Evidence map›Paper›PMID 24936796›Full record

ArticlePloS one2014

Analysis and comparison of somatic mutations in paired primary and recurrent epithelial ovarian cancer samples.

Yong-Man Kim, Shin-Wha Lee, Sung-Min Chun, Dae-Yeon Kim, Jong-Hyeok Kim, Kyu-Rae Kim, Young-Tak Kim, Joo-Hyun Nam, Paul van Hummelen, Laura E MacConaill and 2 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

10 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
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  4. Review
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  6. Article
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  8. Article
  9. TP53 mutations in epithelial ovarian cancer.Translational cancer research · 2016
    Article
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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

12 authors at 3 institutions in 2 countries.

Yong-Man KimDepartment of Obstetrics & Gynecology, University of Ulsan, ASAN Medical Center, Seoul, Korea; ASAN Center for Cancer Genome Discovery, ASAN Medical Center, Seoul, Korea.
Shin-Wha LeeDepartment of Obstetrics & Gynecology, University of Ulsan, ASAN Medical Center, Seoul, Korea; ASAN Center for Cancer Genome Discovery, ASAN Medical Center, Seoul, Korea.
Sung-Min ChunDepartment of Pathology, University of Ulsan, ASAN Medical Center, Seoul, Korea; ASAN Center for Cancer Genome Discovery, ASAN Medical Center, Seoul, Korea.
Dae-Yeon KimDepartment of Obstetrics & Gynecology, University of Ulsan, ASAN Medical Center, Seoul, Korea.
Jong-Hyeok KimDepartment of Obstetrics & Gynecology, University of Ulsan, ASAN Medical Center, Seoul, Korea.
Kyu-Rae KimDepartment of Pathology, University of Ulsan, ASAN Medical Center, Seoul, Korea.
Young-Tak KimDepartment of Obstetrics & Gynecology, University of Ulsan, ASAN Medical Center, Seoul, Korea.
Joo-Hyun NamDepartment of Obstetrics & Gynecology, University of Ulsan, ASAN Medical Center, Seoul, Korea.
Paul van HummelenCenter for Cancer Genome Discovery and Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, United States of America.
Laura E MacConaillCenter for Cancer Genome Discovery and Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, United States of America.
William C HahnCenter for Cancer Genome Discovery and Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, United States of America.
Se Jin JangDepartment of Pathology, University of Ulsan, ASAN Medical Center, Seoul, Korea; ASAN Center for Cancer Genome Discovery, ASAN Medical Center, Seoul, Korea.
Asan Medical Center · KRDana-Farber Cancer Institute · USUniversity of Ulsan · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The TP53 mutations have been proved to be predominated in ovarian cancer in a study from The Cancer Genome Atlas (TCGA). However, the molecular characteristics of recurrent ovarian cancers following initial treatment have been poorly estimated. This study was to investigate the pattern of somatic point mutations in matched paired samples of primary and recurrent epithelial ovarian cancers, using the OncoMap mutation detection protocol. We have adapted a high-throughput genotyping platform to determine the mutation status of a large panel of known cancer genes. OncoMap v.4.4 was used to evaluate genomic DNA isolated from a set of 92 formalin-fixed, paraffin-embedded (FFPE) tumors, consisting of matched paired samples of initially diagnosed and recurrent tumors from 46 epithelial ovarian cancer (EOC) patients. Mutations were observed in 33.7% of the samples, with 29.3% of these samples having a single mutation and the remaining 4.3% having two or more mutations. Among the 41 genes analyzed, 35 mutations were found in four genes, namely, CDKN2A (2.2%), KRAS (6.5%), MLH1 (8.2%) and TP53 (20.7%). TP53 was the most frequently mutated gene, but there was no correlation between the presence of mutation in any gene and clinical prognosis. Furthermore, somatic mutations did not differ between primary and recurrent ovarian carcinomas. Every mutation present in recurrent samples was detected in the corresponding primary sample. In conclusion, these OncoMap data of Korean EOC samples provide that somatic mutations were found in CDKN2A, KRAS, MLH1, and TP53. No differences in mutational status between primary and recurrent samples were detected. To understand the biology of tumor recurrence in epithelial ovarian cancer, more studies are necessary, including epigenetic modifications or additional mutations in other genes.

Indexed as

Adaptor Proteins, Signal TransducingAdolescentAdultAgedColorectal NeoplasmsCyclin-Dependent Kinase Inhibitor p16Disease-Free SurvivalDNA Mutational AnalysisFemaleGenetic Association StudiesGenetic Predisposition to DiseaseHumansKaplan-Meier EstimateMiddle AgedMutL Protein Homolog 1Neoplasm Recurrence, LocalAdaptor Proteins, Signal TransducingCyclin-Dependent Kinase Inhibitor p16KRAS protein, humanMLH1 protein, humanMutL Protein Homolog 1Nuclear ProteinsProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)ras ProteinsTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID24936796
PMCPMC4060993
OpenAlexW1967113174

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.