Gene Products of Chromosome 11q and Tamoxifen Resistance in Breast Cancer
Author Information
Author(s): Katja Lundgren, Karolina Holm, Bo Nordenskjöld, Åke Borg, Göran Landberg
Primary Institution: Lund University
Hypothesis
The study investigates the association between gene amplification at chromosome 11q and tamoxifen resistance in premenopausal breast cancer patients.
Conclusion
The study found that while many gene products associated with 11q13 amplification are over-expressed, they are not linked to an agonistic effect of tamoxifen, and deletion of distal 11q may impair tamoxifen response.
Supporting Evidence
- Cortactin and FADD over-expression was linked to CCND1 amplification but not to a diminished effect of tamoxifen.
- Deletion of distal chromosome 11q was associated with an impaired tamoxifen response.
- The study analyzed 500 primary breast cancer samples to assess gene expression and treatment response.
Takeaway
Some genes on chromosome 11 can make breast cancer harder to treat with tamoxifen, a common medicine for this disease.
Methodology
Array comparative genomic hybridization analysis was used to identify gene expression changes in breast cancer samples, and protein expression was examined in a clinical material of 500 primary breast cancers.
Potential Biases
Potential bias due to the retrospective nature of the study and the reliance on previously collected data.
Limitations
The study had a limited number of tumor samples analyzed for both CGH and IHC, which reduced statistical power.
Participant Demographics
The study involved premenopausal breast cancer patients with invasive stage II disease.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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