Evidence map›Paper›PMID 34746885›Full record

ArticleJTO clinical and research reports2021

CADM1 and SPC25 Gene Mutations in Lung Cancer Patients With Idiopathic Pulmonary Fibrosis.

Aya Fukuizumi, Rintaro Noro, Masahiro Seike, Akihiko Miyanaga, Yuji Minegishi, Miwako Omori, Mamiko Hirao, Kuniko Matsuda, Shinobu Kunugi, Kazutaka Nishiwaki and 5 more

Open access · goldAbstract read
In one paragraph

Article in JTO clinical and research reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

7 citing papers in PubMed, 9 citations in OpenAlex.

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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

15 authors at 2 institutions in 1 country.

Aya FukuizumiDepartment of Pulmonary Medicine and Oncology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.
Rintaro NoroDepartment of Pulmonary Medicine and Oncology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.
Masahiro SeikeDepartment of Pulmonary Medicine and Oncology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.
Akihiko MiyanagaDepartment of Pulmonary Medicine and Oncology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.
Yuji MinegishiDepartment of Pulmonary Medicine and Oncology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.
Miwako OmoriDepartment of Pulmonary Medicine and Oncology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.
Mamiko HiraoDepartment of Pulmonary Medicine and Oncology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.
Kuniko MatsudaDepartment of Pulmonary Medicine and Oncology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.
Shinobu KunugiDepartment of Analytic Human Pathology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.
Kazutaka NishiwakiDepartment of Industrial Administration, Faculty of Science and Technology, Tokyo University of Science, Chiba, Japan.
Masahiro MorimotoDepartment of Industrial Administration, Faculty of Science and Technology, Tokyo University of Science, Chiba, Japan.
Haruka MotohashiDepartment of Industrial Administration, Faculty of Science and Technology, Tokyo University of Science, Chiba, Japan.
Hayato OhwadaDepartment of Industrial Administration, Faculty of Science and Technology, Tokyo University of Science, Chiba, Japan.
Jitsuo UsudaDepartment of Thoracic Surgery, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.
Akihiko GemmaDepartment of Pulmonary Medicine and Oncology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.
Nippon Medical School · JPTokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionTo investigate the genomic profiles of patients with lung cancer with idiopathic pulmonary fibrosis (IPF-LC), mechanism of carcinogenesis, and potential therapeutic targets.

methodsWe analyzed 29 matched, surgically resected, cancerous and noncancerous lung tissues (19 IPF-LC and 10 non-IPF-LC) by whole-exome sequencing and bioinformatics analysis and established a medical-engineering collaboration with the Department of Engineering of the Tokyo University of Science.

resultsIn IPF-LC, CADM1 and SPC25 were mutated at a frequency of 47% (9 of 19) and 53% (10 of 19), respectively. Approximately one-third of the IPF-LC cases (7 of 19; 36%) had both mutations. Pathway analysis revealed that these two genes are involved in transforming growth factor-β1 signaling. CADM1 and SPC25 gene mutations decreased the expression of CADM1 and increased that of SPC25 revealing transforming growth factor-β1-induced epithelial-to-mesenchymal transition and cell proliferation in lung cancer cells. Furthermore, treatment with paclitaxel and DNMT1 inhibitor suppressed SPC25 expression.

conclusionsCADM1 and SPC25 gene mutations may be novel diagnostic markers and therapeutic targets for IPF-LC.

Indexed as

CADM1Idiopathic pulmonary fibrosisLung cancerSPC25Whole-exome sequencing

Identifiers

PMID34746885
PMCPMC8551854
OpenAlexW3202095432

What OpenQuestion holds

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Registered trials

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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.