ArticleDigestive diseases and sciences2000
Combination analysis of genetic alterations and cell proliferation in small intestinal carcinomas.
Article in Digestive diseases and sciences, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 23 citations in OpenAlex.
- Genetic analysis of Japanese patients with small bowel adenocarcinoma using next-generation sequencing.BMC cancer · 2022Article
- Clinicopathologic and prognostic associations of KRAS and BRAF mutations in small intestinal adenocarcinoma.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2016Article
- Decoding the Molecular and Mutational Ambiguities of Gastroenteropancreatic Neuroendocrine Neoplasm Pathobiology.Cellular and molecular gastroenterology and hepatology · 2015Review
- Small bowel adenocarcinoma phenotyping, a clinicobiological prognostic study.British journal of cancer · 2013Article
- KRAS G>A mutation favors poor tumor differentiation but may not be associated with prognosis in patients with curatively resected duodenal adenocarcinoma.International journal of cancer · 2013Article
- The diversity and commonalities of gastroenteropancreatic neuroendocrine tumors.Langenbeck's archives of surgery · 2011Review
- Oral contrast agents for small bowel MRI: comparison of different additives to optimize bowel distension.European radiology · 2004Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We analyzed K-ras and p53 mutations, microsatellite instability (MSI), and loss of heterozygosity (LOH) using the polymerase chain reaction (PCR) methods, as well as p53 expression and the Ki-67 labeling index (LI) using immunohistochemistry in 10 duodenal and 10 jejunal/ileal carcinomas. K-ras mutations were detected in two duodenal (20%) and three jejunal/ileal (30%) carcinomas and p53 mutations in one (10%) and three (30%), respectively. LOH of 17p was detected in two duodenal (20%) and two jejunal/ileal (20%) carcinomas and p53 expression in four duodenal (40%) and four jejunal/ileal (40%). One duodenal (10%) and two jejunal/ileal (20%) carcinomas demonstrated MSI. LOH of APC was detected in three jejunal/ileal (30%), but none of the duodenal carcinomas. The Ki-67 LI was 44% in duodenal and 52.6% in jejunal/ileal carcinomas. A subset of small intestinal carcinomas showed involvement of K-ras and p53 mutations, LOH of APC, and MSI. A difference was also apparent for LOH of APC between duodenal and jejunal/ileal carcinomas.
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Registered trials
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