Evidence map›Paper›PMID 17483321›Full record

ArticleCancer research2007

Identification of novel amplification gene targets in mouse and human breast cancer at a syntenic cluster mapping to mouse ch8A1 and human ch13q34.

Martin C Abba, Victoria T Fabris, Yuhui Hu, Frances S Kittrell, Wei-Wen Cai, Lawrence A Donehower, Aysegul Sahin, Daniel Medina, C Marcelo Aldaz

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. CUL4The American journal of pathology · 2021
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  19. Oncogenic function of SCCRO5/DCUN1D5 requires its Neddylation E3 activity and nuclear localization.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014
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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

9 authors at 2 institutions in 1 country.

Martin C AbbaDepartment of Carcinogenesis, The University of Texas M. D. Anderson Cancer Center, Science Park-Research Division, Smithville, Texas 78957, USA.
Victoria T Fabris
Yuhui Hu
Frances S Kittrell
Wei-Wen Cai
Lawrence A Donehower
Aysegul Sahin
Daniel Medina
C Marcelo Aldaz
The University of Texas MD Anderson Cancer Center · USBaylor College of Medicine · US

Funding

Pilot Project ProgramP30ES007784 · NIEHS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI RICHIE, ELLEN R · 1996 to 2011
$16.4M
MOUSE MODELS OF HUMAN BREAST CANCERU01CA084243 · NCI · BAYLOR COLLEGE OF MEDICINE · PI ROSEN, JEFFREY MARK · 1999 to 2009
$7.3M
High resolution transcriptome analysis: lnn breast cancerU19CA084978 · NCI · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI ALDAZ, C. MARCELO · 2001 to 2004
$4.8M
NCI NIH HHS U01 CA084243NCI NIH HHS U01CA84243NCI NIH HHS U19 CA084978NCI NIH HHS U19 CA84978NIEHS NIH HHS ES07784NIEHS NIH HHS P30 ES007784
6 · The paper itself

Abstract

Serial analysis of gene expression from aggressive mammary tumors derived from transplantable p53 null mouse mammary outgrowth lines revealed significant up-regulation of Tfdp1 (transcription factor Dp1), Lamp1 (lysosomal membrane glycoprotein 1) and Gas6 (growth arrest specific 6) transcripts. All of these genes belong to the same linkage cluster, mapping to mouse chromosome band 8A1. BAC-array comparative genomic hybridization and fluorescence in situ hybridization analyses revealed genomic amplification at mouse region ch8A1.1. The minimal region of amplification contained genes Cul4a, Lamp1, Tfdp1, and Gas6, highly overexpressed in the p53 null mammary outgrowth lines at preneoplastic stages, and in all its derived tumors. The same amplification was also observed in spontaneous p53 null mammary tumors. Interestingly, this region is homologous to human chromosome 13q34, and some of the same genes were previously observed amplified in human carcinomas. Thus, we further investigated the occurrence and frequency of gene amplification affecting genes mapping to ch13q34 in human breast cancer. TFDP1 showed the highest frequency of amplification affecting 31% of 74 breast carcinomas analyzed. Statistically significant positive correlation was observed for the amplification of CUL4A, LAMP1, TFDP1, and GAS6 genes (P < 0.001). Meta-analysis of publicly available gene expression data sets showed a strong association between the high expression of TFDP1 and decreased overall survival (P = 0.00004), relapse-free survival (P = 0.0119), and metastasis-free interval (P = 0.0064). In conclusion, our findings suggest that CUL4A, LAMP1, TFDP1, and GAS6 are targets for overexpression and amplification in breast cancers. Therefore, overexpression of these genes and, in particular, TFDP1 might be of relevance in the development and/or progression in a significant subset of human breast carcinomas.

Indexed as

Gene AmplificationAnimalsBlotting, NorthernBreast NeoplasmsChromosome MappingChromosomes, Human, Pair 13DNA, NeoplasmGene ExpressionGene Expression ProfilingHumansIn Situ Hybridization, FluorescenceMammary Neoplasms, ExperimentalMiceMultigene FamilyNucleic Acid HybridizationReverse Transcriptase Polymerase Chain ReactionDNA, Neoplasm

Identifiers

PMID17483321
PMCPMC4166497
OpenAlexW2145730148

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.