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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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Pu, N., Chen, Q., Gao, S., Liu, G., Zhu, Y., Yin, L., Hu, H., Wei, L., Wu, Y., Maeda, S., et al. (2019) · Annals of Translational Medicine · doi:10.21037/atm.2019.10.91 · Cited by 36
“The s tudy o f tumor gene expres s ion prof i l e s contributes to the identification of molecular subtypes and the establishment of predictive prognostic models, enriching our understanding of the molecular pathways of tumorigenesis (6).”
BackgroundCreeden, J. F., Alganem, K., Imami, A. S., Brunicardi, F. C., Liu, S., Shukla, R., Tomar, T., Naji, F., & McCullumsmith, R. E. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21228679 · Cited by 36
“PDCL5 Patient Derived Age: 56; Gender: Male; Ethnicity: Caucasian; Disease: Pancreatic Ductal Adenocarcinoma Surgical resection with or without post-surgical adjuvant therapy KRAS_G12V; TP53_G245S [7,9,11,108] Data Repo”
BackgroundLiu, M., Qin, Y., Hu, Q., Liu, W., Ji, S., Xu, W., Fan, G., Zeng, Y., Zhang, Z., Xu, X., et al. (2020) · Cancer Letters · doi:10.1016/j.canlet.2020.11.023 · Cited by 36
N 6 -methyladenosine (m 6 A) in pancreatic cancer: Regulatory mechanisms and future direction
Li, J., Wang, F., Liu, Y., Wang, H., & Ni, B. (2021) · International Journal of Biological Sciences · doi:10.7150/ijbs.60115 · Cited by 36
“The protein encoded by TP53 plays a crucial role in multicellular organisms, where it prevents tumor formation [5, 6].”
BackgroundHistone methylation in pancreatic cancer and its clinical implications
Liu, X., Guo, C.-H., Xi, Z.-Y., Xu, X.-Q., Zhao, Q.-Y., Li, L., & Wang, Y. (2021) · World Journal of Gastroenterology · doi:10.3748/wjg.v27.i36.6004 · Cited by 36
Cell Lineage Infidelity in PDAC Progression and Therapy Resistance
Malinova, A., Veghini, L., Real, F. X., & Corbo, V. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.795251 · Cited by 39
Self-citationp53 regulates expression of nuclear envelope components in cancer cells
Panatta, E., Butera, A., Celardo, I., Leist, M., Melino, G., & Amelio, I. (2022) · Biology Direct · doi:10.1186/s13062-022-00349-3 · Cited by 34
“Pancreatic ductal carcinoma shows > 70% inactivation of the tumour suppressor p53 [47, 48].”
BackgroundPancreatic cancer: disease dynamics, tumor biology and the role of the microenvironment
Ansari, D., Frieß, H., Bauden, M. P., Samnegård, J., & Andersson, R. E. (2018) · Oncotarget · doi:10.18632/oncotarget.24019 · Cited by 35
Pentose conversions support the tumorigenesis of pancreatic cancer distant metastases
Bechard, M. E., Word, A. E., Tran, A. V., Liu, X., Locasale, J. W., & McDonald, O. G. (2018) · Oncogene · doi:10.1038/s41388-018-0346-5 · Cited by 35
“Because PGD is not genetically altered [11, 12, 15, 17] and expression levels did not explain these findings [12, 13], we”
Bechard, M. E., Smalling, R., Hayashi, A., Zhong, Y., Word, A. E., Campbell, S. L., Tran, A. V., Weiss, V. L., Iacobuzio-Donahue, C., Wellen, K. E., et al. (2020) · Nature Communications · doi:10.1038/s41467-020-17839-5 · Cited by 33
Self-citationPancreatic cancer and exosomes: role in progression, diagnosis, monitoring, and treatment
Fang, X., Lan, H., Jin, K., & Qian, J. (2023) · Frontiers in Oncology · doi:10.3389/fonc.2023.1149551 · Cited by 35
Li, Y., Tang, S., Wang, H., Zhu, H., Lu, Y., Zhang, Y., Guo, S., He, J., Li, Y., Zhang, Y., et al. (2025) · Cell stem cell · doi:10.1016/j.stem.2025.07.008 · Cited by 45
Fang, B. (2015) · Acta Biochimica et Biophysica Sinica · doi:10.1093/abbs/gmv090 · Cited by 37
“Whole-genome analysis on pancreatic cancer revealed that, although KRAS is mutated in ∼95% of PDACs, PDACs can be classified into four classes based on patterns of chromosomal rearrangements: stable, locally rearranged, scattered, and unstable [138].”
Zhao, S., Cao, Y., Liu, S., Wang, X.-A., Bao, R., Shu, Y., Hu, Y., Zhang, Y., Jiang, L., Zhang, F., et al. (2016) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-016-0370-7 · Cited by 35
“Previous studies have identified the E545K mutation of PIK3CA in various carcinomas, including colorectal cancer, glioblastoma, gastric cancer, breast cancer, lung cancer [17], esophageal squamous cell cancer [18], pancreatic cancer [19], intrahepatic cholangiocarcinoma [20] and GBC [21].”
BackgroundTargeting tumor tolerance: A new hope for pancreatic cancer therapy?
Delitto, D., Wallet, S. M., & Hughes, S. J. (2016) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2016.06.008 · Cited by 37
Extended RAS analysis and correlation with overall survival in advanced pancreatic cancer
Haas, M., Ormanns, S., Baechmann, S., Remold, A., Krüger, S., Westphalen, C. B., Siveke, J. T., Wenzel, P., Schlitter, A. M., Esposito, I., et al. (2017) · British Journal of Cancer · doi:10.1038/bjc.2017.115 · Cited by 33
“KRAS mutations are described as nearly ubiquitous in PC (Waddell et al, 2015).”
Backgroundβ-catenin-activated autocrine PDGF/Src signaling is a therapeutic target in pancreatic cancer
Kuo, T., Cheng, K., Shan, Y., Chen, L., & Hung, W.-C. (2018) · Theranostics · doi:10.7150/thno.28201 · Cited by 35
“It is noteworthy that the deregulation of genes involved in cell cycle control, transforming growth factor beta signaling, and epigenetic modification frequently co-exist with K-ras mutation and p53 inactivation in patients with pancreatic cancer [3-5].”
BackgroundImmunotherapy in pancreatic cancer: New hope or mission impossible?
Jiang, J., Zhou, H., Ni, C., Hu, X., Mou, Y., Huang, D., & Yang, L. (2019) · Cancer Letters · doi:10.1016/j.canlet.2018.10.045 · Cited by 37
Cheng, H., Luo, G., Jin, K., Fan, Z., Huang, Q., Gong, Y., Xu, J., Yu, X., & Liu, C. (2020) · Cancer Medicine · doi:10.1002/cam4.2895 · Cited by 35
Targeting Mutant KRAS in Pancreatic Cancer: Futile or Promising?
Nollmann, F. I., & Ruess, D. A. (2020) · Biomedicines · doi:10.3390/biomedicines8080281 · Cited by 33
Recent advances in precision medicine for pancreatic ductal adenocarcinoma
Hayashi, H., Higashi, T., Miyata, T., Yamashita, Y., & Baba, H. (2021) · Annals of Gastroenterological Surgery · doi:10.1002/ags3.12436 · Cited by 36
The Function of cGAS-STING Pathway in Treatment of Pancreatic Cancer
Mohseni, G., Li, J., Gabriel, A. N. A., Du, L., Wang, Y., & Wang, C. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.781032 · Cited by 36
“However, the tumor suppressors are also modified, such as CDKN2A (6), p53 (7), and DPC4/ SMAD4 (8).”
BackgroundRecent advances in artificial intelligence for pancreatic ductal adenocarcinoma
Hayashi, H., Uemura, N., Matsumura, K., Liu, Z., Sato, H. R., Shiraishi, Y., Yamashita, Y., & Baba, H. (2021) · World Journal of Gastroenterology · doi:10.3748/wjg.v27.i43.7480 · Cited by 40
Baleeiro, R. B., Bouwens, C. J., Liu, P., Gioia, C. D., Chard, L. S., Nagano, A., Gangeswaran, R., Chelala, C., Kocher, H. M., Lemoine, N. R., et al. (2022) · OncoImmunology · doi:10.1080/2162402x.2022.2080329 · Cited by 35
Eberle-Singh, J. A., Sagalovskiy, I. R., Maurer, H. C., Sastra, S. A., Palermo, C. F., Decker-Farrell, A. R., Kim, M. J., Sheedy, J., Mollin, A., Cao, L., et al. (2019) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-18-3281 · Cited by 36
“As p53 is mutated in approximately 78% of human ductal adenocarcinomas (20), we examinedDNA content in three p53-mutant human PDA lines following treatment with PTC596.”
BackgroundPrincipe, D. R., Underwood, P. W., Kumar, S., Timbers, K. E., Koch, R. M., Trevino, J. G., Munshi, H. G., & Rana, A. (2022) · Frontiers in Oncology · doi:10.3389/fonc.2022.806963 · Cited by 35
“In that regard, the mutational landscape of PDAC is highly varied (29).”
Backgroundp53-driven lipidome influences non-cell-autonomous lysophospholipids in pancreatic cancer
Butera, A., Roy, M. K., Zampieri, C., Mammarella, E., Panatta, E., Melino, G., D’Alessandro, A., & Amelio, I. (2022) · Biology Direct · doi:10.1186/s13062-022-00319-9 · Cited by 34
“The subsequent inactivating mutations of TP53, occurring in > 70% of cases, usually drives the final steps of malignancy towards the formation of a metastatic tumour [1, 2].”
BackgroundA mucus production programme promotes classical pancreatic ductal adenocarcinoma
Tonelli, C., Yordanov, G. N., Hao, Y., Deschênes, A., Hinds, J., Belleau, P., Klingbeil, O., Brosnan, E., Doshi, A., Park, Y., et al. (2024) · Gut · doi:10.1136/gutjnl-2023-329839 · Cited by 34
Self-citationHuang, Y., Cheng, W., Kuo, T.-T., Yang, J., Wu, Y., Wu, H., Lo, C.-C., Hsieh, C.-Y., Wong, S., Lu, C., et al. (2024) · Nature Cancer · doi:10.1038/s43018-023-00720-x · Cited by 34
Targeting ATM-deficient CLL through interference with DNA repair pathways
Knittel, G., Liedgens, P., & Reinhardt, H. C. (2015) · Frontiers in Genetics · doi:10.3389/fgene.2015.00207 · Cited by 34
“Coherent with its role in checkpoint signaling and genome maintenance, ATM is frequently mutated in various human cancer entities, ranging from solid tumors to lymphomas and leukemias (Haidar et al., 2000; Ripolles et al., 2006; Ding et al., 2008; Waddell et al., 2015).”
BackgroundState of the art biological therapies in pancreatic cancer
Marco, M. D. (2016) · World Journal of Gastrointestinal Oncology · doi:10.4251/wjgo.v8.i1.55 · Cited by 34
Quirin, K. A., Kwon, J. J., Alioufi, A., Factora, T. D., Temm, C. J., Jacobsen, M. H., Sandusky, G. E., Shontz, K., Chicoine, L. G., Clark, K. R., et al. (2017) · Molecular Therapy — Methods & Clinical Development · doi:10.1016/j.omtm.2017.09.006 · Cited by 35
Pancreatic cancer and associated exosomes
Zhao, C., Gao, F., Weng, S., & Liu, Q. (2017) · Cancer Biomarkers · doi:10.3233/cbm-170258 · Cited by 34
“Median survival and 5-year survival of pancreatic cancer are 6 months and less than 5%, respectively, despite 50 years of research and therapeutic development [6].”
Riva, G., Pea, A., Pilati, C., Fiadone, G., Lawlor, R. T., Scarpa, A., & Luchini, C. (2018) · World Journal of Gastrointestinal Oncology · doi:10.4251/wjgo.v10.i10.317 · Cited by 34
Self-citationCoordinately Targeting Cell-Cycle Checkpoint Functions in Integrated Models of Pancreatic Cancer
Chung, S., Vail, P. J., Witkiewicz, A. K., & Knudsen, E. S. (2018) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-18-1620 · Cited by 34
“While it has beenproposed that TP53mutation is associatedwith sensitivity to CHK1 inhibition (47–50), we observed that none of the common genetic alterations present in pancreatic cancer (e.g., TP53, CDKN2A, or SMAD4) were associated with response.”
BackgroundTian, G., Li, G., Liu, P., Wang, Z., & Li, N. (2020) · DNA and Cell Biology · doi:10.1089/dna.2019.5089 · Cited by 34
“%) and exhibits oncogene biological effects (Waddell et al. , 2015).”
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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