Evidence map›Paper›PMID 20300178›Full record

ArticlePloS one2010

A novel translocation breakpoint within the BPTF gene is associated with a pre-malignant phenotype.

Yosef Buganim, Ido Goldstein, Doron Lipson, Michael Milyavsky, Sylvie Polak-Charcon, Corine Mardoukh, Hilla Solomon, Eyal Kalo, Shalom Madar, Ran Brosh and 6 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 23% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. BPTF is essential for vaccine-induced germinal center B cell responses.Journal of immunology (Baltimore, Md. : 1950) · 2026
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  14. The emerging role of ISWI chromatin remodeling complexes in cancer.Journal of experimental & clinical cancer research : CR · 2021
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. SAR by (Protein-Observed)Accounts of chemical research · 2019
    Review
  20. 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

16 authors at 3 institutions in 1 country.

Yosef BuganimDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Ido Goldstein
Doron Lipson
Michael Milyavsky
Sylvie Polak-Charcon
Corine Mardoukh
Hilla Solomon
Eyal Kalo
Shalom Madar
Ran Brosh
Marina Perelman
Roy Navon
Naomi Goldfinger
Iris Barshack
Zohar Yakhini
Varda Rotter
Weizmann Institute of Science · ILSheba Medical Center · ILTechnion – Israel Institute of Technology · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Partial gain of chromosome arm 17q is an abundant aberrancy in various cancer types such as lung and prostate cancer with a prominent occurrence and prognostic significance in neuroblastoma--one of the most common embryonic tumors. The specific genetic element/s in 17q responsible for the cancer-promoting effect of these aberrancies is yet to be defined although many genes located in 17q have been proposed to play a role in malignancy. We report here the characterization of a naturally-occurring, non-reciprocal translocation der(X)t(X;17) in human lung embryonal-derived cells following continuous culturing. This aberrancy was strongly correlated with an increased proliferative capacity and with an acquired ability to form colonies in vitro. The breakpoint region was mapped by fluorescence in situ hybridization (FISH) to the 17q24.3 locus. Further characterization by a custom-made comparative genome hybridization array (CGH) localized the breakpoint within the Bromodomain PHD finger Transcription Factor gene (BPTF), a gene involved in transcriptional regulation and chromatin remodeling. Interestingly, this translocation led to elevation in the mRNA levels of the endogenous BPTF. Knock-down of BPTF restricted proliferation suggesting a role for BPTF in promoting cellular growth. Furthermore, the BPTF chromosomal region was found to be amplified in various human tumors, especially in neuroblastomas and lung cancers in which 55% and 27% of the samples showed gain of 17q24.3, respectively. Additionally, 42% percent of the cancer cell lines comprising the NCI-60 had an abnormal BPTF locus copy number. We suggest that deregulation of BPTF resulting from the translocation may confer the cells with the observed cancer-promoting phenotype and that our cellular model can serve to establish causality between 17q aberrations and carcinogenesis.

Indexed as

Translocation, GeneticAntigens, NuclearBase SequenceBromodomain Containing ProteinsCarcinogensCell ProliferationChromosomes, Human, Pair 17Comparative Genomic HybridizationHumansIn Situ Hybridization, FluorescenceLungLung NeoplasmsModels, GeneticMolecular Sequence DataNerve Tissue ProteinsNeuroblastomaAntigens, NuclearBromodomain Containing ProteinsCarcinogensfetal Alzheimer antigenNerve Tissue ProteinsTranscription Factors

Identifiers

PMID20300178
PMCPMC2836376
OpenAlexW1978431886

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.