Breast cancer is the second leading cause of cancer death in women around the world, after lung cancer.

By JNS

A newly developed antibody-based treatment for the most aggressive type of breast cancer could also be used to treat many other cancers, the Weizmann Institute of Science announced on Sunday.

The researchers at the university in the central Israeli city of Rehovot, which offers postgraduate-only degrees in the natural and exact sciences, discovered that aggressive breast cancer prompts nearby immune cells to build “molecular bridges” between themselves, which causes these cells to refrain from attacking the cancer and leads to suppression of the immune response.

An antibody treatment that blocks the building of these bridges was shown in a mouse model at the university’s laboratories to restore the immune system’s ability to attack with force, inhibiting the cancer’s progression, the university said.

In the past, cancer treatment focused on destroying the malignant cells, using radiation treatment or chemotherapy.

In recent decades, however, it has become evident that a tumor’s development depends on the communication between the cancer and the nearby noncancerous cells.

Triple-negative breast cancer (TNBC), which the study focused on, is the most aggressive type of breast cancer and represents up to 20% of all new cases, the university said.

A significant proportion of these cancers occurs in patients with mutations in two genes, which are especially common among Ashkenazi Jews.

The City of Hope cancer treatment and research center in Duarte, Calif., in Los Angeles County, is working with the Weizmann Institute to develop therapies based on the antibody, the university said.

Breast cancer is the second leading cause of cancer death in women around the world, after lung cancer. While steadily on the decline over the last several decades, the chances are that one in 39 women, or 2.5%, will succumb to the disease.

TNBC accounts for 15% to 20% of breast cancer cases. They lack or show low levels of estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2) overexpression and/or gene amplification.

The study is being published in the peer-reviewed scientific journal Cell Reports.

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