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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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“(%), y Median (range) 46 (15-50) 46 (24-50) 45(25-50) 30 9 (2.”
BackgroundSelf-citationWNT Ligand Dependencies in Pancreatic Cancer
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“Mutations in BRCA1 and BRCA2 enhance tumor sensitivity to platinum-based chemotherapy in breast (9), ovarian (10, 11), and pancreatic cancer (12, 13).”
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“Disruption of either PTIP or Artemis resulted in partial restoration ofHR and reduced PARPi sensitivity of BRCA1-deficient cells, independently of RIF1 (Callen et al. 2013, Wang et al. 2014).”
BackgroundROBO2 is a stroma suppressor gene in the pancreas and acts via TGF-β signalling
Pinho, A. V., Bulck, M. V., Chantrill, L. A., Arshi, M., Sklyarova, T., Herrmann, D., Vennin, C., Gallego‐Ortega, D., Mawson, A., Giry-Laterrière, M., et al. (2018) · Nature Communications · doi:10.1038/s41467-018-07497-z · Cited by 66
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Pancreatic Cancer Heterogeneity Can Be Explained Beyond the Genome
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“(39) classified samples in four subtypes (stable, locally rearranged, scattered, and unstable) with potential clinical utility.”
BackgroundInterplays of glucose metabolism and KRAS mutation in pancreatic ductal adenocarcinoma
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Genomic signatures as predictive biomarkers of homologous recombination deficiency in ovarian cancer
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“This signature was enriched in a subset of breast, ovarian, pancreatic and gastric cancers [32e35] that displayed other clinical and genetic features of HRD such as better responses to platinum chemotherapy [34,35] and a large degree of structural variation [33,35].”
UTX is an escape from X-inactivation tumor-suppressor in B cell lymphoma
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Methylated DNA in Pancreatic Juice Distinguishes Patients With Pancreatic Cancer From Controls
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“However KRAS mutations were also present in 19% of healthy controls and in 50% of patients without PDAC who had a known risk factor for pancreatic malignancy (14).”
BackgroundCurrent prognostic and predictive biomarkers for gastrointestinal tumors in clinical practice
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Self-citationIntegrin alpha-V is an important driver in pancreatic adenocarcinoma progression
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“Hezel et al. used a genetically engineered mouse model with KrasG12D-initiated, SMAD4-deficient murine PDAs reflecting an early disease state and identified increased tumor cell proliferation through the blockade of integrin αvβ6 [34].”
BackgroundInfluentialCharacterization of the genomic landscape in large-scale Chinese patients with pancreatic cancer
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Pancreatic cancer chemo-resistance is driven by tumor phenotype rather than tumor genotype
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“Several alterations in key oncogenes and tumor suppressors have been identified in PDAC with KRAS being the most frequently mutated oncogene [21, 22].”
BackgroundLiquid biopsies for management of pancreatic cancer
Samandari, M., Juliá, M. G., Rice, A. J., Chronopoulos, A., & Hernández, A. E. D. R. (2018) · Translational research · doi:10.1016/j.trsl.2018.07.008 · Cited by 66
Pancreatic Cancer and Cellular Senescence: Tumor Microenvironment under the Spotlight
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“histone methyltransferase, and histone demethylases, are indeed frequently mutated in PDAC [24,29].”
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“MYC copy number was quantified relative to ALB based on the relative stability of ALB chromosomal locus 4q11-q13 in PDAC[3].”
BackgroundMethodInfluentialRecurrent noncoding regulatory mutations in pancreatic ductal adenocarcinoma
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Self-citationGermline and somatic variant identification using BGISEQ-500 and HiSeq X Ten whole genome sequencing
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Self-citationSatellite RNAs promote pancreatic oncogenic processes via the dysfunction of YBX1
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“[15] classified 4 subtypes PC based on the structural variation in the mutational landscape 1.”
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“Consequently, the loss-of-function mutations in KDM6A probably has effects analogous to EZH2 gain-of-function mutations [153,182,183,202,221].”
BackgroundPreclinical Models of Pancreatic Ductal Adenocarcinoma and Their Utility in Immunotherapy Studies
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“Genomic studies support the notion of homogeneity in diseaseinitiation events identifying common mutations in four genes: KRAS, TP53, CDKN2A, and SMAD4 (14).”
BackgroundReceptor-interacting Protein Kinase 2 Is an Immunotherapy Target in Pancreatic Cancer
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CELF2 suppresses non-small cell lung carcinoma growth by inhibiting the PREX2-PTEN interaction
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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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