Evidence map›Paper›PMID 28424422›Full record

ArticleOncotarget2017

Limited impact of intratumour heterogeneity on molecular risk assignment in endometrial cancer.

Manouk van Esterik, Inge C Van Gool, Cor D de Kroon, Remi A Nout, Carien L Creutzberg, Vincent T H B M Smit, Tjalling Bosse, Ellen Stelloo

Abstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Improving response to progestin treatment of low-grade endometrial cancer.International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · 2020
    Review
  4. Endometrial Carcinoma Diagnosis: Use of FIGO Grading and Genomic Subcategories in Clinical Practice: Recommendations of the International Society of Gynecological Pathologists.International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists · 2019
    Review
  5. Article
  6. 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

8 authors.

Manouk van EsterikDepartment of Pathology, Leiden University Medical Centre, Leiden, The Netherlands.
Inge C Van GoolDepartment of Pathology, Leiden University Medical Centre, Leiden, The Netherlands.
Cor D de KroonDepartment of Gynaecology, Leiden University Medical Centre, Leiden, The Netherlands.
Remi A NoutDepartment of Radiation Oncology, Leiden University Medical Centre, Leiden, The Netherlands.
Carien L CreutzbergDepartment of Radiation Oncology, Leiden University Medical Centre, Leiden, The Netherlands.
Vincent T H B M SmitDepartment of Pathology, Leiden University Medical Centre, Leiden, The Netherlands.
Tjalling BosseDepartment of Pathology, Leiden University Medical Centre, Leiden, The Netherlands.
Ellen StellooDepartment of Pathology, Leiden University Medical Centre, Leiden, The Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionIndividual prediction of tumour behaviour based on molecular markers may refine adjuvant treatment strategies in endometrial cancer (EC). As these molecular alterations are determined in a small tumour fraction, high intratumour heterogeneity may interfere with correct risk prediction. This study aimed to investigate to which extent intratumour heterogeneity exists for molecular markers and whether it affects the molecular risk assignment in EC.

methodsForty-nine ECs (three tumour blocks/case) were selected with alterations in POLE (n=10), CTNNB1 (n=8), p53 (n=10), mismatch repair (n=11), L1CAM (n=10), and ECs without any of these markers (n=9). Nine ECs carried more than one molecular marker. All 147 blocks were analysed for POLE exonuclease domain and CTNNB1 exon 3 mutations, and for p53, mismatch repair and L1CAM protein expression. All blocks were assigned to a favourable, intermediate or unfavourable risk group, based on a molecular risk assignment.

resultsConcordance between the three tumour blocks for POLE and CTNNB1 mutational status, and p53, mismatch repair and L1CAM protein expression was found in 100% (48/48), 95.9% (47/49), 93.9% (46/49), 98.0% (48/49), and 91.8% (45/49) of tumours, respectively. These discordances were found in a total of nine cases (18.4%). The intratumour heterogeneity impacted the risk assignment in five cases (10.2%).

conclusionIntratumour heterogeneity of prognostic molecular markers in EC without morphologic heterogeneity is uncommon among three tumour fractions, affecting the molecular risk allocation in a limited number of cases. This low intratumour heterogeneity facilitates the implementation of the molecular risk assignment, advocating its use in clinical decision making.

Indexed as

Biomarkers, TumorGenetic VariationAgedbeta CateninEndometrial NeoplasmsExonsFemaleGene ExpressionHumansMiddle AgedMutationMutL Protein Homolog 1Neoplasm GradingNeoplasm StagingNeural Cell Adhesion Molecule L1Tumor Suppressor Protein p53beta CateninBiomarkers, TumorCTNNB1 protein, humanMutL Protein Homolog 1Neural Cell Adhesion Molecule L1Tumor Suppressor Protein p53endometrial cancerintratumour heterogeneitymolecular markersprognosticrisk stratification

Identifiers

PMID28424422
PMCPMC5421949

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.