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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Clinicopathologic and Molecular Features of Pancreatic Ductal Adenocarcinomas Harboring Alterations in COMPASS-like Complex Genes
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Extensive molecular profiling of KRAS wild-type as compared to KRAS mutated pancreatic ductal adenocarcinoma on 318 patients
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Background
Endoscopic ultrasound-guided tissue acquisition for comprehensive genomic profiling
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“7 In recent years, the introduction of molecularly targeted therapies, such as those directed against BRCA1/2 mutations, NTRK fusions, and microsatellite instability-high (MSI-high) status, has begun to offer new therapeutic options for a subset of patients with pancreatic cancer, reinforcing the…”
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Emelyanova, M., Ikonnikova, A. Y., Pushkov, A. A., Pudova, E. A., Krasnov, G. S., As, P., Zhanin, I. S., Khomich, D., Abramov, I. S., Tjulandin, S., et al. (2024) · Cancers · doi:10.3390/cancers16112111 · Cited by 4
“Our results are in line with those obtained by Singhi et al., who identified somatic mutations in about 1.2% of 3594 PCs [60].”
BackgroundResultInfluential
Current status of cancer genome medicine for pancreatic ductal adenocarcinoma
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EUS-guided fine-needle biopsy sampling of solid pancreatic masses with and without rapid onsite evaluation for commercial next-generation genomic profiling
Dbouk, M. H., Davis, B. G., Peller, M. T., Sloan, E., Hollander, T. G., Genere, J. P. R., Bazarbashi, A. N., Ismail, M. T., Lang, G. D., Kushnir, V. M., et al. (2025) · Gastrointestinal Endoscopy · doi:10.1016/j.gie.2025.03.1208 · Cited by 3
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“In summary, our current model and future improvements will provide an analytical tool to examine approaches to the treatment of pancreatic ductal adenocarcinoma, including the chemotherapy, surgery, reinvigoration of exhausted CTLs, and the CAR-T cell therapies [24,25,28,29].”
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Identifying Actionable Alterations in KRAS Wild-Type Pancreatic Cancer
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“Many studies have indicated that the gene encoding the proto-oncogenic GTPase KRAS as well as several tumor suppressor genes, consisting of tumor suppressor p53 (TP53), cyclin-dependent kinase inhibitor 2A (CDKN2A), and mothers against decapentaplegic homologue 4 (SMAD4), exhibit the most frequent alterations and/or m…”
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Recommendation: Treatment of pancreatic cancer in 2022 — R1/PR8
(2023) · Cambridge Prisms Precision Medicine · doi:10.1017/pcm.2023.2.pr8
Decision: Treatment of pancreatic cancer in 2022 — R1/PR9
(2023) · Cambridge Prisms Precision Medicine · doi:10.1017/pcm.2023.2.pr9
Review: Treatment of pancreatic cancer in 2022 — R1/PR7
(2022) · Cambridge Prisms Precision Medicine · doi:10.1017/pcm.2023.2.pr7
Author comment: Treatment of pancreatic cancer in 2022 — R1/PR6
Casolino, R. (2022) · Cambridge Prisms Precision Medicine · doi:10.1017/pcm.2023.2.pr6
Decision: Treatment of pancreatic cancer in 2022 — R0/PR5
(2022) · Cambridge Prisms Precision Medicine · doi:10.1017/pcm.2023.2.pr5
Recommendation: Treatment of pancreatic cancer in 2022 — R0/PR4
(2022) · Cambridge Prisms Precision Medicine · doi:10.1017/pcm.2023.2.pr4
Review: Treatment of pancreatic cancer in 2022 — R0/PR2
(2022) · Cambridge Prisms Precision Medicine · doi:10.1017/pcm.2023.2.pr2
Review: Treatment of pancreatic cancer in 2022 — R0/PR3
(2022) · Cambridge Prisms Precision Medicine · doi:10.1017/pcm.2023.2.pr3
Author comment: Treatment of pancreatic cancer in 2022 — R0/PR1
Casolino, R. (2022) · Cambridge Prisms Precision Medicine · doi:10.1017/pcm.2023.2.pr1

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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