Evidence map›Paper›PMID 30218172›Full record

Trial reportMedical oncology (Northwood, London, England)2018

DNA methylation marker to estimate the breast cancer cell fraction in DNA samples.

Hiroki Ishihara, Satoshi Yamashita, Satoshi Fujii, Kazunari Tanabe, Hirofumi Mukai, Toshikazu Ushijima

Abstract readClinical Trial
PubMed Publisher
In one paragraph

Trial report in Medical oncology (Northwood, London, England), 2018. 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
0.6field-weighted citation impact, top 31% 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

6 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. DNA methylation marker to estimate ovarian cancer cell fraction.Medical oncology (Northwood, London, England) · 2022
    Article
  3. Article
  4. Article
  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

6 authors at 3 institutions in 3 countries.

Hiroki IshiharaDivision of Epigenomics, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan.
Satoshi YamashitaDivision of Epigenomics, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan.
Satoshi FujiiDivision of Pathology, Exploratory Oncology Research and Clinical Trial Center, National Cancer Center, Kashiwa, Chiba, Japan.
Kazunari TanabeDepartment of Urology, Tokyo Women's Medical University, Tokyo, Japan.
Hirofumi MukaiDepartment of Breast and Medical Oncology, National Cancer Center Hospital East, Kashiwa, Chiba, Japan.
Toshikazu UshijimaDivision of Epigenomics, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan. tushijim@ncc.go.jp.ORCID http://orcid.org/0000-0003-3405-7817
Tokyo Women's Medical University · JPNational Cancer Center Hospital East · JPNational Cancer Research Institute · GB

Funding

The Japan Agency for Medical Research and Development 18kk0305004h0003
6 · The paper itself

Abstract

Estimation of the cancer cell fraction in breast cancer tissue is important for exclusion of samples unsuitable for multigene prognostic assays and a variety of molecular analyses for research. Here, we aimed to establish a breast cancer cell fraction marker based on DNA methylation. First, we screened genes unmethylated in non-cancerous mammary tissues and methylated in breast cancer tissues using microarray data from the TCGA database, and isolated 12 genes. Among them, four genes were selected as candidate marker genes without a high incidence of copy number alterations and with broad coverage across patients. Bisulfite pyrosequencing analysis of additional breast cancer biopsy specimens purified by laser capture microdissection (LCM) excluded two genes, and a combination of SIM1 and CCDC181 was finally selected as a fraction marker. In further additional specimens without LCM purification, the fraction marker was substantially methylated (≥ 20%) with high incidence (50/51). The cancer cell fraction estimated by the fraction marker was significantly correlated with that estimated by microscopic examination (p < 0.0001). Performance of a previously established marker, HSD17B4 methylation, which predicts therapeutic response of HER2-positive breast cancer to trastuzumab, was improved after the correction of cancer cell fraction by the fraction marker. In conclusion, we successfully established a breast cancer cell fraction marker based on DNA methylation.

Indexed as

Biomarkers, TumorBreast NeoplasmsCell Line, TumorDatabases, GeneticDNA MethylationErb-b2 Receptor Tyrosine KinasesFemaleGenetic MarkersHumansBiomarkers, TumorERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesGenetic MarkersBreast cancerCancer cell contentCancer cell fractionDNA methylationHER2HSD17B4Trastuzumab

Identifiers

PMID30218172
OpenAlexW2890432141

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.