Evidence map›Paper›PMID 26702755›Full record

ArticleOncotarget2015

TMSB4Y is a candidate tumor suppressor on the Y chromosome and is deleted in male breast cancer.

Hong Yuen Wong, Grace M Wang, Sarah Croessmann, Daniel J Zabransky, David Chu, Joseph P Garay, Justin Cidado, Rory L Cochran, Julia A Beaver, Anita Aggarwal and 6 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
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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

16 authors at 4 institutions in 1 country.

Hong Yuen WongThe Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Grace M WangThe Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Sarah CroessmannThe Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Daniel J ZabranskyThe Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
David ChuThe Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Joseph P GarayThe Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Justin CidadoThe Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Rory L CochranThe Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Julia A BeaverThe Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Anita AggarwalVeterans Affairs Medical Center, Washington, DC, USA.
Min-Ling LiuVeterans Affairs Medical Center, Washington, DC, USA.
Pedram ArganiThe Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Alan MeekerThe Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Paula J HurleyThe Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Josh LauringThe Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Ben Ho ParkThe Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Johns Hopkins University · USSidney Kimmel Comprehensive Cancer Center · USGeorgetown University · USVeterans Health Administration · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007309 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI COX, ANDREA L · 1985 to 2019
$43.2M
Training Program in Cellular and Molecular MedicineT32GM008752 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI RAO, RAJINI · 2000 to 2019
$11.7M
Surgical Oncology Training GrantT32CA106183 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI James Richard Goldenring · 2004 to 2026
$6.0M
Cooperation of Mutant TP53 and PIK3CA in Breast CarcinogensisF31CA167939 · NCI · JOHNS HOPKINS UNIVERSITY · PI CROESSMANN, SARAH E · 2013 to 2015
$88k
A novel model system for risk assessment of BRCA carriersF31CA168180 · NCI · JOHNS HOPKINS UNIVERSITY · PI COCHRAN, RORY LANDON · 2012 to 2013
$84k
NCI NIH HHS CA167939NCI NIH HHS CA168180NCI NIH HHS F31 CA167939NCI NIH HHS F31 CA168180NCI NIH HHS NIH P30 CA006973NCI NIH HHS P30 CA006973NCI NIH HHS T32 CA106183NIGMS NIH HHS NIH GM007309NIGMS NIH HHS T32 GM007309NIGMS NIH HHS T32 GM008752
6 · The paper itself

Abstract

Male breast cancer comprises less than 1% of breast cancer diagnoses. Although estrogen exposure has been causally linked to the development of female breast cancers, the etiology of male breast cancer is unclear. Here, we show via fluorescence in situ hybridization (FISH) and droplet digital PCR (ddPCR) that the Y chromosome was clonally lost at a frequency of ~16% (5/31) in two independent cohorts of male breast cancer patients. We also show somatic loss of the Y chromosome gene TMSB4Y in a male breast tumor, confirming prior reports of loss at this locus in male breast cancers. To further understand the function of TMSB4Y, we created inducible cell lines of TMSB4Y in the female human breast epithelial cell line MCF-10A. Expression of TMSB4Y resulted in aberrant cellular morphology and reduced cell proliferation, with a corresponding reduction in the fraction of metaphase cells. We further show that TMSB4Y interacts directly with β-actin, the main component of the actin cytoskeleton and a cell cycle modulator. Taken together, our results suggest that clonal loss of the Y chromosome may contribute to male breast carcinogenesis, and that the TMSB4Y gene has tumor suppressor properties.

Indexed as

Chromosomes, Human, YGene DeletionActinsBreast Neoplasms, MaleCell LineCell ProliferationCell ShapeCell Transformation, NeoplasticFemaleGene Expression Regulation, NeoplasticHumansIn Situ Hybridization, FluorescenceMaleMammary Glands, HumanPhenotypePolymerase Chain ReactionActinsThymosinThymosin beta(4)Tumor Suppressor Proteinscancer geneticsmale breast cancerTMSB4Ytumor suppressorY chromosome

Identifiers

PMID26702755
PMCPMC4792601
OpenAlexW2203305073

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.