ArticleCancer research2016
Integrated Genomic Analysis of Pancreatic Ductal Adenocarcinomas Reveals Genomic Rearrangement Events as Significant Drivers of Disease.
Article in Cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- Comprehensive genome sequencing associates elevated mitochondrial DNA and homoplasmy with early stage I of pancreatic cancer.iScience · 2026Article
- Functional impact of the hyperduplication genomophenotype in high copy number endometrial cancer.iScience · 2025Article
- Unlocking the Genetic Secrets of Pancreatic Cancer:Cancers · 2025Review
- Deletion of 17p in cancers: Guilt by (p53) association.Oncogene · 2025Review
- Article
- Metabolic pathways, genomic alterations, and post-translational modifications in pulmonary hypertension and cancer as therapeutic targets and biomarkers.Frontiers in pharmacology · 2024Article
- Review
- Multi-omics analysis of intra-tumoural and inter-tumoural heterogeneity in pancreatic ductal adenocarcinoma.Clinical and translational medicine · 2022Article
- Article
- Theragnostic chromosomal rearrangements in treatment-naive pancreatic ductal adenocarcinomas obtained via endoscopic ultrasound.Journal of cellular and molecular medicine · 2021Article
- Upregulation of amplified in breast cancer 1 contributes to pancreatic ductal adenocarcinoma progression and vulnerability to blockage of hedgehog activation.Theranostics · 2021Article
- Adjuvant Treatment in Pancreatic Cancer: Shaping the Future of the Curative Setting.Frontiers in oncology · 2021Review
- Growth of pancreatic cancers with hemizygous chromosomal 17p loss ofScience advances · 2020Article
- Pancreatic cancers suppress negative feedback of glucose transport to reprogram chromatin for metastasis.Nature communications · 2020Article
- Phase 1 trial of Vismodegib and Erlotinib combination in metastatic pancreatic cancer.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2020Article
- Rituximab Decreases Lymphoproliferative Tumor Formation in Hepatopancreaticobiliary and Gastrointestinal Cancer Patient-Derived Xenografts.Scientific reports · 2019Article
- Pentose conversions support the tumorigenesis of pancreatic cancer distant metastases.Oncogene · 2018Article
- Genome-Wide Somatic Copy Number Alterations and Mutations in High-Grade Pancreatic Intraepithelial Neoplasia.The American journal of pathology · 2018Article
- Patient-derived xenograft cryopreservation and reanimation outcomes are dependent on cryoprotectant type.Laboratory investigation; a journal of technical methods and pathology · 2018Article
- Mut2Vec: distributed representation of cancerous mutations.BMC medical genomics · 2018Article
Corrections and comments
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Authors and funding
18 authors at 1 institution in 1 country.
Funding
Abstract
Many somatic mutations have been detected in pancreatic ductal adenocarcinoma (PDAC), leading to the identification of some key drivers of disease progression, but the involvement of large genomic rearrangements has often been overlooked. In this study, we performed mate pair sequencing (MPseq) on genomic DNA from 24 PDAC tumors, including 15 laser-captured microdissected PDAC and 9 patient-derived xenografts, to identify genome-wide rearrangements. Large genomic rearrangements with intragenic breakpoints altering key regulatory genes involved in PDAC progression were detected in all tumors. SMAD4, ZNF521, and FHIT were among the most frequently hit genes. Conversely, commonly reported genes with copy number gains, including MYC and GATA6, were frequently observed in the absence of direct intragenic breakpoints, suggesting a requirement for sustaining oncogenic function during PDAC progression. Integration of data from MPseq, exome sequencing, and transcriptome analysis of primary PDAC cases identified limited overlap in genes affected by both rearrangements and point mutations. However, significant overlap was observed in major PDAC-associated signaling pathways, with all PDAC exhibiting reduced SMAD4 expression, reduced SMAD-dependent TGFβ signaling, and increased WNT and Hedgehog signaling. The frequent loss of SMAD4 and FHIT due to genomic rearrangements strongly implicates these genes as key drivers of PDAC, thus highlighting the strengths of an integrated genomic and transcriptomic approach for identifying mechanisms underlying disease initiation and progression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.