Evidence map›Paper›PMID 14747944›Full record

ReviewVirchows Archiv : an international journal of pathology2004

Molecular genetic pathways in various types of endometrial carcinoma: from a phenotypical to a molecular-based classification.

Sigurd F Lax

Abstract readReview
PubMed Publisher
In one paragraph

Review in Virchows Archiv : an international journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed, 3 pooled it
14.9field-weighted citation impact, top 1% 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

103 citing papers in PubMed, 3 syntheses or guidelines pooled it, 379 citations in OpenAlex.

  1. Prognostic value of the TCGA molecular classification in uterine carcinosarcoma.International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics · 2022
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43 more citing papers are in PubMed but not listed here.

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.

Sigurd F LaxDepartment of Pathology, General Hospital Graz West, Goestingerstrasse 22, 8020 Graz, Austria. sigurd.lax@meduni-graz.at
Graz University Hospital · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Two types of endometrial carcinoma are distinguished with respect to biology and clinical course. Type-I carcinoma is related to hyperestrogenism by association with endometrial hyperplasia, frequent expression of estrogen and progesterone receptors and younger age, whereas type-II carcinoma is unrelated to estrogen, associated with atrophic endometrium, frequent lack of estrogen and progesterone receptors and older age. Histologically, endometrioid and mucinous carcinomas are considered type I, serous and clear cell carcinomas type II. Molecular data from multiple studies support the hypothesis of different genetic pathways in the development of endometrioid and serous carcinoma. The most frequent genetic alteration in endometrioid carcinoma is PTEN inactivation by mutation, followed by microsatellite instability (MIN) and mutations of K-ras and beta-catenin. PTEN and K-ras mutations and MIN are considered early events, occurring in a subset of atypical endometrial hyperplasia, whereas p53 mutation is considered a late event, during progression of about 10-20% of endometrioid carcinomas. In serous carcinoma, p53 mutation is the most frequent genetic alteration, followed by inactivation of p16 and e-cadherin and amplification of her2/neu. p53 mutation occurs in endometrial intraepithelial carcinoma, the putative precursor of serous carcinoma. Considering these genetic pathways, the current histological classification of endometrial carcinoma is molecular based.

Indexed as

PhenotypeAgingbeta CateninCytoskeletal ProteinsEndometrial HyperplasiaEndometrial NeoplasmsEndometriumFemaleGenes, rasHumansMicrosatellite RepeatsMutationPrognosisReceptors, EstrogenReceptors, ProgesteroneTrans-Activatorsbeta CateninCTNNB1 protein, humanCytoskeletal ProteinsReceptors, EstrogenReceptors, ProgesteroneTrans-Activators

Identifiers

PMID14747944
OpenAlexW2118925298

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.