ArticleCurrent genomics2008
The genomics of colorectal cancer: state of the art.
Article in Current genomics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis 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
3 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Associations between nutritional factors and KRAS mutations in colorectal cancer: a systematic review.BMC cancer · 2020Pooled it
- Clinical and Molecular Assessment of Patients with Lynch Syndrome and Sarcomas Underpinning the Association withCancers · 2020Article
- Tissue Metabonomic Phenotyping for Diagnosis and Prognosis of Human Colorectal Cancer.Scientific 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The concept of the adenoma-carcinoma sequence, as first espoused by Morson et al. whereby the development of colorectal cancer is dependent on a stepwise progression from adenomatous polyp to carcinoma is well documented. Initial studies of the genetics of inherited colorectal cancer susceptibility concentrated on the inherited colorectal cancer syndromes, such as Familial Adenomatous Polyposis (FAP) and Lynch Syndrome (also known as HNPCC). These syndromes, whilst easily characterisable, have a well understood sequence of genetic mutations that predispose the sufferer to developing colorectal cancer, initiated for example in FAP by the loss of the second, normal allelle of the tumour supressor APC gene. Later research has identified other inherited variants such as MUTYH (MYH) polyposis and Hyperplastic Polyposis Syndrome. Recent research has concentrated on the pathways by which colorectal adenomatous polyps not due to one of these known inherited susceptibilities undergo malignant transformation, and determination of the types of polyps most likely to do so. Also, why do individuals in certain families have a predisposition to colorectal cancer. In this article, we will discuss briefly the current state of knowledge of the genomics of the classical inherited colorectal cancer syndromes. We will also discuss in detail the genetic changes in polyps that undergo malignant transformation as well as current knowledge with regards to the epigenomic changes found in colorectal polyps.
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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.