Evidence map›Paper›PMID 24662919›Full record

ArticleCancer research2014

Emergence, involution, and progression to carcinoma of mutant clones in normal endometrial tissues.

George L Mutter, Nicolas M Monte, Donna Neuberg, Alex Ferenczy, Charis Eng

Erratum issuedAbstract read
In one paragraph

Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.2field-weighted citation impact, top 5% 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

23 citing papers in PubMed, 53 citations in OpenAlex.

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  11. Identification of Therapeutic and Prognostic Biomarkers of Lamin C (LAMC) Family Members in Head and Neck Squamous Cell Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  12. Frequent loss of mutation-specific mismatch repair protein expression in nonneoplastic endometrium of Lynch syndrome patients.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020
    Article
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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

5 authors at 4 institutions in 3 countries.

George L MutterAuthors' Affiliations: Department of Pathology at Brigham and Women's Hospital; Department of Biostatistics and Computational Biology, Dana Farber Cancer Institute, Boston, Massachusetts; Departments of Pathology, McGill University and the Jewish General Hospital, Montreal, Canada; Genomic Medicine Institute and Taussig Cancer Institute, Cleveland Clinic; and Department of Genetics and Genome Sciences, and Case Comprehensive Cancer Center, Case Western Reserve University School of Medicine, Cleveland, Ohio gmutter@partners.org.
Nicolas M MonteAuthors' Affiliations: Department of Pathology at Brigham and Women's Hospital; Department of Biostatistics and Computational Biology, Dana Farber Cancer Institute, Boston, Massachusetts; Departments of Pathology, McGill University and the Jewish General Hospital, Montreal, Canada; Genomic Medicine Institute and Taussig Cancer Institute, Cleveland Clinic; and Department of Genetics and Genome Sciences, and Case Comprehensive Cancer Center, Case Western Reserve University School of Medicine, Cleveland, Ohio.
Donna NeubergAuthors' Affiliations: Department of Pathology at Brigham and Women's Hospital; Department of Biostatistics and Computational Biology, Dana Farber Cancer Institute, Boston, Massachusetts; Departments of Pathology, McGill University and the Jewish General Hospital, Montreal, Canada; Genomic Medicine Institute and Taussig Cancer Institute, Cleveland Clinic; and Department of Genetics and Genome Sciences, and Case Comprehensive Cancer Center, Case Western Reserve University School of Medicine, Cleveland, Ohio.
Alex FerenczyAuthors' Affiliations: Department of Pathology at Brigham and Women's Hospital; Department of Biostatistics and Computational Biology, Dana Farber Cancer Institute, Boston, Massachusetts; Departments of Pathology, McGill University and the Jewish General Hospital, Montreal, Canada; Genomic Medicine Institute and Taussig Cancer Institute, Cleveland Clinic; and Department of Genetics and Genome Sciences, and Case Comprehensive Cancer Center, Case Western Reserve University School of Medicine, Cleveland, Ohio.
Charis EngAuthors' Affiliations: Department of Pathology at Brigham and Women's Hospital; Department of Biostatistics and Computational Biology, Dana Farber Cancer Institute, Boston, Massachusetts; Departments of Pathology, McGill University and the Jewish General Hospital, Montreal, Canada; Genomic Medicine Institute and Taussig Cancer Institute, Cleveland Clinic; and Department of Genetics and Genome Sciences, and Case Comprehensive Cancer Center, Case Western Reserve University School of Medicine, Cleveland, OhioAuthors' Affiliations: Department of Pathology at Brigham and Women's Hospital; Department of Biostatistics and Computational Biology, Dana Farber Cancer Institute, Boston, Massachusetts; Departments of Pathology, McGill University and the Jewish General Hospital, Montreal, Canada; Genomic Medicine Institute and Taussig Cancer Institute, Cleveland Clinic; and Department of Genetics and Genome Sciences, and Case Comprehensive Cancer Center, Case Western Reserve University School of Medicine, Cleveland, Ohio.
Cancer Institute (WIA) · INCase Comprehensive Cancer CenterCase Western Reserve University · USCleveland Clinic · US

Funding

Hormonal modulation of latent endometrial precancersR01CA100833 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI MUTTER, GEORGE L · 2004 to 2008
$1.3M
NCI NIH HHS R01 CA100833NCI NIH HHS R01-CA100833
6 · The paper itself

Abstract

Sporadic somatic inactivation of genes such as PTEN within histologically normal endometrium (latent precancers) is an early step in endometrial carcinogenesis. We have used clone-specific mutations of PTEN to determine the fate of latent precancers over time in women who do (high risk) and do not (low risk) develop endometrial neoplasia. PTEN immunohistochemistry was performed on 45 occurrences of endometrial neoplasia and their paired antecedent benign biopsies, along with age matched sample pairs from 167 patients who did not develop a neoplasm. When PTEN-deficient cells were present at both time points, DNA sequencing was performed to determine whether they were single or multiple independent events. Loss of PTEN protein in isolated glands was common in the initial normal biopsies of high- and low-risk groups (42% and 27%, respectively, P = 0.066). Protein-deficient glands have a tendency to disappear over time in low-risk women (P = 0.047) and, even when "persistent," are infrequently (19%, 3/16) confirmed to be the same clone. Similarly, only a small proportion (6.7%, 1/15) of latent precancers seen in high-risk women are the direct progenitors of subsequent neoplasia. There is a high rate of latent precancer turnover in both low- and high-risk patients, with rare long-term persistence of unique clones, which may or may not progress to a histologic lesion. The temporal dynamics of clonal emergence, persistence, and involution are sufficiently complex that in the individual patient, the presence of a latent precancer has an unknown contribution to long-term cancer risk.

Indexed as

AdultAgedAged, 80 and overBiopsyCarcinoma, EndometrioidDisease ProgressionEndometrial NeoplasmsEndometriumFemaleHumansImmunohistochemistryMiddle AgedMutationPrecancerous ConditionsPTEN PhosphohydrolaseRisk FactorsPTEN PhosphohydrolasePTEN protein, human

Identifiers

PMID24662919
PMCPMC4058864
OpenAlexW2137349242

What OpenQuestion holds

Textmetadata
LicenceTDM
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.