Evidence map›Paper›PMID 35707843›Full record

ArticleCancer science2022

The prognosis of endometrial cancers stratified with conventional risk factors and modified molecular classification.

Hiroyuki Yamazaki, Hiroshi Asano, Kanako C Hatanaka, Ryosuke Matsuoka, Yosuke Konno, Yoshihiro Matsuno, Yutaka Hatanaka, Hidemichi Watari

Abstract read
In one paragraph

Article in Cancer science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

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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

8 authors.

Hiroyuki YamazakiDepartment of Obstetrics and Gynecology, Graduate School of Medicine and Faculty of Medicine, Hokkaido University, Sapporo, Japan.ORCID https://orcid.org/0000-0001-8759-9607
Hiroshi AsanoDepartment of Obstetrics and Gynecology, Graduate School of Medicine and Faculty of Medicine, Hokkaido University, Sapporo, Japan.
Kanako C HatanakaCenter for Development of Advanced Diagnostics, Institute of Health Science Innovation for Medical Care Hokkaido University Hospital, Sapporo, Japan.
Ryosuke MatsuokaDepartment of Pathology, International University of Health and Welfare Narita Hospital, Narita, Japan.
Yosuke KonnoDepartment of Obstetrics and Gynecology, Graduate School of Medicine and Faculty of Medicine, Hokkaido University, Sapporo, Japan.
Yoshihiro MatsunoDepartment of Surgical Pathology, Hokkaido University Hospital, Sapporo, Japan.
Yutaka HatanakaCenter for Development of Advanced Diagnostics, Institute of Health Science Innovation for Medical Care Hokkaido University Hospital, Sapporo, Japan.
Hidemichi WatariDepartment of Obstetrics and Gynecology, Graduate School of Medicine and Faculty of Medicine, Hokkaido University, Sapporo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study aimed to validate the Proactive Molecular Risk Classifier for Endometrial Cancer, a modified version of The Cancer Genome Atlas, using data from 184 patients with endometrial cancer (median age: 57.5 years; median follow-up period: 109 months) who had undergone radical surgery (including systemic lymphadenectomy) and subsequent adjuvant chemotherapy (patients with intermediate or high recurrence risk) from 2003 to 2015. Tissue microarrays were prepared from surgical specimens and classified using the conventional clinical risk classifier. Immunohistochemistry was used to detect mismatch repair proteins, L1 cell adhesion molecule, and p53. Direct sequencing was used to identify hotspot mutations in the polymerase-epsilon gene. Forty-five patients were identified as having high L1 cell adhesion molecule expression, 41 as low risk, 34 as mismatch repair-deficient, 13 as polymerase-epsilon gene-mutated, five as having abnormal p53, and 46 as other. Patients were stratified into significantly different prognostic groups (p < 0.0001): favorable (low risk and polymerase-epsilon gene-mutated), intermediate (mismatch repair-deficient and other), and unfavorable (high L1 cell adhesion molecule expression and abnormal p53) with 5-year disease-specific survival rates of 100%, 93.8%, and 75.1%, respectively (Kaplan-Meier method). The combination of conventional recurrent risk classification, sequencing for polymerase-epsilon gene mutations and immunohistochemistry for L1 cell adhesion molecule, p53, and mismatch repair proteins can be used to determine the prognoses of patients with endometrial cancer.

Indexed as

Endometrial NeoplasmsNeural Cell Adhesion Molecule L1Biomarkers, TumorDNA Mismatch RepairFemaleHumansMiddle AgedPrognosisRisk FactorsTumor Suppressor Protein p53Biomarkers, TumorNeural Cell Adhesion Molecule L1Tumor Suppressor Protein p53adjuvant chemotherapyendometrial cancerlymphadenectomymolecular classificationsurvival

Identifiers

PMID35707843
PMCPMC9459414

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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.