ReviewDer Pathologe2011
[Chromosomal instability, microsatellite instability and CpG island methylator phenotype: roles in small intestinal carcinogenesis].
Review in Der Pathologe, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 1 citations in OpenAlex.
- Microsatellite polymorphism in the P1 promoter region of the IGF‑1 gene is associated with endometrial cancer.Molecular medicine reports · 2016Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsIntestinal carcinogenesis is associated with genetic instability affecting either the chromosomal level (CIN) or microsatellite DNA sequences (MIN). In addition, epigenetic alterations, such as aberrant CpG island methylation (CIMP) may contribute to tumor development. While these single genetic alterations have frequently been addressed in intestinal carcinogenesis little is known about the interaction of the epigenetics and genetics in tumorigenesis. This investigation therefore aimed to define the synergistic effects of CIN, MSI and CIMP in small bowel adenocarcinomas.
methodsA total of 37 primary small bowel adenocarcinomas were investigated for CIN, MSI, CIMP, KRAS and BRAF mutations. The results showed that CIN was found in 22 out of 37 (57%) tumors (3 out of 9 microsatellite instable and 19 out of 28 microsatellite stable carcinomas) and 9 carcinomas (24%) were microsatellite and chromosomally stable. Aberrant CIMP was detected in 16% of chromosomal instable tumors and in 44% of both microsatellite instable and microsatellite and chromosomally stable carcinomas, KRAS was mutated in 55%, 0% and 10% of chromosomal instable, microsatellite instable and microsatellite and chromosomal stable tumors, respectively, while BRAF mutations occurred in 6% of chromosomal instable and 22% of both microsatellite instable and microsatellite and chromosomal stable carcinomas.
conclusionChromosomal instable carcinomas of the small intestine are distinguished from microsatellite instable and microsatellite and chromosomal stable tumors by a high frequency of KRAS mutations and low frequencies of CIMP and BRAF mutations. In microsatellite instable and microsatellite and chromosomally stable cancers, CIMP and BRAF/KRAS mutations are similarly distributed indicating common mechanisms of tumor initiation or progression in the molecular pathogenesis.
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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.