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Whole genomes redefine the mutational landscape of pancreatic cancer
Open accessAbstract
Pancreatic cancer remains one of the most lethal of malignancies and a major health burden. We performed whole-genome sequencing and copy number variation (CNV) analysis of 100 pancreatic ductal adenocarcinomas (PDACs). Chromosomal rearrangements leading to gene disruption were prevalent, affecting genes known to be important in pancreatic cancer (TP53, SMAD4, CDKN2A, ARID1A and ROBO2) and new candidate drivers of pancreatic carcinogenesis (KDM6A and PREX2). Patterns of structural variation (variation in chromosomal structure) classified PDACs into 4 subtypes with potential clinical utility: the subtypes were termed stable, locally rearranged, scattered and unstable. A significant proportion harboured focal amplifications, many of which contained druggable oncogenes (ERBB2, MET, FGFR1, CDK6, PIK3R3 and PIK3CA), but at low individual patient prevalence. Genomic instability co-segregated with inactivation of DNA maintenance genes (BRCA1, BRCA2 or PALB2) and a mutational signature of DNA damage repair deficiency. Of 8 patients who received platinum therapy, 4 of 5 individuals with these measures of defective DNA maintenance responded.
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“the genomic landscape of PDAC is also dominated by loss of function alterations of TP53, SMAD4 (also known as DPC4), and CDKN2A45,48–50.”
From Pancreatic cancer: Advances and challenges (2023) · cites this paper as [49]
In the citing paper
“supporting previous studies linking loss of PALB2 function with BRCA-deficient signatures [7, 10, 13].”
From Whole-genome sequencing reveals clinically relevant insights into the aetiology of familial breast cancers (2019) · cites this paper as [10]
In the citing paper
“Loss of function of BRCA1, BRCA2 and PALB2 yield a high mutation burden and specific signatures inferring defective HR [7, 9, 10, 13].”
From Whole-genome sequencing reveals clinically relevant insights into the aetiology of familial breast cancers (2019) · cites this paper as [10]
In the citing paper
“G12V is frequently identified in pancreatic ductal adenocarcinomas and is associated with aggressive disease biology [16,21].”
From The Role of KRAS Mutations in Colorectal Cancer: Biological Insights, Clinical Implications, and Future Therapeutic Perspectives (2025) · cites this paper as [21]
In the citing paper
“Chromatin remodeling and SWI/SNF complex genes are one of the most frequently altered class of genes in PDAC45,48–50, and can occur via somatic deletions of the associated chromosomal loci94.”
From Pancreatic cancer: Advances and challenges (2023) · cites this paper as [49]
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“Discussion The pronounced inter- and intrapatient heterogeneity, distinct morphologic and molecular subtypes, and the fact that most mutations occur with a frequency of under 5% in pancreatic cancer (22) requires analyses of large patient cohorts for definition and characterization of clinically relevant pancreatic ca…”
BackgroundEpigenetic Alterations in Pancreatic Cancer Metastasis
Wang, S. S., Xu, J., Ji, K. Y., & Hwang, C. (2021) · Biomolecules · doi:10.3390/biom11081082 · Cited by 50
“While KRAS, TP53, SMAD4, and CDKN2A driver mutations are core to early PDA progression, there is a vast genetic heterogeneity among PDA patients, harboring a range of less frequent genetic mutations that facilitate carcinogenesis [6,7].”
BackgroundInfluentialMolecular characteristics of BRCA1/2 and PALB2 mutations in pancreatic ductal adenocarcinoma
Seeber, A., Zimmer, K., Kocher, F., Puccini, A., Xiu, J., Nabhan, C., Elliott, A., Goldberg, R. M., Grothey, A. F., Shields, A. F., et al. (2020) · ESMO Open · doi:10.1136/esmoopen-2020-000942 · Cited by 52
TP53 mutations in head and neck cancer
Nathan, C. O., Khandelwal, A. R., Wolf, G. T., Rodrigo, J. P., Mäkitie, A. A., Saba, N. F., Forastiere, A. A., Bradford, C. R., & Ferlito, A. (2022) · Molecular Carcinogenesis · doi:10.1002/mc.23385 · Cited by 55
“Beyond exerting dominant repression over the wild‐type counterpart due to loss of heterozygosity, some mutants might exert new malignant abilities distinct from those caused by the loss of the wild‐type function.(25,26) Most TP53 missense mutants acquire oncogenic gain‐of‐function (GOF) activities.”
BackgroundThe Promise of Epigenomic Therapeutics in Pancreatic Cancer
Lomberk, G. A., Iovanna, J., & Urrutia, R. A. (2016) · Epigenomics · doi:10.2217/epi-2015-0016 · Cited by 50
The role of cancer stem cells in tumor heterogeneity and resistance to therapy
Konrad, C. V., Murali, R., Varghese, B. A., & Nair, R. (2016) · Canadian Journal of Physiology and Pharmacology · doi:10.1139/cjpp-2016-0079 · Cited by 51
“…Myeloid Leukemia (AML) (Walter et al. 2012), 323 chronic lymphocytic leukaemia (CLL) (Schuh et al. 2012), breast cancer (Navin et al. 2011; 324 Nik-Zainal et al. 2012; Shah et al. 2012), renal cell carcinoma (Xu et al. 2012) and pancreatic 325 cancers (Campbell et al. 2010; Waddell et al. 2015).”
BackgroundGemenetzis, G., Groot, V. P., Blair, A. B., Ding, D., Thakker, S. S., Fishman, E. K., Cameron, J. L., Makary, M. A., Weiss, M. J., Wolfgang, C. L., et al. (2018) · Journal of Surgical Oncology · doi:10.1002/jso.25288 · Cited by 51
“Both duodenal and biliary bypass interventions may result in effective long‐term palliation in metastatic PDAC patients.(8,42) A celiac plexus block for future management of malignant pain was also performed selectively in patients with large tumors of the pancreatic neck, body, and tail.”
BackgroundSelf-citationExosomal microRNA in Pancreatic Cancer Diagnosis, Prognosis, and Treatment: From Bench to Bedside
Uddin, M. H., Hallak, M. N. A., Philip, P. A., Mohammad, R. M., Viola, N. T., Wagner, K., & Azmi, A. S. (2021) · Cancers · doi:10.3390/cancers13112777 · Cited by 51
“Alterations in other tumor suppressor genes include CDKN2A [13], TP53 [14], and DPC4/SMAD4 [15].”
BackgroundMurphy, K. J., Reed, D. A., Vennin, C., Conway, J. R. W., Nobis, M., Yin, J. X. M., Chambers, C. R., Pereira, B., Lee, V., Filipe, E. C., et al. (2021) · Science Advances · doi:10.1126/sciadv.abh0363 · Cited by 54
Self-citationExploiting the p53 Pathway for TherapyPreprint
Cheok, C. F., & Lane, D. P. (2017) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a026310 · Cited by 53
“…found to be selectively up-regulated by mutant p53, and mutant p53 expression was required to maintain the prometastatic phenotype of the murine model of pancreatic cancer, which is a highly metastatic cancer that is frequently linked with p53 mutations (Morton et al. 2010; Waddell et al. 2015).”
BackgroundMolecular Subtyping and Precision Medicine for Pancreatic Cancer
Froeling, F. E. M., Casolino, R., Pea, A., Biankin, A. V., Chang, D. K.-F., & Precision-Panc, O. B. O. (2021) · Journal of Clinical Medicine · doi:10.3390/jcm10010149 · Cited by 52
“Furthermore, DNA repair defects extended beyond germline variations in BRCA1/2 genes and included other genes that contribute to the DDR signature, such as germline and somatic mutations in PALB2 and somatic mutations in BRCA1, BRCA2, ATM, RPA1, REV3L, XRCC4 and XRCC.”
BackgroundInfluentialSelf-citationMass spectrometry‐based targeted proteomics for analysis of protein mutations
Lin, T., Zhang, T., Kitata, R. B., Liu, T., Smith, R. D., Qian, W., & Shi, T. (2021) · Mass Spectrometry Reviews · doi:10.1002/mas.21741 · Cited by 51
Stossel, C., Raitses‐Gurevich, M., Atias, D., Beller, T., Gorman, Y. G., Halperin, S., Peer, E., Denroche, R. E., Zhang, A. X. W., Notta, F., et al. (2023) · Cancer Discovery · doi:10.1158/2159-8290.cd-22-0412 · Cited by 53
Reese, K.-L., Pantel, K., & Smit, D. J. (2024) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-024-03166-w · Cited by 56
ccmGDB: a database for cancer cell metabolism genes
Kim, P., Cheng, F., Zhao, J., & Zhao, Z. (2015) · Nucleic Acids Research · doi:10.1093/nar/gkv1128 · Cited by 52
Circulating tumor DNA as a liquid biopsy target for detection of pancreatic cancer
Takai, E., & Yachida, S. (2016) · World Journal of Gastroenterology · doi:10.3748/wjg.v22.i38.8480 · Cited by 53
Pancreas–Microbiota Cross Talk in Health and Disease
Adolph, T. E., Mayr, L., Grabherr, F., Schwärzler, J., & Tilg, H. (2019) · Annual Review of Nutrition · doi:10.1146/annurev-nutr-082018-124306 · Cited by 48
Rebelatto, T. F., Falavigna, M., Pozzari, M., Spada, F., Cella, C. A., Laffi, A., Pellicori, S., & Fazio, N. (2019) · Cancer Treatment Reviews · doi:10.1016/j.ctrv.2019.101895 · Cited by 50
Li, S., Lavrijsen, M., Bakker, A., Magierowski, M., Magierowska, K., Liu, P., Wang, W., Peppelenbosch, M. P., & Smits, R. (2020) · Oncogene · doi:10.1038/s41388-020-1232-5 · Cited by 49
Cameron, D., Schröder, J., Penington, J. S., Do, H., Molania, R., Dobrovic, A., Speed, T. P., & Papenfuss, A. T. (2017) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/110387 · Cited by 50
Li, F., Ling, X., Chakraborty, S., Fountzilas, C. K., Wang, J., Jamroze, A., Liu, X., Kaliński, P., & Tang, D. G. (2023) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-023-02787-x · Cited by 51
“It is well known that pancreatic cancer is the most-dif-ficult-to-treat lethal malignancy with high genome DNA instability persistence and genetic heterogeneity among metastatic cells [43, 44].”
BackgroundOvercoming treatment resistance in cancer: Current understanding and tactics
Wu, G. J., Wilson, G., George, J., Liddle, C., Hebbard, L., & Qiao, L. (2016) · Cancer Letters · doi:10.1016/j.canlet.2016.04.018 · Cited by 49
Drosos, Y., Escobar, D., Chiang, M.-Y., Roys, K., Valentine, V. A., Valentine, M. B., Rehg, J. E., Sahai, V., Begley, L., Ye, J., et al. (2017) · Scientific Reports · doi:10.1038/s41598-017-11661-8 · Cited by 51
Epithelial-Stromal Interactions in Pancreatic Cancer
Zhang, Y., Crawford, H. C., & di Magliano, M. P. (2018) · Annual Review of Physiology · doi:10.1146/annurev-physiol-020518-114515 · Cited by 52
Non-coding RNAs in Pancreatic Ductal Adenocarcinoma
Gong, R., & Jiang, Y. (2020) · Frontiers in Oncology · doi:10.3389/fonc.2020.00309 · Cited by 49
Targeting the Metabolic Rewiring in Pancreatic Cancer and Its Tumor Microenvironment
Yamamoto, K., Iwadate, D., Kato, H., Nakai, Y., Tateishi, K., & Fujishiro, M. (2022) · Cancers · doi:10.3390/cancers14184351 · Cited by 52
“These include patients with mutations in DNA damage repair (DDR) pathway genes (4–7%), such as BRCA1/2, who are responsive to platinumbased chemotherapy [15,16] or maintenance therapy with the poly-ADP ribose polymerase (PARP) inhibitor, olaparib, after disease stabilization with platinum-based therapy (POLO study) [1…”
BackgroundPancreatic Ductal Adenocarcinoma: Molecular Pathology and Predictive Biomarkers
Taherian, M., Wang, H., & Wang, H. (2022) · Cells · doi:10.3390/cells11193068 · Cited by 52
Mitochondrial DNA damage, repair, and replacement in cancer
Vodička, P., Vodenková, S., Danesova, N., Vodičková, L., Zobalová, R., Tomášová, K., Boukalová, Š., Berridge, M. V., & Neužil, J. (2024) · Trends in cancer · doi:10.1016/j.trecan.2024.09.010 · Cited by 50
Zhong, Y., Macgregor‐Das, A. M., Saunders, T., Whittle, M. C., Makohon-Moore, A. P., Kohutek, Z. A., Poling, J., Herbst, B. T., Javier, B. M., Cope, L., et al. (2016) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-15-1615 · Cited by 46
“Future studies aimed at understanding the gains of function of different mutant TP53 proteins versus TP53 deletion, another common event in PDA (39), in modulating these mechanisms are expected to provide additional insights for eventual therapeutic exploitation.”
Self-citationGermline mutations in pancreatic cancer and potential new therapeutic options
Pihlak, R., Valle, J. W., & McNamara, M. G. (2017) · Oncotarget · doi:10.18632/oncotarget.17291 · Cited by 48
“These data suggest that if defective DNA maintenance could be identified in addition to the mutations in the BRCA pathway genes, one could identify a wider group of patients with BRCAness that could then be potentially treated with new therapeutics targeting that pathway [32, 51].”
BackgroundInfluentialP-Rex1 and P-Rex2 RacGEFs and cancer
Srijakotre, N., Man, J., Ooms, L. M., LUCATO, C. M. A., Ellisdon, A. M., & Mitchell, C. A. (2017) · Biochemical Society Transactions · doi:10.1042/bst20160269 · Cited by 48
Targeted deep sequencing of circulating tumor DNA in metastatic pancreatic cancer
Berger, A. W., Schwerdel, D., Ettrich, T. J., Hann, A., Schmidt, S. A., Kleger, A., Marienfeld, R. B., & Seufferlein, T. T. W. (2017) · Oncotarget · doi:10.18632/oncotarget.23330 · Cited by 48
“The mentioned genes were selected according to previously published data, covering the most frequently mutated genes in PDAC [5, 6].”
BackgroundGermline Variants and Risk for Pancreatic Cancer
Zhan, W., Shelton, C. A., Greer, P. J., Brand, R. E., & Whitcomb, D. C. (2018) · Pancreas · doi:10.1097/mpa.0000000000001136 · Cited by 50
Hu, H., Tu, W., Chen, Y., Zhu, M., Jin, H., Huang, T., Zou, Z., & Xia, Q. (2020) · Journal of Cancer · doi:10.7150/jca.38981 · Cited by 48
“Rapid progress has been made in researches toward the genomics and proteomics of PDAC [3, 4]; however, it brings few benefits in the clinical settings [4].”
BackgroundHuang, B., Trujillo, M. A. M., Fujikura, K., Qiu, M., Chen, F., Felsenstein, M., Zhou, C., Skaro, M. F., Gauthier, C. D., Macgregor‐Das, A. M., et al. (2020) · The Journal of Pathology · doi:10.1002/path.5515 · Cited by 48
Self-citationGonzález, R. S., Raza, A., Propst, R., Adeyi, O. A., Bateman, J., Sopha, S. C., Shaw, J. C., & Auerbach, A. (2020) · Archives of Pathology & Laboratory Medicine · doi:10.5858/arpa.2020-0047-ra · Cited by 48
HMGA1 induces FGF19 to drive pancreatic carcinogenesis and stroma formation
Chia, L., Wang, B., Kim, J., Luo, L., Shuai, S., Herrera, I., Chen, S. Y., Li, L., Xian, L., Huso, T. H., et al. (2023) · Journal of Clinical Investigation · doi:10.1172/jci151601 · Cited by 52
“Although previous studies identified mutant KRAS and molecular alterations inactivating CDKN2A , TP53 , and TGF-β pathway components, these findings have not translated into improved therapies, nor have they led to effective screening strategies (3, 4, 5).”
Metadata
- Authors
- Initiative, A. P. C. G., Waddell, N., Pajic, M., Patch, A.-M., Chang, D. K., Kassahn, K. S., Bailey, P., Johns, A. L., Miller, D., Nones, K., Quek, K., Quinn, M. C. J., Robertson, A. J., Fadlullah, M. Z. H., Bruxner, T. J. C., Christ, A. N., Harliwong, I., Idrisoglu, S., Manning, S., Nourse, C., Nourbakhsh, E., Wani, S., Wilson, P. J., Markham, E., Cloonan, N., Anderson, M. J., Fink, J. L., Holmes, O., Kazakoff, S. H., Leonard, C., Newell, F., Poudel, B., Song, S., Taylor, D., Waddell, N., Wood, S., Xu, Q., Wu, J., Pinese, M., Cowley, M. J., Lee, H. C., Jones, M. D., Nagrial, A. M., Humphris, J., Chantrill, L. A., Chin, V., Steinmann, A. M., Mawson, A., Humphrey, E. S., Colvin, E. K., Chou, A., Scarlett, C. J., Pinho, A. V., Giry-Laterriere, M., Rooman, I., Samra, J. S., Kench, J. G., Pettitt, J. A., Merrett, N. D., Toon, C., Epari, K., Nguyen, N. Q., Barbour, A., Zeps, N., Jamieson, N. B., Graham, J. S., Niclou, S. P., Bjerkvig, R., Grützmann, R., Aust, D., Hruban, R. H., Maitra, A., Iacobuzio-Donahue, C. A., Wolfgang, C. L., Morgan, R. A., Lawlor, R. T., Corbo, V., Bassi, C., Falconi, M., Zamboni, G., Tortora, G., Tempero, M. A., Gill, A. J., Eshleman, J. R., Pilarsky, C., Scarpa, A., Musgrove, E. A., Pearson, J. V., Biankin, A. V., & Grimmond, S. M.
- Affiliations
- The University of Queensland (AU)
- Garvan Institute of Medical Research (AU)
- The University of Sydney (AU)
- Royal Adelaide Hospital (AU)
- The University of Western Australia (AU)
- St John of God Subiaco Hospital (AU)
- Glasgow Royal Infirmary (GB)
- Beatson West of Scotland Cancer Centre (GB)
- Centre de Recherche Public de la Santé (LU)
- University of Bergen (NO)
- Technische Universität Dresden (DE)
- Johns Hopkins University (US)
- The University of Texas MD Anderson Cancer Center (US)
- Memorial Sloan Kettering Cancer Center (US)
- University of Verona (IT)
- QIMR Berghofer Medical Research Institute (AU)
- Corresponding author
- Grimmond, Sean M.
- ORCID
- Waddell, Nicola
- Pajic, Marina
- Patch, Ann-Marie
- Chang, David K.
- Kassahn, Karin S.
- Bailey, Peter
- Johns, Amber L.
- Quek, Kelly
- Quinn, Michael C. J.
- Robertson, Alan J.
- Fadlullah, Muhammad Z. H.
- Christ, Angelika N.
- Harliwong, Ivon
- Manning, Suzanne
- Nourbakhsh, Ehsan
- Wani, Shivangi
- Wilson, Peter J.
- Cloonan, Nicole
- Anderson, Matthew J.
- Fink, J. Lynn
- Holmes, Oliver
- Kazakoff, Stephen H.
- Leonard, Conrad
- Newell, Felicity
- Poudel, Barsha
- Song, Sarah
- Wood, Scott
- Wu, Jianmin
- Pinese, Mark
- Cowley, Mark J.
- Jones, Marc D.
- Nagrial, Adnan M.
- Chantrill, Lorraine A.
- Chin, Venessa
- Mawson, Amanda
- Colvin, Emily K.
- Chou, Angela
- Scarlett, Christopher J.
- Pinho, Andreia V.
- Rooman, Ilse
- Samra, Jaswinder S.
- Kench, James G.
- Pettitt, Jessica A.
- Merrett, Neil D.
- Toon, Christopher
- Nguyen, Nam Q.
- Barbour, Andrew
- Zeps, Nikolajs
- Jamieson, Nigel B.
- Graham, Janet S.
- Niclou, Simone P.
- Bjerkvig, Rolf
- Grützmann, Robert
- Aust, Daniela
- Hruban, Ralph H.
- Maitra, Anirban
- Wolfgang, Christopher L.
- Lawlor, Rita T.
- Corbo, Vincenzo
- Falconi, Massimo
- Zamboni, Giuseppe
- Tortora, Giampaolo
- Tempero, Margaret A.
- Gill, Anthony J.
- Eshleman, James R.
- Pilarsky, Christian
- Scarpa, Aldo
- Pearson, John V.
- Biankin, Andrew V.
- Grimmond, Sean M.
- Venue
- Nature
- Published
- 2015-02-25
- Volume
- 518
- Issue
- 7540
- Pages
- 495-501
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC4523082
- OpenAlex
- W1987313243
- Cited by
- 2,642
- References
- 57
- Citations by year
- 2026: 118 · 2025: 171 · 2024: 185 · 2023: 234 · 2022: 259 · 2021: 301 · 2020: 292 · 2019: 251 · 2018: 260 · 2017: 242 · 2016: 226 · 2015: 96
- FWCI
- 120.10
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (acceptedVersion)
- Open Repository and Bibliography (University of Luxembourg) (submittedVersion, cc-by)
- University of Southern Queensland ePrints (University of Southern Queensland) (submittedVersion)
- UWA Profiles and Research Repository (UWA) (submittedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- eSpace (Curtin University) (submittedVersion)
- Archivio Istituzionale della Ricerca - Università Vita-Salute San Raffaele (submittedVersion)
- VUBIR (Vrije Universiteit Brussel) (submittedVersion)
- NOVA (University of Newcastle Australia) (submittedVersion)
- Funders
- American Association for Cancer Research
- Johns Hopkins University
- Royal College of Pathologists of Australasia
- Wellcome Trust (103721/Z/14/Z, 103721)
- Australian Government
- Cancer Research UK (C596/A18076, C29717/A17263, 17263, A18076, A17263)
- Academy of Medical Sciences (AMS-SGCL9-Jamieson)
- University of Glasgow (C596/A18076)
- Australian Cancer Research Foundation
- Cancer Institute NSW (11/REG/1-10, 09/CDF/2-40, 10/CRF/1-01, 10/TPG/1‐04, 06/ECF/1-24, 08/RSA/1-15, 10/CDF/2-26, 06/RSA/1-05, 11/CDF/3-26, 07/CDF/1-28, 07/CDF/1-03, 10/ECF/2-26, 09/RIG/1-02)
- Gastroenterological Society of Australia
- Royal Australasian College of Physicians
- Petre Foundation
- Queensland Government
- R.T. Hall Trust
- Università degli Studi di Verona
- National Institutes of Health (CA62924)
- Medical Research Council
- National Health and Medical Research Council (631701, 535903, 427601)
- Cancer Council NSW (SRP06-01)
- National Cancer Institute (P50CA-62924, P50CA062924, P30CA006973)
- 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, mutational landscape, chromosomal rearrangements, copy number variation, structural variants, tumor subtypes, focal amplification, genomic instability, DNA repair deficiency, TP53, SMAD4, CDKN2A, ARID1A, Robo2, KDM6A, PREX2, BRCA1, BRCA2, PALB2, platinum-based chemotherapy, therapeutic biomarkers
- MeSH terms
- Poly(ADP-ribose) Polymerase Inhibitors, Adenocarcinoma, Animals, DNA Mutational Analysis, DNA Repair, Female, Genetic Markers, Genotype, Humans, Mutation, Pancreatic Neoplasms, Platinum, Genome, Human, Point Mutation, Genes, BRCA1, Carcinoma, Pancreatic Ductal, Xenograft Model Antitumor Assays, Genomics, Genes, BRCA2, Genomic Instability, Mice
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