Elevated Activity of MYC and E2F in Basal Breast Cancer Subgroup
Author Information
Author(s): Alles M. Chehani, Gardiner-Garden Margaret, Nott David J., Wang Yixin, Foekens John A., Sutherland Robert L., Musgrove Elizabeth A., Ormandy Christopher J.
Primary Institution: Garvan Institute of Medical Research, Sydney, Australia
Hypothesis
The study investigates the pathways that allow estrogen receptor-negative (ER−) breast cancers to proliferate and their potential therapeutic targets.
Conclusion
The study found that increased transcriptional activity of MYC is a characteristic of basal breast cancers, suggesting a mechanism for estrogen-independence and a potential therapeutic target.
Supporting Evidence
- ER− tumors show higher expression of proliferation genes than ER+ tumors of the same grade.
- MYC and E2F activity are significantly enriched in ER− tumors.
- Direct transcriptional targets of ER are significantly depleted in ER− tumors.
Takeaway
Some breast cancers don't have a hormone receptor that helps them grow, but they can still grow fast because of other factors like MYC. This study looks at how these cancers work and what we can do to treat them.
Methodology
The study conducted a meta-analysis of gene expression from five large microarray datasets relative to ER status and used Gene Set Enrichment Analysis (GSEA) to identify pathways associated with ER− tumors.
Potential Biases
The meta-analysis approach minimizes individual study biases but may still be influenced by the datasets used.
Limitations
The study is limited to Grade 3 tumors and may not generalize to other grades.
Participant Demographics
The study included 82 ER− and 101 ER+ patients, all Grade 3 tumors.
Statistical Information
P-Value
p<0.01
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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