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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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Pancreatic Cancer: Yesterday, Today and Tomorrow
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“WGS analysis for breast, ovarian and pancreatic cancers indicated that signatures were related with inactivation of DNA maintenance genes (BRCA1, BRCA2 and PALB2), and also related with high response to DNA-damaging agents and PARP inhibitors.(75,78) Recent studies have demonstrated that somatic substitution, insertio…”
BackgroundReal-time Genomic Characterization of Advanced Pancreatic Cancer to Enable Precision Medicine
Aguirre, A. J., Nowak, J. A., Camarda, N. D., Moffitt, R. A., Ghazani, A. A., Hazar-Rethinam, M., Raghavan, S., Kim, J., Brais, L. K., Ragon, D., et al. (2018) · Cancer Discovery · doi:10.1158/2159-8290.cd-18-0275 · Cited by 367
“As has been suggested in prior studies of primary PDAC resection specimens (7,9,12), we observed a striking prevalence of germline and somatic mutations in DDR genes in our cohort of advanced PDAC patients.”
BackgroundResultInfluentialEvaluating Mismatch Repair Deficiency in Pancreatic Adenocarcinoma: Challenges and Recommendations
Hu, Z. I., Shia, J., Stadler, Z. K., Varghese, A. M., Capanu, M., Salo‐Mullen, E. E., Lowery, M. A., Diaz, L. A., Mandelker, D. L., Yu, K. H., et al. (2018) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-17-3099 · Cited by 377
“NGShas alsobeenused to identify distinct mutational signatures, including a MMR-D subtype, in PDACs (4, 38).”
BackgroundSelf-citationWhole Genome Sequencing Defines the Genetic Heterogeneity of Familial Pancreatic Cancer
Roberts, N. J., Norris, A. L., Petersen, G. M., Bondy, M. L., Brand, R., Gallinger, S., Kurtz, R. C., Olson, S. H., Rustgi, A. K., Schwartz, A. G., et al. (2016) · Cancer Discovery · doi:10.1158/2159-8290.cd-15-0402 · Cited by 361
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“In addition, ~31–38% of pancreatic cancers have mutations in SMAD4, which can occur in the late stages of pancreatic carcinogenesis.(23,25) In pancreatic cancer, the frequent loss of SMAD4 via homozygous deletion or mutation leads to decreasing SMAD4-dependent inhibition of transforming growth factor-β (TGF-β) and the…”
BackgroundPancreatic cancer evolution and heterogeneity: integrating omics and clinical data
Connor, A. A., & Gallinger, S. (2022) · Nature Reviews Cancer · doi:10.1038/s41568-021-00418-1 · Cited by 369
Fibroblast growth factor receptors as treatment targets in clinical oncology
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Self-citationLKB1 loss links serine metabolism to DNA methylation and tumorigenesis
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Andricovich, J., Perkail, S., Kai, Y., Casasanta, N., Peng, W., & Tzatsos, A. (2018) · Cancer Cell · doi:10.1016/j.ccell.2018.02.003 · Cited by 320
Whole-genome landscape of mucosal melanoma reveals diverse drivers and therapeutic targets
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Self-citationSequencing thousands of single-cell genomes with combinatorial indexing
Vitak, S. A., Torkenczy, K. A., Rosenkrantz, J. L., Fields, A. J., Christiansen, L., Wong, M. H., Carbone, L., Steemers, F. J., & Adey, A. (2017) · Nature Methods · doi:10.1038/nmeth.4154 · Cited by 294
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Compensatory metabolic networks in pancreatic cancers upon perturbation of glutamine metabolism
Biancur, D. E., Paulo, J. A., Małachowska, B., Quiles Del Rey, M., Sousa, C. M., Wang, X., Sohn, A. S. W., Chu, G. C., Gygi, S. P., Harper, J. W., et al. (2017) · Nature Communications · doi:10.1038/ncomms15965 · Cited by 315
“For combination studies with BSO, MPDAC-4 subcutaneous xenografts were generated as above in 8-week-old female NCr nude mice and were randomized to one of four treatment arms: (1) Vehicle oral gavage twice daily/Normal saline IP injection once daily, (2) CB-839 200 mg kg 1 oral gavage twice daily/normal saline IP inje…”
MethodDetecting the mutational signature of homologous recombination deficiency in clinical samples
Gulhan, D., Lee, J. J.-K., Melloni, G. E. M., Cortés‐Ciriano, I., & Park, P. J. (2019) · Nature Genetics · doi:10.1038/s41588-019-0390-2 · Cited by 318
CAF Subpopulations: A New Reservoir of Stromal Targets in Pancreatic Cancer
Pereira, B., Vennin, C., Papanicolaou, M., Chambers, C. R., Herrmann, D., Morton, J. P., Cox, T. R., & Timpson, P. (2019) · Trends in cancer · doi:10.1016/j.trecan.2019.09.010 · Cited by 320
α-Ketoglutarate links p53 to cell fate during tumour suppression
Morris, J. P., Yashinskie, J. J., Koche, R., Chandwani, R., Tian, S., Chen, C.-C., Baslan, T., Marinkovic, Z. S., Sánchez-Rivera, F. J., Leach, S. D., et al. (2019) · Nature · doi:10.1038/s41586-019-1577-5 · Cited by 296
Therapeutic targeting of tumour myeloid cells
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Molecular alterations and targeted therapy in pancreatic ductal adenocarcinoma
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“PDAC has been divided into four subtypes according to the structural rearrangements, and the unstable subtype is most sensitive to DNA-damaging agents [140].”
BackgroundCell-free DNA next-generation sequencing in pancreatobiliary carcinomas
Zill, O. A., Greene, C., Sebisanovic, D., Siew, L. M., Leng, J., Vu, M., Hendifar, A. E., Wang, Z., Atreya, C. E., Kelley, R. K., et al. (2015) · Cancer Discovery · doi:10.1158/2159-8290.cd-15-0274 · Cited by 282
“As a result, most genomic research in PDA has centered around tumor-derived cell lines or xenografts in lieu of direct tumor sequencing(7), and expert bodies currently make no recommendations regarding molecular profiling for clinical decision-making in PDA(8), despite potentially sensitive subsets identified by seque…”
BackgroundPatient-centric trials for therapeutic development in precision oncology
Biankin, A. V., Piantadosi, S., & Hollingsworth, S. J. (2015) · Nature · doi:10.1038/nature15819 · Cited by 286
Self-citationVennin, C., Mélénec, P., Rouet, R., Nobis, M., Cazet, A. S., Murphy, K. J., Herrmann, D., Reed, D. A., Lucas, M. C., Warren, S. C., et al. (2019) · Nature Communications · doi:10.1038/s41467-019-10968-6 · Cited by 268
Self-citationLi, J., Woods, S. L., Healey, S. C., Beesley, J., Chen, X., Lee, J. S., Sivakumaran, H., Wayte, N., Nones, K., Waterfall, J. J., et al. (2016) · The American Journal of Human Genetics · doi:10.1016/j.ajhg.2016.03.001 · Cited by 270
Self-citationMartinelli, P., Pau, E. C. D. S., Cox, T. F., Sáinz, B., Dusetti, N., Greenhalf, W., Rinaldi, L., Costello, E., Ghaneh, P., Malats, N., et al. (2016) · Gut · doi:10.1136/gutjnl-2015-311256 · Cited by 273
Self-citationPishvaian, M. J., Bender, R. J., Halverson, D., Rahib, L., Hendifar, A. E., Mikhail, S., Chung, V., Picozzi, V. J., Sohal, D., Blais, E. M., et al. (2018) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-18-0531 · Cited by 245
“This was consistent with the frequency of KRAS mutations in published studies (5, 6, 9).”
ResultVennin, C., Chin, V. T., Warren, S. C., Lucas, M. C., Herrmann, D., Magenau, A., Mélénec, P., Walters, S. N., del Monte‐Nieto, G., Conway, J. R. W., et al. (2017) · Science Translational Medicine · doi:10.1126/scitranslmed.aai8504 · Cited by 266
Self-citationPlasma Circulating Tumor DNA in Pancreatic Cancer Patients Is a Prognostic Marker
Pietrasz, D., Pécuchet, N., Garlan, F., Didelot, A., Dubreuil, O., Doat, S., Imbert‐Bismut, F., Karoui, M., Vaillant, J., Taly, V., et al. (2016) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-16-0806 · Cited by 272
Castillo, J., Bernard, V., Lucas, F. A. S., Allenson, K., Capello, M., Kim, D. U., Gascoyne, P. R. C., Mulu, F. C., Stephens, B. M., Huang, J. H., et al. (2017) · Annals of Oncology · doi:10.1093/annonc/mdx542 · Cited by 267
“An emerging body of literature demonstrates that comprehensive characterization of cancer genomes has both diagnostic and prognostic utility, and may provide insights into formulating individualized treatment strategies [1, 2].”
BackgroundSelf-citationChiou, S., Winters, I. P., Wang, J., Naranjo, S., Dudgeon, C., Tamburini, F. B., Brady Jennifer, J., Yang, D., Grüner, B. M., Chuang, C.-H., et al. (2015) · Genes & Development · doi:10.1101/gad.264861.115 · Cited by 267
“Given the frequent down-regulation and genomic loss of LKB1/STK11 in human PDAC (Morton et al. 2010; Waddell et al. 2015), the predisposition of Peutz-Jeghers syndrome patients to develop pancreatic tumors (Su et al. 1999), and the impact of Lkb1 inactivation in other pancreatic tumor models (Hezel…”
BackgroundHayes, T. K., Neel, N. F., Hu, C., Gautam, P., Chénard, M., Long, B. J., Aziz, M., Kassner, M., Bryant, K. L., Pierobon, M., et al. (2015) · Cancer Cell · doi:10.1016/j.ccell.2015.11.011 · Cited by 266
“This striking heterogeneity is not unexpected in light of the fact that there are numerous alterations in non-KRAS genes that are not widely shared among PDAC tumors (Waddell et al., 2015).”
BackgroundSelf-citationThe current state of molecular testing in the treatment of patients with solid tumors, 2019
El‐Deiry, W. S., Goldberg, R. M., Lenz, H., Shields, A. F., Gibney, G. T., Tan, A. R., Brown, J., Eisenberg, B., Heath, E. I., Phuphanich, S., et al. (2019) · CA: A Cancer Journal for Clinicians · doi:10.3322/caac.21560 · Cited by 264
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Drug resistance in pancreatic cancer: Impact of altered energy metabolism
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“High throughput sequencing and copy number studies of PDAC genome have identified and validated the known driver mutations in K-RAS, TP53, CDKN2A, and SMAD4, as well as novel gene mutations that may be involved in cell growth, DNA repair, invasiveness, angiogenesis and metabolism.(31) These studies can”
BackgroundTranslational advances in pancreatic ductal adenocarcinoma therapy
Hosein, A. N., Dougan, S. K., Aguirre, A. J., & Maitra, A. (2022) · Nature Cancer · doi:10.1038/s43018-022-00349-2 · Cited by 255
Self-citationThe Immune Microenvironment in Pancreatic Cancer
Huber, M., Brehm, C. U., Gress, T. M., Buchholz, M., Alhamwe, B. A., von Strandmann, E. P., Slater, E. P., Bartsch, J. W., Bauer, C. A., & Lauth, M. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21197307 · Cited by 250
“PDAC driver mutations have proven difficult to target in the clinical setting, with the exception of microsatellite instability with immune check point inhibitors [17] or BRCA1/2 mutations with platinum-based chemotherapies and PARP-inhibitors [18,19]; however, these concern only a small number of patients.”
BackgroundKindler, H. L., Hammel, P., Reni, M., Van Cutsem, E., Macarulla, T., Hall, M. J., Park, J. O., Hochhauser, D., Arnold, D., Oh, D.-Y., et al. (2022) · Journal of Clinical Oncology · doi:10.1200/jco.21.01604 · Cited by 244
Self-citationOrdered and deterministic cancer genome evolution after p53 loss
Baslan, T., Morris, J. P., Zhao, Z., Reyes, J., Ho, Y.-J., Tsanov, K. M., Bermeo, J., Tian, S., Zhang, S., Askan, G., et al. (2022) · Nature · doi:10.1038/s41586-022-05082-5 · Cited by 221
Self-citationPark, W., Chen, J., Chou, J. F., Varghese, A. M., Yu, K. H., Wong, W., Capanu, M., Balachandran, V. P., McIntyre, C. A., Dika, I. E., et al. (2020) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-20-0418 · Cited by 247
Self-citation
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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