Evidence map›Paper›PMID 20960194›Full record

ArticleDer Pathologe2010

[Differential diagnostics of hereditary colorectal cancer syndromes. The role of pathology].

J Rüschoff, E Heinmöller, A Hartmann, R Büttner, T Rau

Abstract readEnglish Abstract
PubMed Publisher
In one paragraph

Article in Der Pathologe, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. [Surgical aspects of indications and techniques for adenomatous polyposis variants].Der Chirurg; Zeitschrift fur alle Gebiete der operativen Medizen · 2016
    Review
  4. Review
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

5 authors.

J RüschoffInstitut für Pathologie Nordhessen, Germaniastr. 7, 34119, Kassel. rueschoff@patho-nordhessen.de
E Heinmöller
A Hartmann
R Büttner
T Rau

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

One third of colorectal carcinomas (CRC) show familial clustering of which about 5% have a monogenetic trait. Distinction between disease with and without polyposis, tumor histology and tumor spectrum in a given patient are all of diagnostic relevance. Familial adenomatous polyposis (FAP) underlies approximately 1% of CRC characterized by rapidly forming (>100) adenomas. In contrast to these about 2%-3% of CRC have a hereditary background without polyposis (HNPCC). This is the only hereditary tumour syndrome to date for which a tissue-based molecular screening test is available. Accordingly, expression analysis of mismatch repair genes (MSH2, MSH6 and MLH1, PMS2) is performed first. In the case of an equivocal result with no complete loss of expression testing of microsatellite instability (MSI) is added. In contrast to the other diseases MYH-associated polyposis (MAP) follows a recessive trait with polyp numbers usually between 15-30 adenomas and should be distinguished from attenuated forms of FAP with <100 polyps in the differential diagnosis. In the case of suspected familial cancer syndrome genetic counseling is warranted in order to decide ultimately whether there is an indication for genetic testing (evidence of a germ-line mutation).

Indexed as

AdenomaAdenomatous Polyposis ColiColorectal NeoplasmsColorectal Neoplasms, Hereditary NonpolyposisDiagnosis, DifferentialDNA Mismatch RepairGenetic Diseases, InbornHumansImmunohistochemistryMicrosatellite InstabilityMutationSyndrome

Identifiers

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.