Cited by 348Pancreatic and Hepatic Oncology ResearchCancer Genomics and DiagnosticsChromatin Remodeling and Cancer

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Real-Time Targeted Genome Profile Analysis of Pancreatic Ductal Adenocarcinomas Identifies Genetic Alterations That Might Be Targeted With Existing Drugs or Used as Biomarkers

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Singhi, Aatur D., George, Ben, Greenbowe, Joel R., Chung, Jon, Suh, James, Maitra, Anirban, Klempner, Samuel J., Hendifar, Andrew, Milind, Javle M., Golan, Talia, Brand, Randall E., Zureikat, Amer H., Roy, Somak, Schrock, Alexa B., Miller, Vincent A., Ross, Jeffrey S., Ali, Siraj M., Bahary, Nathan·2019·Gastroenterology

DOI 10.1053/j.gastro.2019.02.037

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Abstract

BACKGROUND & AIMS: It has been a challenge to select treatment for patients with pancreatic ductal adenocarcinomas (PDACs) based on genome alterations. We performed targeted genomic profile analyses of a large number of PDACs to assess the full spectrum of actionable genomic alterations. METHODS: We performed targeted genomic profile analyses of 3594 PDAC samples from an international cohort, including capture-based targeted genomic profiling of as many as 315 cancer-associated genes and intron regions of 28 genes that are rearranged in cancer cells. Tumor mutation burden (TMB) and microsatellite instability (MSI) status were also assessed. TMB was calculated across a 1.14-megabase region; TMB-high was defined as ≥20 mutations/megabase. MSI-high status was assigned based on analysis of 114 intron homopolymer loci. RESULTS: KRAS, TP53, CDKN2A, and SMAD4 were the most frequently altered genes in PDAC. We found KRAS mutations in 88% of samples. Among PDACs without mutations in KRAS, we found alterations in genes whose products are in the mitogen-activated protein kinase signaling pathway and are candidate drug targets (actionable targets, n = 132; 4%), as well as gene fusions (n = 51), gene amplifications (n = 35), genes with missense mutations (n = 30), and genes that contain deletions (n = 16). Many of these encode proteins in receptor tyrosine kinase, RAS, or mitogen-activated protein kinase signaling pathways. Aside from TP53, alterations in genes encoding DNA damage repair proteins (BRCA and FANC) were detected in 14% of PDACs. Among PDACs evaluated for MSI (n = 2563) and TMB (n = 1021), MSI-high and/or TMB-high phenotypes were detected in 0.5% of samples. Alterations in FGF23, CCND2, PIK3CA, and FGF6 were more commonly detected in intraductal papillary mucinous neoplasm-associated PDACs. CONCLUSIONS: In targeted genomic profile analyses of 3594 PDACs, we found 17% to contain genomic alterations that might make the tumor cells susceptible to currently used anticancer agents. We identified mutations in genes that could contribute to progression of intraductal papillary mucinous neoplasms into malignancies. These alterations might be used as biomarkers for early detection.

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Background
Molecular characteristics of early‐onset pancreatic ductal adenocarcinoma
Debernardi, S., Liszka, Ł., Ntala, C., Steiger, K., Esposito, I., Carlotti, E., Baker, A., McDonald, S. A. C., Graham, T. A., Dmitrović, B., et al. (2023) · Molecular Oncology · doi:10.1002/1878-0261.13576 · Cited by 11
“Overall, although alternative pathways in KRAS wild-type tumours were described [15,55,57], these are not age-associated [54] and so are unlikely to be the speciﬁc underlying cause of EOPC.”
Background
Circulating Tumor DNA-Based Detection of Microsatellite Instability and Response to Immunotherapy in Pancreatic Cancer
Kamatham, S., Shahjehan, F., & Kasi, P. M. (2020) · Frontiers in Pharmacology · doi:10.3389/fphar.2020.00023 · Cited by 11
“MSI results from mismatch repair deficiency (dMMR) and consists of repetitive 1–6 base pairs of DNA (Umar and Kunkel, 1996; Humphris et al., 2017). dMMR or loss of functional ability of any of the mismatch repair proteins (MLH1, MSH2, MSH6, and PMS2) hinders the effective DNA replication process.”
Background
Molecular advances in pancreatic cancer: A genomic, proteomic and metabolomic approach
Rajesh, S., Cox, M. J., & Runau, F. (2021) · World Journal of Gastroenterology · doi:10.3748/wjg.v27.i31.5171 · Cited by 11
The Use of Genetically Engineered Mouse Models for Studying the Function of Mutated Driver Genes in Pancreatic Cancer
Weng, C., Lin, Y., & Cheng, K. (2019) · Journal of Clinical Medicine · doi:10.3390/jcm8091369 · Cited by 12
Beyond the Genomic Mutation: Rethinking the Molecular Biomarkers of K-RAS Dependency in Pancreatic Cancers
Mottini, C., & Cardone, L. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21145023 · Cited by 11
Phase I trial of Bermekimab with nanoliposomal irinotecan and 5-fluorouracil/folinic acid in advanced pancreatic ductal adenocarcinoma
Gong, J., Thomassian, S., Kim, S., Gresham, G. K., Moshayedi, N., Ye, J. Y., Yang, J. C., Jacobs, J. P., Lo, S., Nissen, N., et al. (2022) · Scientific Reports · doi:10.1038/s41598-022-19401-3 · Cited by 11
Self-citation
Emerging Therapeutic Approaches to Pancreatic Adenocarcinoma: Advances and Future Directions
Peng, C., & Oberstein, P. E. (2025) · Current Treatment Options in Oncology · doi:10.1007/s11864-025-01352-2 · Cited by 14
“Hepa - totoxicity appeared lower when adagrasib was combined with pembrolizumab in a phase Ib/II trial which showed grade 3 liver toxicity of 8–9%[65 initial studies focused on germline mutations in BRCA1/2 , which lead to DNA homologous recombination deficiency (HRD).”
Improved predictability of pancreatic ductal adenocarcinoma diagnosis using a blood immune cell biomarker panel developed from bulk mRNA sequencing and single-cell RNA-sequencing
Jang, S. I., Lee, H. K., Chang, E., Kim, S., Kim, S. Y., Hong, I. Y., Kim, J. K., Lee, H. S., Yang, J., Cho, J. H., et al. (2023) · Cancer Immunology Immunotherapy · doi:10.1007/s00262-023-03458-8 · Cited by 10
FoundationOne® CDx gene profiling in Japanese pancreatic ductal adenocarcinoma patients: a single-institution experience
Kimura, R., Ohtsuka, T., Kubo, M., Kajihara, A., Fujii, A., Watanabe, Y., Mori, Y., Ikenaga, N., Nakata, K., Shindo, K., et al. (2020) · Surgery Today · doi:10.1007/s00595-020-02123-2 · Cited by 10
“Previous reports have shown that > 95% of PDACs have KRAS mutations (G12D being the most common allele) [24, 25], and approximately 50–70% of PDACs have TP53 mutations [26, 27].”
Background
Practical Considerations Relating to Routine Clinical Biomarker Testing for Non–small Cell Lung Cancer: Focus on Testing for RET Fusions
Herbst, R. S., Aisner, D. L., Sonett, J. R., Turk, A. T., Weintraub, J. L., & Lindeman, N. I. (2021) · Frontiers in Medicine · doi:10.3389/fmed.2020.562480 · Cited by 10
“Although outside of the scope of this review, RET fusions have also been identified in ∼20% of papillary thyroid carcinomas (17, 18), and at a lower frequency (≤1%) in other tumor types including breast (19), colorectal (20), and pancreatic (21) cancers.”
Background
Predictors of Long-Term Survival in Pancreatic Ductal Adenocarcinoma after Pancreatectomy: TP53 and SMAD4 Mutation Scoring in Combination with CA19-9
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Molecular assessment of endoscopically collected pancreatic juice and duodenal fluid from patients with pancreatic diseases
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Germline mutations of homologous recombination genes and clinical outcomes in pancreatic cancer: a multicenter study in Taiwan
Cheng, S. M., Su, Y., Chiang, N., Wang, C., Chao, Y., Huang, C., Tsai, H., Chen, S., Chang, C.-Y., Tsai, C., et al. (2024) · Journal of Biomedical Science · doi:10.1186/s12929-024-01008-7 · Cited by 9
“%) populations [13, 48].”
Triple Blockade of Oncogenic RAS Signaling Using KRAS and MEK Inhibitors in Combination with Irradiation in Pancreatic Cancer
Wang, X., Breuer, J., Garbe, S., Giordano, F. A., Brossart, P., Feldmann, G., & Bisht, S. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25116249 · Cited by 10
“Pancreatic cancer is driven by oncogenic KRAS variants in more than 90% of cases [29], and even those cases with wild type KRAS often show alternative alterations that activate oncogenic signaling through the RAS/MAPK pathway [48].”
Background
Real‐world genome profiling in Japanese patients with pancreatic ductal adenocarcinoma focusing on HRD implications
Doi, T., Ishikawa, T., Sakakida, T., Itani, J., Sone, D., Morita, R., Kataoka, S., Miyake, H., Seko, Y., Yamaguchi, K., et al. (2024) · Cancer Science · doi:10.1111/cas.16329 · Cited by 9
“15,16 Consistent with the re-sults of this study, according to a meta-analysis, the following genes were most common in PDAC with respect to HRD-related gene mutations (germline and somatic): BRCA1 , 0.9%; BRCA2 , 3.5%; PALB2 , 0.2%; ATM , 2.2%; ATR , 0.1%; and CHEK2 , 0.3%.”
BackgroundResultInfluential
FGF6 inhibits oral squamous cell carcinoma progression by regulating PI3K/AKT and MAPK pathways
Zhang, X., Xu, Y., Shi, L., Chen, X., Hu, M., Zhang, M., Nie, M., & Liu, X. (2024) · Scientific Reports · doi:10.1038/s41598-024-78552-7 · Cited by 9
“Singhi et al. conducted targeted genome analysis of a large number of pancreatic ductal adenocarcinomas (PDAC) and found that FGF6 may be related to the pathogenesis of PDAC 19 .”
Switch II Pocket Inhibitor Allosterically Freezes KRASG12D Nucleotide-binding Site and Arrests the GTPase Cycle
Kim, H., Gasmi-Seabrook, G. M. C., Uchida, A., Gebregiworgis, T., Marshall, C. B., & Ikura, M. (2025) · Journal of Molecular Biology · doi:10.1016/j.jmb.2025.169162 · Cited by 10
Tetrandrine synergizes with MAPK inhibitors in treating KRAS-mutant pancreatic ductal adenocarcinoma via collaboratively modulating the TRAIL-death receptor axis
Tang, S., Duan, Y., Yuan, T., Hu, Y., Yuan, L., Shen, N., Fu, Y., Pu, C., Wang, X., Xu, J. Q., et al. (2023) · Pharmacological Research · doi:10.1016/j.phrs.2023.106955 · Cited by 9
An activity-based functional test for identifying homologous recombination deficiencies across cancer types in real time
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Ex vivo modeling of acquired drug resistance in BRAF - mutated pancreatic cancer organoids uncovers individual therapeutic vulnerabilities
Steiner, S., Pliego‐Mendieta, A., Haberecker, M., Hussung, S., Kollár, A., Fritsch, R., Arnold, F. M., Lenggenhager, D. M., Planas‐Paz, L., & Pauli, C. (2024) · Cancer Letters · doi:10.1016/j.canlet.2024.216650 · Cited by 10
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].”
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
Loss of p53 and SMAD4 induces adenosquamous subtype pancreatic cancer in the absence of an oncogenic KRAS mutation
Yang, D., Sun, X., Moniruzzaman, R., Wang, H., Citu, C., Zhao, Z., Wistuba, I. I., Wang, H., Maitra, A., & Chen, Y. (2024) · Cell Reports Medicine · doi:10.1016/j.xcrm.2024.101711 · Cited by 7
Self-citation
Liquid Biopsy in Pancreatic Ductal Adenocarcinoma: A Review of Methods and Applications
Dubrovsky, G., Ross, A., Jalali, P., & Lotze, M. T. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252011013 · Cited by 11
“About 88% of all PDAC cases will have a KRAS mutation, typically at the G12/13 and Q61 loci [62,63].”
Background
Feasibility and clinical utility of endoscopic ultrasound-guided tissue acquisition for comprehensive genomic profiling in pancreatic cancer: A systematic review and meta-analysis
Ko, S. W., Jo, I. H., & Yoon, S. B. (2024) · Pancreatology · doi:10.1016/j.pan.2024.12.012 · Cited by 9
Germline Pathogenic Variants in Patients with Pancreatic Ductal Adenocarcinoma and Extra-Pancreatic Malignancies: A Nationwide Database Analysis
Kryklyva, V., Pflüger, M. J., Ouchene, H., Volleberg-Gorissen, H., Mensenkamp, A. R., Jonker, M. A., van de Water, C., Nagtegaal, I. D., Ligtenberg, M. J. L., & Brosens, L. A. A. (2025) · Modern Pathology · doi:10.1016/j.modpat.2025.100709 · Cited by 8
Ten‐year experience in optimizing neoadjuvant therapy for localized pancreatic cancer—Medical college of Wisconsin perspective
Ward, E. P., Evans, D. B., & Tsai, S. (2021) · Journal of Surgical Oncology · doi:10.1002/jso.26395 · Cited by 8
“5%, respectively).(37) Instead, the vast majority of pancreatic cancers require a more complex molecular characterization which can only be performed on a more substantial amount of tumor tissue; certainly more than is typically achieved with a fine needle biopsy.”
Background
Store-Operated Calcium Entry: Shaping the Transcriptional and Epigenetic Landscape in Pancreatic Cancer
Kutschat, A. P., Johnsen, S. A., & Hamdan, F. H. (2021) · Cells · doi:10.3390/cells10050966 · Cited by 9
“Tumors with such alterations displayed higher sensitivity to receptor tyrosine kinase inhibitors, suggesting that these tumors show a greater dependence on MAPK signaling [17,18].”
Background
EUS-FNA Biopsies to Guide Precision Medicine in Pancreatic Cancer: Results of a Pilot Study to Identify KRAS Wild-Type Tumours for Targeted Therapy
Lundy, J., Harris, M., Zalcberg, J. R., Zimet, A. S., Goldstein, D., Gebski, V., Borsaru, A., Desmond, C., Swan, M. P., Jenkins, B. J., et al. (2021) · Frontiers in Oncology · doi:10.3389/fonc.2021.770022 · Cited by 8
Rational testing for gene fusion in colorectal cancer: MSI and RAS-BRAF wild-type metastatic colorectal cancer as target population for systematic screening
Delaye, M., Ibadioune, S., Julié, C., Marin, C., Peschaud, F., Lupinacci, R. M., Vacher, S., Ahmanache, L., Antonio, S., Schnitzler, A., et al. (2022) · European Journal of Cancer · doi:10.1016/j.ejca.2022.04.024 · Cited by 9
Risk of pancreatic ductal adenocarcinoma associated with carriage of BRCA1 and/or BRCA2 mutation: A systematic review and meta‐analysis
McGarry, J., Creavin, B., Kelly, M. E., & Gallagher, T. K. (2022) · Journal of Surgical Oncology · doi:10.1002/jso.26994 · Cited by 8
The Role of Endoscopic Ultrasound in Pancreatic Cancer Staging in the Era of Neoadjuvant Therapy and Personalised Medicine
Bispo, M., Marques, S., Rio‐Tinto, R., Fidalgo, P. O., & Deviere, J. M. E. (2020) · GE Portuguese Journal of Gastroenterology · doi:10.1159/000509197 · Cited by 8
Germline pathogenic variants of cancer predisposition genes in a multicentre Italian cohort of pancreatic cancer patients.
Orsi, G., Carconi, C., Ghiorzo, P., Carrera, P., Pastorino, L., Presi, S., Chiaravalli, M., Barbieri, E., Giordano, G., Sciallero, S., et al. (2024) · European Journal of Cancer · doi:10.1016/j.ejca.2024.114226 · Cited by 7
Stress and Obesity Signaling Converge on CREB Phosphorylation to Promote Pancreatic Cancer
Sun, X., Teper, Y., Sinnett‐Smith, J. W., Markarian, M., Hines, O. J., Li, G., Eibl, G., & Rozengurt, E. (2024) · Molecular Cancer Research · doi:10.1158/1541-7786.mcr-24-0785 · Cited by 7
Combined Omipalisib and MAPK Inhibition Suppress PDAC Growth
Bye, B. A., Jack, J. L., Pierce, A., Walsh, R. M., Eades, A. E., Chalise, P., Olou, A. A., & VanSaun, M. N. (2025) · Cancers · doi:10.3390/cancers17071152 · Cited by 15
Generation of T cell responses against broad KRAS hotspot neoantigens for cell therapy or TCR discovery
Conn, B. P., Dietze, J. L., Yee, C. J., Hallisey, M., Ortiz-Caraveo, I., van Buuren, M. M., Gaynor, R. B., Foley, K. C., Choi, J., & Juneja, V. R. (2025) · Cell Reports Methods · doi:10.1016/j.crmeth.2025.101049 · Cited by 9
Nouvelle AMM : olaparib — cancer du pancréas avec mutation germinale de BRCA
Hilmi, M., & Neuzillet, C. (2020) · Bulletin du Cancer · doi:10.1016/j.bulcan.2020.06.009 · Cited by 7
Lorlatinib Induces Durable Disease Stabilization in a Pancreatic Cancer Patient with a ROS1 p.L1950F Mutation: Case Report
Velthaus, J.-L., Iglauer, P., Simon, R., Bokemeyer, C., Bannas, P., Beumer, N., Imbusch, C. D., Goekkurt, E., & Loges, S. (2021) · Oncology Research and Treatment · doi:10.1159/000517616 · Cited by 7
Beyond the Front Line: Emerging Data for Maintenance Therapy in Pancreatic Cancer
Singh, H., Perez, K. J., Wolpin, B. M., & Aguirre, A. J. (2021) · Journal of Clinical Oncology · doi:10.1200/jco.21.01510 · Cited by 7
Ras Variant Biology and Contributions to Human Disease
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The EUS molecular evaluation of pancreatic cancer: A prospective multicenter cohort trial
Croagh, D. G., Masoumi-Moghaddam, S., Lundy, J., Gao, H., Rathi, V., Swan, M. P., Desmond, C., Bhutani, M., Southey, M., Vaughan, R., et al. (2021) · Endoscopic Ultrasound · doi:10.4103/eus-d-20-00230 · Cited by 7
Combined PI3K and MAPK inhibition synergizes to suppress PDACPreprint
Bye, B. A., Jack, J. L., Pierce, A., Walsh, R. M., Eades, A. E., Chalise, P., Olou, A. A., & VanSaun, M. N. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.08.15.553438 · Cited by 7
“Since the vast majority of PDAC presents with mutant KRAS (5-8), dual therapeutics targeting PI3K and direct inhibitors of mutant KRAS (13, 53) may prove more synergistic than therapeutics targeting downstream targets of mutant RAS (19, 26).”
Background
Advances in Drug Therapy for Metastatic Pancreatic Ductal Adenocarcinoma
Gao, J., Wang, J., Guan, C., Shi, W., Dong, Q., Sheng, J., Zou, X., Xu, Z., Ge, Y., Huang, Z., et al. (2024) · Journal of Cancer · doi:10.7150/jca.89788 · Cited by 7
How to find a needle in a haystack: a systematic review on targeting KRAS wild-type pancreatic cancer
Mouawad, A., Habib, S., Boutros, M., Attieh, F., & Kourié, H. R. (2024) · Future Oncology · doi:10.1080/14796694.2024.2355078 · Cited by 6
Survival of Patients with Resected Microsatellite Instability-High, Mismatch Repair Deficient, and Lynch Syndrome-Associated Pancreatic Ductal Adenocarcinomas
Eikenboom, E. L., Nasar, N. F., Seier, K., Gönen, M., Spaander, M. C. W., O'Reilly, E. M., Jarnagin, W. R., Drebin, J. A., D'Angelica, M. I., Kingham, T. P., et al. (2024) · Annals of Surgical Oncology · doi:10.1245/s10434-024-16621-x · Cited by 6
Precision Medicine and Pancreatic Cancer
George, B. (2021) · Surgical Oncology Clinics of North America · doi:10.1016/j.soc.2021.06.008 · Cited by 6
Self-citation
How to select the most appropriate adjuvant treatment after neoadjuvant treatment and resection for locally advanced pancreatic cancer?
Rangelova, E. B., & Bratlie, S. O. (2021) · Journal of Gastrointestinal Oncology · doi:10.21037/jgo-21-474 · Cited by 6
Microsatellite instability in patients with hepato-biliary-pancreatic malignancies in clinical practice (KHBO 1903)
Kubo, S., Nagano, H., Tsujie, M., Seo, S., Gotoh, K., Wada, H., Nakashima, S., & Ioka, T. (2022) · International Journal of Clinical Oncology · doi:10.1007/s10147-022-02187-9 · Cited by 6
A multicenter comparative study of endoscopic ultrasound-guided fine-needle biopsy using a Franseen needle versus conventional endoscopic ultrasound-guided fine-needle aspiration to evaluate microsatellite instability in patients with unresectable pancreatic cancer
Takagi, T. J., Sugimoto, M., Imamura, H., Takahata, Y., Nakajima, Y., Suzuki, R., Konno, N., Asama, H., Sato, Y., Irie, H., et al. (2023) · Clinical Endoscopy · doi:10.5946/ce.2022.019 · Cited by 6
Uso de paneles de genes en pacientes con alto riesgo de cáncer digestivo hereditario: documento de posicionamiento de la AEG, SEOM, AEGH y consorcio IMPaCT-GENÓMICA
Carballal, S., Balaguer, F., Bujanda, L., Capellá, G., Santiago, S. G., Jover, R., Moreira, L., Pineda, M., Ruíz-Ponte, C., Sánchez‐Heras, A. B., et al. (2023) · Gastroenterología y Hepatología · doi:10.1016/j.gastrohep.2023.06.004 · Cited by 6
Feasibility of BRCA1/2 Testing of Formalin-Fixed and Paraffin-Embedded Pancreatic Tumor Samples: A Consecutive Clinical Series
Bruno, R., Sensi, E., Lupi, C., Giordano, M., Bernardini, L., Vivaldi, C., Fornaro, L., Vasile, E., Campani, D., & Fontanini, G. (2021) · Diagnostics · doi:10.3390/diagnostics11061046 · Cited by 6
“The high genomic heterogeneity of PDAC can explain the relatively slow progress in the development and approval of effective targeted therapies [10].”
Background
Prostate Ductal Adenocarcinoma Revisited: Clinicopathological and Genomic Characterization Identifies Heterogenous Group of Diseases with Implications for Patient Management
Cai, Q., Meng, X., Sun, J., Gagan, J., Aggarwal, A., Khanshour, A. M., Bhanvadia, R. R., Xu, J., Mohanty, S. K., & Shah, R. B. (2025) · Modern Pathology · doi:10.1016/j.modpat.2025.100743 · Cited by 5
Novel therapeutic strategies in pancreatic cancer: moving beyond cytotoxic chemotherapy
Geerinckx, B., Teuwen, L.-A. M. N., Foo, T., Vandamme, T., Smith, A., Peeters, M., & Price, T. J. (2023) · Expert Review of Anticancer Therapy · doi:10.1080/14737140.2023.2270161 · Cited by 5
“Compared to KRAS mutant (KRAS MT ) PDAC, KRAS wild-type (KRAS WT ) tumors represent a minority of PDAC (8–12% of all [70,71], up to 16% of patients younger than 50 years [72]) but they may harbor alternative oncogenic drivers with the potential for tailored treatments, making their identification a…”
Background
Mutational profiling of 103 unresectable pancreatic ductal adenocarcinomas using EUS-guided fine-needle biopsy
Buchberg, J., de Stricker, K., Pfeiffer, P., Mortensen, M. B., & Detlefsen, S. (2024) · Endoscopic Ultrasound · doi:10.1097/eus.0000000000000072 · Cited by 6

Authors: Singhi, A. D., George, B., Greenbowe, J. R., Chung, J., Suh, J., Maitra, A., Klempner, S. J., Hendifar, A., Milind, J. M., Golan, T., Brand, R. E., Zureikat, A. H., Roy, S., Schrock, A. B., Miller, V. A., Ross, J. S., Ali, S. M., & Bahary, N.
Affiliations: University of Pittsburgh Medical Center (US)
Medical College of Wisconsin (US)
Foundation Medicine (United States) (US)
The University of Texas MD Anderson Cancer Center (US)
Cedars-Sinai Medical Center (US)
Tel Aviv University (IL)
Corresponding author: Singhi, Aatur D.
ORCID: Singhi, Aatur D.
George, Ben
Chung, Jon
Suh, James
Maitra, Anirban
Klempner, Samuel J.
Hendifar, Andrew
Golan, Talia
Brand, Randall E.
Zureikat, Amer H.
Roy, Somak
Schrock, Alexa B.
Miller, Vincent A.
Ross, Jeffrey S.
Ali, Siraj M.
Bahary, Nathan
Venue: Gastroenterology
Publisher: Elsevier BV
Published: 2019-06
Volume: 156
Issue: 8
Pages: 2242-2253.e4
ISSN: 0016-5085 (ISSN-L)
DOI: 10.1053/j.gastro.2019.02.037
OpenAlex: W2919944461
Cited by: 348
References: 60
Citations by year: 2026: 27 · 2025: 43 · 2024: 51 · 2023: 55 · 2022: 56 · 2021: 63 · 2020: 43 · 2019: 9
FWCI: 17.87
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-nd
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
creativecommons.org/licenses/by-nc-nd/4.0/ (vor)
Locations: Gastroenterology (publishedVersion, cc-by-nc-nd)
PubMed (publishedVersion)
Funders: Pancreatic Cancer Action Network
Association for Molecular Pathology
Topics: Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
Keywords: pancreatic ductal adenocarcinoma, actionable genomic alterations, KRAS mutation, TP53, CDKN2A, SMAD4, MAPK signaling, gene fusion, gene amplification, microsatellite instability, tumor mutational burden, DNA repair, intraductal papillary mucinous neoplasm, biomarkers, therapeutic target
MeSH terms: Fibroblast Growth Factor-23, Adult, Aged, Aged, 80 and over, Antineoplastic Agents, Adenocarcinoma, Mucinous, Chromosome Mapping, Female, Humans, Male, Middle Aged, Neoplasm Invasiveness, Neoplasm Staging, Pancreatic Neoplasms, Retrospective Studies, Biomarkers, Tumor, Genetic Variation, Cohort Studies, Gene Expression Regulation, Neoplastic, Carcinoma, Pancreatic Ductal, Young Adult, Genomic Structural Variation, Molecular Targeted Therapy, Real-Time Polymerase Chain Reaction

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Real-Time Targeted Genome Profile Analysis of Pancreatic Ductal Adenocarcinomas Identifies Genetic Alterations That Might Be Targeted With Existing Drugs or Used as Biomarkers

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