Evidence map›Paper›PMID 9765621›Full record

ArticleJapanese journal of cancer research : Gann1998

Somatic mutations of the PTEN/MMAC1 gene in fifteen Japanese endometrial cancers: evidence for inactivation of both alleles.

K Kurose, K Bando, K Fukino, Y Sugisaki, T Araki, M Emi

Open access · bronzeAbstract read
In one paragraph

Article in Japanese journal of cancer research : Gann, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

7 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. The tumor-suppressor activity of PTEN is regulated by its carboxyl-terminal region.Proceedings of the National Academy of Sciences of the United States of America · 1999
    Article
  7. 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

6 authors at 2 institutions in 1 country.

K KuroseDepartment of Molecular Biology, Nippon Medical School, Kawasaki.
K Bando
K Fukino
Y Sugisaki
T Araki
M Emi
Nippon Medical School · JPNippon Medical School Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Loss of heterozygosity (LOH) of chromosome 10q is observed in approximately 40% of endometrial cancers. Mutations in PTEN/MMAC1, a gene recently isolated from the 10q23 region, are responsible for two dominantly inherited neoplastic syndromes, Cowden disease and Bannayan-Zonana syndrome. Somatic mutations of this gene have also been detected in sporadic cancers of the brain, prostate and breast. To investigate the potential role of this putative tumor suppressor gene in endometrial carcinogenesis as well, we examined 46 primary endometrial cancers for LOH at the 10q23 region, and for mutations in the entire coding region and exon-intron boundaries of the PTEN/MMAC1 gene. LOH was identified in half of the 38 informative cases, and subtle somatic mutations were detected in 15 tumors (33%). Our results suggest that of the genes studied so far in endometrial carcinomas, PTEN/MMAC1 is the most commonly mutated one, and that inactivation of both copies by allelic loss and/or mutation, a pattern that defines genes as "tumor suppressors," contributes to tumorigenesis in endometrial cancers.

Indexed as

AllelesGene Expression Regulation, NeoplasticMutationPhosphoric Monoester HydrolasesTumor Suppressor ProteinsChromosomes, Human, Pair 10Endometrial NeoplasmsFemaleGenes, Tumor SuppressorHumansLoss of HeterozygosityNeoplasm ProteinsProtein Tyrosine PhosphatasesPTEN PhosphohydrolaseNeoplasm ProteinsPhosphoric Monoester HydrolasesProtein Tyrosine PhosphatasesPTEN PhosphohydrolasePTEN protein, humanTumor Suppressor Proteins

Identifiers

PMID9765621
PMCPMC5921910
OpenAlexW2080842507

What OpenQuestion holds

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Registered trials

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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.