Evidence map›Paper›PMID 26081045›Full record

ArticleCancer science2015

Somatic alteration and depleted nuclear expression of BAP1 in human esophageal squamous cell carcinoma.

Takahiro Mori, Makiko Sumii, Fumiyoshi Fujishima, Kazuko Ueno, Mitsuru Emi, Masao Nagasaki, Chikashi Ishioka, Natsuko Chiba

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  13. International journal of molecular sciences · 2019
    Article
  14. Germline BAP1 mutations induce a Warburg effect.Cell death and differentiation · 2017
    Article
  15. Article
  16. Article
  17. Mesothelioma: recent highlights.Annals of translational medicine · 2017
    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

8 authors at 4 institutions in 2 countries.

Takahiro MoriTohoku Community Cancer Services Program, Tohoku University Graduate School of Medicine, Sendai, Japan.
Makiko SumiiTohoku Community Cancer Services Program, Tohoku University Graduate School of Medicine, Sendai, Japan.
Fumiyoshi FujishimaDepartment of Pathology, Tohoku University Hospital, Sendai, Japan.
Kazuko UenoDepartment of Integrative Genomics, Tohoku Medical Megabank Organization, Tohoku University, Sendai, Japan.
Mitsuru EmiThoracic Oncology Program, University of Hawaii Cancer Center, Honolulu, Hawaii, USA.
Masao NagasakiDepartment of Integrative Genomics, Tohoku Medical Megabank Organization, Tohoku University, Sendai, Japan.
Chikashi IshiokaDepartment of Clinical Oncology, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan.
Natsuko ChibaDepartment of Cancer Biology, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan.
Tohoku University · JPTohoku Medical Megabank Organization · JPTohoku University Hospital · JPUniversity of Hawaiʻi at Mānoa · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BRCA1-associated protein 1 (BAP1) is a deubiquitinating enzyme that is involved in the regulation of cell growth. Recently, many somatic and germline mutations of BAP1 have been reported in a broad spectrum of tumors. In this study, we identified a novel somatic non-synonymous BAP1 mutation, a phenylalanine-to-isoleucine substitution at codon 170 (F170I), in 1 of 49 patients with esophageal squamous cell carcinoma (ESCC). Multiplex ligation-dependent probe amplification (MLPA) of BAP1 gene in this ESCC tumor disclosed monoallelic deletion (LOH), suggesting BAP1 alterations on both alleles in this tumor. The deubiquitinase activity and the auto-deubiquitinase activity of F170I-mutant BAP1 were markedly suppressed compared with wild-type BAP1. In addition, wild-type BAP1 mostly localizes to the nucleus, whereas the F170I mutant preferentially localized in the cytoplasm. Microarray analysis revealed that expression of the F170I mutant drastically altered gene expression profiles compared with expressed wild-type BAP1. Gene-ontology analyses indicated that the F170I mutation altered the expression of genes involved in oncogenic pathways. We found that one candidate, TCEAL7, previously reported as a putative tumor suppressor gene, was significantly induced by wild-type BAP1 as compared to F170I mutant BAP1. Furthermore, we found that the level of BAP1 expression in the nucleus was reduced in 44% of ESCC examined by immunohistochemistry (IHC). Because the nuclear localization of BAP1 is important for its tumor suppressor function, BAP1 may be functionally inactivated in a substantial portion of ESCC. Taken together, BAP1 is likely to function as a tumor suppressor in at least a part of ESCC.

Indexed as

AdultAgedCarcinoma, Squamous CellCell Line, TumorCell NucleusCell ProliferationCytoplasmEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaFemaleHumansImmunohistochemistryMaleMiddle AgedMutationNuclear ProteinsBAP1 protein, humanNuclear ProteinsTCEAL7 protein, humanTumor Suppressor ProteinsUbiquitin ThiolesteraseBAP1deubiquitinaseesophageal squamous cell carcinomagene expression profilingsomatic mutation

Identifiers

PMID26081045
PMCPMC4582980
OpenAlexW1863979973

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.