Evidence map›Paper›PMID 27785690›Full record

ReviewHuman cell2017

Small cell lung cancer, an epithelial to mesenchymal transition (EMT)-like cancer: significance of inactive Notch signaling and expression of achaete-scute complex homologue 1.

Takaaki Ito, Shinji Kudoh, Takaya Ichimura, Kosuke Fujino, Wael Ahmed Maher Abdo Hassan, Naoko Udaka

Abstract readReview
PubMed Publisher
In one paragraph

Review in Human cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

57 citing papers in PubMed, 101 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

6 authors at 4 institutions in 2 countries.

Takaaki ItoDepartment of Pathology and Experimental Medicine, Kumamoto University Graduate School of Medical Sciences, 1-1-1 Honjo, Chuo-ku, Kumamoto, 860-8556, Japan. takaito@kumamoto-u.ac.jp.ORCID http://orcid.org/0000-0001-5528-3464
Shinji KudohDepartment of Pathology and Experimental Medicine, Kumamoto University Graduate School of Medical Sciences, 1-1-1 Honjo, Chuo-ku, Kumamoto, 860-8556, Japan.
Takaya IchimuraDepartment of Pathology, Saitama Medical University Faculty of Medicine, Saitama, Japan.
Kosuke FujinoDepartment of Thoracic Surgery, Kumamoto University Graduate School of Medical Sciences, Kumamoto, Japan.
Wael Ahmed Maher Abdo HassanDepartment of Pathology, Faculty of Medicine, Suez Canal University, Ismailia, Egypt.
Naoko UdakaDepartment of Diagnostic Pathology, Yokohama City University Hospital, Yokohama, Japan.
Kumamoto University · JPSaitama Medical University · JPSuez Canal University · EGYokohama City University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Small cell lung cancer (SCLC) is one of the most malignant neoplasms in common human cancers. The tumor is composed of small immature-looking cells with a round or fusiform shape, which possesses weak adhesion features among them, suggesting that SCLC shows the morphological characteristics of epithelial to mesenchymal transition (EMT). SCLC is characterized by high metastatic and recurrent rates, sensitivity to the initial chemotherapy, and easy acquirement of chemoresistance afterwards. These characters may be related to the EMT phenotype of SCLC. Notch signaling is an important signaling pathway, and could have roles in regulating neuroendocrine differentiation, proliferation, cell adhesion, EMT, and chemoresistance. Notch1 is usually absent in SCLC in vivo, but could appear after chemotherapy. Notch1 can enhance cell adhesion by induction of E-cadherin in SCLC, which indicates mesenchymal to epithelial transition. On the other hand, achaete-scute complex homologue 1 (ASCL1), negatively regulated by Notch signaling, is a lineage-specific gene of SCLC, and functions to promote neuroendocrine differentiation as well as EMT. ASCL1-transfected adenocarcinoma cell lines induced neuroendocrine phenotypes and lost epithelial cell features. SCLC is characterized by neuroendocrine differentiation and EMT-like features, which could be produced by inactive Notch signaling and ASCL1 expression. In addition, chemical and radiation treatments can activate Notch signaling, which suppress neuroendocrine differentiation and induces chemoradioresistance, accompanied by secession from EMT. Thus, the status of Notch signaling and ASCL1 expression may determine the cell behaviors of SCLC partly through modifying EMT phenotypes.

Indexed as

Basic Helix-Loop-Helix ProteinsEpithelial-Mesenchymal TransitionGene ExpressionHumansLung NeoplasmsReceptor, Notch1Signal TransductionSmall Cell Lung CarcinomaASCL1 protein, humanBasic Helix-Loop-Helix ProteinsNOTCH1 protein, humanReceptor, Notch1Achaete-scute complex homologue 1 (ASCL1)Epithelial-mesenchymal transition (EMT)NeuroendocrineNotch signalingSmall cell lung cancer

Identifiers

PMID27785690
OpenAlexW2540338380

What OpenQuestion holds

Textmetadata
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.