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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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Citations
Cites
Fast and accurate short read alignment with Burrows-Wheeler transform
Li, H., & Durbin, R. (2009) · Bioinformatics · doi:10.1093/bioinformatics/btp324 · Cited by 58,607
New response evaluation criteria in solid tumours: revised RECIST guideline (version 1.1)
Eisenhauer, E. A., Therasse, P., Bogaerts, J., Schwartz, L. H., Sargent, D., Ford, R., Dancey, J., Arbuck, S., Gwyther, S., Mooney, M., et al. (2009) · European Journal of Cancer · doi:10.1016/j.ejca.2008.10.026 · Cited by 29,534
The Genome Analysis Toolkit: A MapReduce framework for analyzing next-generation DNA sequencing data
McKenna, A., Hanna, M., Banks, E., Sivachenko, A., Cibulskis, K., Kernytsky, A., Garimella, K., Altshuler, D., Gabriel, S., Daly, M., et al. (2010) · Genome Research · doi:10.1101/gr.107524.110 · Cited by 27,895
Circos: An information aesthetic for comparative genomicsPreprint
Krzywinski, M. I., Schein, J. E., Birol, İ., Connors, J. M., Gascoyne, R. D., Horsman, D. E., Jones, S. J. M., & Marra, M. A. (2009) · Genome Research · doi:10.1101/gr.092759.109 · Cited by 11,073
Signatures of mutational processes in human cancer
Initiative, A. P. C. G., Alexandrov, L. B., ICGC Breast Cancer Consortium, ICGC MMML-Seq Consortium, PedBrain, I., Nik-Zainal, S., Wedge, D. C., Aparicio, S. A. J. R., Behjati, S., Biankin, A. V., et al. (2013) · Nature · doi:10.1038/nature12477 · Cited by 9,660
Self-citationIntegrative Genomics Viewer (IGV): high-performance genomics data visualization and exploration
Thorvaldsdottir, H., Robinson, J. T., & Mesirov, J. P. (2013) · Briefings in Bioinformatics · doi:10.1093/bib/bbs017 · Cited by 9,049
Integrated genomic analyses of ovarian carcinoma
Perou, C. M. (2019) · Carolina Digital Repository (University of North Carolina at Chapel Hill) · doi:10.17615/hvp3-wg08 · Cited by 7,927
FOLFIRINOX versus Gemcitabine for Metastatic Pancreatic Cancer
Conroy, T., Desseigne, F., Ychou, M., Bouché, O., Guimbaud, R., Bécouarn, Y., Adenis, A., Raoul, J.-L., Gourgou-Bourgade, S., de la Fouchardière, C., et al. (2011) · New England Journal of Medicine · doi:10.1056/nejmoa1011923 · Cited by 7,810 · cited 1×
“The majority of structural variants were intra-chromosomal (10,114) and were classified into 7 types: intra-chromosomal rearrangements (5,860), deletions (1,393), duplications (128), tandem duplications (179), inversions (1,629), foldback inversions (579) and amplified inversions (346); inter-chromosomal translocation…”
BackgroundMutational heterogeneity in cancer and the search for new cancer-associated genes
Lawrence, M. S., Stojanov, P., Polak, P., Kryukov, G. V., Cibulskis, K., Sivachenko, A., Carter, S. L., Stewart, C., Mermel, C. H., Roberts, S. A., et al. (2013) · Nature · doi:10.1038/nature12213 · Cited by 5,461
Comprehensive genomic characterization of squamous cell lung cancers
The Cancer Genome Atlas Research Network (2012) · Nature · doi:10.1038/nature11404 · Cited by 3,994
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Items 201–300 of 1,006
The biological underpinnings of therapeutic resistance in pancreatic cancerPreprint
Beatty, G. L., Werba, G., Lyssiotis, C. A., & Simeone, D. M. (2021) · Genes & Development · doi:10.1101/gad.348523.121 · Cited by 139
Lawlor, R. T., Mattiolo, P., Mafficini, A., Hong, S., Piredda, M. L., Taormina, S. V., Malleo, G., Marchegiani, G., Pea, A., Salvia, R., et al. (2021) · Cancers · doi:10.3390/cancers13133119 · Cited by 143
Self-citationPancreatic ductal adenocarcinoma: State-of-the-art 2017 and new therapeutic strategies
Chiaravalli, M., Reni, M., & O'Reilly, E. M. (2017) · Cancer Treatment Reviews · doi:10.1016/j.ctrv.2017.08.007 · Cited by 137
Konukiewitz, B., Jesinghaus, M., Steiger, K., Schlitter, A. M., Kasajima, A., Sipos, B., Zamboni, G., Weichert, W., Pfarr, N., & Klöppel, G. (2018) · Human Pathology · doi:10.1016/j.humpath.2018.03.018 · Cited by 135
Self-citationPalam, L. R., Gore, J., Craven, K. E., Wilson, J. L., & Korc, M. (2015) · Cell Death and Disease · doi:10.1038/cddis.2015.264 · Cited by 139
Pea, A., Yu, J., Rezaee, N., Luchini, C., He, J. P., Molin, M. D., Griffin, J. F., Fedor, H. L., Fesharakizadeh, S., Salvia, R., et al. (2016) · Annals of Surgery · doi:10.1097/sla.0000000000001817 · Cited by 132
“In both margin-positive cases with genetically unrelated primary/progressive neoplasms, the IPMN at the resection margin harbored LGD and showed genetic discordance with both the primary and the progressive lesions, suggesting that it was an independent multifocal IPMN.”
BackgroundInfluentialSelf-citationTGF-β induces miR-100 and miR-125b but blocks let-7a through LIN28B controlling PDAC progression
Ottaviani, S., Stebbing, J., Frampton, A. E., Zagorac, S., Krell, J., de Giorgio, A., Trabulo, S. M. D., Nguyen, V. T. M., Magnani, L., Feng, H., et al. (2018) · Nature Communications · doi:10.1038/s41467-018-03962-x · Cited by 132
“Considering this principle, (5) to find bona fide targets of the overexpressed miRNAs we used tools that unbiasedly retrieve enriched words 6–8 bases long within selected regions of sorted transcripts38,40,51 for both AGO2-RIP and RNAseq.”
Stress-Activated NRF2-MDM2 Cascade Controls Neoplastic Progression in Pancreas
Todoric, J., Antonucci, L., Caro, G. D., Li, N., Wu, X., Lytle, N. K., Dhar, D., Banerjee, S., Fagman, J. B., Browne, C. D., et al. (2017) · Cancer Cell · doi:10.1016/j.ccell.2017.10.011 · Cited by 129
“…al., 2008), which controls transcription of cell-cycle inhibitors and apoptosis inducers. p53 also inhibits cellular reprogramming thereby preventing acquisition of stemness (Kawamura et al., 2009; Marion et al., 2009), and is functionally inactivated in >80% of human PDAC (Waddell et al., 2015).”
Surgical and molecular pathology of pancreatic neoplasms
Hackeng, W. M., Hruban, R. H., Offerhaus, G. J. A., & Brosens, L. A. A. (2016) · Diagnostic Pathology · doi:10.1186/s13000-016-0497-z · Cited by 133
“In addition, extensive larger structural variations including intra-chromosomal rearrangements, deletions and amplifications are common in PDAC [21, 28].”
BackgroundSelf-citationMolecular subtypes in cancers of the gastrointestinal tract
Bijlsma, M. F., Sadanandam, A., Tan, P. B. O., & Vermeulen, L. (2017) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/nrgastro.2017.33 · Cited by 134
Buscail, É., Alix‐Panabières, C., Quincy, P., Cauvin, T., Chauvet, A., Degrandi, O., Caumont, C., Verdon, S., Lamrissi‐Garcia, I., Moranvillier, I., et al. (2019) · Cancers · doi:10.3390/cancers11111656 · Cited by 138
“CTC-enrichment methods have been combined with molecular identification such as the detection of mutant KRAS, present in >92% of PDACs [16].”
MethodInfluentialPrecancerous neoplastic cells can move through the pancreatic ductal system
Makohon-Moore, A. P., Matsukuma, K., Zhang, M., Reiter, J. G., Gerold, J. M., Jiao, Y., Sikkema, L., Attiyeh, M. A., Yachida, S., Sandone, C., et al. (2018) · Nature · doi:10.1038/s41586-018-0481-8 · Cited by 120
Self-citationCerrato, A., Morra, F., & Celetti, A. (2016) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-016-0456-2 · Cited by 132
Rath, N., Morton, J. P., Julian, L., Helbig, L., Kadir, S. R., McGhee, E. J., Anderson, K. I., Kalna, G., Mullin, M., Pinho, A. V., et al. (2016) · EMBO Molecular Medicine · doi:10.15252/emmm.201606743 · Cited by 125
“© EMBO 1 ROCK signaling promotes collagen remodeling to facilitate invasive pancreatic ductal adenocarcinoma tumor cell growth”
BackgroundSelf-citationPDX-derived organoids model in vivo drug response and secrete biomarkers
Huang, L., Bockorny, B., Paul, I., Akshinthala, D., Frappart, P., Gandarilla, O., Bose, A., Sanchez‐Gonzalez, V., Rouse, E. E., Lehoux, S. D., et al. (2020) · JCI Insight · doi:10.1172/jci.insight.135544 · Cited by 138
“To build a set of matched PDX and tumor organoid models, we identified eight PDX models that have heterogeneous combination of alterations in the common pancreatic cancer oncogenes such as KRAS, TP53, CDKN2A, SMAD4, c-MYC, GATA6, ERBB2, as well as other genetic alterations in SWI/SNF, DNA damage repair and axon guidan…”
Recent advances in organoid development and applications in disease modeling
Rauth, S., Karmakar, S., Batra, S. K., & Ponnusamy, M. P. (2021) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2021.188527 · Cited by 135
“Inactivating mutations of chromatin modifiers are frequent genetic events in pancreatic tumors [125].”
BackgroundEarly detection of pancreatic cancer using DNA-based molecular approaches
Singhi, A. D., & Wood, L. D. (2021) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-021-00470-0 · Cited by 127
Krieger, T. G., Blanc, S. L., Jabs, J., Ten, F. W., Ishaque, N., Jechow, K., Debnath, O., Leonhardt, C.-S., Giri, A., Eils, R., et al. (2021) · Nature Communications · doi:10.1038/s41467-021-26059-4 · Cited by 131
Loss of ATM accelerates pancreatic cancer formation and epithelial–mesenchymal transition
Russell, R., Perkhofer, L., Liebau, S., Lin, Q., Lechel, A., Feld, F. M., Heßmann, E., Gaedcke, J., Güthle, M., Zenke, M., et al. (2015) · Nature Communications · doi:10.1038/ncomms8677 · Cited by 125
“Herein we examine the role of ATM in PDAC tumour biology in both mice and men and provide evidence that loss of ATM (1) enhances acinar-to-ductal reprogramming (ADR) via altered TGFb-superfamily signalling, (2) is associated with epithelial-tomesenchymal transition (EMT) and a gain in tumour initiating properties and…”
BackgroundPancreatic cancer in 2021: What you need to know to win
Tonini, V., & Zanni, M. (2021) · World Journal of Gastroenterology · doi:10.3748/wjg.v27.i35.5851 · Cited by 133
Patra, K. C., Bardeesy, N. M., & Mizukami, Y. (2017) · Clinical and Translational Gastroenterology · doi:10.1038/ctg.2017.3 · Cited by 127
“93 The issues of clonality and field defect are presently under discussion as potentially having more general importance in PDA.”
BackgroundInfluentialPancreatic Cancer: Molecular Characterization, Clonal Evolution and Cancer Stem Cells
Pelosi, E., Castelli, G., & Testa, U. (2017) · Biomedicines · doi:10.3390/biomedicines5040065 · Cited by 128
“The pattern of chromosomal structural variation allowed the classification of ductal pancreatic adenocarcinomas in four groups: a stable subtype (20% of total), containing ≤50% structural variation events and often exhibiting extended aneuploidy and with a frequency of TP53, SMAD4 and KRAS mutation in the range; a loc…”
BackgroundInfluentialHNF4A and GATA6 Loss Reveals Therapeutically Actionable Subtypes in Pancreatic Cancer
Brunton, H., Caligiuri, G., Cunningham, R., Upstill‐Goddard, R., Bailey, U., Garner, I., Nourse, C., Dreyer, S. B., Jones, M. D., Moran‐Jones, K., et al. (2020) · Cell Reports · doi:10.1016/j.celrep.2020.107625 · Cited by 121
Self-citationDefining the molecular pathology of pancreatic body and tail adenocarcinoma
Initiative, A. P. C. G., Dreyer, S. B., Jamieson, N. B., Upstill‐Goddard, R., Bailey, P. J., McKay, C. J., Biankin, A. V., & Chang, D. K.-F. (2018) · British journal of surgery · doi:10.1002/bjs.10772 · Cited by 125
Self-citationImmune therapies in pancreatic ductal adenocarcinoma: Where are we now?
Hilmi, M., Bartholin, L., & Neuzillet, C. (2018) · World Journal of Gastroenterology · doi:10.3748/wjg.v24.i20.2137 · Cited by 126
Combinatorial CRISPR screen identifies fitness effects of gene paralogues
Thompson, N., Ranzani, M., van der Weyden, L., Iyer, V., Offord, V., Droop, A., Behan, F. M., Gonçalves, E., Speak, A. O., Iorio, F., et al. (2021) · Nature Communications · doi:10.1038/s41467-021-21478-9 · Cited by 120
Prognostic and predictive markers in pancreatic adenocarcinoma
Le, N. N. H., Sund, M., Vinci, A., Beyer, G., Javed, M., Krug, S., Neessee, A., & Schober, M. (2015) · Digestive and Liver Disease · doi:10.1016/j.dld.2015.11.001 · Cited by 122
“Their results showed hat DNA maintenance defect can predict chemosensitivity to latinum-based therapy, giving this marker a potential to be further nvestigated in the future [92].”
BackgroundA Multidisciplinary Approach to Pancreas Cancer in 2016: A Review
Fogel, E. L., Shahda, S., Sandrasegaran, K., DeWitt, J. M., Easler, J. J., Agarwal, D. M., Eagleson, M. A., Zyromski, N. J., House, M. G., Ellsworth, S. G., et al. (2017) · The American Journal of Gastroenterology · doi:10.1038/ajg.2016.610 · Cited by 122
Neuroendocrine Neoplasms of the Small Bowel and Pancreas
Clift, A. K., Kidd, M. S., Bodei, L., Toumpanakis, C., Baum, R. P., Öberg, K., Modlin, I. M., & Frilling, A. (2019) · Neuroendocrinology · doi:10.1159/000503721 · Cited by 125
The Evolutionary Origins of Recurrent Pancreatic Cancer
Sakamoto, H., Attiyeh, M. A., Gerold, J. M., Makohon-Moore, A. P., Hayashi, A., Hong, J., Kappagantula, R. L., Zhang, L., Melchor, J. P., Reiter, J. G., et al. (2020) · Cancer Discovery · doi:10.1158/2159-8290.cd-19-1508 · Cited by 123
“8 9 10 Discussion 11 To date genomic studies of PDA have primarily relied on resections or biopsies of 12 treatment naïve disease (9,36,37).”
BackgroundSelf-citationEmerging roles for the IL-6 family of cytokines in pancreatic cancer
van Duijneveldt, G., Griffin, M. D. W., & Putoczki, T. L. (2020) · Clinical Science · doi:10.1042/cs20191211 · Cited by 126
SerpinB2 regulates stromal remodelling and local invasion in pancreatic cancer
Initiative, A. P. C. G., Harris, N. L. E., Vennin, C., Conway, J. R. W., Vine, K. L., Pinese, M., Cowley, M. J., Shearer, R. F., Lucas, M. C., Herrmann, D., et al. (2017) · Oncogene · doi:10.1038/onc.2017.63 · Cited by 121
Self-citationNile, A. H., Mukund, S., Stanger, K., Wang, W., & Hannoush, R. N. (2017) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1618293114 · Cited by 117
Chou, A. S. Y., Froio, D., Nagrial, A. M., Parkin, A., Murphy, K. J., Chin, V. T., Wohl, D., Steinmann, A. M., Stark, R., Drury, A., et al. (2017) · Gut · doi:10.1136/gutjnl-2017-315144 · Cited by 121
Self-citationAdvances in pancreatic cancer biomarkers
Hasan, S. M., Jacob, R., Manne, U., & Paluri, R. K. (2019) · Oncology Reviews · doi:10.4081/oncol.2019.410 · Cited by 124
Analysis of Mucosal Melanoma Whole-Genome Landscapes Reveals Clinically Relevant Genomic Aberrations
Zhou, R., Shi, C., Tao, W., Li, J., Wu, J., Han, Y., Yang, G., Gu, Z., Xu, S., Wang, Y., et al. (2019) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-18-3442 · Cited by 120
“the structural variant type and the copy-number status in breakpoints (30), all variants were further classified into eight groups: deletions, duplications, tandem duplications, fold-back inversions, amplified inversions, inversions, intrachromosomal, or interchromosomal translocations.”
BackgroundSelf-citationCurrent Clinical Strategies of Pancreatic Cancer Treatment and Open Molecular Questions
Brunner, M., Wu, Z., Krautz, C., Pilarsky, C. P., Grützmann, R., & Weber, G. F. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20184543 · Cited by 121
“A recent whole genome sequencing and copy number analysis identified KDM6A and MLL2 as the most frequently altered histone methylation regulatory genes in pancreatic cancers [146].”
BackgroundSelf-citationTu, M., Klein, L., Espinet, E., Georgomanolis, T., Wegwitz, F., Li, X., Urbach, L., Danieli‐Mackay, A., Küffer, S., Bojarczuk, K., et al. (2021) · Nature Cancer · doi:10.1038/s43018-021-00258-w · Cited by 115
Efficient Genome-Wide, Privacy-Preserving Similar Patient Query based on Private Edit Distance
Wang, X. S., Huang, Y., Zhao, Y., Tang, H., Wang, X., & Bu, D. (2015) · ACM SIGSAC Conference on Computer and Communications Security (CCS) · doi:10.1145/2810103.2813725 · Cited by 115
“Among the indicators of genetic similarity, editdistance is one of the most important metrics, which is very useful in the biomedical research for the diagnosis and treatment of cancer, Alzheimer’s disease, Schizophrenia, etc [44, 49, 22, 51].”
BackgroundBlasco, M. T., Navas, C., Martín-Serrano, G., Graña-Castro, O., Lechuga, C. G., Martín-Díaz, L., Djurec, M., Li, J., Morales-Cacho, L., Esteban-Burgos, L., et al. (2019) · Cancer Cell · doi:10.1016/j.ccell.2019.03.002 · Cited by 115
Serum Concentrations of Selenium and Copper in Patients Diagnosed with Pancreatic Cancer
Lener, M. R., Scott, R. J., Wiechowska–Kozłowska, A., Serrano‐Fernández, P., Baszuk, P., Jaworska–Bieniek, K., Sukiennicki, G., Marciniak, W., Muszyńska, M., Kładny, J., et al. (2015) · Cancer Research and Treatment · doi:10.4143/crt.2015.282 · Cited by 116
Kirby, M. K., Ramaker, R. C., Gertz, J., Davis, N. S., Johnston, B. E., Oliver, P. G., Sexton, K. C., Greeno, E. W., Christein, J. D., Heslin, M. J., et al. (2016) · Molecular Oncology · doi:10.1016/j.molonc.2016.05.004 · Cited by 110
Pan-cancer analysis of whole genomesPreprint
Campbell, P. J., Getz, G., Stuart, J. M., Korbel, J. O., & Stein, L. D. (2017) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/162784 · Cited by 117
Schlitter, A. M., Segler, A., Steiger, K., Michalski, C. W., Jäger, C., Konukiewitz, B., Pfarr, N., Endris, V., Bettstetter, M., Kong, B., et al. (2017) · Scientific Reports · doi:10.1038/srep41064 · Cited by 122
Perkhofer, L., Schmitt, A., Carrasco, M. C. R., Ihle, M., Hampp, S., Ruess, D. A., Heßmann, E., Russell, R., Lechel, A., Azoitei, N., et al. (2017) · Cancer Research · doi:10.1158/0008-5472.can-17-0634 · Cited by 113
“Whole genome sequencing studies could also define subgroups of PDAC including a genomically instable type (2).”
BackgroundInfluentialA unified haplotype-based method for accurate and comprehensive variant calling
Cooke, D. P., Wedge, D. C., & Lunter, G. A. (2021) · Nature Biotechnology · doi:10.1038/s41587-021-00861-3 · Cited by 117
Comprehensive Genomic Profiling of Neuroendocrine Carcinomas of the Gastrointestinal System
Yachida, S., Totoki, Y., Noë, M., Nakatani, Y., Horie, M., Kawasaki, K., Nakamura, H. K., Saito-Adachi, M., Suzuki, M., Takai, E., et al. (2022) · Utrecht University Repository (Utrecht University) · Cited by 112
Self-citationThe Landscape of Pancreatic Cancer Therapeutic Resistance Mechanisms
Chand, S. N., O’Hayer, K., Blanco, F. F., Winter, J. M., & Brody, J. R. (2016) · International Journal of Biological Sciences · doi:10.7150/ijbs.14951 · Cited by 117
“as well as identifying novel gene mutations that may be involved in cell growth, DNA repair, invasiveness and angiogenesis[15, 32-34] (Fig.”
BackgroundWallez, Y., Dunlop, C. R., Johnson, T. I., Koh, S., Fornari, C., Yates, J. W. T., Fernández, S. B. D. Q., Lau, A., Richards, F. M., & Jodrell, D. I. (2018) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-18-0010 · Cited by 114
“org Mol Cancer Ther; 17(8) August 2018 1673”
BackgroundInfluentialNever let it go: Stopping key mechanisms underlying metastasis to fight pancreatic cancer
Giovannetti, E., van der Borden, C. L., Frampton, A. E., Ali, A., Firuzi, O., & Peters, G. J. (2017) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2017.04.006 · Cited by 114
Strijker, M., Soer, E. C., Pastena, M. D., Creemers, A., Balduzzi, A., Beagan, J. J., Busch, O. R., van Delden, O. M., Halfwerk, H., van Hooft, J. E., et al. (2019) · International Journal of Cancer · doi:10.1002/ijc.32586 · Cited by 107
“PDAC shows a very homogeneous mutational landscape with KRAS mutations in approximately 90% of cases, barring the need for extensive coverage and patient-tailored primers.(18,38,39) This implies that ddPCR, which has a lower limit of detection than NGS, would be eminently suited to PDAC.”
BackgroundMekonnen, N., Yang, H., & Shin, Y. K. (2022) · Frontiers in Oncology · doi:10.3389/fonc.2022.880643 · Cited by 117
Genetic Diversity of Pancreatic Ductal Adenocarcinoma and Opportunities for Precision Medicine
Knudsen, E. S., O'Reilly, E. M., Brody, J. R., & Witkiewicz, A. K. (2015) · Gastroenterology · doi:10.1053/j.gastro.2015.08.056 · Cited by 115
Cancer whole-genome sequencing: present and future
Nakagawa, H., Wardell, C. P., Furuta, M., Taniguchi, H., & Fujimoto, A. (2015) · Oncogene · doi:10.1038/onc.2015.90 · Cited by 111
Nanoparticle cancer vaccines: Design considerations and recent advances
Liu, J., Miao, L., Sui, J., Hao, Y., & Huang, G. (2019) · Asian Journal of Pharmaceutical Sciences · doi:10.1016/j.ajps.2019.10.006 · Cited by 113
“[63] Waddell N , Pajic M , Patch AM , Chang DK , Kassahn KS , Bailey P , et al.”
BackgroundMolecular profiling of biliary tract cancer: a target rich disease
Jain, A., & Javle, M. M. (2016) · Journal of Gastrointestinal Oncology · doi:10.21037/jgo.2016.09.01 · Cited by 106
“In case of pancreatic cancer, similarly four subgroups have been proposed: (I) stable (20% aneuploidy); (II) locally rearranged (30%, focal event in one or two chromosomes); (III) scattered (36%, <200 structural variation events); and (IV) unstable (14%, >200 structural variation events, defects in DNA repair and main…”
BackgroundThe Role of PALB2 in the DNA Damage Response and Cancer Predisposition
Nepomuceno, T. C., Gregoriis, G. D., de Oliveira, F. M. B., Suarez‐Kurtz, G., Monteiro, Á. N. A., & Carvalho, M. A. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms18091886 · Cited by 117
“Frequencies of ~4% have been described in familial PC patients in European, Australian and Japanese cohorts [43,44,47,48].”
BackgroundState of the art and future directions of pancreatic ductal adenocarcinoma therapy
Neuzillet, C., Tijeras‐Raballand, A., Bourget, P., Cros, J. F., Couvelard, A., Sauvanet, A., Vullierme, M., Tournigand, C., & Hammel, P. R. (2015) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2015.08.006 · Cited by 114
ATM Deficiency Is Associated with Sensitivity to PARP1- and ATR Inhibitors in Lung Adenocarcinoma
Schmitt, A., Knittel, G., Welcker, D., Yang, T.-P., George, J., Nowak, M., Leeser, U., Büttner, R., Perner, S., Peifer, M., et al. (2017) · Cancer Research · doi:10.1158/0008-5472.can-16-3398 · Cited by 109
“In keeping with the prominent role of ATM in cell cycle control, DNA repair and genome maintenance, the ATM gene is recurrently inactivated through mutations and/or deletions in various cancer entities, ranging from hematological malignancies to solid tumors, including lung adenocarcinoma (3, 5, 16-19).”
BackgroundIdentification of Targetable ALK Rearrangements in Pancreatic Ductal Adenocarcinoma
Singhi, A. D., Ali, S. M., Lacy, J., Hendifar, A. E., Nguyen, K., Koo, J., Chung, J., Greenbowe, J. R., Ross, J. S., Nikiforova, M. N., et al. (2017) · Journal of the National Comprehensive Cancer Network · doi:10.6004/jnccn.2017.0058 · Cited by 106
Varghese, A. M., Perry, M., Chou, J. F., Nandakumar, S., Muldoon, D. M., Erakky, A., Zucker, A., Fong, C. J., Mehine, M. M., Nguyen, B., et al. (2025) · Nature Medicine · doi:10.1038/s41591-024-03362-3 · Cited by 122
Self-citationNones, K., Johnson, J., Newell, F., Patch, A. M., Thorne, H., Kazakoff, S. H., de Luca, X. M., Parsons, M. T., Ferguson, K., Reid, L. E., et al. (2019) · Annals of Oncology · doi:10.1093/annonc/mdz132 · Cited by 93
“The tumour was ‘BRCA2-like’ with a high burden of substitution signature 3 and rearrangement signature 5 supporting previous studies linking loss of PALB2 function with BRCAdeficient signatures [7, 10, 13].”
BackgroundSelf-citationPreclinical models of pancreatic ductal adenocarcinoma
Hwang, C., Boj, S. F., Clevers, H. C., & Tuveson, D. A. (2015) · The Journal of Pathology · doi:10.1002/path.4651 · Cited by 105
“Recent genome-wide approaches have comprehensively characterized the human PDA genome and have identified additional genes and pathways operant in disease pathogenesis [9,10].”
BackgroundWu, D., Wen, X., Han, X., Wang, S., Wang, Y., Shen, M., Fan, S., Zhang, Z.-F., Shan, Q., Li, M., et al. (2019) · Molecular Therapy — Nucleic Acids · doi:10.1016/j.omtn.2019.02.022 · Cited by 105
RetractedTargeting KRAS in pancreatic cancer: new drugs on the horizon
Bannoura, S. F., Uddin, M. H., Nagasaka, M., Fazili, F., Hallak, M. N. A., Philip, P. A., El‐Rayes, B. F., & Azmi, A. S. (2021) · Cancer and Metastasis Reviews · doi:10.1007/s10555-021-09990-2 · Cited by 112
Dawkins, J. B. N., Wang, J., Maniati, E., Heward, J. A., Koniali, L., Kocher, H. M., Martin, S. A., Chelala, C., Balkwill, F. R., Fitzgibbon, J., et al. (2016) · Cancer Research · doi:10.1158/0008-5472.can-16-0481 · Cited by 104
“Four of these genes were selected for validation based on their previous associations with pancreatic cancer [c-MET (2, 41), Calumenin (42), Claudin-1 (43, 44), and PTPN14 (45)], with Western blot analysis confirming expression changes of each at the protein level (Fig.”
BackgroundCui, L., Nakano, K., Obchoei, S., Setoguchi, K., Matsumoto, M., Yamamoto, T., Obika, S., Shimada, K., & Hiraoka, N. (2017) · Gastroenterology · doi:10.1053/j.gastro.2017.03.050 · Cited by 103
Moreira, L., Bakir, B. S., Chatterji, P., Dantes, Z., Reichert, M., & Rustgi, A. K. (2017) · Cellular and Molecular Gastroenterology and Hepatology · doi:10.1016/j.jcmgh.2017.12.004 · Cited by 112
The involvement of exosomes in the diagnosis and treatment of pancreatic cancer
Gabriel, A. N. A., Wang, F., Jiao, Q., Umwali, Y., Yang, X., Al-Ameri, S. A. A.-E., Du, L., Wang, Y., & Wang, C. (2020) · Molecular Cancer · doi:10.1186/s12943-020-01245-y · Cited by 108
“1Department of Clinical Laboratory, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250033, People’s Republic of China Full list of author information is available at the end of the article as CDKN2A [17], p53 [18], and DPC4/SMAD4 [19] are also altered in above 95%, between 50 an…”
BackgroundMTOR signaling orchestrates stress-induced mutagenesis, facilitating adaptive evolution in cancer
Cipponi, A., Goode, D. L., Bedo, J., McCabe, M. J., Pajic, M., Croucher, D. R., Rajal, A. G., Junankar, S. R., Saunders, D. N., Lobachevsky, P., et al. (2020) · Science · doi:10.1126/science.aau8768 · Cited by 103
Self-citationPancreatic cancer subtypes: a roadmap for precision medicine
Torres, C., & Grippo, P. J. (2018) · Annals of Medicine · doi:10.1080/07853890.2018.1453168 · Cited by 104
“performed whole-genome sequencing and copy number variation analysis of 100 PDAC samples showing that variation in chromosomal structure is an important mechanism of DNA damage in pancreatic carcinogenesis and employed structural variation profiles to classify PDAC into four subtypes (stable, locally rearranged, scatt…”
BackgroundStromal barriers to nanomedicine penetration in the pancreatic tumor microenvironment
Tanaka, H. Y., & Kano, M. R. (2018) · Cancer Science · doi:10.1111/cas.13630 · Cited by 106
A quarter century of EUS-FNA: Progress, milestones, and future directions
Bhutani, M., Cazacu, I. M., Chavez, A. L., Săftoiu, A., & Vilmann, P. (2018) · Endoscopic Ultrasound · doi:10.4103/eus.eus_19_18 · Cited by 104
“[247,249] Whole-genome sequencing and whole-exome sequencing analyses have confirmed that mutations in four genes are most commonly seen in pancreatic adenocarcinoma: K-ras, SMAD4, TP53, and CDKN2A/p16.”
BackgroundEmerging epigenomic landscapes of pancreatic cancer in the era of precision medicine
Lomberk, G. A., Dusetti, N., Iovanna, J., & Urrutia, R. A. (2019) · Nature Communications · doi:10.1038/s41467-019-11812-7 · Cited by 101
Pishvaian, M. J., Blais, E. M., Brody, J. R., Rahib, L., Lyons, E. E., Arbeloa, P., Hendifar, A. E., Mikhail, S., Chung, V. M., Sohal, D. P. S., et al. (2019) · JCO Precision Oncology · doi:10.1200/po.19.00115 · Cited by 105
Truong, L.-H., & Pauklin, S. (2021) · Cancers · doi:10.3390/cancers13195028 · Cited by 102
Tumor Heterogeneity in Pancreatic Adenocarcinoma
Cros, J. F., Raffenne, J., Couvelard, A., & Poté, N. (2017) · Pathobiology · doi:10.1159/000477773 · Cited by 106
Steentoft, C., Migliorini, D., King-Peoples, T. R., Mandel, U., June, C. H., & Posey, A. D. (2018) · Glycobiology · doi:10.1093/glycob/cwy008 · Cited by 102
Single-cell profiling to explore pancreatic cancer heterogeneity, plasticity and response to therapy
Bärthel, S., Falcomatà, C., Rad, R., Theis, F. J., & Saur, D. (2023) · Nature Cancer · doi:10.1038/s43018-023-00526-x · Cited by 105
“(3) Immunosuppressive microenvironment”
BackgroundPancreatic cancer: Current research and future directions
Falasca, M., Kim, M., & Casari, I. (2016) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2016.01.001 · Cited by 101
Rho GTPases: Anti- or pro-neoplastic targets?
Zandvakili, I., Lin, Y., Morris, J. C., & Zheng, Y. (2016) · Oncogene · doi:10.1038/onc.2016.473 · Cited by 103
Knudsen, E. S., Balaji, U., Mannakee, B. K., Vail, P. J., Eslinger, C. R., Moxom, C., Mansour, J. C., & Witkiewicz, A. K. (2017) · Gut · doi:10.1136/gutjnl-2016-313133 · Cited by 101
SUMO pathway inhibition targets an aggressive pancreatic cancer subtype
Biederstädt, A., Hassan, Z., Schneeweis, C., Schick, M., Schneider, L., Muckenhuber, A., Hong, Y., Siegers, G., Nilsson, L. M., Wirth, M., et al. (2020) · Gut · doi:10.1136/gutjnl-2018-317856 · Cited by 105
SMAD4 and the TGFβ Pathway in Patients with Pancreatic Ductal Adenocarcinoma
Dardare, J., Witz, A., Merlin, J.-L., Gilson, P., & Harlé, A. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21103534 · Cited by 101
“Genomic analyses of PDAC revealed a large panel of molecular alterations particularly affecting Kirsten rat sarcoma viral oncogene (KRAS), tumor protein P53 (TP53), Mothers Against Decapentaplegic Homolog 4 (SMAD4), and cyclin-dependent kinase inhibitor 2A (CDKN2A) genes [10,11].”
BackgroundIwatate, Y., Hoshino, I., Yokota, H., Ishige, F., Itami, M., Mori, Y., Chiba, S., Arimitsu, H., Yanagibashi, H., Nagase, H., et al. (2020) · British Journal of Cancer · doi:10.1038/s41416-020-0997-1 · Cited by 101
KRAS wild-type pancreatic ductal adenocarcinoma: molecular pathology and therapeutic opportunities
Luchini, C., Paolino, G., Mattiolo, P., Piredda, M. L., Cavaliere, A., Gaule, M., Melisi, D., Salvia, R., Malleo, G., Shin, J. I., et al. (2020) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-020-01732-6 · Cited by 105
Self-citationLu, C., Liu, Z., Klement, J. D., Yang, D., Merting, A. D., Poschel, D. B., Albers, T., Waller, J. L., Shi, H., & Liu, K. (2021) · Journal for ImmunoTherapy of Cancer · doi:10.1136/jitc-2021-002624 · Cited by 103
Shi, X., Li, Y., Yuan, Q., Tang, S., Guo, S., Zhang, Y., He, J., Zhang, X., Han, M., Liu, Z., et al. (2022) · Nature Communications · doi:10.1038/s41467-022-29857-6 · Cited by 103
Genome-wide DNA methylation analysis reveals molecular subtypes of pancreatic cancer
Mishra, N. K., & Guda, C. (2017) · Oncotarget · doi:10.18632/oncotarget.15993 · Cited by 99
“[2] proposed molecular sub-types of pancreatic cancer on the basis of point mutation and structural variation using PC data from ICGC resource.”
Wei, T., Zhang, Q., Li, X., Su, W., Li, G., Ma, T., Gao, S., Lou, J., Que, R., Zheng, L., et al. (2018) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-17-1298 · Cited by 102
“Numerous evidence has revealed complicated mutational landscape in various types of cancer and genetic heterogeneity among patients (1, 2).”
BackgroundSinkala, M., Mulder, N., & Martin, D. P. (2020) · Scientific Reports · doi:10.1038/s41598-020-58290-2 · Cited by 100
Kanteti, R., Mirzapoiazova, T., Riehm, J., Dhanasingh, I., Mambetsariev, B., Wang, J., Kulkarni, P., Kaushik, G., Seshacharyulu, P., Ponnusamy, M. P., et al. (2018) · Cancer Biology & Therapy · doi:10.1080/15384047.2017.1416937 · Cited by 98
“Previously it has been shown that PDAC is a very complex genetic disease and could be due to successive accumulation of mutations in the KRAS, CDKN2A, TP53 and SMAD4 genes.(9) Among these, KRAS somatic mutations are observed in 90% of PDAC cases.”
BackgroundSystemic treatment of pancreatic cancer revisited
Ducreux, M. P., Seufferlein, T. T. W., Laethem, J. V., Laurent‐Puig, P., Smolenschi, C., Malka, D., Boige, V., Hollebecque, A., & Conroy, T. (2018) · Seminars in Oncology · doi:10.1053/j.seminoncol.2018.12.003 · Cited by 105
Hypoxia: Friend or Foe for drug delivery in Pancreatic Cancer
Shah, V. M., Sheppard, B. C., Sears, R. C., & Alani, A. W. G. (2020) · Cancer Letters · doi:10.1016/j.canlet.2020.07.041 · Cited by 101
USP21 deubiquitinase promotes pancreas cancer cell stemness via Wnt pathway activation
Hou, P., Ma, X., Zhang, Q., Wu, C.-J., Liao, W., Li, J., Wang, H., Zhao, J., Zhou, X., Guan, C., et al. (2019) · Genes & Development · doi:10.1101/gad.326314.119 · Cited by 96
Wang, Y., Li, Z., Zheng, S., Zhou, Y., Zhao, L., Ye, H., Zhao, X., Gao, W., Fu, Z., Zhou, Q., et al. (2015) · Oncotarget · doi:10.18632/oncotarget.5533 · Cited by 98
“Despite the great efforts on the research of molecular alterations involved in PC [3–6], due to the sophistication and heterogeneity of this disease [7], the situation for PC is still deplorable.”
Therapeutic trends in pancreatic ductal adenocarcinoma (PDAC)
Chandana, S. R., Babiker, H. M., & Mahadevan, D. (2018) · Expert Opinion on Investigational Drugs · doi:10.1080/13543784.2019.1557145 · Cited by 102
“erate range of chromosomal damage, 50 to 200 structural variants; 36% of all samples), and unstable (>200 structural variants; 14% of all samples) [18,20].”
BackgroundInfluentialClinical correlates of blood-derived circulating tumor DNA in pancreatic cancer
Patel, H., Okamura, R., Fanta, P. T., Patel, C., Lanman, R. B., Raymond, V. M., Kato, S., & Kurzrock, R. (2019) · Journal of Hematology & Oncology · doi:10.1186/s13045-019-0824-4 · Cited by 99
Cancer of the Pancreas: Molecular Pathways and Current Advancement in Treatment
Polireddy, K., & Chen, Q. (2016) · Journal of Cancer · doi:10.7150/jca.14922 · Cited by 103
“The mutational landscape of pancreatic cancer has been explored using whole genome sequencing analysis (5), and revealed average of 119 somatic chromosomal structural variants per individual patient, which exceeded the previously reported average of 63 mutations by another comprehensive genetic analysis (6).”
BackgroundGleeson, F. C., Kerr, S. E., Kipp, B. R., Voss, J. S., Minot, D. M., Tu, Z. J., Henry, M. R., Graham, R. P., Vasmatzis, G., Cheville, J. C., et al. (2016) · Oncotarget · doi:10.18632/oncotarget.9440 · Cited by 97
“[24–26] The absolute multigene mutational profile concordance was 83%.”
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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