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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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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]
In the citing paper
“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]
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“This is an overstatement, since researchers believed that the number of mutations already exceeds 63 [12].”
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“Loss of miR-34a expression may play a critical role in the development of PDAC.”
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Self-citationCirculating lncRNA ABHD11-AS1 serves as a biomarker for early pancreatic cancer diagnosis
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“Pancreatic cancer (PC) is the fourth leading cause of cancer death in Western societies, and despite recent research and therapeutic developments, its median 5-year survival remains less than 5% [1].”
BackgroundKeratin 17 identifies the most lethal molecular subtype of pancreatic cancer
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“Large-scale data sets have helped to better understand the mutagenic landscape of PDAC and allowed subgrouping of this tumor.(4) Thus, novel and more tailored treatment algorithms are warranted to eventually reach a higher response rate in a subset of patients with PDAC.”
BackgroundWhen Genome Maintenance Goes Badly Awry
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“They have been observed in multiple tumor types and, surprisingly, even constitutionally in rare individuals (Kloosterman et al., 2012; Weckselblatt et al., 2015).”
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Wu, S., Ou, T., Xing, N., Jiang, L., Wan, S., Wang, C., Zhang, X., Yang, F., Huang, Y. F., & Cai, Z. (2019) · Nature Communications · doi:10.1038/s41467-019-08576-5 · Cited by 87
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“As previously reported, the majority of these alterations were located at the hotspot codon 12, the spectrum was concordant with the distribution of KRAS tumor mutation types from ICGC data [34–36], suggesting that KRAS mutations in the circulating DNA mainly originate from tumor cells.”
ResultFive key lncRNAs considered as prognostic targets for predicting pancreatic ductal adenocarcinoma
Song, J., Xu, Q., Zhang, H., Yin, X., Zhu, C. Y., Zhao, K., & Zhu, J. (2017) · Journal of Cellular Biochemistry · doi:10.1002/jcb.26598 · Cited by 83
Self-citationA pancreatic cancer organoid platform identifies an inhibitor specific to mutant KRAS
Duan, X., Zhang, T., Feng, L., de Silva, N., Greenspun, B. C., Wang, X., Moyer, J. E., Martin, M. L., Chandwani, R., Elemento, O., et al. (2023) · Cell stem cell · doi:10.1016/j.stem.2023.11.011 · Cited by 85
McIntyre, C. A., Grimont, A., Park, J., Meng, Y., Sisso, W. J., Seier, K. P., Jang, G. H., Walch, H. S., Aveson, V. G., Falvo, D. J., et al. (2024) · Cancer Cell · doi:10.1016/j.ccell.2024.08.002 · Cited by 85
Cheng, H., Fan, K., Luo, G., Fan, Z., Yang, C., Huang, Q., Jin, K., Xu, J., Yu, X., & Liu, C. (2019) · Cancer Letters · doi:10.1016/j.canlet.2019.01.013 · Cited by 83
Concepts to Target MYC in Pancreatic Cancer
Wirth, M., Mahboobi, S., Krämer, O. H., & Schneider, G. (2016) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-16-0050 · Cited by 81
“Beyond a few exceptions (4), it is unclear how genetic lesions translate into effective therapies, and deciphering vulnerabilities arising from genetic lesions remains challenging.”
BackgroundPancreatic cancer survival analysis defines a signature that predicts outcome
Raman, P., Maddipati, R., Lim, K., & Tözeren, A. (2018) · PLoS ONE · doi:10.1371/journal.pone.0201751 · Cited by 84
Knudsen, E. S., Kumarasamy, V. M., Chung, S., Ruiz, A., Vail, P. J., Tzetzo, S. L., Wu, J., Nambiar, R., Sivinski, J., Chauhan, S. S., et al. (2020) · Gut · doi:10.1136/gutjnl-2020-321000 · Cited by 83
“5 Clinical trials of agents targeting RAS pathway in pancreatic cancer via MEK or other effector pathway inhibitors have largely failed to demonstrate improved outcome.”
Self-citationModeling pancreatic cancer in mice for experimental therapeutics
Mallya, K. B., Gautam, S. K., Aithal, A., Batra, S. K., & Jain, M. (2021) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2021.188554 · Cited by 88
Molecular principles underlying aggressive cancers
Nussinov, R., Yavuz, B. R., & Jang, H. (2025) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-025-02129-7 · Cited by 91
Implication of PI3K/Akt pathway in pancreatic cancer: When PI3K isoforms matter?
Baer, R., Cintas, C., Therville, N., & Guillermet‐Guibert, J. (2015) · Advances in Biological Regulation · doi:10.1016/j.jbior.2015.05.001 · Cited by 85
High immune cell score predicts improved survival in pancreatic cancer
Tahkola, K., Mecklin, J., Wirta, E., Ahtiainen, M., Helminen, O., Böhm, J., & Kellokumpu, I. (2018) · Archiv für Pathologische Anatomie und Physiologie und für Klinische Medicin · doi:10.1007/s00428-018-2297-1 · Cited by 79
“The accumulation of successive genetic mutations seems to be the preliminary step for the development of PDAC [5].”
BackgroundDijk, F., Veenstra, V. L., Soer, E. C., Dings, M. P. G., Zhao, L., Halfwerk, J. B. G., Hooijer, G. K. J., Damhofer, H., Marzano, M., Steins, A., et al. (2020) · Scientific Reports · doi:10.1038/s41598-019-56826-9 · Cited by 77
Golan, T., Barenboim, A., Lahat, G., Nachmany, I., Goykhman, Y., Shacham‐Shmueli, E., Halpern, N., Brazowski, E., Geva, R., Wolf, I., et al. (2020) · Annals of Surgical Oncology · doi:10.1245/s10434-020-08469-8 · Cited by 79
Gout, J., Perkhofer, L., Morawe, M., Arnold, F., Ihle, M., Biber, S., Lange, S., Roger, É., Kraus, J. M., Stifter, K., et al. (2020) · Gut · doi:10.1136/gutjnl-2019-319970 · Cited by 83
Hirt, C., Booij, T. H., Grob, L., Simmler, P., Toussaint, N. C., Keller, D., Taube, D., Ludwig, V., Goryachkin, A., Pauli, C., et al. (2022) · Cell Genomics · doi:10.1016/j.xgen.2022.100095 · Cited by 92
Takeda, M., Yoshida, S., Inoue, T., Sekido, Y., Hata, T., Hamabe, A., Ogino, T., Miyoshi, N., Uemura, M., Yamamoto, H., et al. (2025) · Cancers · doi:10.3390/cancers17030428 · Cited by 82
“For example, G12V is frequently identified in pancreatic ductal adenocarcinomas and is associated with aggressive disease biology [16,21].”
Sehdev, A., Gbolahan, O. B., Hancock, B. A., Stanley, M., Shahda, S., Wan, J., Wu, H. H., Radovich, M., & O’Neil, B. H. (2018) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-18-1472 · Cited by 82
“In addition, our study also validates the association of germline BRCA1/2 mutations and sensitivity to platinum-based chemotherapy reported by others in PDAC patients (16, 17) and expands the hypothesis beyond germline BRCA1/2 mutations to both somatic and germline mutation in DDR genes.”
BackgroundResultLanfredini, S., Thapa, A., & O’Neill, E. E. (2019) · Biochemical Society Transactions · doi:10.1042/bst20170521 · Cited by 78
Schaefer, D., Tomiuk, S., Kuester, L. N., Rawashdeh, W. A., Henze, J., Tischler-Höhle, G., Agorku, D., Brauner, J., Linnartz, C., Lock, D., et al. (2021) · Nature Communications · doi:10.1038/s41467-021-21774-4 · Cited by 80
Digestive cancers: mechanisms, therapeutics and management
Zhan, T., Betge, J., Schulte, N., Dreikhausen, L., Hirth, M., Li, M., Weidner, P., Leipertz, A., Teufel, A., & Ebert, M. P. A. (2025) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-02097-4 · Cited by 90
BRCA1 and BRCA2 mutations sensitize to chemotherapy in patient-derived pancreatic cancer xenografts
Lohse, I., Borgida, A., Cao, P., Cheung, M., Pintilie, M., Bianco, T., Hölter, S. M., Ibrahimov, E., Kumareswaran, R., Bristow, R. G., et al. (2015) · British Journal of Cancer · doi:10.1038/bjc.2015.220 · Cited by 79
“Although Waddell et al used both agents at their maximum-tolerated dose, we used significantly lower doses in our treatments (140mg kg 1 vs 100mg kg 1 gemcitabine, 6mg kg 1 vs 4mg kg 1 cisplatin).”
ResultOrganoid models for translational pancreatic cancer research
Tiriac, H., Plenker, D., Baker, L. A., & Tuveson, D. A. (2019) · Current Opinion in Genetics & Development · doi:10.1016/j.gde.2019.02.003 · Cited by 81
Argentiero, A., Summa, S. D., Fonte, R., Iacobazzi, R. M., Porcelli, L., Vià, M. D., Brunetti, O., Azzariti, A., Silvestris, N., & Solimando, A. G. (2019) · Cancers · doi:10.3390/cancers11070942 · Cited by 78
Synthetic lethality strategies: Beyond BRCA1/2 mutations in pancreatic cancer
Hu, Y., & Guo, M. (2020) · Cancer Science · doi:10.1111/cas.14565 · Cited by 82
Ashrafizadeh, M., Zhang, W., Zou, R., Sethi, G., Klionsky, D. J., & Zhang, X. (2023) · Pharmacological Research · doi:10.1016/j.phrs.2023.106822 · Cited by 79
Rho Kinase Inhibition by AT13148 Blocks Pancreatic Ductal Adenocarcinoma Invasion and Tumor Growth
Rath, N., Munro, J., Cutiongco, M. F. A., Jagiełło, A., Gadegaard, N., McGarry, L., Unbekandt, M., Michalopoulou, E., Kamphorst, J. J., Sumpton, D. P., et al. (2018) · Cancer Research · doi:10.1158/0008-5472.can-17-1339 · Cited by 79
“One challenge for chemotherapy is that the mostly commonly mutated driver genes (KRAS, TP53, SMAD4 and CDKN2A (4,5)) are not targeted by current drugs.”
Self-citationCurrent and future biomarkers for pancreatic adenocarcinoma
Loosen, S. H., Neumann, U. P., Trautwein, C., Roderburg, C., & Luedde, T. (2017) · Tumor Biology · doi:10.1177/1010428317692231 · Cited by 81
Martens, S., Lefesvre, P., Nicolle, R., Biankin, A. V., Puleo, F., Laethem, J. V., & Rooman, I. (2019) · Annals of Oncology · doi:10.1093/annonc/mdz181 · Cited by 78
Self-citationPancreatic cancer cachexia: three dimensions of a complex syndrome
Kordes, M., Larsson, L., Engstrand, L., & Löhr, M. J. (2021) · British Journal of Cancer · doi:10.1038/s41416-021-01301-4 · Cited by 83
Clinical Impact of Molecular Subtyping of Pancreatic Cancer
Zhou, X., Hu, K., Bailey, P. J., Springfeld, C., Roth, S., Kurilov, R., Brors, B., Gress, T. M., Buchholz, M., An, J., et al. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.743908 · Cited by 84
“It is estimated that 24% of all pancreatic cancers may be sensitive to platinum therapy based on an unstable genomic structural variation subtype, and/or somatic and germline mutations in BRCA genes, and/or a BRCA-type mutational signature (Waddell et al., 2015).”
BackgroundMethodInfluentialSelf-citationZhang, X., Zheng, S., Hu, C., Li, G., Lin, H., Xia, R., Ye, Y., He, R., Li, Z., Lin, Q., et al. (2022) · Oncogene · doi:10.1038/s41388-022-02253-6 · Cited by 80
“were platinum-sensitive, which is consistent with previous finding [17, 42, 43].”
ResultFGFR families: biological functions and therapeutic interventions in tumors
Liu, Q., Huang, J., Yan, W., Liu, Z., Liu, S., & Fang, W. (2023) · MedComm · doi:10.1002/mco2.367 · Cited by 77
Co-clinical Assessment of Tumor Cellularity in Pancreatic Cancer
Heid, I., Steiger, K., Trajkovic‐Arsic, M., Settles, M., Eßwein, M. R., Erkan, M., Kleeff, J. H., Jäger, C., Friess, H., Haller, B., et al. (2016) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-15-2432 · Cited by 78
Pishvaian, M. J., Biankin, A. V., Bailey, P. J., Chang, D. K.-F., Laheru, D. A., Wolfgang, C. L., & Brody, J. R. (2017) · British Journal of Cancer · doi:10.1038/bjc.2017.40 · Cited by 80
Self-citationHNF1A recruits KDM6A to activate differentiated acinar cell programs that suppress pancreatic cancer
Kalisz, M., Bernardo, E., Beucher, A., Maestro, M. A., del Pozo, N., Millán, I., Haeberle, L., Schlensog, M., Safi, S. A., Knoefel, W. T., et al. (2020) · The EMBO Journal · doi:10.15252/embj.2019102808 · Cited by 77
“Up to 18% of PDAC tumors carry mutations in KDM6A (Waddell et al, 2015), which encodes Lysine-specific demethylase 6A (KDM6A), a component of the MLL/COMPASS transcriptional co-regulatory complex (Cho et al, 2007).”
BackgroundJameson, G., Borazanci, E. H., Babiker, H. M., Poplin, E. A., Niewiarowska, A. A., Gordon, M. S., Barrett, M. T., Rosenthal, A., Stoll-D'Astice, A. C., Crowley, J. J., et al. (2019) · JAMA Oncology · doi:10.1001/jamaoncol.2019.3394 · Cited by 78
Patil, S., Steuber, B., Kopp, W., Kari, V., Urbach, L., Wang, X., Küffer, S., Bohnenberger, H., Spyropoulou, D., Zhang, Z., et al. (2020) · Cancer Research · doi:10.1158/0008-5472.can-20-0672 · Cited by 79
“Indeed, genome-wide sequencing studies have revealed genetic amplification of GATA6 in approximately 8% of PDAC (1), possibly relieving the expression of the TF from epigenetic repression by EZH2.”
BackgroundNel, A. E., Mei, K., Liao, Y., & Liu, X. (2022) · ACS Nano · doi:10.1021/acsnano.2c01252 · Cited by 81
McIntyre, C. A., Lawrence, S., Richards, A. L., Chou, J. F., Wong, W., Capanu, M., Berger, M. F., Donoghue, M. T. A., Yu, K. H., Varghese, A. M., et al. (2020) · Cancer · doi:10.1002/cncr.33038 · Cited by 75
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Malik, R., Luong, T., Cao, X., Han, B., Shah, N., Franco-Barraza, J., Han, L., Shenoy, V. B., Lelkes, P. I., & Cukierman, E. (2019) · Matrix Biology · doi:10.1016/j.matbio.2018.11.001 · Cited by 74
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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