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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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Höfer, S., Frasch, L., Brajkovic, S., Putzker, K., Lewis, J., Schürmann, H., Leone, V., Sakhteman, A., The, M., Bayer, F. P., et al. (2025) · Molecular Systems Biology · doi:10.1038/s44320-025-00085-6 · Cited by 29
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Genomic alterations in pancreatic cancer and their relevance to therapy
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“Mutations that affect breast cancer pathway components, and especially the tumor suppressor gene breast cancer-2 (BRCA2) gene, which is associated with hereditary predisposition to breast, ovarian and pancreatic cancer are known to promote deficiency in DNA damage repair mechanisms and also induce genome instability (…”
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Luchini, C., Pea, A., Yu, J., He, J. P., Salvia, R., Riva, G., Weiss, M. J., Bassi, C., Cameron, J. L., Hruban, R. H., et al. (2018) · Modern Pathology · doi:10.1038/s41379-018-0183-7 · Cited by 27
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“Overall, approximately 55% of PDAC patients harbor inactivation or loss of the Smad4 gene [121].”
BackgroundEvaluation of KRAS inhibitor-directed therapies for pancreatic cancer treatment
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“However, structural rearrangements are relatively uncommon in the pancreatic cancer genome [13,14].”
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“Further, the authors used variation in chromosomal structure to group these PDAC patients into 4 subtypes: stable, locally rearranged, scattered, and unstable (43).”
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Mutant KRAS drives metabolic reprogramming and autophagic flux in premalignant pancreatic cells
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Long Non-Coding RNAs in Epithelial-Mesenchymal Transition of Pancreatic Cancer
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“Mutations in KRAS and TP53, which are frequently observed in type 1 and type 2 ECs, respectively, are common in PDAC as well (Waddell et al., 2015).”
BackgroundLongitudinal profiling of circulating tumour DNA for tracking tumour dynamics in pancreatic cancer
Sivapalan, L., Thorn, G. J., Gadaleta, E., Kocher, H. M., Ross‐Adams, H., & Chelala, C. (2022) · BMC Cancer · doi:10.1186/s12885-022-09387-6 · Cited by 26
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Homologous Recombination Deficiency Scar: Mutations and Beyond—Implications for Precision Oncology
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“Single-base substitution Signature 3 (SBS3)—a uniform pattern of mutations across all 96 possible substitution types—is one of the mutational signatures discovered to be correlated with HRD—specifically with BRCA1/2 mutations [12,50]—in breast cancer, and was later extended to pancreatic [51,52], ovarian [53], and gas…”
BackgroundLogsdon, C. D., Arumugam, T., & Ramachandran, V. (2015) · American Journal of Physiology-Gastrointestinal and Liver Physiology · doi:10.1152/ajpgi.00169.2015 · Cited by 27
Xie, H., Rachakonda, P. S., Heidenreich, B., Nagore, E., Sucker, A., Hemminki, K., Schadendorf, D., & Kumar, R. (2016) · Oncotarget · doi:10.18632/oncotarget.7503 · Cited by 28
CA19-9-Low&Lewis (+) pancreatic cancer: A unique subtype
Luo, G., Liu, C., Guo, M., Long, J., Liu, Z., Xiao, Z., Jin, K., Cheng, H., Yu, L., Ni, Q., et al. (2016) · Cancer Letters · doi:10.1016/j.canlet.2016.10.046 · Cited by 28
Grixti, J. M., O’Hagan, S., Day, P. J., & Kell, D. B. (2017) · Frontiers in Pharmacology · doi:10.3389/fphar.2017.00155 · Cited by 27
“…(2’,2’-difluorodeoxycytidine, Gemzar R©) (Alvarellos et al., 2014) is one of the most commonly used chemotherapeutic agents in pancreatic adenocarcinoma, the carcinoma with arguably the least favorable prognosis (5- year survival time) of any (Bhattacharjee et al., 2014; Waddell et al., 2015).”
BackgroundOncological and genetic factors impacting PDX model construction with NSG mice in pancreatic cancer
Guo, S., Gao, S., Liu, R., Shen, J., Shi, X., Bai, S., Wang, H., Zheng, K., Shao, Z., Liang, C., et al. (2018) · The FASEB Journal · doi:10.1096/fj.201800617r · Cited by 26
Transforming growth factor-β in pancreatic diseases: Mechanisms and therapeutic potential
Zhou, Q., Xia, S., Guo, F., Hu, F., Wang, Z., Ni, Y., Wei, T., Xiang, H., & Shang, D. (2019) · Pharmacological Research · doi:10.1016/j.phrs.2019.01.038 · Cited by 26
Li, Z., Shao, C., Liu, X., Lu, X., Jia, X., Zheng, X., Wang, S., Zhu, L., Li, K., Pang, Y., et al. (2019) · Carcinogenesis · doi:10.1093/carcin/bgz086 · Cited by 26
Medullary Pancreatic Carcinoma Due to Somatic POLE Mutation
Kryklyva, V., ter Linden, E., Kroeze, L. I., de Voer, R. M., Kolk, B., Stommel, M. W. J., Hermans, J. J., Luchini, C., Wood, L. D., Hruban, R. H., et al. (2020) · Pancreas · doi:10.1097/mpa.0000000000001588 · Cited by 26
Self-citationBusch, E., Kreutzfeldt, S., Agaimy, A., Mechtersheimer, G., Horak, P., Brors, B., Hutter, B., Fröhlich, M., Uhrig, S., Mayer, P., et al. (2020) · Molecular Case Studies · doi:10.1101/mcs.a005553 · Cited by 26
“Other molecular predictors of platinum response, such as the very low HRD, LST, and TAI scores (Waddell et al. 2015) and the rather low level of the mutational signature 3 (Telli et al. 2016), did not point to a major defect in homologous recombination DNA repair mechanisms and were therefore in…”
BackgroundShah, D. N., Wells, A., Cox, M. C., Dawravoo, K., Abad, J., D’Souza, A., Suh, G. K., Bayer, R., Chaudhry, S., Zhang, Q., et al. (2024) · Annals of Surgery · doi:10.1097/sla.0000000000006209 · Cited by 30
“47 Studies have shown PDAC patients with SMAD4 mutations had a shorter OS and disease-free survival.”
The Evolutionary Forest of Pancreatic Cancer
Mullen, K. M., Hong, J., Attiyeh, M. A., Hayashi, A., Sakamoto, H., Kohutek, Z. A., McIntyre, C. A., Zhang, H., Makohon-Moore, A. P., Zucker, A., et al. (2024) · Cancer Discovery · doi:10.1158/2159-8290.cd-23-1541 · Cited by 26
Self-citationNext-generation sequencing and empowering personalised cancer medicine
McDermott, U. (2015) · Drug Discovery Today · doi:10.1016/j.drudis.2015.10.008 · Cited by 25
Werner syndrome through the lens of tissue and tumour genomics
Tokita, M., Kennedy, S. R., Risques, R. A., Chun, S. G., Pritchard, C. C., Oshima, J., Liu, Y., BRYANT-GREENWOOD, P. K., Welcsh, P. L., & Monnat, R. J. (2016) · Scientific Reports · doi:10.1038/srep32038 · Cited by 26
Carcinosarcoma of the Pancreas
Ruess, D. A., Kayser, C., Neubauer, J., Fichtner‐Feigl, S., Hopt, U. T., & Wittel, U. A. (2017) · Pancreas · doi:10.1097/mpa.0000000000000904 · Cited by 25
Ghurburrun, E., Borbath, I., Lemaigre, F. P., & Jacquemin, P. (2018) · Gene Expression · doi:10.3727/105221618x15216414278706 · Cited by 25
Integrated multi-omics analysis of genomics, epigenomics, and transcriptomics in ovarian carcinoma
Zheng, M., Hu, Y., Gou, R., Wang, J., Nie, X., Li, X., Liu, Q., Liu, J., & Lin, B. (2019) · Aging · doi:10.18632/aging.102047 · Cited by 23
Characterization of genetic subclonal evolution in pancreatic cancer mouse models
Niknafs, N., Zhong, Y., Moral, J. A., Zhang, L., Shao, M. X., Lo, A., Makohon-Moore, A. P., Iacobuzio–Donahue, C. A., & Karchin, R. (2019) · Nature Communications · doi:10.1038/s41467-019-13100-w · Cited by 26
Self-citationWang, Y., Du, C., Zhao, Y., Nie, G., & Yang, Y. (2020) · Nano Today · doi:10.1016/j.nantod.2020.100877 · Cited by 25
Hashimoto, A., Handa, H., Hata, S., Tsutaho, A., Yoshida, T., Hirano, S., Hashimoto, S., & Sabe, H. (2021) · Cell Communication and Signaling · doi:10.1186/s12964-021-00733-y · Cited by 27
Targeting DNA Damage Repair Mechanisms in Pancreas Cancer
Perkhofer, L., Golan, T., Cuyle, P.-J. A., Matysiak‐Budnik, T., Laethem, J. V., Macarulla, T. M., Cauchin, E., Kleger, A., Beutel, A. K., Gout, J., et al. (2021) · Cancers · doi:10.3390/cancers13174259 · Cited by 25
“Waddell and colleagues defined four PDAC subtypes: (i) stable, (ii) locally rearranged, (iii) scattered and (iv) unstable [4].”
BackgroundOu, K., Liu, X., Li, W., Yang, Y., Ying, J., & Yang, L. (2021) · Frontiers in Oncology · doi:10.3389/fonc.2021.724815 · Cited by 25
Sekita‐Hatakeyama, Y., Fujii, T., Nishikawa, T., Mitoro, A., Sawai, M., Itami, H., Morita, K., Uchiyama, T., Takeda, M., Sho, M., et al. (2021) · Cancer Cytopathology · doi:10.1002/cncy.22525 · Cited by 24
Zhan, Q., Wen, C., Zhao, Y., Fang, L., Jin, Y., Zhang, Z., Zou, S., Li, F., Yang, Y., Wu, L., et al. (2021) · EBioMedicine · doi:10.1016/j.ebiom.2021.103716 · Cited by 25
“Intriguingly, Waddell et al observed that PAAD with high BRCAmutational signature burden had much better response to platinum-based chemotherapy [57].”
BackgroundDalmasso, B., Puccini, A., Catalano, F., Borea, R., Iaia, M. L., Bruno, W., Fornarini, G., Sciallero, S., Rebuzzi, S. E., & Ghiorzo, P. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23094709 · Cited by 25
Pancreatic Cancer: BRCA Targeted Therapy and Beyond
Keane, F., O'Connor, C. A., Park, W., Seufferlein, T. T. W., & O'Reilly, E. M. (2023) · Cancers · doi:10.3390/cancers15112955 · Cited by 26
“’s whole genome sequencing and copy number variation analysis on 100 patients with PDAC identified two with a somatic BRCA1 mutation and three with a somatic BRCA2 alteration [12].”
BackgroundApplication of glycoscience to the early detection of pancreatic cancer
Miyoshi, E., & Kamada, Y. (2016) · Cancer Science · doi:10.1111/cas.13011 · Cited by 25
Martínez‐Useros, J., & García‐Foncillas, J. (2016) · BioMed Research International · doi:10.1155/2016/1869304 · Cited by 25
“The milestone of DNA strand exchange is RAD51 protein which is closely related to other tumour suppressor genes such as TP53, ATM, BRCA1, BLM, and FANCD2.”
BackgroundNeuzillet, C., Rousseau, B., Kocher, H. M., Bourget, P., & Tournigand, C. (2017) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2017.02.028 · Cited by 25
“salts, mitomycin C) and PARP inhibitors in familial pancreatic cancer (de Mestier et al., 2016; Lowery et al., 2011; Waddell et al., 2015).”
BackgroundMolecular subtype specific efficacy of MEK inhibitors in pancreatic cancers
Brauswetter, D., Gurbi, B., Varga, A., Várkondi, E., Schwab, R. B., Bánhegyi, G., Fábián, O., Kéri, G., Valyi-Nagy, I. T., & Peták, I. (2017) · PLoS ONE · doi:10.1371/journal.pone.0185687 · Cited by 26
Reviewing the Utility of EUS FNA to Advance Precision Medicine in Pancreatic Cancer
Berry, W., Lundy, J., Croagh, D. G., & Jenkins, B. J. (2018) · Cancers · doi:10.3390/cancers10020035 · Cited by 27
“FGFR1 amplification FGFR inhibitors 1% [27,30]”
BackgroundYoon, K., Woo, S. M., Kim, Y., Kong, S., Lee, M. K., Han, S., Kim, T. H., Lee, W. J., & Park, S. (2019) · Gut and Liver · doi:10.5009/gnl18355 · Cited by 25
“In addition, SWI/SNF-mediated chromatin remodeling, including alterations in the ARID1A, KDM6A and SMARCA2 genes, has emerged as the basis for additional pathways affected by somatic mutations in PDA.(10,11) Genome analyses of PDAs have revealed considerable genetic diversity and a complex mutational landscape, making…”
BackgroundResultInfluentialPDAC as an immune evasive disease: can 3D model systems aid to tackle this clinical problem?
Narayanan, S., Vicent, S., & Ponz-Sarvisé, M. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.787249 · Cited by 24
“Mutations in KRAS occur early in PDAC tumorigenesis and function as an initiating event of the disease (Biankin et al., 2012; Waddell et al., 2015; Witkiewicz et al., 2015; Frappart and Hofmann, 2020).”
BackgroundLost in translation: returning germline genetic results in genome-scale cancer research
Initiative, A. P. C. G., Johns, A. L., McKay, S. H., Humphris, J. L., Pinese, M., Chantrill, L. A., Mead, R. S., Tucker, K., Andrews, L., Goodwin, A., et al. (2017) · Genome Medicine · doi:10.1186/s13073-017-0430-4 · Cited by 79
“We performed whole-genome (n = 184) and exome (n = 208) sequencing of matched tumour-normal DNA pairs from eligible patients to an average depth of 65× (tumour) and 35× (germline) under conditions previously described by this group [1, 32, 33].”
MethodSelf-citationStigliani, A., Ialchina, R., Yao, J., Czaplińska, D., Dai, Y., Andersen, H. B., Rennie, S., Andersson, R., Pedersen, S. F., & Sandelin, A. (2024) · Cell Reports · doi:10.1016/j.celrep.2024.114409 · Cited by 27
Yavas, A., Özcan, K., Adsay, V. N., Balcı, S., Tarcan, Z. C., Hechtman, J. F., Luchini, C., Scarpa, A., Lawlor, R. T., Mafficini, A., et al. (2024) · Modern Pathology · doi:10.1016/j.modpat.2024.100585 · Cited by 24
Self-citationXiao, M., Yang, H. J., Dong, M., Mao, X., Pan, H., Lei, Y., Tong, X., Yu, X., Yu, X., & Shi, S. (2024) · Cell Death and Disease · doi:10.1038/s41419-024-06984-0 · Cited by 26
Li, P., Huang, M., Li, M., Li, G., Ma, Y., Zhao, Y. X., Wang, X., Zhang, Y., & Shi, C. (2025) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-025-03332-8 · Cited by 26
“The advent of next-generation sequencing (NGS) has revolutionized the landscape of PDAC treatment by identifying genomic tumor drivers and potential targeted therapies [4–5].”
Changing the course of pancreatic cancer – Focus on recent translational advances
Javle, M. M., Golan, T., & Maitra, A. (2016) · Cancer Treatment Reviews · doi:10.1016/j.ctrv.2016.01.004 · Cited by 24
“Genomic instability correlated with inactivation of DNA repair genes (BRCA1, BRCA2 or PALB2) and a mutational signature of DNA damage repair deficiency [65].”
BackgroundSelf-citationc-Myc downregulation is required for preacinar to acinar maturation and pancreatic homeostasis
Lobo, V. J. S.-A., Fernández, L. C., Pau, E. C. D. S., Richart, L., Cobo, I., Cendrowski, J., Moreno‐Celis, U., del Pozo, N., Megı́as, D., Bréant, B., et al. (2017) · Gut · doi:10.1136/gutjnl-2016-312306 · Cited by 24
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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