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In Vitro Evaluation of Oncogenic Transformation in Human Mammary Epithelial Cells
Published on: September 24, 2020
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c-MYC is a radiosensitive locus in human breast cells
M A Wade1, N J Sunter1, S E Fordham1
1Northern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne, UK.
Oncogene
|December 23, 2014
Summary
Ionizing radiation increases breast cancer risk, especially in young women. This study identifies c-MYC gene amplification as a key molecular driver in radiation-induced breast cancer development.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Ionizing radiation is a known human carcinogen.
- Young women exposed to radiation face a higher risk of breast cancer.
- The molecular mechanisms of radiation-induced breast cancer are not fully understood.
Purpose of the Study:
- To identify genetic alterations driving radiation-induced breast cancer.
- To investigate the role of c-MYC in radiogenic breast carcinogenesis.
Main Methods:
- Exposed human breast epithelial cells (MCF-10A) to fractionated X-ray doses.
- Analyzed copy number and cytogenetic alterations.
- Examined c-MYC amplification and protein expression in cell lines and primary tissues.
Main Results:
- Identified high-level c-MYC amplification and increased protein expression following radiation exposure.
- Observed c-MYC amplification in primary human mammary epithelial cells post-radiation.
- Found significantly higher c-MYC amplification and expression in radiation-associated breast cancers.
Conclusions:
- c-MYC is a radiosensitive locus and a key factor in radiation-induced breast cancer.
- The findings implicate c-MYC in the etiology of radiogenic breast cancer.
- Intratumor heterogeneity in c-MYC copy number suggests ongoing genetic evolution.
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