ArticlePancreas2008
Mutational analyses of multiple oncogenic pathways in intraductal papillary mucinous neoplasms of the pancreas.
Article in Pancreas, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 3 of them syntheses that pooled it.
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
18 citing papers in PubMed, 3 syntheses or guidelines pooled it, 40 citations in OpenAlex.
- Signal transduction pathway mutations in gastrointestinal (GI) cancers: a systematic review and meta-analysis.Scientific reports · 2020Pooled it
- Can we better predict the biologic behavior of incidental IPMN? A comprehensive analysis of molecular diagnostics and biomarkers in intraductal papillary mucinous neoplasms of the pancreas.Langenbeck's archives of surgery · 2018Pooled it
- Genetic markers of malignant transformation in intraductal papillary mucinous neoplasm of the pancreas: a meta-analysis.Pancreas · 2012Pooled it
- Molecular Pathology of Pancreatic Cystic Lesions with a Focus on Malignant Progression.Cancers · 2024Review
- BRAF V600E and Novel Somatic Mutations in Thyroid Cancer of Libyan Patients.Asian Pacific journal of cancer prevention : APJCP · 2022Article
- Cystic pancreatic lesions, the endless dilemma.World journal of gastroenterology · 2021Article
- Intraductal Pancreatic Mucinous Neoplasms: A Tumor-Biology Based Approach for Risk Stratification.International journal of molecular sciences · 2020Review
- From somatic mutation to early detection: insights from molecular characterization of pancreatic cancer precursor lesions.The Journal of pathology · 2018Review
- KRAS, GNAS, and RNF43 mutations in intraductal papillary mucinous neoplasm of the pancreas: a meta-analysis.SpringerPlus · 2016Review
- The genetic classification of pancreatic neoplasia.Journal of gastroenterology · 2015Review
- Pancreatic cancer genomes: toward molecular subtyping and novel approaches to diagnosis and therapy.Molecular diagnosis & therapy · 2013Review
- Mutation and genomic amplification of the PIK3CA proto-oncogene in pituitary adenomas.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2012Article
- Intraductal papillary mucinous neoplasm of the pancreas: an update.Scientifica · 2012Review
- Recurrent GNAS mutations define an unexpected pathway for pancreatic cyst development.Science translational medicine · 2011Article
- Genetic and epigenetic alterations in pancreatic carcinogenesis.Current genomics · 2011Article
- Pulmonary mucinous cystadenoma: a rare benign tumor of the lung.General thoracic and cardiovascular surgery · 2010Article
- Molecular biology of pancreatic cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2008Review
- Pathology and molecular genetics of pancreatic neoplasms.Cancer journal (Sudbury, Mass.)Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 2 countries.
Funding
Abstract
objectiveThere is much accumulated evidence that EGFR, HER2, and their downstream signaling pathway members such as KRAS, BRAF, and PIK3CA are strongly implicated in cancer development and progression. Recently, mutations in the kinase domains of EGFR and HER2, associated with increased sensitivity to tyrosine kinase inhibitors, have been described.
methodsTo evaluate the mutational status of these genes in intraductal papillary mucinous neoplasm (IPMN)/intraductal papillary mucinous carcinoma (IPMC), EGFR and HER2 were analyzed in 36 IPMN/IPMC, and the results were correlated to the mutational status of the KRAS, BRAF, and PIK3CA genes in the samples.
resultsTogether, we identified 1 silent mutation of HER2, 17 (43%) KRAS mutations, 1 (2.7%) BRAF mutation, and 4 (11%) mutations of PIK3CA in the IPMN/IPMC samples.
conclusionsThe EGFR and ERBB2 (HER2) mutations are very infrequent in IPMN/IPMC, suggesting the limited possibility of targeting mutated ERBB2 and EGFR for therapy for these lesions. The KRAS, BRAF, and PIK3CA, however, could represent interesting targets for future therapies in these lesions.
Indexed as
Identifiers
What OpenQuestion holds
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.