ReviewInternational journal of molecular sciences2013
Carcinogenesis of pancreatic adenocarcinoma: precursor lesions.
Review in International journal of molecular sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed.
- PR55α subunit of protein phosphatase 2A supports KRASOncogene · 2025Article
- Oncolytic viral therapy as a novel potential solution for treatment of pancreatic cancer.Gastroenterology and hepatology from bed to bench · 2025Review
- Regulation of ubiquitin-proteasome system and its relative pathways in pancreatic adenocarcinoma.BioImpacts : BI · 2025Review
- The cross-talk between the macro and micro-environment in precursor lesions of pancreatic cancer leads to new and promising circulating biomarkers.Journal of experimental & clinical cancer research : CR · 2024Review
- Bile Acids in Pancreatic Carcinogenesis.Metabolites · 2024Review
- Analytical Validation of Loss of Heterozygosity and Mutation Detection in Pancreatic Fine-Needle Aspirates by Capillary Electrophoresis and Sanger Sequencing.Diagnostics (Basel, Switzerland) · 2024Article
- Advances in Pancreatic Cancer Treatment by Nano-Based Drug Delivery Systems.Pharmaceutics · 2023Review
- Clinical and Molecular Attributes and Evaluation of Pancreatic Cystic Neoplasm.Biochimica et biophysica acta. Reviews on cancer · 2023Review
- Intraductal Papillary Mucinous Neoplasms of the Pancreas: A Review of Their Genetic Characteristics and Mouse Models.Cancers · 2021Review
- From Oncogenic Signaling Pathways to Single-Cell Sequencing of Immune Cells: Changing the Landscape of Cancer Immunotherapy.Molecules (Basel, Switzerland) · 2021Review
- Digoxin use is associated with pancreatic cancer risk but does not affect survival.Cancer causes & control : CCC · 2021Article
- Complete Response of Synchronous Liver Metastasis in a Pancreatic Ductal Adenocarcinoma, When Surgery Could Represent a Therapeutic Option.Canadian journal of gastroenterology & hepatology · 2020Article
- Role of BRAF in Hepatocellular Carcinoma: A Rationale for Future Targeted Cancer Therapies.Medicina (Kaunas, Lithuania) · 2019Review
- Systematic Review of Irreversible Electroporation Role in Management of Locally Advanced Pancreatic Cancer.Cancers · 2019Review
- AreCancers · 2019Article
- Common features between neoplastic and preneoplastic lesions of the biliary tract and the pancreas.World journal of gastroenterology · 2019Review
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- Ampullary and pancreatic adenocarcinoma-a comparative study.Journal of gastrointestinal oncology · 2019Article
- The active role of the transcription factor Sp1 in NFATc2-mediated gene regulation in pancreatic cancer.BMC biochemistry · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic adenocarcinoma displays a variety of molecular changes that evolve exponentially with time and lead cancer cells not only to survive, but also to invade the surrounding tissues and metastasise to distant sites. These changes include: genetic alterations in oncogenes and cancer suppressor genes; changes in the cell cycle and pathways leading to apoptosis; and also changes in epithelial to mesenchymal transition. The most common alterations involve the epidermal growth factor receptor (EGFR) gene, the HER2 gene, and the K-ras gene. In particular, the loss of function of tumor-suppressor genes has been documented in this tumor, especially in CDKN2a, p53, DPC4 and BRCA2 genes. However, other molecular events involved in pancreatic adenocarcinoma pathogenesis contribute to its development and maintenance, specifically epigenetic events. In fact, key tumor suppressors that are well established to play a role in pancreatic adenocarcinoma may be altered through hypermethylation, and oncogenes can be upregulated secondary to permissive histone modifications. Indeed, factors involved in tumor invasiveness can be aberrantly expressed through dysregulated microRNAs. This review summarizes current knowledge of pancreatic carcinogenesis from its initiation within a normal cell until the time that it has disseminated to distant organs. In this scenario, highlighting these molecular alterations could provide new clinical tools for early diagnosis and new effective therapies for this malignancy.
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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.