Evidence map›Paper›PMID 12096344›Full record

ArticleOncogene2002

The cyclin D1 high and cyclin E high subgroups of breast cancer: separate pathways in tumorogenesis based on pattern of genetic aberrations and inactivation of the pRb node.

Martin Lodén, Maria Stighall, Niels Hilmer Nielsen, Göran Roos, Stefan O Emdin, Hanna Ostlund, Göran Landberg

Abstract read
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In one paragraph

Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

40 citing papers in PubMed, 105 citations in OpenAlex.

  1. Multicenter Phase II Trial of the WEE1 Inhibitor Adavosertib in Refractory Solid Tumors HarboringJournal of clinical oncology : official journal of the American Society of Clinical Oncology · 2023
    Trial
  2. Organic extract ofOncology letters · 2022
    Article
  3. Review
  4. Article
  5. Article
  6. Cytoplasmic Cyclin E Predicts Recurrence in Patients with Breast Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
    Article
  7. Article
  8. Article
  9. Article
  10. Synergistic effects of AKAP95, Cyclin D1, Cyclin E1, and Cx43 in the development of rectal cancer.International journal of clinical and experimental pathology · 2015
    Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
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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.

Martin LodénDepartment of Pathology, Umeå University, S-901 87 Umeå, Sweden.
Maria Stighall
Niels Hilmer Nielsen
Göran Roos
Stefan O Emdin
Hanna Ostlund
Göran Landberg
Umeå University · SEMalmö University · SELund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In an attempt to identify subtypes of breast cancer and pinpoint patterns of cell cycle regulatory defects associated with clinical behaviour, proliferation and other transformation associated events, a multitude of cell cycle regulatory proteins were analysed in a material of 113 primary breast cancers. Increased proliferation was observed in two different scenarios; (1) with high cyclin D1 and elevated retinoblastoma protein (pRb) phosphorylation, (cyclin D1(high) tumours) or (2) with high cyclin E protein but low cyclin D1 and lack of corresponding pRb phosphorylation (cyclin E(high) tumours) indicative of an interrupted pRb pathway. Characteristic for cyclin E(high) tumours were further defects in p53, p27 and bcl-2, while c-erbB2 overexpression and c-myc amplification was found in both cyclin D1(high) and E(high) tumours. Using transfected cell lines overexpressing cyclin E, cyclin E(high) and D1(high) tumours were mimicked and the cyclin D1(high) cell line normalized the cyclin E kinase activity by an induction and redirection of p21 and p27 to the cyclin E complex whereas cyclin E(high) cell lines obtained increased kinase activity without redirection of inhibitors. Based on differences in genetic aberrations as well as function of the pRb node we therefore propose a model in which cyclin D1(high) and cyclin E(high) tumours represent two alternative mechanisms to inactivate the pRb pathway and thereby achieve unrestrained growth in the tumorogenesis of breast cancer.

Indexed as

Blotting, WesternBreast NeoplasmsCell DivisionCyclin D1Cyclin-Dependent KinasesCyclin EFollow-Up StudiesHumansIn Situ Hybridization, FluorescenceModels, BiologicalReceptors, EstrogenRetinoblastoma ProteinSignal TransductionSurvival RateTumor Cells, CulturedCyclin D1Cyclin-Dependent KinasesCyclin EReceptors, EstrogenRetinoblastoma Protein

Identifiers

PMID12096344
OpenAlexW2083035492

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.