Evidence map›Paper›PMID 34680910›Full record

ReviewGenes2021

The Second Allele: A Key to Understanding the Timing of Sporadic and Hereditary Colorectal Tumorigenesis.

Mohammed Ali Abbass, Brandie Leach, James Michael Church

Open access · goldAbstract readReview
In one paragraph

Review in Genes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.8field-weighted citation impact, top 29% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 7 citations in OpenAlex.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 1 country.

Mohammed Ali AbbassNorthwestern Medicine Digestive Health Center, Chicago, IL 60611, USA.
Brandie LeachInvitae, San Francisco, CA 94103, USA.
James Michael ChurchDivision of Colorectal Surgery, Columbia University Medical Center, New York, NY 10032, USA.
Columbia University Irving Medical Center · USInvitae (United States) · USNorthwestern Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our understanding of the molecular basis of colorectal neoplasia is derived from Mendelian genetics, with tumor suppressor genes contributing more to the deregulation of growth than oncogenes. In patients with hereditary syndromes, expression of one allele of a key tumor suppressor gene is absent at birth. The loss of the expression of the second allele precipitates tumorigenesis. However, there are multiple ways in which the expression of the second allele of a tumor suppressor gene is lost. Here, we review these ways and their possible effect on phenotype.

Indexed as

Loss of HeterozygosityAdenomatous Polyposis ColiAdenomatous Polyposis Coli ProteinAnimalsCarcinogenesisHumansAdenomatous Polyposis Coli Proteinallelic losscolorectal cancerhereditary syndromesmethylationmolecular geneticssecond hittumor suppression gene

Identifiers

PMID34680910
PMCPMC8536005
OpenAlexW3204354846

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.