Evidence map›Paper›PMID 27677402›Full record

ArticleScientific reports2016

FAIM2, as a novel diagnostic maker and a potential therapeutic target for small-cell lung cancer and atypical carcinoid.

Hio Chung Kang, Jong In Kim, Hee Kyung Chang, Gavitt Woodard, Young Sik Choi, Ja-Lok Ku, David M Jablons, Il-Jin Kim

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

10 citing papers in PubMed, 24 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

8 authors at 4 institutions in 2 countries.

Hio Chung KangThoracic Oncology Laboratory, Department of Surgery, University of California San Francisco, San Francisco, CA, USA.
Jong In KimThoracic Oncology Laboratory, Department of Surgery, University of California San Francisco, San Francisco, CA, USA.
Hee Kyung ChangDepartment of Pathology, Kosin University College of Medicine, Busan, Republic of Korea.
Gavitt WoodardThoracic Oncology Laboratory, Department of Surgery, University of California San Francisco, San Francisco, CA, USA.
Young Sik ChoiDepartment of Internal Medicine, Kosin University College of Medicine, Busan, Republic of Korea.
Ja-Lok KuLaboratory of Cell Biology, Cancer Research Institute, Seoul National University College of Medicine, Seoul, Republic of Korea.
David M JablonsThoracic Oncology Laboratory, Department of Surgery, University of California San Francisco, San Francisco, CA, USA.
Il-Jin KimThoracic Oncology Laboratory, Department of Surgery, University of California San Francisco, San Francisco, CA, USA.
University of California, San Francisco · USKosin University · KRUCSF Helen Diller Family Comprehensive Cancer Center · USSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung neuroendocrine (NE) tumors are a heterogeneous group of tumors arising from neuroendocrine cells that includes typical carcinoid, atypical carcinoid, small cell lung cancer (SCLC), and large cell NE cancer. The subtyping of NE tumors is based on the number of mitoses per high powered field and the presences of necrosis. However, the best diagnostic criteria to differentiate various subtypes of lung NE tumors remains controversial and few diagnostic markers distinguish typical and atypical carcinoid. In this study, we show that FAIM2, an inhibitory molecule in the Fas-apoptosis pathway, is significantly overexpressed in SCLC compared to non-small cell lung cancer. In addition, FAIM2 expression is significantly higher in atypical carcinoid than typical carcinoid. As atypical carcinoid has been shown to have worse clinical outcomes than typical carcinoid, our data suggests that FAIM2 may be a useful diagnostic marker for atypical carcinoid. Knockdown of FAIM2 expression increases Fas-induced apoptotic cell death in SCLC cells. Etoposide treatment combined with FAIM2 inhibition also shows modest but significant reduction of viable SCLC cells. Taken together, our results suggest that FAIM2 is a potential NE tumor marker with higher expression in atypical carcinoid and SCLC, and could be a new therapeutic target for SCLC.

Identifiers

PMID27677402
PMCPMC5039724
OpenAlexW2524448644

What OpenQuestion holds

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LicenceCC BY
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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.