Evidence map›Paper›PMID 38104198›Full record

ArticleNature communications2023

Genomic and epigenomic integrative subtypes of renal cell carcinoma in a Japanese cohort.

Akihiko Fukagawa, Natsuko Hama, Yasushi Totoki, Hiromi Nakamura, Yasuhito Arai, Mihoko Saito-Adachi, Akiko Maeshima, Yoshiyuki Matsui, Shinichi Yachida, Tetsuo Ushiku and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

17 citing papers in PubMed, 20 citations in OpenAlex.

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  6. Interferon Epsilon Loss Is Elusive 9p21 Link to Immune-Cold Tumors, Resistant to Immune Checkpoint Therapy, and Endogenous CXCL9/10 Induction.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2025
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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

11 authors at 4 institutions in 2 countries.

Akihiko FukagawaDivision of Cancer Genomics, National Cancer Center Research Institute, Tokyo, Japan.
Natsuko HamaDivision of Cancer Genomics, National Cancer Center Research Institute, Tokyo, Japan.
Yasushi TotokiDivision of Cancer Genomics, National Cancer Center Research Institute, Tokyo, Japan.ORCID 0000-0003-1876-6859
Hiromi NakamuraDivision of Cancer Genomics, National Cancer Center Research Institute, Tokyo, Japan.
Yasuhito AraiDivision of Cancer Genomics, National Cancer Center Research Institute, Tokyo, Japan.ORCID 0000-0001-6306-9409
Mihoko Saito-AdachiDivision of Cancer Genomics, National Cancer Center Research Institute, Tokyo, Japan.ORCID 0000-0001-9213-0184
Akiko MaeshimaDepartment of Diagnostic Pathology, National Cancer Center Hospital, Tokyo, Japan.
Yoshiyuki MatsuiDepartment of Urology, National Cancer Center Hospital, Tokyo, Japan.
Shinichi YachidaDepartment of Cancer Genome Informatics, Graduate School of Medicine, Osaka University, Osaka, Japan.ORCID 0000-0001-5507-4566
Tetsuo UshikuDepartment of Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID 0000-0002-1763-8380
Tatsuhiro ShibataDivision of Cancer Genomics, National Cancer Center Research Institute, Tokyo, Japan. tshibata2010@gmail.com.ORCID 0000-0002-0477-210X
The University of Osaka · JPThe University of Tokyo · JPTokyo National Hospital · JPNational Cancer Research Institute · GB

Funding

Japan Agency for Medical Research and Development (AMED) 21ck0106547h000
6 · The paper itself

Abstract

Renal cell carcinoma (RCC) comprises several histological types characterised by different genomic and epigenomic aberrations; however, the molecular pathogenesis of each type still requires further exploration. We perform whole-genome sequencing of 128 Japanese RCC cases of different histology to elucidate the significant somatic alterations and mutagenesis processes. We also perform transcriptomic and epigenomic sequencing to identify distinguishing features, including assay for transposase-accessible chromatin sequencing (ATAC-seq) and methyl sequencing. Genomic analysis reveals that the mutational signature differs among the histological types, suggesting that different carcinogenic factors drive each histology. From the ATAC-seq results, master transcription factors are identified for each histology. Furthermore, clear cell RCC is classified into three epi-subtypes, one of which expresses highly immune checkpoint molecules with frequent loss of chromosome 14q. These genomic and epigenomic features may lead to the development of effective therapeutic strategies for RCC.

Indexed as

Carcinoma, Renal CellKidney NeoplasmsChromatinEpigenomicsGenomicsHumansJapanChromatin

Identifiers

PMID38104198
PMCPMC10725467
OpenAlexW4389832170

What OpenQuestion holds

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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.