Evidence map›Paper›PMID 37179440›Full record

ArticleBritish journal of cancer2023

Whole-exome and targeted gene sequencing of large-cell lung carcinoma reveals recurrent mutations in the PI3K pathway.

Jun-Hong Guo, Yu-Shui Ma, Jie-Wei Lin, Geng-Xi Jiang, Juan He, Hai-Min Lu, Wei Wu, Xun Diao, Qi-Yu Fan, Chun-Yan Wu and 3 more

Open access · greenAbstract read
In one paragraph

Article in British journal of cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. TEP RNA: a new frontier for early diagnosis of NSCLC.Journal of cancer research and clinical oncology · 2024
    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

13 authors at 4 institutions in 1 country.

Jun-Hong Guo *Department of Pathology, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, 200433, China.
Yu-Shui Ma *Institute of Oncology, Affiliated Tumor Hospital of Nantong University, Nantong, 226631, China.
Jie-Wei Lin *Department of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, 200433, China.
Geng-Xi Jiang *Department of Thoracic Surgery, Navy Military Medical University Affiliated Changhai Hospital, Shanghai, 200433, China.
Juan He *Pharmacy Department, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200025, China.
Hai-Min Lu *Department of Thoracic Surgery, Affiliated Tumor Hospital of Nantong University, Nantong, 226631, China.
Wei WuDepartment of Pathology, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, 200433, China.
Xun DiaoInstitute of Oncology, Affiliated Tumor Hospital of Nantong University, Nantong, 226631, China.
Qi-Yu FanInstitute of Oncology, Affiliated Tumor Hospital of Nantong University, Nantong, 226631, China.
Chun-Yan WuDepartment of Pathology, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, 200433, China. wuchunyan581@163.com.
Ji-Bin LiuInstitute of Oncology, Affiliated Tumor Hospital of Nantong University, Nantong, 226631, China. tians2008@ntu.edu.cn.
Da FuInstitute of Oncology, Affiliated Tumor Hospital of Nantong University, Nantong, 226631, China. fu800da900@126.com.ORCID http://orcid.org/0000-0002-0878-2575
Li-Kun HouDepartment of Pathology, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, 200433, China. hlk9575@163.com.
Nantong University · CNTongji University · CNRuijin Hospital · CNSecond Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLarge cell lung carcinoma (LCLC) is an exceptionally aggressive disease with a poor prognosis. At present, little is known about the molecular pathology of LCLC.

methodsUltra-deep sequencing of cancer-related genes and exome sequencing were used to detect the LCLC mutational in 118 tumor-normal pairs. The cell function test was employed to confirm the potential carcinogenic mutation of PI3K pathway.

resultsThe mutation pattern is determined by the predominance of A > C mutations. Genes with a significant non-silent mutation frequency (FDR) < 0.05) include TP53 (47.5%), EGFR (13.6%) and PTEN (12.1%). Moreover, PI3K signaling (including EGFR, FGRG4, ITGA1, ITGA5, and ITGA2B) is the most mutated pathway, influencing 61.9% (73/118) of the LCLC samples. The cell function test confirmed that the potential carcinogenic mutation of PI3K pathway had a more malignant cell function phenotype. Multivariate analysis further revealed that patients with the PI3K signaling pathway mutations have a poor prognosis (P = 0.007).

conclusionsThese results initially identified frequent mutation of PI3K signaling pathways in LCLC and indicate potential targets for the treatment of this fatal type of LCLC.

Indexed as

Carcinoma, Large CellCarcinoma, Non-Small-Cell LungLung NeoplasmsErbB ReceptorsExomeHumansLungMutationPhosphatidylinositol 3-KinasesErbB ReceptorsPhosphatidylinositol 3-Kinases

Identifiers

PMID37179440
PMCPMC10338432
OpenAlexW4376598356

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.