Evidence map›Paper›PMID 11884607›Full record

ArticleMolecular and cellular biology2002

ErbB2/Neu-induced, cyclin D1-dependent transformation is accelerated in p27-haploinsufficient mammary epithelial cells but impaired in p27-null cells.

Rebecca S Muraoka, Anne E G Lenferink, Brian Law, Elizabeth Hamilton, Dana M Brantley, L Renee Roebuck, Carlos L Arteaga

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

51 citing papers in PubMed, 118 citations in OpenAlex.

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  20. Hunk is required for HER2/neu-induced mammary tumorigenesis.The Journal of clinical investigation · 2011
    Article
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 1 institution in 1 country.

Rebecca S MuraokaDepartment of Cancer Biology, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.
Anne E G Lenferink
Brian Law
Elizabeth Hamilton
Dana M Brantley
L Renee Roebuck
Carlos L Arteaga
Vanderbilt University · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
MULTIDISCIPLINARY BASIC RESEARCH TRAINING IN CANCERT32CA009592 · NCI · VANDERBILT UNIVERSITY · PI Justin M Balko, Julie A Rhoades (Sterling) · 1987 to 2026
$10.4M
ERBB2 TARGETED ANTITUMOR STRATEGIES IN BREAST CANCERR01CA080195 · NCI · VANDERBILT UNIVERSITY · PI ARTEAGA, CARLOS L · 1999 to 2014
$3.9M
NCI NIH HHS CA68485NCI NIH HHS P30 CA068485NCI NIH HHS R01 CA080195NCI NIH HHS R01 CA80195NCI NIH HHS T32 CA009592NCI NIH HHS T32 CA09592
6 · The paper itself

Abstract

ErbB2/Neu destabilizes the cyclin-dependent kinase (Cdk) inhibitor p27 and increases expression of cyclin D1. Therefore, we studied the roles of p27 and cyclin D1 in ErbB2-mediated mammary epithelial cell transformation. Overexpression of ErbB2 or cyclin D1 in p27(+/-) primary murine mammary epithelial cells resulted in increased proliferation, cyclin D1 nuclear localization, and colony formation in soft agar compared to those in p27(+/+) cells. In contrast, ErbB2- or cyclin D1-overexpressing p27(-/-) cells displayed reduced proliferation, anchorage-independent growth, Cdk4 activity, cyclin D1 expression, and cyclin D1 nuclear localization compared to wild-type cells. A cyclin D1 mutation in its nuclear export sequence (T286A) partially rescued nuclear localization of cyclin D1 in p27(-/-) cells but did not increase proliferation or Cdk4 kinase activity. Overexpression of E2F1, however, increased proliferation to the same degree in p27(+/+), p27(+/-), and p27(-/-) cells. Mammary glands from MMTV (mouse mammary tumor virus)-neu/p27(+/-) mice exhibited alveolar hyperplasia, enhanced proliferation, decreased apoptosis, and accelerated tumor formation compared to MMTV-neu/p27(+/+) glands. However, MMTV-neu/p27(-/-) glands showed decreased proliferation, cyclin D1 expression, and Cdk4 activity, as well as markedly prolonged tumor latency, compared to MMTV-neu/p27(+/+) glands. These results suggest that p27(+/-) mammary epithelium may be more susceptible to oncogene-induced tumorigenesis, whereas p27-null glands, due to severely impaired cyclin D1/Cdk4 function, are more resistant to transformation.

Indexed as

Gene DeletionProto-Oncogene ProteinsActive Transport, Cell NucleusAmino Acid SequenceAnimalsApoptosisBase SequenceCell Cycle ProteinsCell DivisionCell NucleusCell Transformation, NeoplasticCyclin D1Cyclin-Dependent Kinase 4Cyclin-Dependent Kinase Inhibitor p27Cyclin-Dependent KinasesErb-b2 Receptor Tyrosine KinasesCdk4 protein, mouseCdkn1b protein, mouseCell Cycle ProteinsCyclin D1Cyclin-Dependent Kinase 4Cyclin-Dependent Kinase Inhibitor p27Cyclin-Dependent KinasesErb-b2 Receptor Tyrosine KinasesProto-Oncogene ProteinsRNA, MessengerTumor Suppressor Proteins

Identifiers

PMID11884607
PMCPMC133673
OpenAlexW2121038486

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.