Evidence map›Paper›PMID 19667180›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

Chromosome 14 transfer and functional studies identify a candidate tumor suppressor gene, mirror image polydactyly 1, in nasopharyngeal carcinoma.

Arthur Kwok Leung Cheung, Hong Lok Lung, Josephine Mun Yee Ko, Yue Cheng, Eric J Stanbridge, Eugene R Zabarovsky, John M Nicholls, Daniel Chua, Sai Wah Tsao, Xin-Yuan Guan and 1 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
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  13. EBV infection is associated with histone bivalent switch modifications in squamous epithelial cells.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  14. Journal of Cancer · 2019
    Article
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  19. A pathway from chromosome transfer to engineering resulting in human and mouse artificial chromosomes for a variety of applications to bio-medical challenges.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2015
    Review
  20. 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

11 authors at 5 institutions in 4 countries.

Arthur Kwok Leung CheungDepartment of Biology and Center for Cancer Research, Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong SAR, People's Republic of China.
Hong Lok Lung
Josephine Mun Yee Ko
Yue Cheng
Eric J Stanbridge
Eugene R Zabarovsky
John M Nicholls
Daniel Chua
Sai Wah Tsao
Xin-Yuan Guan
Maria Li Lung
Chinese University of Hong Kong · CNUniversity of Hong Kong · HKHong Kong University of Science and Technology · HKKarolinska Institutet · SEUniversity of California, Irvine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chromosome 14 allelic loss is common in nasopharyngeal carcinoma (NPC) and may reflect essential tumor suppressor gene loss in tumorigenesis. An intact chromosome 14 was transferred to an NPC cell line using a microcell-mediated chromosome transfer approach. Microcell hybrids (MCHs) containing intact exogenously transferred chromosome 14 were tumor suppressive in athymic mice, demonstrating that intact chromosome 14 NPC MCHs are able to suppress tumor growth in mice. Comparative analysis of these MCHs and their derived tumor segregants identified 4 commonly eliminated tumor-suppressive CRs. Here we provide functional evidence that a gene, Mirror-Image POLydactyly 1 (MIPOL1), which maps within a single 14q13.1-13.3 CR and that hitherto has been reported to be associated only with a developmental disorder, specifically suppresses in vivo tumor formation. MIPOL1 gene expression is down-regulated in all NPC cell lines and in approximately 63% of NPC tumors via promoter hypermethylation and allelic loss. SLC25A21 and FOXA1, 2 neighboring genes mapping to this region, did not show this frequent down-regulated gene expression or promoter hypermethylation, precluding possible global methylation effects and providing further evidence that MIPOL1 plays a unique role in NPC. The protein localizes mainly to the nucleus. Re-expression of MIPOL1 in the stable transfectants induces cell cycle arrest. MIPOL1 tumor suppression is related to up-regulation of the p21(WAF1/CIP1) and p27(KIP1) protein pathways. This study provides compelling evidence that chromosome 14 harbors tumor suppressor genes associated with NPC and that a candidate gene, MIPOL1, is associated with tumor development.

Indexed as

AnimalsCell CycleCell Line, TransformedCell Line, TumorChromosomes, Human, Pair 14Cyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27DNA MethylationFlow CytometryFluorescent Antibody TechniqueGenes, Tumor SuppressorGenetic Predisposition to DiseaseGene Transfer TechniquesHumansImmunohistochemistryIntracellular Signaling Peptides and ProteinsCDKN1A protein, humanCDKN1B protein, humanCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Intracellular Signaling Peptides and ProteinsMIPOL1 protein, humanTumor Suppressor Proteins

Identifiers

PMID19667180
PMCPMC2732794
OpenAlexW2131883173

What OpenQuestion holds

Textmetadata
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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.