Evidence map›Paper›PMID 35815661›Full record

ArticleThoracic cancer2022

Comprehensive genetic analysis of histological components of combined small cell carcinoma.

Yuko Iida, Yoko Nakanishi, Tetsuo Shimizu, Masayuki Nomoto, Yoshiko Nakagawa, Reiko Ito, Noriaki Takahashi, Shinobu Masuda, Yasuhiro Gon

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

Article in Thoracic cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. 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

9 authors at 1 institution in 1 country.

Yuko IidaDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.ORCID 0000-0002-1807-7781
Yoko NakanishiDivision of Oncologic Pathology, Department of Pathology and Microbiology, Nihon University School of Medicine, Tokyo, Japan.
Tetsuo ShimizuDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.ORCID 0000-0003-3405-9652
Masayuki NomotoDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
Yoshiko NakagawaDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.ORCID 0000-0003-4807-3797
Reiko ItoDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
Noriaki TakahashiDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
Shinobu MasudaDivision of Oncologic Pathology, Department of Pathology and Microbiology, Nihon University School of Medicine, Tokyo, Japan.ORCID 0000-0002-0361-8071
Yasuhiro GonDivision of Respiratory Medicine, Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
Nihon University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCombined small-cell lung cancer (cSCLC) is a rare type of small-cell lung cancer (SCLC) that includes both SCLC and non-small-cell lung cancer (NSCLC). The molecular biological mechanisms underlying the heterogeneity of histological types in combined or metachronously transformed SCLC (mtSCLC) remain unclear. This study aimed to investigate the relationship between genetic alterations and each histological component heterogeneously detected in cSCLC and mtSCLC.

methodsThis study included four cSCLC cases and one mtSCLC case. Formalin-fixed and paraffin-embedded sections of each histological component of these tumors were subjected to next-generation sequencing (NGS) and quantitative reverse transcription-polymerase chain reaction to investigate the genetic mutations and expression levels of neuroendocrine cell-specific transcription factors (achaete-scute homolog-1 [ASCL1], brain-2 [BRN2] also known as POU domain class 3 transcription factor 2, nuclear factor 1 B [NF1B], insulinoma-associated protein 1 [INSM1], and thyroid transcription factor-1 [TTF-1]).

resultsNGS analysis revealed that SCLC and NSCLC components share the same somatic mutations detected most frequently in TP53, and also in RB1 and EGFR. Gene expression analysis showed ASCL1 expression was significantly lower in the NSCLC component than in the SCLC component.

conclusionWe conclude that the morphological evolution of heterogeneous histological components in cSCLC may be associated with differences in ASCL1 expression levels, but not in acquired somatic gene mutations.

Indexed as

Carcinoma, Non-Small-Cell LungCarcinoma, Small CellLung NeoplasmsSmall Cell Lung CarcinomaHumansRepressor ProteinsTranscription FactorsINSM1 protein, humanRepressor ProteinsTranscription Factorsachaete-scute homolog-1heterogeneitynext-generation sequencingsmall-cell lung cancersomatic mutations

Identifiers

PMID35815661
PMCPMC9376179
OpenAlexW4285025444

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.