Evidence map›Paper›PMID 30053869›Full record

ArticleDiagnostic pathology2018

Difference in transducin-like enhancer of split 1 protein expression between basal cell adenomas and basal cell adenocarcinomas - an immunohistochemical study.

Yuzo Oyama, Haruto Nishida, Takahiro Kusaba, Hiroko Kadowaki, Motoki Arakane, Junpei Wada, Shogo Urabe, Takashi Hirano, Kenji Kawano, Masashi Suzuki and 2 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in Diagnostic pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 47% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
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

12 authors at 1 institution in 1 country.

Yuzo OyamaDepartment of Diagnostic Pathology, Faculty of Medicine, Oita University, 1-1, Idaigaoka, Hasama-machi, Yufu, 879-5593, Japan.
Haruto NishidaDepartment of Diagnostic Pathology, Faculty of Medicine, Oita University, 1-1, Idaigaoka, Hasama-machi, Yufu, 879-5593, Japan. nharuto@oita-u.ac.jp.
Takahiro KusabaDepartment of Diagnostic Pathology, Faculty of Medicine, Oita University, 1-1, Idaigaoka, Hasama-machi, Yufu, 879-5593, Japan.
Hiroko KadowakiDepartment of Diagnostic Pathology, Faculty of Medicine, Oita University, 1-1, Idaigaoka, Hasama-machi, Yufu, 879-5593, Japan.
Motoki ArakaneDepartment of Diagnostic Pathology, Faculty of Medicine, Oita University, 1-1, Idaigaoka, Hasama-machi, Yufu, 879-5593, Japan.
Junpei WadaOita Preferectual Hospital, Oita, Japan.
Shogo UrabeOita Preferectual Hospital, Oita, Japan.
Takashi HiranoDepartment of Otolaryngology, Faculty of Medicine, Oita University, Yufu, Japan.
Kenji KawanoDepartment of Oral and Maxillofacial Surgery, Faculty of Medicine, Oita University, Yufu, Japan.
Masashi SuzukiDepartment of Otolaryngology, Faculty of Medicine, Oita University, Yufu, Japan.
Shigeo YokoyamaDepartment of Diagnostic Pathology, Faculty of Medicine, Oita University, 1-1, Idaigaoka, Hasama-machi, Yufu, 879-5593, Japan.
Tsutomu DaaDepartment of Diagnostic Pathology, Faculty of Medicine, Oita University, 1-1, Idaigaoka, Hasama-machi, Yufu, 879-5593, Japan.
Oita University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBasal cell adenoma (BCA) and basal cell adenocarcinoma (BCAC) are benign and malignant, basaloid salivary gland neoplasms, respectively. These tumors show a dual-cell proliferation of inner luminal/ductal cells and outer abluminal/myoepithelial or basal cells. The only difference between them is defined as a malignant morphology such as invasion. Recently, the nuclear expression of β-catenin and a catenin beta-1 (CTNNB1) mutation were found in BCA. Transducin-like enhancer of split 1 (TLE1) belongs to the Groucho/TLE family, and it functions in the "off" state in the Wnt/β-catenin signaling pathway. We hypothesized that if the dysregulation of the Wnt/β-catenin signaling pathway could be attributed to the tumorigenesis of BCA/BCAC, there might be differences in TLE1 expression between BCA and BCAC.

methodThe study included 35 BCA and 4 BCAC cases. We performed immunohistochemistry to detect TLE1 and β-catenin and investigated the catenin beta-1 (CTNNB1) mutational profile among BCA and BCAC cases.

resultsIn BCA, the expression of TLE1 was confined to luminal cells of glandular structures, in contrast to the expression of β-catenin in abluminal cells. The BCA cases harbored CTNNB1 gene mutations (12/35). In BCAC, luminal cell staining of TLE1 was identical to BCA in non-invasive areas (4/4) but indistinct in invasive areas (3/4). The BCAC cases were β-catenin positive for abluminal cells in both areas. The BCAC cases had CTNNB1 mutation (2/4) and the laser-captured microdissection allowed the separate collection of infiltrative and non-infiltrative areas to detect the same mutation.

conclusionsImmunohistochemical analysis for TLE1 can identify BCA and BCAC by luminal cell staining difference, especially indistinct luminal cell expression for TLE1 in invasive areas of BCAC. Moreover, TLE1 can be luminal/ductal cell markers.

Indexed as

ImmunohistochemistryAdenocarcinomaAdenomaAdultAgedAged, 80 and overbeta CateninBiomarkers, TumorCo-Repressor ProteinsDiagnosis, DifferentialFemaleHumansMaleMiddle AgedMutationNeoplasm Invasivenessbeta CateninBiomarkers, TumorCo-Repressor ProteinsCTNNB1 protein, humanRepressor ProteinsTLE1 protein, humanBasal cell adenocarcinomaBasal cell adenomaTLE1β-catenin

Identifiers

PMID30053869
PMCPMC6064148
OpenAlexW2884627409

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.