The DOI matches its Crossref record; 58 of the 58 references it cites were found in a registry or an index.
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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
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]
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]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
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
Flagged first, then by citations
Cited by
Sorted by citations
Items 601–700 of 1,006
Distal pancreatectomy with celiac axis resection: what are the added risks?
Beane, J. D., House, M. G., Pitt, S. C., Kilbane, E. M., Hall, B. L., Parmar, A. D., Riall, T. S., & Pitt, H. A. (2015) · HPB · doi:10.1111/hpb.12453 · Cited by 47
“PDACs into four subtypes: stable, locally rearranged, scattered and unstable.(31) While the implications of these findings are broad, their clinical utility in selecting patients that would benefit from a more aggressive surgical approach remains to be seen.”
BackgroundTargeting mTOR in Pancreatic Ductal Adenocarcinoma
Iriana, S., Ahmed, S., Gong, J., Annamalai, A., Tuli, R., & Hendifar, A. E. (2016) · Frontiers in Oncology · doi:10.3389/fonc.2016.00099 · Cited by 48
“In one evaluation, utilizing whole genome sequencing and copy number variation of PDAC, combining structural variation events with deleterious point mutations increased the prevalence of inactivation events to 74% for TP53, 31% for SMAD4, and 35% for CDKN2A (9).”
BackgroundInfluentialKameta, E., Sugimori, K., Kaneko, T., Ishii, T., Miwa, H., Sato, T. A., Ishii, Y., Sue, S., Sasaki, T., Yamashita, Y., et al. (2016) · Oncology Letters · doi:10.3892/ol.2016.5168 · Cited by 47
“A number of studies have assessed the genetic changes in resected PDAC specimens by NGS (15,17).”
Glycoprotein biomarkers for the detection of pancreatic ductal adenocarcinoma
Llop, E., Guerrero, P. E., Duran, A., Barrabés, S., Massaguer, A., Ferri, M. J., Albiol-Quer, M., Llorens, R., & Peracaula, R. (2018) · World Journal of Gastroenterology · doi:10.3748/wjg.v24.i24.2537 · Cited by 47
Napolitano, F., Formisano, L., Giardino, A., Girelli, R., Servetto, A., Santaniello, A., Foschini, F., Marciano, R., Mozzillo, E., Carratù, A. C., et al. (2019) · Cancers · doi:10.3390/cancers11070981 · Cited by 47
“First of all, almost 10% of the PDAC patients demonstrated a familial predisposition by BRCA, and related genes, mutations [59].”
BackgroundLi, F., Dai, L., & Niu, J. (2019) · Journal of Cellular Physiology · doi:10.1002/jcp.29391 · Cited by 47
“Pancreatic cancer is one common fatal disease and a major health burden (Waddell et al., 2015).”
BackgroundFrappart, P., & Hofmann, T. G. (2020) · Cancers · doi:10.3390/cancers12102750 · Cited by 48
“, using whole genome sequencing (WGS), identified 4 groups based mainly on their variation on chromosomal structure: The “stable”, the “scattered”, the “unstable”, and the “locally arranged” [20].”
MethodLarge, T. Y. S. L., Bijlsma, M. F., Hassouni, B. E., Mantini, G., Lagerweij, T., Henneman, A. A., Funel, N., Kok, B., Pham, T. V., Haas, R. D. G.-D., et al. (2021) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-021-01892-z · Cited by 44
“The typical panel of mutated genes present in PDAC is further completed by inactivating mutations in TP53, SMAD4 and CDKN2A [9, 10].”
BackgroundOncogenic Drivers and Therapeutic Vulnerabilities in KRAS Wild-Type Pancreatic Cancer
Singh, H., Keller, R. B., Kapner, K. S., Dilly, J., Raghavan, S., Yuan, C., Cohen, E. F., Tolstorukov, M. Y., Andrews, E., Brais, L. K., et al. (2023) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-22-3930 · Cited by 53
Next-generation therapies for pancreatic cancer
Buckley, C. W., & O'Reilly, E. M. (2024) · Expert Review of Gastroenterology & Hepatology · doi:10.1080/17474124.2024.2322648 · Cited by 49
“[31].”
BackgroundBiallelic BRCA2 Mutations Shape the Somatic Mutational Landscape of Aggressive Prostate Tumors
Decker, B. J., Karyadi, D. M., Davis, B. W., Karlins, E., Tillmans, L. S., Stanford, J. L., Thibodeau, S. N., & Ostrander, E. A. (2016) · The American Journal of Human Genetics · doi:10.1016/j.ajhg.2016.03.003 · Cited by 48
Allele-Specific Quantification of Structural Variations in Cancer Genomes
Li, Y., Zhou, S., Schwartz, D. C., & Ma, J. (2016) · Cell Systems · doi:10.1016/j.cels.2016.05.007 · Cited by 46
Decoster, C., Gilabert, M., Autret, A., Turrini, O., Oziel-Taïeb, S., Poizat, F., Giovannini, M. F., Viens, P., Iovanna, J., & Raoul, J. (2016) · Oncotarget · doi:10.18632/oncotarget.9861 · Cited by 46
“According to a whole-genome sequencing analysis [13] of PDAC, an average of 119 somatic structural variants were detected per tumor.”
BackgroundExome-Wide Association Study of Pancreatic Cancer Risk
Grant, R. C., Denroche, R. E., Borgida, A., Virtanen, C., Cook, N., Smith, A. L., Connor, A. A., Wilson, J. M., Peterson, G., Roberts, N. J., et al. (2017) · Gastroenterology · doi:10.1053/j.gastro.2017.10.015 · Cited by 46
Self-citationAdaptive and Reversible Resistance to Kras Inhibition in Pancreatic Cancer Cells
Chen, P., Muzumdar, M. D., Dorans, K. J., Robbins, R., Bhutkar, A. J., Rosario, A. M. D., Mertins, P., Qiao, J., Schäfer, C., Gertler, F. B., et al. (2017) · Cancer Research · doi:10.1158/0008-5472.can-17-2129 · Cited by 47
“We used murine cells with defined genetic alterations frequently observed in human PDACs (Kras and p53) (6,35) to minimize genetic variability in our analyses.”
Er, J. L., Goh, P. N., Lee, C. Y., Tan, Y. J., Hii, L., Mai, C., Chung, F. F., & Leong, C. (2018) · APOPTOSIS · doi:10.1007/s10495-018-1459-6 · Cited by 48
Poly (ADP) Ribose Glycohydrolase Can Be Effectively Targeted in Pancreatic Cancer
Jain, A., Agostini, L. C., McCarthy, G. A., Chand, S. N., Ramirez, A., Nevler, A., Cozzitorto, J. A., Schultz, C. W., Lowder, C. Y., Smith, K. M., et al. (2019) · Cancer Research · doi:10.1158/0008-5472.can-18-3645 · Cited by 46
“Initial results from the “Know Your Tumor Initiative” for PDAC patients, as well as several related publications [5-8], have identified certain patient populations with 27% highly actionable mutations.”
Cives, M., Partelli, S., Palmirotta, R., Lovero, D., Mandriani, B., Quaresmini, D., Pellè, E., Andreasi, V., Castelli, P., Strosberg, J., et al. (2019) · Scientific Reports · doi:10.1038/s41598-019-55156-0 · Cited by 46
Self-citationGao, H.-L., Wang, W., Yu, X., & Liu, L. (2020) · Experimental Hematology and Oncology · doi:10.1186/s40164-020-00184-0 · Cited by 47
“The most common driver genes found in PDAC are KRAS (88–100% of cases), TP53 (85% of cases), CDKN2A (90% of cases) and SMAD4 (55% of cases) [20, 21].”
BackgroundSMAD4 represses FOSL1 expression and pancreatic cancer metastatic colonization
Dai, C., Rennhack, J. P., Arnoff, T. E., Thaker, M., Younger, S. T., Doench, J. G., Huang, A. Y., Yang, A., Aguirre, A. J., Wang, B. L., et al. (2021) · Cell Reports · doi:10.1016/j.celrep.2021.109443 · Cited by 45
Kattan, W. E., Liu, J., Montufar‐Solis, D., Hong, L., Barathi, B. B., van der Hoeven, R., Zhou, Y., & Hancock, J. F. (2021) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2114126118 · Cited by 45
Datta, J., Bianchi, A., Silva, I. D. C., Deshpande, N., Cao, L., Mehra, S., Singh, S. P., Rafie, C. I., Sun, X., Chen, X., et al. (2022) · Oncogene · doi:10.1038/s41388-022-02368-w · Cited by 46
“Although next-generation sequencing (NGS) has allowed comprehensive characterization of the dominant drivers of PDAC tumorigenesis—namely mutant KRAS, TP53, SMAD4, CDKN2A—these molecular alterations are not currently therapeutically actionable [1].”
BackgroundSmall molecule inhibitors in pancreatic cancer
Sun, J., Russell, C. C., Scarlett, C. J., & McCluskey, A. (2020) · RSC Medicinal Chemistry · doi:10.1039/c9md00447e · Cited by 45
Self-citationGastric Cancer Risk and Pathogenesis in BRCA1 and BRCA2 Carriers
Buckley, K. H., Niccum, B. A., Maxwell, K. N., & Katona, B. W. (2022) · Cancers · doi:10.3390/cancers14235953 · Cited by 46
“Such approaches have been shown to be efficacious in treatment of breast and ovarian cancers of BRCA1/2 carriers [60–66], as well pancreatic cancers with an inactivation of BRCA1, BRCA2, or PALB2 and an HR deficiency tumor mutation signature [67].”
BackgroundMandelker, D. L., Marra, A., Zheng-Lin, B., Selenica, P., Blanco-Heredia, J., Zhu, Y., Gazzo, A. M., Wong, D., Yelskaya, Z., Rai, V., et al. (2023) · Journal of Clinical Oncology · doi:10.1200/jco.23.00561 · Cited by 45
Guo, J., Wang, S., & Gao, Q. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1258538 · Cited by 47
“Genetic mutations are the primary driver of PDAC initiation and progression (11, 25).”
BackgroundInfluentialMiR-377 inhibits the proliferation of pancreatic cancer by targeting Pim-3
Chang, W., Liu, M., Xu, J., Fu, H., Zhou, B., Yuan, T., & Chen, P. (2016) · Tumor Biology · doi:10.1007/s13277-016-5295-4 · Cited by 45
Bringing 3D tumor models to the clinic – predictive value for personalized medicine
Halfter, K., & Mayer, B. (2017) · Biotechnology Journal · doi:10.1002/biot.201600295 · Cited by 48
Chamberlain, C. E., German, M. S., Yang, K. Y., Wang, J., VanBrocklin, H. F., Regan, M., Shokat, K. M., Ducker, G. S., Kim, G., Hann, B. C., et al. (2018) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-17-1204 · Cited by 45
“We did not observe mutations in genes commonly associated with pancreatic ductal adenocarcinoma,suchas KRAS,TP53,CDKN2A, SMAD3,SMAD4 , and TGFBR1 (49, 50).”
Vendrely, V., Amintas, S., Noel, C., Moranvillier, I., Lamrissi‐Garcia, I., Rousseau, B., Coulibaly, S., Bedel, A., Moreau‐Gaudry, F., Buscail, É., et al. (2019) · Cancer Letters · doi:10.1016/j.canlet.2019.02.038 · Cited by 47
Next-Generation Sequencing in Pancreatic Cancer
Shen, G.-Q., Aleassa, E. M., Walsh, R. M., & Morris‐Stiff, G. J. (2019) · Pancreas · doi:10.1097/mpa.0000000000001324 · Cited by 45
“The authors' proof-of-concept data suggested that mutations in the BRCA pathway component genes and surrogate measures of defects in DNA maintenance (genomic instability and the BRCA mutational signature) have potential implications for therapeutic selection in patients with PDAC.(67) These data define a putative biom…”
BackgroundSinn, M., Sinn, B. V., Treue, D., Keilholz, U., Damm, F., Schmuck, R. B., Lohneis, P., Klauschen, F., Striefler, J. K., Bahra, M., et al. (2020) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-19-3034 · Cited by 45
A novel sensitive detection method for DNA methylation in circulating free DNA of pancreatic cancer
Shinjo, K., Hara, K., Nagae, G., Umeda, T., Katsushima, K., Suzuki, M. M., Murofushi, Y., Umezu, Y., Takeuchi, I., Takahashi, S., et al. (2020) · PLoS ONE · doi:10.1371/journal.pone.0233782 · Cited by 45
Parsels, L. A., Engelke, C. G., Parsels, J. D., Flanagan, S. A., Zhang, Q., Tanska, D. M., Wahl, D. R., Canman, C. E., Lawrence, T. S., & Morgan, M. A. (2020) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-20-0365 · Cited by 46
“While the findings of this trial are a major advancement in therapy for these patients, BRCA1/2 mutations or homologous recombination (HR) repair deficiencies only occur in about 10% of all pancreatic cancers (4).”
BackgroundThe State-of-the-Art of Phase II/III Clinical Trials for Targeted Pancreatic Cancer Therapies
García-Sampedro, A., Gaggia, G., Ney, A., Mahamed, I., & Acedo, P. (2021) · Journal of Clinical Medicine · doi:10.3390/jcm10040566 · Cited by 47
“Different targeting approaches have been directed against PDAC genetic aberrations with great importance for DDR mechanisms such as the BRCA1, PALB2, BRC2, and RAD51 genes [74].”
BackgroundPancreatic cancer intrinsic PI3Kα activity accelerates metastasis and rewires macrophage component
Thibault, B., Ramos‐Delgado, F., Tostivint, E. P., Therville, N., Cintas, C., Arcucci, S., Cassant‐Sourdy, S., Reyes‐Castellanos, G., Tosolini, M., Villard, A. V., et al. (2021) · EMBO Molecular Medicine · doi:10.15252/emmm.202013502 · Cited by 46
Biankin, A. V., & Maitra, A. (2015) · Cancer Cell · doi:10.1016/j.ccell.2015.09.020 · Cited by 45
“…mutational profile, with activating mutations of KRAS present in over 90%, mutations of TP53, CDKN2A, and SMAD4 in over 50% of cases among a sea of diverse infrequently mutated genes mostly at a prevalence of less than 5% (Biankin et al., 2012; Waddell et al., 2015; Witkiewicz et al., 2015).”
BackgroundSelf-citationLiu, X., Wang, W., Liu, X., Zhang, Z., Yu, L., Li, R., Guo, D., Cai, W., Quan, X., Wu, H., et al. (2022) · Clinical and Translational Medicine · doi:10.1002/ctm2.670 · Cited by 45
“45 SNVs called by Strelka2 were further filtered by the following criteria: (1) sequencing depth ≥20 at variant sites in both control and tumour samples; (2) ≤5 alternative reads support the variant in germline sample; (3)≥5 alternative reads support the variant in tumour sample Filtered variantswere then annotated by…”
MethodThe Role of the Microbiome in Pancreatic Cancer
Miyabayashi, K., Ijichi, H., & Fujishiro, M. (2022) · Cancers · doi:10.3390/cancers14184479 · Cited by 48
Advances in Liquid Biopsy Technology and Implications for Pancreatic Cancer
Raufi, A. G., May, M. S., Hadfield, M. J., Seyhan, A. A., & El‐Deiry, W. S. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24044238 · Cited by 47
“In addition, 10–20% of patients with PDAC will carry a germline mutation in a gene encoding a DNA damage response protein such as ATM, BRCA1/2, or PALB2 [20].”
BackgroundInfluentialThe Multifaceted Role of miR-21 in Pancreatic Cancers
Chen, C., Demirkhanyan, L. H., & Gondi, C. S. (2024) · Cells · doi:10.3390/cells13110948 · Cited by 49
“In at least 95% of all PDAC cases, the KRAS gene is mutated [202,203].”
BackgroundYokode, M., Akita, M., Fujikura, K., Kim, M., Morinaga, Y., Yoshikawa, S., Terada, T., Matsukiyo, H., Tajiri, T., Abe‐Suzuki, S., et al. (2018) · Histopathology · doi:10.1111/his.13629 · Cited by 44
“Before PanIN progresses to an invasive malignancy, genetic abnormalities accumulate in a multistep manner, with mutations in KRAS, p16/CDKN2A, TP53 and SMAD4/DPC4 playing major roles in the carcinogenetic process.(10,11) KRAS mutations occur first, followed by molecular alterations in p16/CDKN2A, TP53 and SMAD4/DPC4,…”
BackgroundFollia, L., Ferrero, G., Mandili, G., Beccuti, M., Giordano, D., Spadi, R., Satolli, M. A., Evangelista, A., Katayama, H., Hong, W., et al. (2019) · Frontiers in Oncology · doi:10.3389/fonc.2019.00115 · Cited by 44
“, gene expression profiles (17–19) or genomic alteration signatures (20), or metabolic data (21).”
BackgroundGoldstein, J. B., Zhao, L., Wang, X., Ghelman, Y., Overman, M. J., Javle, M. M., Shroff, R. T., Varadhachary, G. R., Wolff, R. A., McAllister, F. M., et al. (2019) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-19-0224 · Cited by 46
“In those with BRCA-mutated cancers, previous predictive data has largely been based on treatment with cisplatin, a chemotherapeutic agent that is less frequently used with current SOC chemotherapy regimens (27).”
BackgroundMechanisms of drug resistance of pancreatic ductal adenocarcinoma at different levels
Du, J., Gu, J., & Li, J. (2020) · Bioscience Reports · doi:10.1042/bsr20200401 · Cited by 44
Ono, H., Kato, T., Murase, Y., Nakamura, Y., Ishikawa, Y., Watanabe, S., Akahoshi, K., Ogura, T., Ogawa, K., Ban, D., et al. (2021) · Scientific Reports · doi:10.1038/s41598-021-89530-8 · Cited by 45
Epigenetics of Most Aggressive Solid Tumors: Pathways, Targets and Treatments
Martínez‐Useros, J., Martin-Galan, M., Florez-Cespedes, M., & García‐Foncillas, J. (2021) · Cancers · doi:10.3390/cancers13133209 · Cited by 46
KDM6A regulates cell plasticity and pancreatic cancer progression by noncanonical activin pathway
Yi, Z., Wei, S., Jin, L., Jeyarajan, S., Yang, J., Gu, Y., Kim, H. S., Schechter, S., Lu, S., Paulsen, M. T., et al. (2022) · Cellular and Molecular Gastroenterology and Hepatology · doi:10.1016/j.jcmgh.2021.09.014 · Cited by 41
“Collectively, these results showed that loss of KDM6A was associated with worse prognosis and metastasis in human PDAC.”
BackgroundInfluentialTargeting DNA damage repair pathways in pancreas cancer
Crowley, F., Park, W., & O’Reilly, E. M. (2021) · Cancer and Metastasis Reviews · doi:10.1007/s10555-021-09983-1 · Cited by 43
Differential activity of MAPK signalling defines fibroblast subtypes in pancreatic cancer
Veghini, L., Pasini, D., Fang, R., Delfino, P., Filippini, D., Neander, C., Vicentini, C., Fiorini, E., Lupo, F., D’Agosto, S. L., et al. (2024) · Nature Communications · doi:10.1038/s41467-024-54975-8 · Cited by 46
“Activating mutations of KRAS are nearly universal in PDAC 24 and result in the hyperactivation of the RAS/MEK/ERK (Mitogen-activated protein kinase, MAPK) pathway, which plays a central role in tumour initiation and maintenance 25,26 .”
Self-citationBhaw‐Luximon, A., & Jhurry, D. (2015) · Cancer Letters · doi:10.1016/j.canlet.2015.09.007 · Cited by 43
Gore, J., Imasuen, I., Conteh, A. M., Craven, K. E., Cheng, M., & Korc, M. (2016) · Cancer Letters · doi:10.1016/j.canlet.2016.05.037 · Cited by 43
Tesfaye, A. A., Kamgar, M., Azmi, A. S., & Philip, P. A. (2017) · Expert Review of Anticancer Therapy · doi:10.1080/14737140.2018.1417844 · Cited by 43
Advances in oncolytic adenovirus therapy for pancreatic cancer
Nattress, C. B., & Halldén, G. (2018) · Cancer Letters · doi:10.1016/j.canlet.2018.07.006 · Cited by 43
Dreyer, S. B., Jamieson, N. B., Evers, L., Duthie, F. R., Cooke, S., Marshall, J., Beraldi, D., Knight, S. R., Upstill‐Goddard, R., Dickson, E. J., et al. (2019) · Chinese Clinical Oncology · doi:10.21037/cco.2019.04.06 · Cited by 43
Self-citationMüller, D., Shin, S., de Rugy, T. G., Samain, R., Baer, R., Strehaïano, M., Masvidal, L., Guillermet‐Guibert, J., Jean, C., Tsukumo, Y., et al. (2019) · JCI Insight · doi:10.1172/jci.insight.121951 · Cited by 42
T-Cell Immunity in Pancreatic Cancer
Ajina, R., & Weiner, L. M. (2020) · Pancreas · doi:10.1097/mpa.0000000000001621 · Cited by 46
Yadav, S., Kasi, P. M., Bamlet, W. R., Ho, T. P., Polley, E. C., Hu, C., Hart, S. N., Rabe, K. G., Boddicker, N. J., Gnanaolivu, R. D., et al. (2020) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-20-1788 · Cited by 44
“It is not entirely clearwhether germlinemutation–associatedPDACshave Clin Cancer Res; 26(24) December 15, 2020 CLINICAL CANCER RESEARCH6508 similar landscapes of somatic mutations and mutational signatures as sporadic PDAC, but differences in tumor biology have been reported from smaller series.”
BackgroundInfluentialTargeting eIF4A-Dependent Translation of KRAS Signaling Molecules
Singh, K., Lin, J., Lecomte, N., Mohan, P., Gokce, A., Sanghvi, V. R., Jiang, M., Grbovic-Huezo, O., Burčul, A., Stark, S. G., et al. (2021) · Cancer Research · doi:10.1158/0008-5472.can-20-2929 · Cited by 39
“Genomic studies have catalogued the genetic drivers of PDAC and show nearly ubiquitous activation of KRAS and loss of tumor suppressor genes p53, p16/INK4A, and SMAD4 (13-17).”
BackgroundTargeting DNA Damage Response and Immune Checkpoint for Anticancer Therapy
Huang, J.-L., Chang, Y.-T., Hong, Z.-Y., & Lin, C.-S. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23063238 · Cited by 42
“The DDR deficiency occurs in up to 24% pancreatic cancer [49,136].”
BackgroundNeoadjuvant multimodal treatment of pancreatic ductal adenocarcinoma
Silvestris, N., Longo, V., Cellini, F., Reni, M., Bittoni, A., Cataldo, I., Partelli, S., Falconi, M., Scarpa, A., Brunetti, O., et al. (2015) · Critical Reviews in Oncology/Hematology · doi:10.1016/j.critrevonc.2015.11.016 · Cited by 41
Self-citationCraven, K. E., Gore, J., Wilson, J. L., & Korc, M. (2015) · Oncotarget · doi:10.18632/oncotarget.6345 · Cited by 42
“However, mutations were similar across the PDAC subgroups, and consistent with PDAC genome sequencing studies [3, 4, 16, 17], KRAS (~86%), TP53 (~55%), SMAD4 (19”
Pancreatic Cancer: “A Riddle Wrapped in a Mystery inside an Enigma”
Borazanci, E. H., Dang, C. V., Robey, R. W., Bates, S. E., Chabot, J. A., & Hoff, D. D. V. (2017) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-16-2070 · Cited by 42
“A TCGA study published in 2015 examined 100 different PDAC specimens, extending the analysis to include copy number variation (CNV) analysis (22).”
MethodGene Therapy for Pancreatic Cancer: Specificity, Issues and Hopes
Rouanet, M., Lebrin, M., Gross, F., Bournet, B., Cordelier, P., & Buscail, L. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms18061231 · Cited by 47
Chan, E. W., Chiorean, E. G., O'Dwyer, P. J., Gabrail, N. Y., Alcindor, T., Potvin, D., Chao, R. C., & Hurwitz, H. I. (2017) · Cancer Chemotherapy and Pharmacology · doi:10.1007/s00280-017-3494-3 · Cited by 42
Alcaide, M., Cheung, M. C., Bushell, K. R., Arthur, S. E., Wong, H., Karasinska, J. M., Renouf, D. J., Schaeffer, D. F., McNamara, S., du Tertre, M. C., et al. (2018) · Journal of Molecular Diagnostics · doi:10.1016/j.jmoldx.2018.09.007 · Cited by 41
Pancreatic Cancer Diagnosis and Management: Has the Time Come to Prick the Bubble?
Moutinho-Ribeiro, P., Macedo, G., & Melo, S. A. (2019) · Frontiers in Endocrinology · doi:10.3389/fendo.2018.00779 · Cited by 43
Low P4HA2 and high PRTN3 expression predicts poor survival in patients with pancreatic cancer
Hu, D., Ansari, D., Zhou, Q., Sasor, A., Hilmersson, K. S., & Andersson, R. E. (2019) · Scandinavian Journal of Gastroenterology · doi:10.1080/00365521.2019.1574360 · Cited by 42
“To overcome therapeutic resistance in pancreatic cancer, it has been proposed to subgroup patients based on biomarker profiles in tumor tissue [3,4].”
BackgroundPrecision medicine in pancreatic cancer: treating every patient as an exception
Herbst, B. T., & Zheng, L. (2019) · The Lancet. Gastroenterology & hepatology · doi:10.1016/s2468-1253(19)30175-x · Cited by 42
Li, W., Zhu, Y., Zhang, K., Yu, X., Lin, H., Wu, W., Peng, Y., & Sun, J. M. (2020) · Experimental & Molecular Medicine · doi:10.1038/s12276-020-0390-4 · Cited by 42
Yu, Y., Yang, G., Huang, H., Fu, Z., Cao, Z., Zheng, L., You, L., & Zhang, T. (2021) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-020-01787-5 · Cited by 42
“For example, wholegenome sequencing was used to classify PDAC into four groups (the stable subtype, locally rearranged subtype, scattered subtype and unstable subtype) according to the frequency and distribution of structural variations [14].”
BackgroundMethodThe Abscission Checkpoint: A Guardian of Chromosomal Stability
Petsalaki, E., & Zachos, G. (2021) · Cells · doi:10.3390/cells10123350 · Cited by 40
Aung, K. L., McWhirter, E., Welch, S. A., Wang, L. E., Lovell, S., Stayner, L.-A., Ali, S., Malpage, A., Makepeace, B., Ramachandran, M., et al. (2022) · Journal of Gastrointestinal Oncology · doi:10.21037/jgo-22-86 · Cited by 41
Pihlak, R., Weaver, J. M. J., Valle, J. W., & McNamara, M. G. (2018) · Cancers · doi:10.3390/cancers10010017 · Cited by 42
“[19] defined four subclasses based on structural variants (SV) patterns; unstable, stable, locally rearranged and scattered.”
BackgroundInfluentialTopham, J. T., Tsang, E. S., Karasinska, J. M., Metcalfe, A. L., Ali, H., Kalloger, S. E., Csizmók, V., Williamson, L., Titmuss, E., Nielsen, K., et al. (2022) · Nature Communications · doi:10.1038/s41467-022-33718-7 · Cited by 41
Costanzo, F. D., Costanzo, F. D., Antonuzzo, L., Mazza, E., & Giommoni, E. (2023) · Cancers · doi:10.3390/cancers15020416 · Cited by 42
“Most mPC carry a mutation in the key driver K-ras, and over half have mutations and/or copy number losses of TP53, SMAD4, and CDKN2A [43,65,66].”
BackgroundMannucci, A., & Goel, A. (2025) · CA A Cancer Journal for Clinicians · doi:10.3322/caac.70035 · Cited by 54
“88 The interplay be-tween genetic and epigenetic alterations 85 is central to PDAC progression.”
Resolution of Novel Pancreatic Ductal Adenocarcinoma Subtypes by Global Phosphotyrosine Profiling
Humphrey, E. S., Su, S., Nagrial, A. M., Hochgräfe, F., Pajic, M., Lehrbach, G. M., Parton, R. G., Yap, A. S., Horvath, L. G., Chang, D. K.-F., et al. (2016) · Molecular & Cellular Proteomics · doi:10.1074/mcp.m116.058313 · Cited by 40
“1, TKCC 04, TKCC 05, TKCC 06, TKCC 07, TKCC 09, TKCC 10, TKCC 12, TKCC 14, TKCC 15, TKCC 16, TKCC 17, TKCC 18, TKCC 19, TKCC 22, TKCC 26, TKCC 27) (4).”
Self-citationFujikura, K., Akita, M., Abe‐Suzuki, S., Itoh, T., & Zen, Y. (2017) · Histopathology · doi:10.1111/his.13271 · Cited by 41
“Large-scale genomic studies have shown that >90% of pancreatic ductal adenocarcinomas carry these specific genetic alterations.(22,23) The reported genetic alterations identified in IPMNs include mutations in KRAS (45–85%) and GNAS (40–70%),(26,27) whereas PanIN harbours KRAS (~95%) and GNAS (6%) mutations.”
BackgroundFrom First Line to Sequential Treatment in the Management of Metastatic Pancreatic Cancer
Martín, A. M., Hidalgo, M. M., Álvarez-Gallego, R., Arrazubi, V., Martínez-Galán, J., Salgado, M., Macarulla, T. M., & Carrato, A. (2018) · Journal of Cancer · doi:10.7150/jca.23716 · Cited by 41
Prioritization and functional assessment of noncoding variants associated with complex diseases
Zhou, L., & Zhao, F. (2018) · Genome Medicine · doi:10.1186/s13073-018-0565-y · Cited by 41
“First, the ANNOTATION part of online platform integrated variants from dbSNP [40], NHLBI-Exome Sequencing Project v2 (ESP) [41], YanHuang Project [42], CNV of 100 pancreatic ductal adenocarcinomas (PDACs) [43], schizophrenia somatic Control variants Functional variants ClinVar 1000 Genomes”
MethodToumpeki, C., Liberis, A., Tsirkas, I., Tsirka, T., Kalagasidou, S., Inagamova, L., Anthoulaki, X., Tsatsaris, G., & Kontomanolis, E. N. (2019) · In Vivo · doi:10.21873/invivo.11524 · Cited by 42
BRCA1 and homologous recombination: implications from mouse embryonic development
Liu, Y., & Lu, L. (2020) · Cell & Bioscience · doi:10.1186/s13578-020-00412-4 · Cited by 44
Localized Pancreatic Cancer: Multidisciplinary Management
Coveler, A. L., Herman, J. M., Simeone, D. M., & Chiorean, E. G. (2016) · American Society of Clinical Oncology Educational Book · doi:10.1200/edbk_160827 · Cited by 40
Grierson, P. M., Tan, B. R., Pedersen, K. S., Park, H., Suresh, R., Amin, M. A., Trikalinos, N. A., Knoerzer, D. L., Kreider, B. L., Reddy, A., et al. (2022) · The Oncologist · doi:10.1093/oncolo/oyac237 · Cited by 41
Frank, K. J., Mulero-Sánchez, A., Berninger, A., Ruiz-Cañas, L., Bosma, A., Görgülü, K., Wu, N., Diakopoulos, K. N., Kaya-Aksoy, E., Ruess, D. A., et al. (2022) · Cell Reports Medicine · doi:10.1016/j.xcrm.2022.100815 · Cited by 40
Yang, X., Ma, Y., Liu, Y., Jiang, X., Ding, H., Shi, Y., Jia, C., Lu, G., Zhang, D., Wang, H., et al. (2021) · Cellular Signalling · doi:10.1016/j.cellsig.2021.110025 · Cited by 40
Latest Advances in the Use of Therapeutic Focused Ultrasound in the Treatment of Pancreatic Cancer
Mouratidis, P., & ter Haar, G. (2022) · Cancers · doi:10.3390/cancers14030638 · Cited by 40
“This is because pancreatic carcinogenesis is driven by a low number of mutations typically ~3 mutations/Megabase [6,18].”
BackgroundConner, J., Mariño‐Enríquez, A., Mino-Kenudson, M. A., Garcia, E. P., Pitman, M. B., Sholl, L. M., Srivastava, A., & Doyle, L. A. (2017) · Pancreas · doi:10.1097/mpa.0000000000000805 · Cited by 40
Shukla, H. D. (2017) · Proteomes · doi:10.3390/proteomes5040028 · Cited by 41
“In a majority of these samples, a specific group of patients exhibited susceptibility to platinum-based chemotherapy [51].”
BackgroundDNA Damage Repair System in Plants: A Worldwide Research Update
Giménez, E., & Manzano-Agugliaro, F. R. (2017) · Genes · doi:10.3390/genes8110299 · Cited by 40
Genomic testing for pancreatic cancer in clinical practice as real-world evidence
Hayashi, H., Tanishima, S., Fujii, K., Mori, R., Okamura, Y., Yanagita, E., Matsuoka, R., Amano, T., Kinoshita, I., Komatsu, Y., et al. (2018) · Pancreatology · doi:10.1016/j.pan.2018.07.006 · Cited by 40
Li, C., Zeng, X., Yu, H., Gu, Y., & Zhang, W. (2018) · World Journal of Surgical Oncology · doi:10.1186/s12957-018-1519-y · Cited by 40
“resulting from chromosomal rearrangements in pancreatic ductal adenocarcinomas patients [6].”
BackgroundParente, P., Parcesepe, P., Covelli, C., Olivieri, N., Remo, A., Pancione, M., Latiano, T. P., Graziano, P., Maiello, E., & Giordano, G. (2018) · Gastroenterology Research and Practice · doi:10.1155/2018/7530619 · Cited by 40
“However, in the presence of oncogenic mutations like KRAS, TP53, SMAD4, and CDKN2A, genetically altered epithelial cells transform into cancer cells and disrupt normal communications between PSCs and immune and vascular cells, creating a favorable microenvironment for cancer progression (Figure 2(c)) [21].”
BackgroundLin, T., Ren, Q., Zuo, W., Jia, R., Xie, L., Lin, R., Zhao, H., Chen, J., Yan, L., Wang, P., et al. (2019) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-019-1160-9 · Cited by 40
RET gene rearrangements occur in a subset of pancreatic acinar cell carcinomas
Chou, A. S. Y., Brown, I., Kumarasinghe, P. M., Perren, A. A., Riley, D., Kim, Y., Pajic, M., Steinmann, A. M., Rathi, V., Jamieson, N. B., et al. (2019) · Modern Pathology · doi:10.1038/s41379-019-0373-y · Cited by 40
Self-citationKumarasamy, V. M., Ruiz, A., Nambiar, R., Witkiewicz, A. K., & Knudsen, E. S. (2019) · Oncogene · doi:10.1038/s41388-019-1102-1 · Cited by 39
Yang, B., Zhang, B., Cao, Z., Xu, X., Huo, Z., Zhang, P., Xiang, S., Zhao, Z., Lv, C., Meng, M., et al. (2020) · Cell Death and Differentiation · doi:10.1038/s41418-020-0514-3 · Cited by 40
Han, X., Fang, Y., Chen, P., Xu, Y., Zhou, W., Rong, Y., Li, J., Chen, W., & Lou, W. (2021) · Cell Cycle · doi:10.1080/15384101.2021.1874684 · Cited by 40
“Pancreatic ductal adenocarcinoma (PDAC), generally regarded as pancreatic cancer, is a highly aggressive and one of the most lethal malignancies with a 5-year overall survival rate of less than 8% [1,2].”
BackgroundWang, H., Ding, Y., Chen, Y., Jiang, J., Chen, Y., Lu, J., Kong, M., Mo, F., Huang, Y., Zhao, W., et al. (2021) · Gastric Cancer · doi:10.1007/s10120-021-01201-9 · Cited by 41
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
