Evidence map›Paper›PMID 19043454›Full record

ArticleOncogene2009

In vitro and in vivo analysis of B-Myb in basal-like breast cancer.

A R Thorner, K A Hoadley, J S Parker, S Winkel, R C Millikan, C M Perou

Abstract 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 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

69 citing papers in PubMed, 99 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Emerging role of MYB transcription factors in cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2024
    Review
  9. Article
  10. Frontiers in genetics · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

9 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 1 country.

A R ThornerCurriculum in Genetics and Molecular Biology, University of North Carolina, Chapel Hill, NC 27599, USA.
K A Hoadley
J S Parker
S Winkel
R C Millikan
C M Perou
UNC Lineberger Comprehensive Cancer CenterUniversity of North Carolina at Chapel Hill · US

Funding

Tissue Procurement & PathologyP50CA058223 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI KATHERINE A. HOADLEY · 1992 to 2026
$59.3M
Molecular Characterization of Breast Basal-like TumorsR01CA101227 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PEROU, CHARLES M · 2003 to 2007
$2.0M
NCI NIH HHS P50 CA058223NCI NIH HHS P50-CA58223-09A1NCI NIH HHS R01 CA101227NCI NIH HHS R01-CA-101227-01
6 · The paper itself

Abstract

A defining feature of basal-like breast cancer, a breast cancer subtype with poor clinical prognosis, is the high expression of 'proliferation signature' genes. We identified B-Myb, a MYB family transcription factor that is often amplified and overexpressed in many tumor types, as being highly expressed in the proliferation signature. However, the roles of B-Myb in disease progression, and its mammary-specific transcriptional targets, are poorly understood. Here, we showed that B-Myb expression is a significant predictor of survival and pathological complete response to neoadjuvant chemotherapy in breast cancer patients. We also identified a significant association between the G/G genotype of a nonsynonymous B-Myb germline variant (rs2070235, S427G) and an increased risk of basal-like breast cancer [OR 2.0, 95% CI (1.1-3.8)]. In immortalized, human mammary epithelial cell lines, but not in basal-like tumor lines, cells ectopically expressing wild-type B-Myb or the S427G variant showed increased sensitivity to two DNA topoisomerase IIalpha inhibitors, but not to other chemotherapeutics. In addition, microarray analyses identified many G2/M genes as being induced in B-Myb overexpressing cells. These results confirm that B-Myb is involved in cell cycle control, and that its dysregulation may contribute to increased sensitivity to a specific class of chemotherapeutic agents. These data provide insight into the influence of B-Myb in human breast cancer, which is of potential clinical importance for determining disease risk and for guiding treatment.

Indexed as

Antigens, NeoplasmAntineoplastic AgentsBasal Cell CarcinomaBreast NeoplasmsCell Cycle ProteinsDNA-Binding ProteinsDNA Topoisomerases, Type IIDrug Resistance, NeoplasmEnzyme InhibitorsGene Expression ProfilingGene Expression Regulation, NeoplasticGenetic Predisposition to DiseaseGerm-Line MutationHumansOligonucleotide Array Sequence AnalysisPolymorphism, Single NucleotideAntigens, NeoplasmAntineoplastic AgentsCell Cycle ProteinsDNA-Binding ProteinsDNA Topoisomerases, Type IIEnzyme InhibitorsMYBL2 protein, humanTopoisomerase II InhibitorsTrans-Activators

Identifiers

PMID19043454
PMCPMC2636852
OpenAlexW2068182875

What OpenQuestion holds

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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.