Evidence map›Paper›PMID 22037875›Full record

ArticleCancer research2011

Cyclin D3 compensates for the loss of cyclin D1 during ErbB2-induced mammary tumor initiation and progression.

Qian Zhang, Kazuhito Sakamoto, Chengbao Liu, Aleata A Triplett, Wan-chi Lin, Hallgeir Rui, Kay-Uwe Wagner

Abstract read
In one paragraph

Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 25% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Clear cell renal carcinoma essentially requires CDKL3 for oncogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  9. The Essential Role of Rac1 Glucosylation inFrontiers in microbiology · 2022
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  15. Regulation and New Treatment Strategies in Breast Cancer.Journal of life sciences (Westlake Village, Calif.) · 2019
    Article
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  18. 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

7 authors at 3 institutions in 1 country.

Qian ZhangEppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, Nebraska 68198, USA.
Kazuhito Sakamoto
Chengbao Liu
Aleata A Triplett
Wan-chi Lin
Hallgeir Rui
Kay-Uwe Wagner
Thomas Jefferson University · USSidney Kimmel Cancer Center · USUniversity of Nebraska Medical Center · US

Funding

Growth-Regulatory Signaling Networks in Breast CancerR01CA117930 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI WAGNER, KAY-UWE · 2006 to 2016
$2.5M
Experimental Modeling of Human Breast Cancer in MiceR01CA118740 · NCI · THOMAS JEFFERSON UNIVERSITY · PI RUI, HALLGEIR · 2008 to 2012
$1.8M
NCI NIH HHS CA117930NCI NIH HHS CA118740NCI NIH HHS R01 CA117930NCI NIH HHS R01 CA118740
6 · The paper itself

Abstract

Cyclin D1 regulates cell proliferation and is a candidate molecular target for breast cancer therapy. This study addresses whether Cyclin D1 is indispensable for ErbB2-associated mammary tumor initiation and progression using a breast cancer model in which this cell-cycle regulator can be genetically ablated prior to or after neoplastic transformation. Deficiency in Cyclin D1 delayed tumor onset but did not prevent the occurrence of mammary cancer in mice overexpressing wild-type ErbB2. The lack of Cyclin D1 was associated with a compensatory upregulation of Cyclin D3, which explains why the targeted downregulation of Cyclin D1 in established mammary tumors had no effect on cancer cell proliferation. Cyclin D1 and D3 are overexpressed in human breast cancer cell lines and primary invasive breast cancers, and Cyclin D3 frequently exceeded the expression of Cyclin D1 in ErbB2-positive cases. The simultaneous inhibition of both cyclins in mammary tumor cells reduced cancer cell proliferation in vitro and decreased the tumor burden in vivo. Collectively, the results of this study suggest that only the combined inhibition of Cyclin D1 and D3 might be a suitable strategy for breast cancer prevention and therapy.

Indexed as

AnimalsBlotting, WesternBreast NeoplasmsCell Line, TumorCell ProliferationCells, CulturedCyclin D1Cyclin D3Disease ProgressionErb-b2 Receptor Tyrosine KinasesFemaleHumansImmunohistochemistryMammary Neoplasms, AnimalMiceMice, KnockoutCyclin D1Cyclin D3Erb-b2 Receptor Tyrosine Kinases

Identifiers

PMID22037875
PMCPMC3242818
OpenAlexW2144681982

What OpenQuestion holds

Textmetadata
LicenceTDM
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.