in ARID1A and RBM10 might have prognostic value.”
Background
Clinical and genetic characteristics in pancreatic cancer from Chinese patients revealed by whole exome sequencing
He, Y., Huang, W. J., Tang, Y., Li, Y., Peng, X., Li, J., Wu, J. Y., You, N., Li, L., Liu, C., et al. (2023) · Frontiers in Oncology · doi:10.3389/fonc.2023.1167144 · Cited by 10
“The aggregation of mutations in these four primary driver genes not only represents the distinctive molecular features of PDAC, but, is also linked to a bad prognosis (9).”
Background
Cellular crosstalk of regulatory T cells in pancreatic ductal adenocarcinoma
Shi, X., Liu, H., & Liang, Z. (2023) · Journal of Pancreatology · doi:10.1097/jp9.0000000000000135 · Cited by 10
“[24] KRAS G12D mutation modulates cytokine IL-10 and TGF β expression in tumor cells to tailor the function of converting naïve CD4+ T cells into Tregs and accumulating Tregs, which is reversed by inhibiting the RAF-MEK-ERK pathway, a pivotal downstream pathway of oncogenic KRAS .”
Background
Recent Anti-KRASG12D Therapies: A “Possible Impossibility” for Pancreatic Ductal Adenocarcinoma
Sobhani, N., Pittacolo, M., D’Angelo, A., & Marchegiani, G. (2025) · Cancers · doi:10.3390/cancers17040704 · Cited by 12
Concurrent inhibition of pBADS99 synergistically improves MEK inhibitor efficacy in KRASG12D-mutant pancreatic ductal adenocarcinoma
Tan, Y. Q., Sun, B., Zhang, X., Zhang, S., Guo, H., Basappa, B., Zhu, T., Sethi, G., Lobie, P. E., & Pandey, V. (2024) · Cell Death and Disease · doi:10.1038/s41419-024-06551-7 · Cited by 10
“Indeed, PDAC patients with wild-type KRAS generally exhibited better prognosis than those harboring mutant KRAS [51], even though patients with wild-type KRAS PDAC frequently harbor activating BRAF mutations, thus similarly generating constitutive activation of the p44/42 MAPK pathway [52].”
The Landscape of Genetic Alterations Stratified Prognosis in Oriental Pancreatic Cancer Patients
Guo, S., Shi, X., Gao, S., Hou, Q., Jiang, L., Li, B., Shen, J., Wang, H., Shen, S., Zhang, G., et al. (2021) · Frontiers in Oncology · doi:10.3389/fonc.2021.717989 · Cited by 9
“Furthermore, heterogeneity brings significant differences in biological behaviors of pancreatic cancer, including malignant proliferation (10), metastasis potential (11), and chemotherapy sensitivity (12), and these differences can affect prognosis (13, 14).”
Background
Incomplete Conflict of Interest Disclosures
(2019) · JAMA Oncology · doi:10.1001/jamaoncol.2019.0286 · Cited by 9
[Retracted] Gene Differential Expression and Interaction Networks Illustrate the Biomarkers and Molecular Biological Mechanisms of Unsaponifiable Matter in Kanglaite Injection for Pancreatic Ductal Adenocarcinoma
Xu, B., Dan, W., Zhang, X., Wang, H., Cao, L., Li, S., & Li, J. (2022) · BioMed Research International · doi:10.1155/2022/6229462 · Cited by 9
Retracted
Postoperative hyperprogression disease of pancreatic ductal adenocarcinoma after curative resection: a retrospective cohort study
Zou, S., Wang, X., Chen, H., Lin, J., Wen, C., Zhan, Q., Chen, H., Lu, X., Deng, X., & Shen, B. (2022) · BMC Cancer · doi:10.1186/s12885-022-09719-6 · Cited by 9
“Previous studies reported KRAS, TP53, SMAD4, and CDKN2A as the four major driver genes associated with poor prognosis of pancreatic cancer [32].”
Result
Driver mutation subtypes involve with differentiated immunophenotypes influencing pancreatic cancer outcomes
Zou, S., Zhang, L., Jiang, C., Li, F., Yang, Y., Deng, X., Zhang, J., Chen, H., Jiang, L., Cheng, X., et al. (2024) · Cancer Letters · doi:10.1016/j.canlet.2024.217134 · Cited by 9
Prognostic value of the TP53 mutation in patients with pancreatic ductal adenocarcinoma receiving FOLFIRINOX
Kim, M. K., Cho, I. R., Kim, Y., Choi, J. H., Jung, K., Kim, J., Kim, S., Yun, H., Yoon, J., Oh, D. Y., et al. (2024) · Therapeutic Advances in Medical Oncology · doi:10.1177/17588359241290482 · Cited by 8
“17,18 Furthermore, a meta-analysis of 17 studies revealed that TP53 mutation overexpression was associated with poorer OS, along with other driver mutations.”
Background
Clinical outcomes and molecular characteristics of lung-only and liver-only metastatic pancreatic cancer: results from a real-world evidence database
Levi, A., Blais, E. M., Davelaar, J., Ebia, M., Minasyan, A., Nikravesh, N., Gresham, G. K., Zheng, L., Chuy, J. W., Shroff, R. T., et al. (2025) · The Oncologist · doi:10.1093/oncolo/oyaf007 · Cited by 8
The Mutational Status of Driver Genes in Patients With Resected Pancreatic Ductal Adenocarcinoma Is Associated With Pathological Characteristics and Overall Survival
Campbell, B. A., Solinas, D., Blackford, A. L., Molin, M. D., Purchla, J., McPhaul, T. J., Chidambaram, S., Cameron, J. L., Lin, M., Hruban, R. H., et al. (2025) · Annals of Surgery · doi:10.1097/sla.0000000000006794 · Cited by 8
Individualized prognostic signature for pancreatic carcinoma validated by integrating immune-related gene pairs (IRGPs)
Li, Y., Yao, P., Zhao, K., Ye, Z., Zhang, H., Cao, J., Zhang, S., & Xing, C. (2021) · Bioengineered · doi:10.1080/21655979.2020.1860493 · Cited by 8
“In some recent studies, some gene alterations (KRAS, TP53, CDKN2A and SMAD4) have been shown to be associated with the OS of pancreatic cancer patients [26], but the proportion of pancreatic cancer patients with mutations in at least one of these four genes was found to be less than 40%[27].”
Background
Inhibition of NAD-GPx4 axis and MEK triggers ferroptosis to suppress pancreatic ductal adenocarcinoma
Jiang, H., Satoh, Y., Yamamura, R., Ooshio, T., Luo, Y., Hai, H., Otsuka, T., Hata, S., Sato, R., Hirata, T., et al. (2025) · Molecular Therapy · doi:10.1016/j.ymthe.2025.05.037 · Cited by 8
Sample-Specific Perturbation of Gene Interactions Identifies Pancreatic Cancer Subtypes
Wei, R., Zhang, H., Cao, J., Qin, D., Li, S., & Deng, W. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23094792 · Cited by 7
“Previous studies have demonstrated that PDAC patients who had CDKN2A or SMAD4 expression loss had worse disease-free survival and overall survival compared with patients with intact CDKN2A/SMAD4 [22,23].”
Result
Comprehensive Genomic Studies on the Cell Blocks of Pancreatic Cancer
da Silva, R. S., Pina, M. J., Cirnes, L., Gouveia, L. B., Albergaria, A., & Schmitt, F. C. (2024) · Diagnostics · doi:10.3390/diagnostics14090906 · Cited by 7
“Quin et al. [27] reported that tumors harboring KRAS G12D mutation exhibited a poorer DFS after surgery when compared to those characterized by wild-type KRAS.”
BackgroundResult
STRAP as a New Therapeutic Target for Poor Prognosis of Pancreatic Ductal Adenocarcinoma Patients Mainly Caused by TP53 Mutation
Hu, S., Chen, X., Xu, X., Zheng, C., Huang, W., Zhou, Y., Akuetteh, P. D. P., Yang, H., Shi, K., Chen, B., et al. (2020) · Frontiers in Oncology · doi:10.3389/fonc.2020.594224 · Cited by 7
“Further, other studies (22, 23) showed that the higher the number of mutations occurring in these driver genes, the worse the prognosis, especially in patient with mutations in more than three genes.”
Result
Unveiling the Molecular Landscape of Pancreatic Ductal Adenocarcinoma: Insights into the Role of the COMPASS-like Complex
Jamali, M., Barar, E., & Shi, J. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25105069 · Cited by 6
Preoperative Prognostic Factors in Resectable Pancreatic Cancer: State of the Art and Prospects
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“OS was defined as the time from diagnosis to either relapse, death, or the last follow-up date 13 .”
Background
Hereditary chronic pancreatitis induced plasticity cooperates with mutant Kras in early pancreatic carcinogenesis
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“30 This mutation has been effectively modelled in Ptf1a Cre ;Kras LSL-G12D (KC) mice, which recapitulate the full spectrum of PDAC progression.”
Development and Validation of the Predictive and Prognostic ChemoResist Signature in Resected Pancreatic Ductal Adenocarcinoma
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“9,10,30 We previously reported that high-frequency mutations of KRAS in tumor and ctDNA (mutation allelic frequency ≥ 30% and ≥ 5% in tumor and ctDNA, respectively) and their dynamic alterations effectively predicted the response of metastatic PDAC to nab-paclitaxel plus S1 chemotherapy, with…”
Self-citation
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“…solid tumors, the progression of pancreatic cancer is driven by the progressive accumulation of mutations in key driver genes, including the oncogene KRAS [34–36], the tumor suppressor gene TP53 [37,38], cyclin-dependent kinase inhibitor 2A ( CDKN2A ), and SMAD family member 4 ( SMAD4 ) [39–41].”
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Tumor copy number instability is a significant predictor for late recurrence after radical surgery of pancreatic ductal adenocarcinoma
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Identification of KRAS G12V associated clonal neoantigens and immune microenvironment in long-term survival of pancreatic adenocarcinoma
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“According to the defined genes of 10 curated signaling pathways in TCGA [22], KRAS G12V mutation was detected in primary foci and all metastatic foci of Pt204, while other common reported driver genes in PDAC (TP53, CDKN2A, SMAD4) were not mutated in the case of Pt204 [4] (Fig.”
BackgroundInfluential
Evaluating the Effect of KRAS Variants on Survival Outcomes and Therapy Response in Pancreatic Cancer
Ebia, M., Blais, E. M., Cui, Y. Y., Petricoin, E. F., Pishvaian, M. J., Gaddam, S., Gong, J., Osipov, A., & Hendifar, A. E. (2025) · JCO Precision Oncology · doi:10.1200/po-24-00684 · Cited by 7
The tumor immune microenvironment in resected treatment-naive pancreatic cancer patients with long-term survival
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Background
Comparing clinical and genomic features based on the tumor location in patients with resected pancreatic cancer
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“With frequent alterations in main driver genes, including KRAS , TP53 , CDKN2A , and SMAD4 , Moffitt et al. (2015) and Bailey et al. (2016) established the molecular subtypes of PDAC, which showed the difference in survival according to tumor biology [7–9].”
Background
Negative p53 Expression Confers Worse Prognosis in Patients With Resected Pancreatic Ductal Adenocarcinoma
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“In addition, we successfully picked out negative p53 expression, which was closely related with complete LOF of TP53, as an independent biomarker to predict worse prognosis of resected PDAC.”
BackgroundResultInfluential
Exploring the differences in the tumor microenvironment and immuno-oncologic targets in pancreatic ductal adenocarcinomas (PDAC) according to KRAS mutational status
Faber, E. B., Baca, Y., Xiu, J., Walker, P., Manji, G. A., Gholami, S., Saeed, A., Prakash, A., Botta, G. P., Sohal, D. P. S., et al. (2024) · ESMO Gastrointestinal Oncology · doi:10.1016/j.esmogo.2024.100042 · Cited by 3
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“19 In PDAC cells, the mKRAS mutation causes major histocompatibility complex class I (MHC-I) to be selectively targeted for lysosomal degradation through an autophagy-dependent mechanism.”
Background
Key Considerations for Targeting KRAS in Pancreatic Cancer: Potential Impact on the Treatment Paradigm
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No Associations between Dairy Intake and Markers of Gastrointestinal Inflammation in Healthy Adult Cohort
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Background
SMAD4 loss predicts worse overall and distant metastasis‐free survival in patients with resected pancreatic adenocarcinoma
Anstadt, E. J., Carmona, R., Berlin, E. E., Yegya‐Raman, N., Venigalla, S., Reddy, V. K., Williams, G. R., Leibensperger, M. R., Wojcieszynski, A. P., Baumann, B. C., et al. (2023) · Cancer · doi:10.1002/cncr.35058 · Cited by 3
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“The accumulation of driver mutations seems however, to be of prognostic significance, as shown more recently by Qian and colleagues [14].”
BackgroundResult
Postoperative hyperprogression disease of pancreatic ductal adenocarcinoma after curative resection: A retrospective cohort study.Preprint
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Clinical utility of comprehensive genomic profiling for advanced pancreatic cancer: insights from real-world data analysis
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“The number of mutations in these genes (three or more) is considered to be associated with a poor prognosis [12, 16, 17].”
Influential
KRAS Mutations in Cancer
Zhang, Y., Ma, Y., Zhang, K., Wang, Y., Sun, X., Kan, C., & Han, F. (2025) · American Journal of Clinical Oncology · doi:10.1097/coc.0000000000001192 · Cited by 2
Potential for Clinical Management of Pancreatic Cancer Through Whole Exome Profiling of Site-Specific Metastases and Matched Primary Tumors
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MTAP in small biopsy samples of pancreatic lesions: a potential diagnostic biomarker. Immunohistochemical, fluorescence in situ hybridization and molecular analysis
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“Approximately CDKN2A is inactivated in 40% of pancreatic cancers by homozygous deletion mutations while another 40% of the patients show loss of one allele coupled with an intragenic mutation, and in an additional 15% by hypermethylation of the gene promoter 12,13 .”
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“[104] Altered TP53 was associated with shorter DFS but was not associated with OS.”
BackgroundInfluential
Multiomic quantification of the KRAS mutation dosage improves the preoperative prediction of survival and recurrence in patients with pancreatic ductal adenocarcinoma
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“Therefore, the alterations of major driver genes are perhaps not suitable to be used as universal biomarkers for evaluating outcomes of those PAAD individuals undergoing radical (mainly for early-stage individuals) or nonradical (mainly for late-stage individuals) resections like previously performed([4]).”
BackgroundInfluential
An amino acid metabolism-based seventeen-gene signature correlates with the clinical outcome and immune features in pancreatic cancer
Hao, J., Zhou, C., Wang, Z., Ma, Z., Wu, Z., Lv, Y., & Wu, R. (2023) · Frontiers in Genetics · doi:10.3389/fgene.2023.1084275 · Cited by 2
“Moreover, numerous studies have revealed that the KRAS mutation adversely influenced the outcomes of patients with pancreatic cancer (Ogura et al., 2013; Qian et al., 2018).”
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Network Pharmacology-based Elucidation of Molecular Biological Mechanisms of Kanglaite Injection for Treatment of Pancreatic Ductal AdenocarcinomaPreprint
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Case report: Diverse immune responses in advanced pancreatic ductal adenocarcinoma treated with immune checkpoint inhibitor-based conversion therapies
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Integrated In silico small molecule drug repurposing approach targeting KRAS G12D therapies for pancreatic ductal adenocarcinoma
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Authors: Qian, Z. R., Rubinson, D. A., Nowak, J. A., Morales-Oyarvide, V., Dunne, R. F., Kozak, M. M., Welch, M. W., Brais, L. K., Da Silva, A., Li, T., Li, W., Masuda, A., Yang, J., Shi, Y., Gu, M., Masugi, Y., Bui, J., Zellers, C. L., Yuan, C., Babic, A., Khalaf, N., Aguirre, A., Ng, K., Miksad, R. A., Bullock, A. J., Chang, D. T., Tseng, J. F., Clancy, T. E., Linehan, D. C., Findeis-Hosey, J. J., Doyle, L. A., Thorner, A. R., Ducar, M., Wollison, B., Laing, A., Hahn, W. C., Meyerson, M., Fuchs, C. S., Ogino, S., Hornick, J. L., Hezel, A. F., Koong, A. C., & Wolpin, B. M.
Affiliations: Harvard University (US)
Brigham and Women's Hospital (US)
Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts
University of Rochester Medicine (US)
Stanford Cancer Institute (US)
Dana-Farber Cancer Institute (US)
Beth Israel Deaconess Medical Center (US)
Broad Institute (US)
The University of Texas MD Anderson Cancer Center (US)
Corresponding author: Wolpin, Brian M.
ORCID: Qian, Zhi Rong
Rubinson, Douglas A.
Nowak, Jonathan A.
Dunne, Richard F.
Kozak, Margaret M.
Brais, Lauren K.
Li, Tingting
Li, Wanwan
Masuda, Atsuhiro
Yang, Juhong
Shi, Yan
Gu, Mancang
Masugi, Yohei
Bui, Justin
Yuan, Chen
Khalaf, Natalia
Aguirre, Andrew
Ng, Kimmie
Miksad, Rebecca A.
Bullock, Andrea J.
Chang, Daniel T.
Tseng, Jennifer F.
Clancy, Thomas E.
Linehan, David C.
Findeis-Hosey, Jennifer J.
Doyle, Leona A.
Thorner, Aaron R.
Ducar, Matthew
Wollison, Bruce
Hahn, William C.
Meyerson, Matthew
Fuchs, Charles S.
Ogino, Shuji
Hornick, Jason L.
Hezel, Aram F.
Koong, Albert C.
Wolpin, Brian M.
Venue: JAMA Oncology
Publisher: American Medical Association (AMA)
Published: 2018-03-08
Volume: 4
Issue: 3
Pages: e173420
ISSN: 2374-2437 (ISSN-L)
DOI: 10.1001/jamaoncol.2017.3420
PMC: PMC5844844
OpenAlex: W2767007332
Cited by: 260
References: 15
Citations by year: 2026: 17 · 2025: 31 · 2024: 38 · 2023: 47 · 2022: 49 · 2021: 28 · 2020: 24 · 2019: 19 · 2018: 7
FWCI: 6.03
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: JAMA Oncology (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Pancreatic Cancer Action Network
National Institutes of Health (UL1TR001102, UL1TR001863)
National Cancer Institute (P50CA127003, R01CA124908, R35CA197735, K07CA148894, U01CA176058, U01CA199253, K08CA218420, U01CA210171)
National Center for Advancing Translational Sciences
Topics: Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
Health Sciences › Medicine › Surgery › Cholangiocarcinoma and Gallbladder Cancer Studies
Keywords: pancreatic ductal adenocarcinoma, pancreatic cancer surgery, driver gene alterations, KRAS mutation, CDKN2A, SMAD4, TP53, disease-free survival, overall survival, prognostic factors, protein expression, DNA alterations, recurrence, postoperative adjuvant therapy, neoadjuvant therapy, tumor-infiltrating lymphocytes, tumor-infiltrating macrophages, tumor-infiltrating neutrophils, tumor-infiltrating T cells, tumor-infiltrating B cells, tumor-infiltrating plasma cells, tumor-infiltrating dendritic cells, tumor-infiltrating NK cells, tumor-infiltrating Treg cells, tumor-infiltrating myeloid cells
MeSH terms: Adenocarcinoma, Aged, DNA Mutational Analysis, Female, Follow-Up Studies, Humans, Immunohistochemistry, Male, Middle Aged, Mutation, Pancreatectomy, Pancreatic Neoplasms, Prognosis, Proto-Oncogene Proteins, Biomarkers, Tumor, Gene Expression Regulation, Neoplastic, Survival Analysis, Treatment Outcome, Gene Expression Profiling, Carcinoma, Pancreatic Ductal, High-Throughput Nucleotide Sequencing

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Association of Alterations in Main Driver Genes With Outcomes of Patients With Resected Pancreatic Ductal Adenocarcinoma

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