By Melissa Weber, from the American Cancer Society

What if there was an easier, faster way to find out whether a breast tumor was malignant or benign? What if a weak spot was finally found in triple-negative breast cancer? What if we knew how breast cancer spreads to bone—and how to stop it?

With funding from the American Cancer Society, scientists are making medical discoveries that could one day turn these what-ifs into reality.

A New Tool to Diagnose Breast Cancer

Society-funded researchers are developing a new tool that can see inside breast tissue and distinguish a cancerous tumor from a harmless lump. Called a hand-held optical mammography device, the noninvasive imaging tool could help some women avoid unnecessary breast biopsies.

The optical mammography device doesn’t use X-rays or press on the breast, as does traditional mammography. Rather, the portable imager uses near-infrared light to create 3D images of breast tissue, and its flexible probe contours to the breast tissue.

But the device doesn’t replace mammography, says researcher Sarah Erickson, PhD, a postdoctoral fellow at Beckman Institute for Advanced Science and Technology at the University of Illinois at Urbana-Champaign. “Mammography is still the gold standard for screening,” she says.

Mammography and other imaging tests can spot a breast tumor, but the only way to know whether it is cancer is to remove a small piece of breast tissue during a biopsy. “Currently, about 80 percent of biopsies turn out to be benign (noncancerous). So that’s causing a patient unnecessary physical and psychological pain,” Erickson says.

Results from lab studies and early research in women with and without breast cancer are promising. Erickson and her co-investigators will soon begin testing the device in a larger group of breast cancer patients to see how many breast cancers the test can find without giving false-positive results.

Erickson says the imaging device could also be used to monitor a breast tumor’s response to chemotherapy. “If a patient’s cancer doesn’t respond and doctors can find that out early, they can change the treatment,” Erickson says.

Triple-Negative Breast Cancer Gene Discovered

Other scientists supported by the Society have pinpointed a new gene that, when found in high amounts, causes normal breast cells to start behaving like cancer. Named FAM83B, the gene specifically drives the growth of triple-negative breast cancers and may finally give researchers a drug target for these hard-to-treat tumors.

“When we eliminated FAM83B from breast cancer cells that had high levels of expression, the cancer cells stopped growing and the [cancer growth] pathway turned off,” says researcher Mark W. Jackson, PhD, assistant professor at Case Western Reserve University in Cleveland.

Jackson and his co-investigators plan to test thousands of chemical compounds that might inhibit the cancer-promoting function of FAM83B. He hopes to see an experimental FAM83B inhibitor in phase 1 clinical trials within a couple of years.

Triple-negative breast cancers account for about 15 percent of all breast cancers. Its name refers to the absence of three main proteins that fuel the growth of most breast cancers: estrogen receptor, progesterone receptor, and HER2 receptor. If researchers can develop a FAM83B-targeted drug that starves triple-negative breast cancers just like Herceptin shuts down the growth of HER2-driven tumors, FAM83B could possibly join their ranks, Jackson says.

“With every discovery of a gene that may play a role in getting cancer, every one of those are new opportunities,” Jackson says. “If we can develop targeted therapies toward new players we’re uncovering in the lab, that is the next generation of treatment options for triple-negative cancers.”

The Answer to How Breast Cancer Invades Bone

Researchers recently solved the mystery of how breast cancer takes root in the bone. Now, the discovery has led to an experimental drug for breast cancer that has spread to the bone.

At Princeton University, Society grantee Yibin Kang, PhD, found breast cancer cells use a protein called Jagged1 to upset the normal balance of bone builders and bone demolishers. Jagged1 recruits cells that normally break down bone to dig deeper into it. This in turn releases molecules that further spur cancer growth.

“We knew the bone is a fertile soil for breast cancer to spread to. But we didn’t know why. We didn’t know how to make bone less fertile soil,” says Kang, Princeton’s Warner-Lambert/Parke-Davis professor of molecular biology. “Now that we know, the next step is to design drugs to break that vicious cycle.”

Breast cancer spreads, or metastasizes, to the bone in 70 to 80 percent of patients with advanced breast cancer. These malignant cells invade the spine, ribs, pelvis and other bones, causing pain, fractures and other complications. Current treatments offer symptom control but little else, Kang says. “The hope is that with more options, more combined agents, we can effectively control bone metastasis and hopefully treat it as a chronic condition,” he says.

Kang and his lab team are now working with drug maker Amgen to test an experimental monoclonal antibody (a man-made protein) that blocks Jagged1 in mice.

Kang hopes his quest in the lab one day results in lives saved in the clinic. “What we try to do in the lab is to figure out what the enemy is capable of and how cancer achieves its goal of spreading and killing patients,” Kang says. “You have to know your enemy to defeat it.”