Evidence map›Paper›PMID 37273076›Full record

ReviewPathologie (Heidelberg, Germany)2023

[Hereditary colorectal carcinogenesis].

Hendrik Bläker

Abstract readEnglish AbstractReview
PubMed Publisher
In one paragraph

Review in Pathologie (Heidelberg, Germany), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 79% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

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

1 author at 1 institution in 1 country.

Hendrik BläkerInstitut für Pathologie, Universitätsklinikum Leipzig AöR, Liebigstraße 26, 04103, Leipzig, Deutschland. hendrik.blaeker@medizin.uni-leipzig.de.
Leipzig University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hereditary cancer is characterized by the development of certain cancer types in combination with pathogenic germline mutations in genes known to predispose to these cancer types. Familial cancer differs from hereditary cancer in that no predisposing germline mutation is detected in affected families. However, familial cancer may have a genetic background of as yet unknown origin. Colorectal cancer is unique among human tumors since almost all cancers derive from macroscopically visible benign polypoid precursors. Molecular mechanisms of precursor development differ from that of malignant transformation. Hereditary colorectal cancer can be categorized into polypous and non-polypous predispositions. While the former elevate cancer risk by increasing the number of cancer precursors, the latter elevate cancer risk by increasing the likeliness of malignant transformation. It is the pathologist's responsibility to use morphologic criteria in combination with clinical data in order to raise suspicion of hereditary tumorigenesis and recommend genetic counselling. This article summarizes the current knowledge on hereditary colorectal cancer.

Indexed as

Adenomatous Polyposis ColiColorectal NeoplasmsPeutz-Jeghers SyndromeCell Transformation, NeoplasticGenetic Predisposition to DiseaseHumansAdenomatous polyposis coliCarcinogenesisGerm-line mutationLynch syndromePeutz-Jeghers syndrome

Identifiers

PMID37273076
OpenAlexW4379375877

What OpenQuestion holds

Textmetadata
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.