Evidence map›Paper›PMID 37691868›Full record

ArticleTranslational lung cancer research2023

Masaki Suzuki, Rika Kasajima, Tomoyuki Yokose, Eigo Shimizu, Seira Hatakeyama, Kiyoshi Yamaguchi, Kazuaki Yokoyama, Kotoe Katayama, Rui Yamaguchi, Yoichi Furukawa and 5 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Translational lung cancer research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.5field-weighted citation impact, top 26% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Review
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

15 authors at 3 institutions in 1 country.

Masaki SuzukiDepartment of Pathology, The University of Tokyo, Tokyo, Japan.
Rika KasajimaMolecular Pathology and Genetics Division, Kanagawa Cancer Center Research Institute, Yokohama, Japan.
Tomoyuki YokoseDepartment of Pathology, Kanagawa Cancer Center, Yokohama, Japan.
Eigo ShimizuDivision of Health Medical Intelligence, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Seira HatakeyamaDivision of Clinical Genome Research, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Kiyoshi YamaguchiDivision of Clinical Genome Research, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Kazuaki YokoyamaDepartment of Hematology/Oncology, Research Hospital, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Kotoe KatayamaDivision of Health Medical Intelligence, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Rui YamaguchiDivision of Health Medical Intelligence, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Yoichi FurukawaDivision of Clinical Genome Research, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Satoru MiyanoDivision of Health Medical Intelligence, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Seiya ImotoDivision of Health Medical Intelligence, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Aya Shinozaki-UshikuDepartment of Pathology, The University of Tokyo, Tokyo, Japan.
Tetsuo UshikuDepartment of Pathology, The University of Tokyo, Tokyo, Japan.
Yohei MiyagiMolecular Pathology and Genetics Division, Kanagawa Cancer Center Research Institute, Yokohama, Japan.
The University of Tokyo · JPKanagawa Prefectural Hospital Organization · JPKanagawa Cancer Center

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: High-grade fetal adenocarcinoma of the lung (H-FLAC) is a rare variant of pulmonary adenocarcinoma. Our previous study showed a high frequency of KMT2C mutations in lung cancers with an H-FLAC component, showing that KMT2C dysfunction may be associated with the biological features of H-FLACs. Methods: In this study, we performed RNA sequencing and immunohistochemical analysis to identify the differentially expressed genes and corresponding pathways associated with H-FLACs, compared with common adenocarcinomas. Results: Ingenuity pathway analysis based on RNA sequencing data revealed that DNA homologous recombination repair (HRR) pathways were significantly inactivated in H-FLAC. Expression of Conclusions: Cancers containing H-FLAC components showed lower levels of KMT2C and HRR factors than common lung adenocarcinomas, and their levels exhibited a positive correlation. These results support the hypothesis that loss of KMT2C function decreases the expression of the HRR factors in H-FLACs. H-FLACs with low

Indexed as

BRCA1BRCA2Fetal adenocarcinomaKMT2Clung adenocarcinoma

Identifiers

PMID37691868
PMCPMC10483084
OpenAlexW4386226205

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.