ArticleGastroenterology2009
Changes in the structure and function of ICC networks in ICC hyperplasia and gastrointestinal stromal tumors.
Article in Gastroenterology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04751591 (Prospective Randomized Controlled Multicenter Clinical Trial For Comparison Of Safety Between Endoscopic Resection And Laparoscopic Partial Gastrectomy In Patients With 2-5cm Gastric Gastrointestinal Stromal Tumor), which is not on this map. Cited by 23 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.
Prospective Randomized Controlled Multicenter Clinical Trial For Comparison Of Safety Between Endoscopic Resection And Laparoscopic Partial Gastrectomy In Patients With 2-5cm Gastric Gastrointestinal Stromal Tumor
Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
- Interstitial Cells of Cajal-Origin, Distribution and Relationship with Gastrointestinal Tumors.Medicina (Kaunas, Lithuania) · 2022Review
- Efficacy and safety of endoscopic resection in treatment of small gastric stromal tumors: A state-of-the-art review.World journal of gastrointestinal oncology · 2021Review
- The V654A second-site KIT mutation increases tumor oncogenesis and STAT activation in a mouse model of gastrointestinal stromal tumor.Oncogene · 2020Article
- The Enteric Nervous System and Its Emerging Role as a Therapeutic Target.Gastroenterology research and practice · 2020Review
- Rapid gastric emptying in diabetes mellitus: Pathophysiology and clinical importance.Journal of diabetes and its complications · 2019Review
- Article
- Direct engagement of the PI3K pathway by mutant KIT dominates oncogenic signaling in gastrointestinal stromal tumor.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- ETV1-Positive Cells Give Rise toCancer research · 2017Article
- Combined inhibition of MAP kinase and KIT signaling synergistically destabilizes ETV1 and suppresses GIST tumor growth.Cancer discovery · 2015Article
- Clinical presentations of gastric small gastrointestinal stromal tumors mimics functional dyspepsia symptoms.World journal of gastroenterology · 2014Article
- Interstitial cells: regulators of smooth muscle function.Physiological reviews · 2014Review
- Responses to enteric motor neurons in the gastric fundus of mice with reduced intramuscular interstitial cells of cajal.Journal of neurogastroenterology and motility · 2014Article
- Establishment of pacemaker activity in tissues allotransplanted with interstitial cells of Cajal.Neurogastroenterology and motility · 2013Article
- Primordial germ cells and gastrointestinal stromal tumors respond distinctly to a cKit overactivating allele.Human molecular genetics · 2013Article
- C-KIT mutations were closely associated with the response to Imatinib in Chinese advanced gastrointestinal stromal tumor patients.Medical oncology (Northwood, London, England) · 2012Article
- Evolution of the cancer genome.Nature reviews. Genetics · 2012Review
- Imatinib resistance and microcytic erythrocytosis in a KitV558Δ;T669I/+ gatekeeper-mutant mouse model of gastrointestinal stromal tumor.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Recent advances in small bowel diseases: Part II.World journal of gastroenterology · 2012Review
- 3-D illustration of network orientations of interstitial cells of Cajal subgroups in human colon as revealed by deep-tissue imaging with optical clearing.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- Visualization of the interstitial cells of cajal (ICC) network in mice.Journal of visualized experiments : JoVE · 2011Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND &
aimsGastrointestinal stromal tumors (GISTs) express the receptor tyrosine kinase c-kit. Approximately 90% of GISTs have gain-of-function mutations in the Kit gene, which leads to its constitutive activation and drives malignant behavior of GISTs. Interstitial cells of Cajal (ICC) express c-kit; however, it is unknown whether uncontrolled hyperplasia of ICC is responsible for GISTs. Here, we sought to determine whether gain-of-function mutations in Kit lead to hyperplasia of all classes of ICC, whether ICC hyperplasia begins before birth, and whether functional defects occur in ICC hyperplasia or the development of GISTs.
methodsHeterozygous mutant Kit(V558Delta)/+ mice that develop symptoms of human familial GISTs and prematurely die from pathology of the gastrointestinal tract were utilized and compared with wild-type controls. C-kit-immunohistochemistry and intracellular electrical recording of spontaneous and nerve-evoked activity were applied to examine the density and functionality of ICC in these mutants.
resultsThere was considerable hyperplasia in all classes of ICC throughout the GI tract of Kit(V558Delta)/+ mice, except for ICC in the deep muscular plexus of the intestine. Spontaneous electrical activity and postjunctional neural responses in hyperplastic ICC tissues appeared normal but were up-regulated in the cecum, where GISTs were commonly found.
conclusionsKit gain-of-function leads to hyperplasia of most classes of ICC throughout the GI tract. ICC retain normal pacemaker function and enteric neural responses well after development of hyperplasia.
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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.