Recent findings by Penn researchers pave a way to target drug treatments for an aggressive form of breast cancer.
In their study published in the Biochima and Biophysical Acta journal, researchers at Penn's School of Veterinary Medicine along with collaborators from the Children's Hospital of Philadelphia, University of Pittsburgh, Kagoshima University in Japan, and the Columbia University Medical Center discovered a mitochondria defect in triple-negative breast cancer that could lead to the first ever targeted treatment for the cancer.
TNBC is a subtype of breast cancer in which the cells lack receptors for estrogen, progesterone, and Her2, traditional drug targets for breast cancer therapies.
The researchers performed the study using tissue samples from patients with different breast cancer subtypes, and also analyzed previously collected genomic data representing 825 breast cancer patients. They found that patients at the most advanced stages of TNBC were more likely to have the lowest copy numbers of mitochondrial DNA.
According to Penn News, this breakthrough could prevent metastasis, or the spread of cancer throughout the body, in TBNC patients. First author and assistant professor of Penn Vet, Manti Guha, and her colleagues have focused on mitochondrial dysfunction in their research and have previously linked it to breast cancer metastasis.
“This particular mtDNA sequence imbalance is fairly unique, and has not been reported in cancers,” Guha said to Penn News. “This could potentially be used to stratify patients into different risk categories.”
Next, the researchers are looking into whether existing breast cancer drug therapies may effectively target TBNC using the characteristics they just discovered.
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