Association of Alterations in Main Driver Genes With Outcomes of Patients With Resected Pancreatic Ductal Adenocarcinoma
Open accessAbstract
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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A previous study of 356 patients with resected PDAC reported that those with KRAS mutations had worse disease-free survival (median 12.3 months) and OS (median 20.3 months) compared with those with wildtype KRAS (DFS 16.2 months and OS 38.6 months), and particularly poor outcomes were observed in patients with KRASG12D mutation (median OS 15.3 months).
“This is consistent with a previous study of 356 patients with resected PDAC, which reported that those with KRAS mutations had worse disease-free survival (DFS) (median 12.3 months) and OS (median 20.3 months) compared with those with wildtype KRAS (DFS 16.2 months and OS 38.6 months), and particularly poor outcomes were observed in patients with KRASG12D mutation (median OS 15.3 months)39.”
From Impact of KRAS mutations and co-mutations on clinical outcomes in pancreatic ductal adenocarcinoma (2024) · cites this paper as [39]
Patients with resected PDAC and somatic CDKN2A loss had worse survival (median DFS 11.5 and OS 19.7) compared to patients with wildtype CDKN2A (median DFS 14.8 and median OS 24.6).
“Patients with resected PDAC and somatic CDKN2A loss had worse survival (median DFS 11.5 and OS 19.7) compared to patients with wildtype CDKN2A (median DFS 14.8 and median OS 24.6)39.”
From Impact of KRAS mutations and co-mutations on clinical outcomes in pancreatic ductal adenocarcinoma (2024) · cites this paper as [39]
Reported results about the prognostic value of SMAD4 have been inconsistent.
“SMAD4 is a tumor suppressor gene, and reported results about the prognostic value of SMAD4 have been inconsistent39,60–62.”
From Impact of KRAS mutations and co-mutations on clinical outcomes in pancreatic ductal adenocarcinoma (2024) · cites this paper as [39]
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“Most studies have concluded that there is a negative influence on prognosis of patients with a KRAS mutation whether or not they have undergone surgery for other solid tumors [24, 25] and a correlation between oncogenic KRAS mutations and PD-L1 expression in cancers has also been emphasized [10, 26, 27].”
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Ma, Z., Li, Z., Wang, S., Zhou, Z., Liu, C., Zhuang, H., Zhou, Q., Huang, S., Zhang, C., & Hou, B. (2022) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-022-02310-8 · Cited by 37 · see citing works
“Almost all PDAC patients carry at least one of four frequently-mutated driver genes including the oncogene KRAS and the tumor suppressors TP53, SMAD4, and CDKN2A [4, 5].”
BackgroundPan, M., Jiang, C., Zhang, Z., Achacoso, N. S., Alexeeff, S., Solorzano, A. V., Tse, P., Chung, E. H., Sundaresan, T. K., Suga, J. M., et al. (2023) · JCO Precision Oncology · doi:10.1200/po.22.00570 · Cited by 36 · see citing works
“22 Qian et al 23 analyzed a cohort of 356 patients with resected PDAC and found that KRAS alteration was associated with worse disease-free survival (DFS) and OS compared with wtKRAS and loss of CDKN2A expression was associated with worse DFS and OS, whereas TP53 alteration was associated with worse DFS but not OS, an…”
Zhang, D., Lindstrom, A. R., Kim, E. J.-H., Hwang, C., Hall, M. L., Lin, T., & Li, Y. (2022) · Frontiers in Oncology · doi:10.3389/fonc.2022.890154 · Cited by 34 · see citing works
“There are several studies on the KRAS mutation related prognosis and multiple studies stated that poor outcomes were identified in patients with KRAS G12D mutant pancreatic cancer (35, 36).”
BackgroundHuang, Y., Cheng, W., Kuo, T.-T., Yang, J., Wu, Y., Wu, H., Lo, C.-C., Hsieh, C.-Y., Wong, S., Lu, C., et al. (2024) · Nature Cancer · doi:10.1038/s43018-023-00720-x · Cited by 34 · see citing works
“A well-known fact in PDAC is that wild-type (WT) KRAS imparts a more favorable prognosis than mutant KRAS 10 .”
Self-citationMoving the Needle on Precision Medicine in Pancreatic Cancer
O'Kane, G. M., & Lowery, M. A. (2022) · Journal of Clinical Oncology · doi:10.1200/jco.21.02514 · Cited by 34 · see citing works
Nagai, K., Mizukami, Y., Omori, Y., Kin, T., Yane, K., Takahashi, K., Ono, Y., Sugitani, A., Karasaki, H., Shinohara, T., et al. (2019) · Modern Pathology · doi:10.1038/s41379-019-0405-7 · Cited by 33 · see citing works
Zhu, X., Peng, S.-Q., Wang, L., Chen, X., Feng, C.-X., Liu, Y.-Y., & Chen, M. (2021) · Cell Death and Disease · doi:10.1038/s41419-021-04201-w · Cited by 33 · see citing works
Lencioni, G., Gregori, A., Toledo, B., Rebelo, R., Immordino, B., Amrutkar, M., Xavier, C. P. R., Kocijancic, A., Pandey, D. P., Perán, M., et al. (2024) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2024.09.002 · Cited by 31 · see citing works
Critical role of KRAS mutation in pancreatic ductal adenocarcinoma
Fan, Z., Fan, K., Yan, C., Huang, Q., Gong, Y., Cheng, H., Jin, K., Liu, C., Ni, Q., Yu, X., et al. (2018) · Translational Cancer Research · doi:10.21037/tcr.2018.10.19 · Cited by 30 · see citing works
Precision oncology for gallbladder cancer: insights from genetic alterations and clinical practice
Lin, J., Dong, K., Bai, Y., Zhao, S., Dong, Y., Shi, J., Shi, W., Long, J., Yang, X., Wang, D., et al. (2019) · Annals of Translational Medicine · doi:10.21037/atm.2019.08.67 · Cited by 29 · see citing works
“Ann Transl Med 2019;7(18):467 | http://dx.”
BackgroundRacu, M.-L., Lebrun, L., Schiavo, A. A., Campenhout, C. V., Clercq, S. D., Absil, L., Minguijón, E., Maris, C., Decaestecker, C., Salmon, I. J., et al. (2022) · Cancers · doi:10.3390/cancers14040973 · Cited by 29 · see citing works
“(2) Although SMAD4 IHC has been described as a reliable tool, discrepancies exist between protein expression and gene which do not always lead to a complete absence of staining [52,69,125].”
MethodEmerging Role of Targeted Therapy in Metastatic Pancreatic Adenocarcinoma
Huffman, B. M., Ellis, H., Jordan, A. C., Freed-Pastor, W. A., Perez, K. J., Rubinson, D. A., Sethi, N. S., Singh, H., Surana, R., Wolpin, B. M., et al. (2022) · Cancers · doi:10.3390/cancers14246223 · Cited by 30 · see citing works
“Interestingly, PDAC with KRAS G12R mutations are more likely to harbor deleterious HR gene alterations and PI3-kinase pathway mutations [52,53].”
BackgroundSelf-citationCharacterization of pancreatic cancer with ultra-low tumor mutational burden
Imamura, T., Ashida, R., Ohshima, K., Uesaka, K., Sugiura, T., Ohgi, K., Yamada, M., Otsuka, S., Hatakeyama, K., Nagashima, T., et al. (2023) · Scientific Reports · doi:10.1038/s41598-023-31579-8 · Cited by 27 · see citing works
Wang, H., Wang, X., Xu, L., Lin, Y., Zhang, J., & Cao, H. (2020) · Aging · doi:10.18632/aging.103958 · Cited by 26 · see citing works
“Furthermore, study of 356 www.aging-us.com 18687 AGING www.aging-us.com 18688 AGING patients from Dana-Farber/Brigham and Women’s Cancer Center [24] and our results derived from the TCGA PAAD datasets showed that the KRAS, TP53 mutation and CDKN2A deletion were synergistically determined the clinical overall survival…”
MethodThe Evolutionary Forest of Pancreatic Cancer
Mullen, K. M., Hong, J., Attiyeh, M. A., Hayashi, A., Sakamoto, H., Kohutek, Z. A., McIntyre, C. A., Zhang, H., Makohon-Moore, A. P., Zucker, A., et al. (2024) · Cancer Discovery · doi:10.1158/2159-8290.cd-23-1541 · Cited by 26 · see citing works
Ardalan, B., Ciner, A., Baca, Y., Hinton, A. C., Darabi, S., Kasi, A., Lou, E., Azqueta, J. I., Xiu, J., Datta, J., et al. (2025) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-24-3149 · Cited by 26 · see citing works
“Prior reports have suggested that the number of mutated driver genes is associated with outcomes (10).”
Self-citationZhan, Q., Wen, C., Zhao, Y., Fang, L., Jin, Y., Zhang, Z., Zou, S., Li, F., Yang, Y., Wu, L., et al. (2021) · EBioMedicine · doi:10.1016/j.ebiom.2021.103716 · Cited by 25 · see citing works
“Although mutated KRAS is a recognized risk factor for PAAD prognosis in previous study [56], we only observed the trend that mutated KRAS was associated with worse prognosis (Figure 1B), which might be due to different ethnic backgrounds and operation methods (notably, all of PAAD patients in our Chinese cohort receiv…”
BackgroundSMAD4 Y353C promotes the progression of PDAC
Wang, Z., Li, Y., Zhan, S., Zhang, L., Zhang, S., Tang, Q., Li, M., Tan, Z., Liu, S., & Xing, X. (2019) · BMC Cancer · doi:10.1186/s12885-019-6251-7 · Cited by 25 · see citing works
Masugi, Y., Takamatsu, M., Tanaka, M., Hara, K., Inoue, Y., Hamada, T., Suzuki, T., Arita, J., Hirose, Y., Kawaguchi, Y., et al. (2023) · The Journal of Pathology: Clinical Research · doi:10.1002/cjp2.323 · Cited by 23 · see citing works
“For SMAD4, tumours were defined as ‘intact’ when there was any nuclear or cytoplasmic staining in carcinoma cells or ‘lost’ when there was a complete loss of staining [5,22].”
BackgroundMethodInfluentialSelf-citationResection of Recurrent Pancreatic Cancer: Who Can Benefit?
Nienhüser, H., Büchler, M. W., & Schneider, M. A. (2021) · Visceral Medicine · doi:10.1159/000519754 · Cited by 22 · see citing works
Suzuki, T., Masugi, Y., Inoue, Y., Hamada, T., Tanaka, M. H., Takamatsu, M., Arita, J., Kato, T., Kawaguchi, Y., Kunita, A., et al. (2022) · Cancer Science · doi:10.1111/cas.15398 · Cited by 21 · see citing works
“Absent/mild 403 (35) 6 (26) 397 (35) 128 (46) 175 (35) 94 (26)”
Self-citationMasuda, S., Yamakawa, K., Masuda, A., Toyama, H., Sofue, K., Nanno, Y., Komatsu, S., Omiya, S., Sakai, A., Kobayashi, T., et al. (2023) · Annals of Surgical Oncology · doi:10.1245/s10434-023-13569-2 · Cited by 22 · see citing works
Self-citationShoucair, S., Habib, J. R., Pu, N., Kinny‐Köster, B., van Oosten, A. F., Javed, A. A., Lafaro, K. J., He, J. P., Wolfgang, C. L., & Yu, J. (2021) · Annals of Surgical Oncology · doi:10.1245/s10434-021-11081-z · Cited by 20 · see citing works
“These conclusions were made using NGS and validated using immunohistochemistry for protein expression, but also did not incorporate the factor of different gene mutation combinations.(31) One study by Zarkavellis et al.”
MethodGower, A., Golestany, B., Gong, J., Singhi, A. D., & Hendifar, A. E. (2020) · JCO Precision Oncology · doi:10.1200/po.19.00365 · Cited by 23 · see citing works
“In patients with resected pancreatic cancer, KRAS mutation is associated with worse overall survival than KRAS wild-type tumors.(34) Additionally, prevalence of KRAS mutation is notably less (80% v 89%) in patients , 50 years old, and 3/19 4/19 5/19 7/19 9/19 12/19 1/20 3/20”
BackgroundBiological Hallmarks and New Therapeutic Approaches for the Treatment of PDAC
Digiacomo, G., Volta, F., Garajová, I., Balsano, R., & Cavazzoni, A. (2021) · Life · doi:10.3390/life11080843 · Cited by 20 · see citing works
Treatment of KRAS-Mutated Pancreatic Cancer: New Hope for the Patients?
Krupa, K., Fudalej, M. M., Włoszek, E., Miski, H., Badowska-Kozakiewicz, A. M., Mękal, D., Budzik, M. P., Czerw, A. I., & Deptała, A. (2025) · Cancers · doi:10.3390/cancers17152453 · Cited by 21 · see citing works
“Less common mutations affect codons 13 and 61, with KRAS Q61H found in about 5% of cases and associated with improved survival, while KRAS G12D is linked to poorer outcomes [44,45].”
Reviews on Current Liquid Biopsy for Detection and Management of Pancreatic Cancers
Kaczor‐Urbanowicz, K. E., Cheng, J. C., King, J. C., Sedarat, A., Pandol, S. J., Farrell, J. J., Wong, D. T., & Kim, Y. H. (2020) · Pancreas · doi:10.1097/mpa.0000000000001662 · Cited by 20 · see citing works
“progression in pancreatic cancer patients.(96) Interestingly, recent studies report that tumor-specific mutations in ctDNA can be a better prognostic marker than CTC count.”
BackgroundHill, C., Rosati, L. M., Wang, H., Tsai, H., He, J. P., Hacker‐Prietz, A., Laheru, D. A., Zheng, L., Sehgal, S., Bernard, V., et al. (2022) · Practical Radiation Oncology · doi:10.1016/j.prro.2022.02.009 · Cited by 19 · see citing works
Advances in immunotherapy and targeted therapy for pancreatic cancer
Zhou, X., Wang, X., Yang, S., & Huang, Z. (2024) · Oncology and Translational Medicine · doi:10.1097/ot9.0000000000000074 · Cited by 19 · see citing works
Kurosaki, H., Nakatake, M., Sakamoto, T., Kuwano, N., Yamane, M., Ishii, K., Fujiwara, Y., & Nakamura, T. (2021) · Cells · doi:10.3390/cells10050985 · Cited by 18 · see citing works
Nanomedicine and epigenetics: New alliances to increase the odds in pancreatic cancer survival
Urbanova, M., Cihova, M., Buociková, V., Slopovský, J., Dubovan, P., Pinďák, D., Tomáš, M., García‐Bermejo, L., Rodríguez-Garrote, M., Earl, J., et al. (2023) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2023.115179 · Cited by 18 · see citing works
Yamakawa, K., Koyanagi‐Aoi, M., Uehara, K., Masuda, A., Yanagimoto, H., Toyama, H., Fukumoto, T., Kodama, Y., & Aoi, T. (2022) · PLoS ONE · doi:10.1371/journal.pone.0266620 · Cited by 16 · see citing works
Self-citationHuang, L., Yang, H., Chen, K., Yuan, J., Li, J., Dai, G., Gu, M., & Shi, Y. X. (2023) · Clinical and Translational Medicine · doi:10.1002/ctm2.1500 · Cited by 17 · see citing works
“32 Notably, the efficacy of anticancer drugs directly targeting KRAS remains uncertain.”
BackgroundSelf-citationLee, M. R., Woo, S. M., Kim, M. K., Han, S., Park, S., Lee, W. J., Lee, D.-E., Choi, S. Y., Choi, W., Yoon, K., et al. (2024) · Cancer Science · doi:10.1111/cas.16104 · Cited by 17 · see citing works
“22 Nevertheless, ctDNA detection is correlated with the clinical tumor burden and thus could be utilized as a biomarker for monitoring the tumor dynamics and more accurately predicting the clinical prognosis.”
BackgroundPrognostic implications of RAS alterations in diverse malignancies and impact of targeted therapies
Kato, S., Okamura, R., Sicklick, J., Daniels, G., Hong, D., Goodman, A., Weihe, E., Lee, S., Khalid, N., Collier, R., et al. (2019) · International Journal of Cancer · doi:10.1002/ijc.32813 · Cited by 16 · see citing works
“This observation is in line with a previous report that showed that a combination of alterations, especially KRAS and CDKN2A abnormalities, had significantly worse disease-free survival and OS among patients with pancreatic adenocarcinoma.(13) Further investigations that incorporate an understanding of RAS downstream…”
ResultFujita, Y., Matsuda, S., Sasaki, Y., Masugi, Y., Kitago, M., Yagi, H., Abe, Y., Shinoda, M., Tokino, T., Sakamoto, M., et al. (2019) · Cancer Science · doi:10.1111/cas.14268 · Cited by 17 · see citing works
Self-citationAffolter, K. E., Hellwig, S., Nix, D. A., Bronner, M. P., Thomas, A., Fuertes, C. L., Hamil, C. L., Garrido‐Laguna, I., Scaife, C. L., Mulvihill, S. J., et al. (2021) · Neoplasia · doi:10.1016/j.neo.2021.06.005 · Cited by 16 · see citing works
Shui, L., Li, X., Peng, Y., Tian, J., Li, S., He, D., Li, A., Tian, B., Mao, L., Gao, H., et al. (2021) · Journal of Translational Medicine · doi:10.1186/s12967-021-02972-6 · Cited by 16 · see citing works
“And the phenomenon that patients with altered driven genes may have worse OS, which was reported in other studies [17, 26], was not observed in our research.”
ResultNoormohamadi, H., Samarkhazan, H. S., Kargar, M., Maroufi, F., Servatian, N., & Davami, F. (2025) · Discover Oncology · doi:10.1007/s12672-025-03383-5 · Cited by 16 · see citing works
“Although frequently mutated driver genes such as KRAS, TP53, CDKN2A, and SMAD4 are associated with a negative outcome in PDAC patients, they cannot currently be targeted by existing agents [125, 126], necessitating the identification of novel drug-gable targets.”
Ashina, S., Masuda, A., Yamakawa, K., Hamada, T., Tsujimae, M., Tanaka, T., Toyama, H., Sofue, K., Shiomi, H., Sakai, A., et al. (2023) · Journal of Gastroenterology · doi:10.1007/s00535-023-02020-8 · Cited by 15 · see citing works
“In this study, we determined alterations in the KRAS , TP53 , CDKN2A , and SMAD4 genes using NGS, ddPCR, and IHC, as reported previously [30, 31].”
BackgroundMethodSelf-citationGarimella, S. V., Gampa, S. C., & Chaturvedi, P. (2023) · Stem Cells and Cloning Advances and Applications · doi:10.2147/sccaa.s417842 · Cited by 15 · see citing works
“However, CSCs can undergo quiescence and resist such treatments, triggering a tumor relapse.(25,26) Hence, it is essential to understand the basic cellular and molecular factors that influence the functioning and survival of CSCs.”
BackgroundLoss of Claudin-1 incurred by DNMT aberration promotes pancreatic cancer progression
Zhu, L., Tang, N., Hang, H., Zhou, Y., Dong, J. P., Yang, Y., Mao, L., Qiu, Y., Fu, X., & Cao, W. (2024) · Cancer Letters · doi:10.1016/j.canlet.2024.216611 · Cited by 15 · see citing works
Sang, M., Ge, J., Ge, J., Tang, G., Wang, Q., Wu, J., Mao, L., Ding, X., & Zhou, X. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2024.1382842 · Cited by 15 · see citing works
“For example, KRAS mutations in pancreatic cancer trigger the constitutive activation of downstream signaling (18).”
Du, C., da Silva, A., Morales‐Oyarvide, V., Costa, A. D., Kozak, M. M., Dunne, R. F., Rubinson, D. A., Perez, K. J., Masugi, Y., Hamada, T., et al. (2020) · Cancer Epidemiology Biomarkers & Prevention · doi:10.1158/1055-9965.epi-19-1315 · Cited by 15 · see citing works
“Massivelyparallel sequencingwasperformed using a customized, hybrid capture–based platform that targets either 422 (version 1) or 428 (version 2) PDAC-associated genes for detection of mutations, copy number alterations, and selected structural variants, as described previously (25).”
BackgroundMethodSelf-citationAgostini, A., Orlacchio, A., Carbone, C., & Guerriero, I. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.876291 · Cited by 14 · see citing works
Treatment of pancreatic cancer in 2022
Casolino, R., & Biankin, A. V. (2023) · Cambridge Prisms Precision Medicine · doi:10.1017/pcm.2023.2 · Cited by 15 · see citing works
“…have elucidated the molecular complexity of PDAC, which challenges the development of effective treatments (Biankin et al., 2012; Chang et al., 2014; Waddell et al., 2015; Cancer Genome Atlas Research, 2017; Connor et al., 2017; Aguirre et al., 2018; Qian et al., 2018; Singhi et al., 2019).”
BackgroundPancreatic cancer: failures and hopes—a review of new promising treatment approaches
Cereda, V., & D'Andrea, M. R. (2025) · Exploration of Targeted Anti-tumor Therapy · doi:10.37349/etat.2025.1002299 · Cited by 15 · see citing works
Xie, W., Li, X., Yang, C., Li, J., Shen, G., Chen, H., Xiao, S., & Li, Y. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23116178 · Cited by 14 · see citing works
“Studies have shown that patient outcomes are associated with alterations of these four main driver genes in resected PC and patients with mutated genes have significantly shorter OS than patients with wild-type genes [53].”
BackgroundCheng, C., Hou, K., Hsu, C., & Chiang, L. (2023) · Advanced Science · doi:10.1002/advs.202304926 · Cited by 14 · see citing works
Till, J. E., McDaniel, L., Chang, C., Long, Q., Pfeiffer, S. M., Lyman, J. P., Padrón, L., Maurer, D. M., Yu, J. X., Spencer, C. N., et al. (2024) · Nature Communications · doi:10.1038/s41467-024-49915-5 · Cited by 15 · see citing works
“Consistent with previous studies 16,17 , a multi-institution study of patients with resectable PDAC reportedthatmedianOSdifferedsigni fi cantlyforpatientswithvarious KRAS mutations compared to KRAS wild-type 18 .”
Self-citation
- 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)
- 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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