ArticleGut and liver2008
Precursor lesions of pancreatic cancer.
Article in Gut and liver, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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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.
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Who cites it
43 citing papers in PubMed, 83 citations in OpenAlex.
- Claudin-18.2 immunohistochemical evaluation in pancreatic cancer specimens: review and recommendations for routine testing and scoring.Virchows Archiv : an international journal of pathology · 2025Review
- Article
- Progress of single-cell RNA sequencing combined with spatial transcriptomics in tumour microenvironment and treatment of pancreatic cancer.Journal of translational medicine · 2024Review
- A pancreatic cancer organoid platform identifies an inhibitor specific to mutant KRAS.Cell stem cell · 2024Article
- The function of p97/valosin-containing protein (VCP) and small VCP-interacting protein (SVIP) in invasion and migration of pancreatic cancer cells.Turkish journal of medical sciences · 2024Article
- Earlier Diagnosis of Pancreatic Cancer: Is It Possible?Cancers · 2023Review
- Antagonism between Prdm16 and Smad4 specifies the trajectory and progression of pancreatic cancer.The Journal of cell biology · 2023Article
- Laser Capture Microdissection: A Gear for Pancreatic Cancer Research.International journal of molecular sciences · 2022Review
- Non-coding RNA biomarkers in pancreatic ductal adenocarcinoma.Seminars in cancer biology · 2021Review
- Review
- Targeting Tumor-Stromal Interactions in Pancreatic Cancer: Impact of Collagens and Mechanical Traits.Frontiers in cell and developmental biology · 2021Review
- CGAT: Cell Graph ATtention Network for Grading of Pancreatic Disease Histology Images.Frontiers in immunology · 2021Article
- Combination Therapies and Drug Delivery Platforms in Combating Pancreatic Cancer.The Journal of pharmacology and experimental therapeutics · 2019Review
- DuctalAnnals of pancreatic cancer · 2019Article
- Characteristics and Clinical Outcomes of Individuals at High Risk for Pancreatic Cancer: A Descriptive Analysis from a Comprehensive Cancer Center.Gastrointestinal disorders (Basel, Switzerland) · 2019Article
- Article
- Karyopherin Alpha 2-Expressing Pancreatic Duct Glands and Intra-Islet Ducts in Aged Diabetic C414A-Mutant-CRY1 Transgenic Mice.Journal of diabetes research · 2019Article
- Pancreatic cancer chemo-resistance is driven by tumor phenotype rather than tumor genotype.Heliyon · 2018Review
- Quantitative proteomic analysis of pancreatic cyst fluid proteins associated with malignancy in intraductal papillary mucinous neoplasms.Clinical proteomics · 2018Article
- Current modalities in cancer immunotherapy: Immunomodulatory antibodies, CARs and vaccines.Pharmacology & therapeutics · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This review article describes morphological aspects, gene abnormalities, and mucin expression profiles in precursor lesions such as pancreatic intraepithelial neoplasia (PanIN), intraductal papillary mucinous neoplasm (IPMN), and mucinous cystic neoplasm (MCN) of the pancreas, as well as their relation to pancreatic ductal adenocarcinoma (PDAC). The gene abnormalities in precursors of PDAC are summarized as follows: (1) KRAS mutation and p16/CDKN2A inactivation are early events whose frequencies increase with the dysplasia grade in both PanIN and IPMN; (2) TP53 mutation and SMAD4/DPC4 inactivation are late events observed in PanIN3 or carcinomatous change of IPMN in both PanIN and IPMN, although the frequency of the TP53 mutation is lower in IPMN than in PDAC; and (3) also in MCN, KRAS mutation is an early event whose frequency increases with the dysplasia grade, whereas TP53 mutation and SMAD4/DPC4 inactivation are evident only in the carcinoma. The mucin expression profiles in precursors of PDAC are summarized as follows: (1) MUC1 expression increases with the PanIN grade, and is high in PDAC; (2) the expression pattern of MUC2 differs markedly between the major subtypes of IPMN with different malignancy potentials (i.e., IPMN-intestinal type with MUC2+ expression and IPMN-gastric type with MUC2- expression); (3) MUC2 is not expressed in any grade of PanINs, which is useful for differentiating PanIN from intestinal-type IPMN; (4) de novo expression of MUC4, which appears to increase with the dysplasia grade; and (5) high de novo expression of MUC5AC in all grades of PanINs, all types of IPMN, MCN, and PDAC.
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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.