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New drug target for triple-negative breast cancer

New drug target for triple-negative breast cancer

A new study has identified a potential drug target for the most aggressive and difficult-to-treat type of breast cancer.

The study, published in the journal Nature Medicine, found that a protein called ROR1 is overexpressed in triple-negative breast cancer and that inhibiting ROR1 halted the growth of these cancer cells in laboratory experiments.

Triple-negative breast cancer is characterized by the absence of three common receptors that are present in other types of breast cancer. These receptors are estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2).

Without these receptors, triple-negative breast cancer cells are more difficult to treat because they are not susceptible to hormone therapy or drugs that target HER2.

The current standard of care for triple-negative breast cancer is chemotherapy, but this treatment is not very effective and often has severe side effects.

The new study provides hope that ROR1 could be a potential target for developing more effective treatments for triple-negative breast cancer.

In the study, the researchers showed that inhibiting ROR1 halted the growth of triple-negative breast cancer cells in laboratory experiments.

The researchers also found that ROR1 is overexpressed in a majority of triple-negative breast tumors.

This suggests that inhibiting ROR1 could be an effective treatment for triple-negative breast cancer.

The study’s findings need to be confirmed in clinical trials, but the new study provides hope that ROR1 could be a potential target for developing more effective treatments for triple-negative breast cancer.

A new study has found a potential target for drugs to treat triple-negative breast cancer, one of the most aggressive forms of the disease.

Triple-negative breast cancer (TNBC) is so named because it lacks the three receptors that are targeted by most breast cancer treatments: estrogen, progesterone, and the HER2 protein. TNBC represents around 20 percent of all breast cancer cases, and is particularly difficult to treat because it doesn’t respond to hormone therapy or drugs that target HER2.

The new study, published in the journal Nature, found that a protein called BAX is a key player in the development of TNBC. When BAX is present in high levels, it drives the growth of TNBC tumors.

“Our study provides the first direct evidence that BAX is a key driver of triple-negative breast cancer,” said study co-leader Rong Li, PhD, of the Johns Hopkins Kimmel Cancer Center. “This discovery opens up a new avenue for the development of much-needed treatments for this aggressive disease.”

The researchers used a technique called CRISPR-Cas9 to disable the BAX gene in TNBC cells. This stopped the cells from growing and also induced cell death.

“Our findings show that BAX is essential for the survival of TNBC cells, and that targeting BAX could be a promising approach for treating this aggressive cancer,” said study co-leader Luis Parada, MD, PhD, also of the Johns Hopkins Kimmel Cancer Center.

The researchers are now working on developing drugs that target BAX, in the hope that they will be able to provide a new treatment option for patients with TNBC.

“The fact that targeting BAX induces cell death in triple-negative breast cancer cells but not in healthy cells is a major advantage, as it reduces the likelihood of side effects,” said Li. “We are optimistic that BAX-targeted therapy will one day help patients with this difficult-to-treat disease.”

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