Evidence map›Paper›PMID 15897883›Full record

ArticleOncogene2005

Gene expression profiling of cancer progression reveals intrinsic regulation of transforming growth factor-beta signaling in ErbB2/Neu-induced tumors from transgenic mice.

Melissa D Landis, Darcie D Seachrist, Marjorie E Montañez-Wiscovich, David Danielpour, Ruth A Keri

Open access · greenAbstract readComparative Study
In one paragraph

Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

27 citing papers in PubMed, 59 citations in OpenAlex.

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  9. Tumor protein D52 (TPD52) and cancer-oncogene understudy or understudied oncogene?Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Review
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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

5 authors at 2 institutions in 1 country.

Melissa D LandisDepartment of Pharmacology, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA.
Darcie D Seachrist
Marjorie E Montañez-Wiscovich
David Danielpour
Ruth A Keri
Case Western Reserve University · USUniversity School · US

Funding

TUMOR METABOLISM PROGRAMP30CA043703 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI MARK R CHANCE · 1987 to 2026
$142.3M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007250 · NIGMS · CASE WESTERN RESERVE UNIVERSITY · PI HUANG, ALEX YEE-CHEN · 1985 to 2023
$33.4M
PREDOCTORAL TRAINING PROGRAM IN MOLECULAR THERAPEUTICST32GM008803 · NIGMS · CASE WESTERN RESERVE UNIVERSITY · PI MIEYAL, JOHN J, NIEMAN, MARVIN THOMAS · 2001 to 2023
$4.2M
Regulation of erbB2/Neu-induced mammary gland cancerR01CA090398 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI KERI, RUTH A. · 2001 to 2011
$2.7M
NCI NIH HHS P30 CA043703NCI NIH HHS P30CA43703NCI NIH HHS R01 CA090398NCI NIH HHS R01-CA90398NIGMS NIH HHS GM08803A1NIGMS NIH HHS T32 GM007250NIGMS NIH HHS T32 GM008803
6 · The paper itself

Abstract

Upregulation of HER2/ErbB2/Neu occurs in 15-30% of human breast cancers and correlates with poor prognosis. Identification of ErbB2/Neu transcriptional targets should facilitate development of novel therapeutic approaches. Development of breast cancer is a multistep process; thus, to identify the transcriptomes associated with different stages of progression of tumorigenesis, we compared expression profiles of mammary tumors and preneoplastic mammary tissue from MMTV-Neu transgenic mice to expression profiles of wild-type mammary glands using Affymetrix microarrays. We identified 324 candidate genes that were unique to ErbB2/Neu-induced tumors relative to normal mammary gland tissue from wild-type controls. Expression of a subset of these genes (82) was also changed in the preneoplastic mammary glands compared to wild-type controls, indicating that they may play a pivotal role during early events of ErbB2/Neu-initiated mammary tumorigenesis. Further analysis of the microarray data revealed that expression of several known transforming growth factor (TGF)-beta target genes was altered, suggesting that the TGF-beta signaling cascade is downregulated in ErbB2/Neu-induced tumors. Western blot analysis for TGF-beta-Receptor-I/ALK5 and immunohistochemistry for TGF-beta-Receptor-I/ALK5 and phosphorylated/activated Smad2 confirmed that the Smad-dependent TGF-beta signaling cascade was inactive in these tumors. Although absent in most of the tumor, phosphorylated Smad2 was present in the periphery of tumors. Interestingly, presence of phosphorylated/activated Smad2 correlated with expression of Activin-Receptor-IB/ALK4, suggesting that although Smad-dependent TGF-beta signaling is absent in ErbB2/Neu-induced tumors, Activin signaling may be active at the leading edge of these tumors. Cumulatively, these data indicate that the TGF-beta pathway is intrinsically suppressed in ErbB2/Neu tumors via a mechanism involving loss of TGF-beta-Receptor-I/ALK5.

Indexed as

Gene Expression ProfilingActivin ReceptorsAnimalsCell Transformation, NeoplasticDisease ProgressionDNA-Binding ProteinsErb-b2 Receptor Tyrosine KinasesFemaleGene Expression Regulation, NeoplasticMammary Neoplasms, AnimalMiceMice, TransgenicOligonucleotide Array Sequence AnalysisPrecancerous ConditionsSignal TransductionSmad2 ProteinActivin ReceptorsDNA-Binding ProteinsErb-b2 Receptor Tyrosine KinasesSmad2 ProteinSmad2 protein, mouseTrans-ActivatorsTransforming Growth Factor beta

Identifiers

PMID15897883
PMCPMC1431507
OpenAlexW2101249719

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.