Identifying Chemotherapy Resistance Factors in Breast Cancer Patients

Chemotherapy is a key component of the standard treatment regimen for triple-negative breast cancer patients whose cancer lacks estrogen and progesterone receptors and the human epidermal growth factor receptor 2 or HER2. While many patients respond positively to chemotherapy, a significant number of those treated are resistant to chemotherapy or will develop recurrent tumors which are resistant to chemo.

The Study:

A research team led by Mercedes Rincon at the University of Vermont recently identified low expressions of methylation-controlled J protein (MCJ) as a marker of poor response to chemotherapy, the results were published in the current edition of JCI Insight.

The study was focused on 62 breast cancer patients, they demonstrated that MCJ expression relates with pathological and clinical responses to neoadjuvant chemotherapy. Furthermore, by reviewing a large clinical data group from breast cancer repositories, the team found that breast cancer patients with low-MCJ expressing tumors had a reduction in relapse-free survival.

Lastly, the team examined a mouse model with a mammary tumor and it showed that mice who were deficient in MCJ had bigger tumors and acquired increased resistance to chemotherapy. This study suggests that MCJ may be useful as a marker of chemotherapy response and it may be a potential therapeutic target for breast cancer treatments.

What is Chemotherapy Resistance?

A resistance to chemotherapy happens when cancer that’s been responding to a therapy suddenly starts to grow. When cancer becomes resistant to chemotherapy, it may be time for a person’s doctor to change the drugs being used. There are many reasons why chemotherapy can fail:

•Some of the cancer cells aren’t being killed by chemotherapy and mutate, becoming resistant to the drug. Once these cells multiply, there may be more resistant cells than cells that are sensitive to chemotherapy.
•Gene amplification. A cancer cell may produce hundreds of copies of a particular gene. This gene will trigger an overproduction of protein that makes the anticancer medication ineffective.
•Cancer cells could pump the drug out of the cell as quickly as it is going in using a molecule called p-glycoprotein.
•The cancer cells could learn how to repair the DNA breaks caused by some cancer drugs.
•Cancer cells may stop absorbing the drug because the protein that transports the drug across the cellular wall quits working.
•Cancer cells might develop a mechanism that inactivates the drug.

Closing:

More research is needed in order to find out how to more easily identify chemotherapy resistant factors, because it can lead to improved treatment and ultimately increased survival rates in cancer patients.

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