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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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“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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“In 2015, the consortium led by Biankin and Grimmond identified a small percentage of PDAC (< 15%) with high genomic instability due to serious defects in DNA integrity maintenance (creating the so called “BRCA signature”) (102).”
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“As TSC2 mutation in PDAC is rare [3, 29], it is likely that BRSK2 downregulates mTORC1 through phosphorylation of TSC2.”
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“The POLO trial provided a milestone in targeted therapy of PDAC albeit tailored to a minimal subgroup of around 3–6% of germline BRCA1/2-mutated patients with pancreatic cancer [7,29].”
BackgroundCircadian Genes as Therapeutic Targets in Pancreatic Cancer
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“3-state (10) >3 state (17) amp (13) subclonal (2)”
Developmental Pathways Direct Pancreatic Cancer Initiation from Its Cellular Origin
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“As controversial as this theory might be, it is one way to explain tumor heterogeneity, and solid tumors, especially pancreatic ductal adenocarcinomas (PDA), are heterogeneous [2, 3].”
Hypoxia, a Targetable Culprit to Counter Pancreatic Cancer Resistance to Therapy
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“This included an “unstable” subtype, which harbors greater than 200 variants [17], and was found to be associated with the HRD signature.”
BackgroundPancreatic ductal adenocarcinoma (PDAC): clinical progress in the last five years
Mosalem, O. M., Abdelhakeem, A. A. F., Abdel-Razeq, N. H., & Babiker, H. M. (2025) · Expert Opinion on Investigational Drugs · doi:10.1080/13543784.2025.2473698 · Cited by 33
“SMAD4 , a regulator of the TGF-β signaling pathway, is also mutated in approximately 50% of PDAC cases, can disrupt the tumor suppressive functions of TGF-β , promoting tumor growth and contributing to the dense, fibrotic stroma characteristic of PDAC [9,10].”
Predictive and prognostic biomarkers in personalized gastrointestinal cancer treatment
Verdaguer, H., Saurí, T., & Macarulla, T. M. (2017) · Journal of Gastrointestinal Oncology · doi:10.21037/jgo.2016.11.15 · Cited by 32
“In a study published by Waddell and colleagues (55), whole-genome sequencing and copy number variation analysis of 100 pancreatic ductal adenocarcinomas was performed.”
BackgroundLin, M., Alnaggar, M., Liang, S., Chen, J., Xu, K., Dong, S., Du, D., & Niu, L. (2018) · Cellular Physiology and Biochemistry · doi:10.1159/000490874 · Cited by 32
Multi-omic molecular comparison of primary versus metastatic pancreatic tumours
Brar, G. S., Blais, E. M., Bender, R. J., Brody, J. R., Sohal, D. P. S., Madhavan, S., Picozzi, V. J., Hendifar, A. E., Chung, V. M., Halverson, D., et al. (2019) · British Journal of Cancer · doi:10.1038/s41416-019-0507-5 · Cited by 30
Yan, W., Liu, X., Wang, Y., Han, S., Wang, F., Liu, X., Xiao, F., & Hu, G. (2020) · Frontiers in Pharmacology · doi:10.3389/fphar.2020.00534 · Cited by 30
“Until now, most of research effort in PDAC has been directed at identifying the important disease-driving genes and pathways (Waddell et al., 2015).”
BackgroundWang, Y., Park, J. Y. P., Pacis, A., Denroche, R. E., Jang, G. H., Zhang, A. X. W., Cuggia, A., Domecq, C., Monlong, J., Raitses‐Gurevich, M., et al. (2020) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-20-1439 · Cited by 29
Exploiting base excision repair to improve therapeutic approaches for pancreatic cancer
Sharbeen, G. (2015) · Frontiers in Nutrition · doi:10.3389/fnut.2015.00010 · Cited by 30
“On this point, recent data from the Australian Pancreatic Genome Initiative showed that 14% of pancreatic cancers display high genomic instability and a further 36% display substantial “scattered” genomic instability (141).”
BackgroundAlterations of Epigenetic Regulators in Pancreatic Cancer and Their Clinical Implications
Silverman, B., & Shi, J. (2016) · International Journal of Molecular Sciences · doi:10.3390/ijms17122138 · Cited by 32
“e t st fre e tl altere ist e et lati re lat r e es i a creatic ca cer are 6 a LL2 [1].”
BackgroundInfluentialObazee, O. M., Archibugi, L., Andriulli, A., Souček, P., Malecka-Panas, E. I., Ivanauskas, A., Johnson, T., Gazouli, M., Pausch, T. M., Lawlor, R. T., et al. (2019) · International Journal of Cancer · doi:10.1002/ijc.32127 · Cited by 29
“J. Cancer: 145, 686–693 (2019) © 2019 UICC C an ce r G en et ic s an d E pi ge n et ic s and BRCA2.”
BackgroundSelf-citationConcentrations of trace elements and KRAS mutations in pancreatic ductal adenocarcinoma
Gómez‐Tomás, Á., Pumarega, J. A., Alguacil, J., Amaral, A. F. S., Malats, N., Pallarés, N., Gasull, M., Porta, M. S., & for the PANKRAS II Study Group (2019) · Environmental and Molecular Mutagenesis · doi:10.1002/em.22296 · Cited by 30
“In PDAC, codon 12 mutations are identified in 70–90% of tumors (Deramaudt and Rustgi, 2005; Porta et al. 1999a; Waddell et al. 2015).”
BackgroundMCL-1 antagonism enhances the anti-invasive effects of dasatinib in pancreatic adenocarcinoma
(APGI), A. P. C. G. I., Castillo, L. E., Young, A. I. J., Mawson, A., Schafranek, P., Steinmann, A. M., Nessem, D., Parkin, A., Johns, A. L., Chou, A. S. Y., et al. (2019) · Oncogene · doi:10.1038/s41388-019-1091-0 · Cited by 29
Self-citationImmune-related somatic mutation genes are enriched in PDACs with diabetes
Wang, K., Zhou, W., Meng, P., Wang, P., Zhou, C., Yao, Y., Wu, S., Wang, Y., Zhao, J., Zou, D., et al. (2019) · Translational Oncology · doi:10.1016/j.tranon.2019.03.006 · Cited by 29
The Role of the Transforming Growth Factor-β Signaling Pathway in Gastrointestinal Cancers
Matsuoka, T., & Yashiro, M. (2023) · Biomolecules · doi:10.3390/biom13101551 · Cited by 32
“Approximately 40% of genetic alterations in mediators of TGF-β signaling occur in gastrointestinal (GI) cancers [2–4].”
BackgroundXiang, J.-F., Wang, W.-Q., Liu, L., Xu, H., Wu, C., Yang, J., Qi, Z.-H., Wang, Y.-Q., Xu, J., Liu, C., et al. (2016) · Scientific Reports · doi:10.1038/srep19222 · Cited by 31
RetractedThe possibility of clinical sequencing in the management of cancer
Kou, T., Kanai, M., Matsumoto, S., Okuno, Y., & Muto, M. (2016) · Japanese Journal of Clinical Oncology · doi:10.1093/jjco/hyw018 · Cited by 30
PALB2: research reaching to clinical outcomes for women with breast cancer
Southey, M. C., Winship, I., & Nguyen‐Dumont, T. (2016) · Hereditary Cancer in Clinical Practice · doi:10.1186/s13053-016-0049-2 · Cited by 29
“deficiency in pancreatic cancers that could benefit from platinum therapies [33].”
BackgroundMollinedo, F., & Gajate, C. (2019) · Annals of Translational Medicine · doi:10.21037/atm.2019.06.40 · Cited by 29
“Additional frequently mutated genes also include TP53, SMAD4, CDKN2A, ARID1A, ROBO2, PREX2, BRCA2 and MLL3 (25,28).”
BackgroundPalacio, S., McMurry, H. S., Ali, R. A., Donenberg, T. R., Silva‐Smith, R., Wideroff, G. A., Sussman, D. A., Lima, C. M. S. R., & Hosein, P. J. (2019) · Journal of Gastrointestinal Oncology · doi:10.21037/jgo.2019.09.12 · Cited by 29
“Patients with pathogenic variants in DNA damage repair (DDR) genes may derive greater benefit with platinum-based chemotherapy in metastatic PDAC (8,9).”
BackgroundInfluentialATM Serine/Threonine Kinase and its Role in Pancreatic Risk
Nanda, N., & Roberts, N. J. (2020) · Genes · doi:10.3390/genes11010108 · Cited by 30
“In addition, a mutation spectrum associated with BRCA1/BRCA2-deficient cancers, including PDAC, was defined [46,58,59].”
BackgroundApplication of liquid biopsy for surgical management of pancreatic cancer
Nagai, M., Sho, M., Akahori, T., Nakagawa, K., & Nakamura, K. (2020) · Annals of Gastroenterological Surgery · doi:10.1002/ags3.12317 · Cited by 29
Yokose, T., Kitago, M., Matsuda, S., Sasaki, Y., Masugi, Y., Nakamura, Y., Shinoda, M., Yagi, H., Abe, Y., Oshima, G., et al. (2020) · Cancer Science · doi:10.1111/cas.14425 · Cited by 28
“Preoperative CA19-9, IU/mL; median (range) 100 (1-2392)”
Current status of targeted microbubbles in diagnostic molecular imaging of pancreatic cancer
Jugniot, N., Bam, R., Meuillet, E. J., Unger, E. C., & Paulmurugan, R. (2020) · Bioengineering & Translational Medicine · doi:10.1002/btm2.10183 · Cited by 26
Current methods in translational cancer research
Lee, M. W., Miljanic, M., Triplett, T., Ramírez, C., Aung, K. L., Eckhardt, S., & Capasso, A. (2020) · Cancer and Metastasis Reviews · doi:10.1007/s10555-020-09931-5 · Cited by 32
Zhu, L., Wu, Z., Li, R., Xing, X., Jiang, Y., Li, J., Wang, Y., Hu, L.-P., Wang, X., Qin, W., et al. (2020) · International Journal of Biological Sciences · doi:10.7150/ijbs.49243 · Cited by 29
“key oncogenes and tumor suppressor genes, including KRAS, TP53, CDKN2A, and SMAD4 [2, 3].”
BackgroundInfluentialPeretti, U., Cavaliere, A., Niger, M., Tortora, G., Marco, M. D., Rodriquenz, M. G., Centonze, F., Rapposelli, I. G., Giordano, G., Vita, F. D., et al. (2021) · ESMO Open · doi:10.1016/j.esmoop.2020.100032 · Cited by 29
“Number 939 820 76 43 Gender Male, n (%) 492 (52) 431 (53) 40 (53) 21 (49) Female, n (%) 447 (48) 389 (47) 36 (47) 22 (51) Age, n (%) Median 62 62 59 64 Range 28-87 28-87 33-73 45-78 <41 35 (4) 29 (4) 6 (8) 0 41-50 115 (12) 100 (12) 12 (16) 3 (7) 51-60 282 (30) 243 (30) 26 (34) 13 (30) 61-70 327 (35) 287 (35) 22 (29) 1…”
Self-citationAdvances in Targeted Therapy and Immunotherapy for Pancreatic Cancer
Liu, X., Li, Z., & Wang, Y. (2021) · Advanced Biology · doi:10.1002/adbi.201900236 · Cited by 29
Tarasiuk, A., Mackiewicz, T., Malecka-Panas, E. I., & Fichna, J. (2021) · Cancer Biology & Therapy · doi:10.1080/15384047.2021.1941584 · Cited by 29
Hendifar, A. E., Blais, E. M., Wolpin, B. M., Subbiah, V., Collisson, E. A., Singh, I., Cannon, T. L., Shaw, K. R. M., Petricoin, E. F., Klempner, S. J., et al. (2021) · JCO Precision Oncology · doi:10.1200/po.20.00494 · Cited by 31
Diehl, J. N., Klomp, J. E., Snare, K. R., Hibshman, P. S., Blake, D. R., Kaiser, Z. D., Gilbert, T. S. K., Baldelli, E., Pierobon, M., Papke, B., et al. (2021) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2021.101335 · Cited by 30
Racu, 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 31
Subtyping for pancreatic cancer precision therapy
Huang, X., Zhang, G., & Liang, T. (2022) · Trends in Pharmacological Sciences · doi:10.1016/j.tips.2022.03.005 · Cited by 32
Targeting autophagy as a therapeutic strategy against pancreatic cancer
Yamamoto, K., Iwadate, D., Kato, H., Nakai, Y., Tateishi, K., & Fujishiro, M. (2022) · Journal of Gastroenterology · doi:10.1007/s00535-022-01889-1 · Cited by 29
“However, unlike other types of cancer, mutations in MHC-I are rare in PDAC [99].”
BackgroundSiret, C., Dobric, A., Մարտիրոսյան, Ա., Terciolo, C., Germain, S., Bonier, R., Dirami, T., Dusetti, N., Tomasini, R., Rubis, M., et al. (2017) · British Journal of Cancer · doi:10.1038/bjc.2017.411 · Cited by 29
“In addition to these commonly recognised genetic drivers of pancreatic carcinogenesis, a recent genomic analysis of PDAC has increased the number of genomic alterations (Waddell et al, 2015; Bailey et al, 2016).”
BackgroundA look at the progress of treating pancreatic cancer over the past 20 years
Göß, R., & Frieß, H. (2018) · Expert Review of Anticancer Therapy · doi:10.1080/14737140.2018.1428093 · Cited by 30
Hopkins, J. F., Denroche, R. E., Aguiar, J. A., Notta, F., Connor, A. A., Wilson, J. M., Stein, L. D., Gallinger, S., & Boutros, P. C. (2018) · Gastroenterology · doi:10.1053/j.gastro.2018.01.029 · Cited by 30
Alver, T. N., Bergholtz, H., Holm, M. B., Dorg, L. T., Skrede, M. L., Kure, E. H., & Verbeke, C. S. (2025) · Modern Pathology · doi:10.1016/j.modpat.2025.100726 · Cited by 28
Sannino, G., Armbruster, N. S., Bodenhöfer, M., Haerle, U., Behrens, D., Buchholz, M., Rothbauer, U., Sipos, B., & Schmees, C. (2016) · Oncotarget · doi:10.18632/oncotarget.12455 · Cited by 28
“Global genomic analyses revealed that, in the prevalence of PDAC cases, the WNT pathway is one of the most strongly altered signaling pathways [16, 17].”
BackgroundAu, T. H., Wang, K., Stenehjem, D. D., & Garrido‐Laguna, I. (2017) · Journal of Gastrointestinal Oncology · doi:10.21037/jgo.2017.01.04 · Cited by 29
“Most PDAC patients present with advanced disease, and therefore they are not candidates for surgical resection.”
BackgroundInfluentialThe CA19-9 and Sialyl-TRA Antigens Define Separate Subpopulations of Pancreatic Cancer Cells
Barnett, D., Liu, Y., Partyka, K. A., Huang, Y., Tang, H., Hostetter, G. H., Brand, R. E., Singhi, A. D., Drake, R. R., & Haab, B. B. (2017) · Scientific Reports · doi:10.1038/s41598-017-04164-z · Cited by 28
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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