Evidence map›Paper›PMID 24375252›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2014

The co-expression of telomerase and ALT pathway in human breast cancer tissues.

Bin Xu, Min Peng, Qibin Song

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In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact, top 83% 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

16 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

3 authors at 2 institutions in 1 country.

Bin XuOncology Center, Renmin Hospital of Wuhan University, Wuhan, Hubei, 430060, People's Republic of China.
Min Peng
Qibin Song
Wuhan University · CNRenmin Hospital of Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, telomerase-targeted therapy was studied intensively; however, many studies have verified the existence of alternative lengthening mechanisms of telomeres in vitro. In the present work, we explored the expression characteristic of the two kinds of telomere-prolonging mechanisms in the breast cancer tissues per se. Furthermore, we studied the relationship between Her-2 expression and ALT pathway. Ninety samples of breast cancer tissues were examined in this research. RT-PCR was used for the detection of the expression of human telomerase reverse transcriptase (hTERT); IHC was used for the detection of the expression of promyelocytic leukemia body (PML) bodies; the co-expression of PML bodies and hTERT was detected using the QDs-based immunofluorescence. The co-expression of PML body and hTERT was found in the same cell in breast cancer tissues, and ten samples expressed neither PML bodies nor hTERT. Additionally, the expression of PML bodies and Her-2 was statistically co-related (P = 0.047). The two kinds of mechanisms of telomere extension can co-exist in the same cell in beast cancer tissues, and there may be other mechanisms of telomere extension functioning in human breast carcinoma.

Indexed as

TelomereAdultAgedAged, 80 and overBreast NeoplasmsErb-b2 Receptor Tyrosine KinasesFemaleHumansImmunohistochemistryMiddle AgedNuclear ProteinsPromyelocytic Leukemia ProteinTelomeraseTranscription FactorsTumor Suppressor ProteinsERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesNuclear ProteinsPML protein, humanPromyelocytic Leukemia ProteinTelomeraseTERT protein, humanTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID24375252
OpenAlexW2163036274

What Socratic holds

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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 Socratic graph.