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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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“…is also amplified (Hingorani et al., 2005), in the SB_PDACmodel, inwhich some tumors exhibit transposon insertions upstream of the Kras locus that are predicted to drive expression (Mann et al., 2012; Perez-Mancera et al., 2012), and from human pancreatic cancer patients (Waddell et al., 2015).”
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Self-citationc-Met and PD-L1 on Circulating Exosomes as Diagnostic and Prognostic Markers for Pancreatic Cancer
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ResultSelf-citationp53 mutations cooperate with oncogenic Kras to promote adenocarcinoma from pancreatic ductal cells
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Dreyer, S. B., Chang, D. K.-F., Bailey, P. J., & Biankin, A. V. (2017) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-16-2411 · Cited by 168
Self-citationArtificial Intelligence and Early Detection of Pancreatic Cancer: 2020 Summative Review
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Orozco, C. A., Martínez‐Bosch, N., Guerrero, P. E., Vinaixa, J., Dalotto‐Moreno, T., Iglesias, M., Moreno, M., Djurec, M., Poirier, F., Gabius, H., et al. (2018) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1722434115 · Cited by 158
Characterizing allele- and haplotype-specific copy numbers in single cells with CHISEL
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Hosoda, W., Chianchiano, P. E., Griffin, J. F., Pittman, M. E., Brosens, L. A. A., Noë, M., Yu, J., Shindo, K., Suenaga, M., Rezaee, N., et al. (2017) · The Journal of Pathology · doi:10.1002/path.4884 · Cited by 158
“A cc ep te d A rti cl e As expected from previous studies, we found that KRAS and CDKN2A are commonly targeted in PanIN lesions [16-19].”
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“This functional distinction of UTX between molecular subtypes of T-ALL was further supported in patientderived xenografts, in which treatment with H3K27 demethylase inhibitor GSK-J4 dramatically reduced percentage of human leukemic blasts and splenomegaly in TAL1-positive models, with no effect on TAL1-negative models…”
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Lowery, M. A., Kelsen, D. P., Capanu, M., Smith, S., Lee, J. W., Stadler, Z. K., Moore, M. J., Kindler, H. L., Golan, T., Segal, A., et al. (2017) · European Journal of Cancer · doi:10.1016/j.ejca.2017.11.004 · Cited by 159
New Treatment Strategies for Metastatic Pancreatic Ductal Adenocarcinoma
Singh, R., & O'Reilly, E. M. (2020) · Drugs · doi:10.1007/s40265-020-01304-0 · Cited by 158
Golan, T., O'Kane, G. M., Denroche, R. E., Raitses‐Gurevich, M., Grant, R. C., Holter, S., Wang, Y., Zhang, A. X. W., Jang, G. H., Stossel, C., et al. (2021) · Gastroenterology · doi:10.1053/j.gastro.2021.01.220 · Cited by 157
Molecular subtyping of cancer: current status and moving toward clinical applications
Zhao, L., Lee, V. H.-F., Ng, M. K., Yan, H., & Bijlsma, M. F. (2018) · Briefings in Bioinformatics · doi:10.1093/bib/bby026 · Cited by 156
The plasticity of pancreatic cancer metabolism in tumor progression and therapeutic resistance
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“The driving oncogene in PDA results from an activating mutation in the KRAS gene which is found in > 90% of tumors [4].”
BackgroundBPTF is required for c-MYC transcriptional activity and in vivo tumorigenesis
Richart, L., Pau, E. C. D. S., Rio‐Machín, A., de Andrés, M. P., Cigudosa, J. C., Lobo, V. J. S.-A., & Real, F. X. (2016) · Nature Communications · doi:10.1038/ncomms10153 · Cited by 155
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Self-citationNoncanonical secondary structures arising from non-B DNA motifs are determinants of mutagenesis
Georgakopoulos-Soares, I., Morganella, S., Jain, N., Hemberg, M., & Nik-Zainal, S. (2018) · Genome Research · doi:10.1101/gr.231688.117 · Cited by 146
The role of hypoxia in pancreatic cancer: a potential therapeutic target?
Erkan, M., Kurtoğlu, M., & Kleeff, J. H. (2015) · Expert Review of Gastroenterology & Hepatology · doi:10.1586/17474124.2016.1117386 · Cited by 157
“most prevalent.[2,3] Recently, whole genome sequencing has deepened our understanding of the mutational landscape of pancreatic cancer.”
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“Pancreatic cancer is characterized by the accumulation of loss of tumor suppressor genes (19–22).”
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3D genomic mapping reveals multifocality of human pancreatic precancers
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Biomarkers of Response and Resistance to DNA Repair Targeted Therapies
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“Genomic sequencing studies have demonstrated frequent DDR alterations in diverse cancers, suggesting that DNA repair targeted agents may be broadly active in cancer therapy and highlighting the need for accurate biomarkers of response (17, 18).”
BackgroundComprehensive Genomic Profiling of Neuroendocrine Carcinomas of the Gastrointestinal System
Yachida, S., Totoki, Y., Noë, M., Nakatani, Y., Horie, M., Kawasaki, K., Nakamura, H., Saito-Adachi, M., Suzuki, M., Takai, E., et al. (2021) · Cancer Discovery · doi:10.1158/2159-8290.cd-21-0669 · Cited by 161
“Unlike PDAC (27), loss of p16 and SMAD4 protein immunolabeling was rare (Supplementary Table S16), indicating a pathway to progression different from PDAC development.”
Self-citationCarugo, A., Genovese, G., Seth, S., Nezi, L., Rose, J. L., Bossi, D., Cicalese, A., Shah, P. K., Viale, A., Pettazzoni, P., et al. (2016) · Cell Reports · doi:10.1016/j.celrep.2016.05.063 · Cited by 140
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“It was reported that the BRCA mutation rate in pancreatic cancer tissues was approximately 5% while other mutations in pancreatic cancer tissues are rare.(8,20) Our data showed that the rate of BRCA2 mutation in ctDNA is 11.”
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“mutation was observed in several types of cancer including pancreatic cancer (15) and colorectal cancer (45, 46).”
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“7,33 The central challenge is that although WGS can de fi ne putative biomarkers of therapeutic response in cohort studies of breast 73 and pancreatic cancer, 19 these methodologies are not currently translatable to the clinic.”
Self-citationTGF-β in pancreatic cancer initiation and progression: two sides of the same coin
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“The data from whole-genome sequencing analyses demonstrated that the common co-mutations detected in pancreatic cancer are SMAD4, KRAS, MED12, TP53, and CDKN2A [37].”
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Mutant p53 proteins counteract autophagic mechanism sensitizing cancer cells to mTOR inhibition
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“Introduction In the presentwork, we ascertain that GOFmutant p53 pro- Mutations in the TP53 gene occur in over 50% of human cancers, where most of them are missense mutations resulting in the expression of mutant forms of p53 (Vousden and Lu, 2002; Waddell et al., 2015).”
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Precision oncology in the age of integrative genomics
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Epigenetic treatment of pancreatic cancer: is there a therapeutic perspective on the horizon?
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Replication protein A: a multifunctional protein with roles in DNA replication, repair and beyond
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“Biallelic somatic mutation of RPA1 has been found in a pancreatic tumor (321).”
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Patient-derived organoid models help define personalized management of gastrointestinal cancer
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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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