Evidence map›Paper›PMID 19330026›Full record

ArticleOncogene2009

Co-amplified genes at 8p12 and 11q13 in breast tumors cooperate with two major pathways in oncogenesis.

S S Kwek, R Roy, H Zhou, J Climent, J A Martinez-Climent, J Fridlyand, D G Albertson

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
7.5field-weighted citation impact, top 3% 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

59 citing papers in PubMed, 109 citations in OpenAlex.

  1. Trial
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  3. Phase separation of DDHD2 remodels lipid metabolism to dictate treatment sensitivity in luminal breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  15. Comprehensive Profiling of Poor-Risk Paired Primary and Recurrent Triple-Negative Breast Cancers Reveals Immune Phenotype Shifts.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020
    Article
  16. Article
  17. Reports of biochemistry & molecular biology · 2019
    Article
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  19. Article
  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

7 authors at 4 institutions in 2 countries.

S S KwekCancer Research Institute, University of California San Francisco, San Francisco, CA 94143-0808, USA.
R Roy
H Zhou
J Climent
J A Martinez-Climent
J Fridlyand
D G Albertson
UCSF Helen Diller Family Comprehensive Cancer Center · USUniversity of California, San Francisco · USCancer Research Institute · USUniversidad de Navarra · ES

Funding

Genomic Analysis of ER Negative Breast CancerR01CA101359 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ALBERTSON, DONNA G. · 2003 to 2007
$1.9M
High Resolution Genomic Analysis of Amplicon StructureR01CA090421 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ALBERTSON, DONNA G. · 2003 to 2007
$1.0M
NCI NIH HHS CA101359NCI NIH HHS CA90421NCI NIH HHS R01 CA090421NCI NIH HHS R01 CA101359
6 · The paper itself

Abstract

Co-amplification at chromosomes 8p11-8p12 and 11q12-11q14 occurs often in breast tumors, suggesting possible cooperation between genes in these regions in oncogenesis. We used high-resolution array comparative genomic hybridization (array CGH) to map the minimal amplified regions. The 8p and 11q amplicons are complex and consist of at least four amplicon cores at each site. Candidate oncogenes mapping to these regions were identified by combining copy number and RNA and protein expression analyses. These studies also suggested that CCND1 at 11q13 induced expression of ZNF703 mapping at 8p12, which was subsequently shown to be mediated by the Rb/E2F pathway. Nine candidate oncogenes from 8p12 and four from 11q13 were further evaluated for oncogenic function. None of the genes individually promoted colony formation in soft agar or collaborated with each other functionally. On the other hand, FGFR1 and DDHD2 at 8p12 cooperated functionally with MYC, whereas CCND1 and ZNF703 cooperated with a dominant negative form of TP53. These observations highlight the complexity and functional consequences of the genomic rearrangements that occur in these breast cancer amplicons, including transcriptional cross-talk between genes in the 8p and 11q amplicons, as well as their cooperation with major pathways of tumorigenesis.

Indexed as

Gene AmplificationBreast NeoplasmsCarrier ProteinsCell Line, TumorChromosomes, Human, Pair 11Chromosomes, Human, Pair 8Comparative Genomic HybridizationCyclin D1Epistasis, GeneticFemaleGene DosageGene Expression Regulation, NeoplasticGenetic Predisposition to DiseaseHumansNeoplastic Stem CellsOncogene Protein p55(v-myc)Carrier ProteinsCCND1 protein, humanCyclin D1DDHD2 protein, humanFGFR1 protein, humanOncogene Protein p55(v-myc)PhospholipasesReceptor, Fibroblast Growth Factor, Type 1RNA, Small InterferingTP53 protein, humanTumor Suppressor Protein p53ZNF703 protein, human

Identifiers

PMID19330026
PMCPMC2722962
OpenAlexW1985160458

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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 OpenQuestion graph.