Evidence map›Paper›PMID 17384672›Full record

ArticleOncogene2007

UTRN on chromosome 6q24 is mutated in multiple tumors.

Y Li, J Huang, Y-L Zhao, J He, W Wang, K E Davies, V Nosé, S Xiao

Abstract read
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In one paragraph

Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

26 citing papers in PubMed, 54 citations in OpenAlex.

  1. Exploring Dystrophin Expression and Mutations in theInternational journal of molecular sciences · 2026
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  9. The Duchenne muscular dystrophy gene and cancer.Cellular oncology (Dordrecht, Netherlands) · 2021
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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

8 authors at 4 institutions in 3 countries.

Y LiDepartment of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
J Huang
Y-L Zhao
J He
W Wang
K E Davies
V Nosé
S Xiao
Brigham and Women's Hospital · USHarvard University · USCornell University · USUniversity of Oxford · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Though deletion of the long arm of chromosome 6 is one of the most common aberrations in tumors, its targeted gene(s) has not been convincingly identified. Using a functional screening approach, we found that UTRN (which encodes utrophin, a dystrophin-related protein) at 6q24, when expressed in an antisense orientation, induced cellular transformation, consistent with a tumor suppressor role. Northern blot analysis, semiquantitative reverse transcription-polymerase chain reaction (RT-PCR), and gene expression arrays all showed that UTRN expression was downregulated in primary tumors compared with matched normal tissues. Several UTRN neighbor genes were not affected in some tumors with UTRN downregulation, suggesting that UTRN was specifically targeted. RT-PCR, coupled with an in vitro transcription and translation assay, revealed inactivation mutations in 21/62 breast cancers, 4/20 neuroblastomas and 4/15 malignant melanomas. Most of the mutations were deletions involving one or more exons that led to the truncation of utrophin. Splicing errors were found in two cases, and nonsense mutation in one case. Overexpression of a wild-type UTRN in breast cancer cells inhibited tumor cell growth in vitro and reduced their tumor potential in nude mice. Our studies suggest that UTRN is a candidate tumor suppressor gene.

Indexed as

AnimalsBase SequenceBreast NeoplasmsChromosomes, Human, Pair 6FemaleHumansMaleMammary Neoplasms, ExperimentalMelanomaMelanoma, ExperimentalMiceMice, NudeNeoplasms, ExperimentalNeuroblastomaNIH 3T3 CellsPoint MutationTumor Suppressor ProteinsUTRN protein, humanUtrophin

Identifiers

PMID17384672
OpenAlexW2080595062

What OpenQuestion holds

Textmetadata
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.