New evidence supports earlier findings that cancer therapy drugs based on a family of enzymes called metalloproteinases (MMPs) failed in clinical trials because they were aimed at the wrong target.

Failure of Highly Touted MMP Cancer Therapies May Be Explained

Berkeley Lab researchers have identified the FAM83A protein as a possible new oncogene and linked it to therapy resistance in breast cancer. This discovery helps explain the clinical correlation between a high expression of FAM83A and a poor prognosis for breast cancer patients, and may also provide a new target for future therapies.

A big step towards understanding the cellular basis for why women over the age of 50 are much more vulnerable to breast cancer has been taken by Berkeley Lab researchers. They determined that aging causes an increase in a type of adult stem cell believed to be at the root of many breast cancers, and a decrease in cells believed to serve as tumor suppressors.

A Berkeley Lab-University of Copenhagen collaboration found that luminal-like breast cancer cells with no detectable stem cell qualities can generate larger tumors than their basal-like counterparts. This contradicts prevailing beliefs and could impact future breast cancer diagnosis and treatment.

Berkeley Lab researchers have discovered a rotational motion that plays a critical role in the ability of breast cells to form the spherical structures in the mammary gland known as acini. This rotation, called “CAMo,” for coherent angular motion, is necessary for the cells to form spheres. Otherwise, cells undergo random motion, leading to loss of structure and malignancy.

Working with a special line of human breast cells, Berkeley Lab researchers have shown that for low dose levels of ionizing radiation, cancer risks may not be directly proportional to dose. This contradicts the standard model for predicting biological damage from ionizing radiation, which holds that risk is directly proportional to dose at all levels of irradiation.

Berkeley Lab researchers have shown that normal breast cells help defend against cancer by producing the protein interleukin 25 to actively and specifically kill breast cancer cells. This important new finding points the way to a new therapeutic target for breast cancer treatment.

A Berkeley Lab study has shown how communities of different types of breast cells self-organize into breast tissue. This helps explain how the processes of stem cell differentiation and tissue architecture maintenance are coordinated, and might lead to a better understanding of what goes wrong in cancer.

Berkeley Lab researchers led by cancer authority Mina Bissell have shown how the protein laminin, long thought to provide only structural support in the microenvironment of breast and other epithelial tissue, can play a leading role in the development of cancer.