Not all cancer cells are created equal. In fact, to call a cancer a cancer, in the singular, is something of a misnomer. Really, a patient could be said to have cancers, as every tumor is actually a mixture of cells with different mutations and capabilities.
One of those capabilities is the ability to escape the main tumor and spread, or metastasize, to other sites in the body. Not every cancer cell has this ability. But just like bacteria can share the ability to resist antibiotics, at least some cancer cells may be able to share the ability to spread.
According to a study by Judy Lieberman, MD, PhD, of Boston Children’s Hospital’s Program in Cellular and Molecular Medicine, breast cancer cells that can metastasize can tell those that can’t to turn that ability on. That conversation takes place via small pieces of RNA called microRNAs, delivered in microscopic packages called extracellular vesicles.
According to Lieberman, not only do her team’s data give insight into the metastatic process, they might also reveal the first example of cancer cells teaching each other. …
You are what you eat, the saying goes. For some conditions (think cardiovascular disease or type 2 diabetes), there are clear connections between diet, health and illness.
For breast cancer, the picture is less clear. Many epidemiologic and laboratory studies have examined the Western diet (in particular, cholesterol) and its relation to breast cancer, with conflicting results.
“There’s been a raging debate in the field,” says Christine Coticchia, PhD, who works in the laboratory of Boston Children’s Hospital’s Vascular Biology Program director, Marsha Moses, PhD. “The biology of cancer and of cholesterol are so complex, and there are many subsets of breast cancer. In order to find any connections, you have to ask very specific questions.”
Banding together with Keith Solomon, PhD, in Boston Children’s Urology Department, Coticchia and Moses asked whether dietary cholesterol might encourage progression of the most aggressive, so-called “triple-negative” breast tumors. As they report in the American Journal of Pathology, they found a big impact, at least in mice. But it’s too early to say just yet that cutting back on cholesterol will help women avoid breast cancer. …
When the drug Velcade® came on the market in 2003, it was seen as a godsend for patients with multiple myeloma, an intractable blood cancer that until then was uniformly fatal. Velcade was the first in a novel family of drugs called proteasome blockers, which make it hard for cancer cells to break down and recycle used, misfolded or excess proteins.
In the last decade, Velcade has been tested against a long list of other cancers, including melanomas, lymphomas, as well as prostate, lung and breast cancers. The results have been mixed, particularly for breast cancer.
But in the case of breast cancer, the uncertain outcomes may in part be because past trials looked in the wrong place. New research by Fabio Petrocca, MD, and Judy Lieberman, MD, PhD, in Boston Children’s Hospital’s Program in Cellular and Molecular Medicine, suggests that proteasome blockers like Velcade may indeed have a place in the breast oncologist’s armamentarium, but just for a particular aggressive kind of breast cancer called basal-like, triple-negative breast cancer (TNBC). …
Breast cancers whose cells carry the HER2 protein are pretty tough customers. They only account for about 20 percent of all breast cancers, but they are some of the most aggressive. While targeted drugs like trastuzumab (Herceptin) and lapatinib (Tykerb) have made these tumors easier to treat, those that resist these drugs, relapse or don’t have HER2 on their cells’ surfaces can still stymie oncologists.
A molecular phenomenon called RNA interference (RNAi)—in which small pieces of RNA silence the expression of individual genes—could provide an alternative solution for breast and other cancers.
Though it was first discovered in plants, researchers have known for about a decade that small interfering RNAs (siRNAs) are active in mammals like us, and are already working on ways to harness them for shutting down genes promoting cancer and other diseases.
The problem with siRNAs for treatment, however, is making sure they get exactly where they need to go. That’s a problem that Judy Lieberman, MD, PhD, has taken a big step toward solving. …
Drugs like cisplatin that break DNA are some of the strongest weapons we have against breast, ovarian and other cancers. The problem, common to every form of chemotherapy, is that cisplatin doesn’t work for everyone. Given the potential side effects that go along with the drug—including vomiting, hearing loss and muscle cramps, just to name a few—the decision to give it to a patient becomes something of a gamble: Does the benefit outweigh the risk?
There are tests that examine individual genes and which can give doctors a limited view as to which tumors might respond best to cisplatin. But a multicenter team co-led by Zoltan Szallasi, MD, of Boston Children’s Hospital’s Informatics Program (CHIP), thinks they may have a solution that looks beyond individual genes to see which tumors might succumb to cisplatin and other drugs like it. …
About two-thirds of breast cancers are fueled by estrogen, making them quite vulnerable to drugs like tamoxifen that interfere with the hormone. But some 50 percent of such hormone-sensitive tumors start shrugging off tamoxifen treatment at some point and continue to grow.
Marsha Moses and her team in Children’s Vascular Biology Program want to turn the tide against these estrogen- or hormone-independent tumors, which are much more difficult to treat. And they think a protein named Adam – or rather, ADAM12 – might hold the key.
The story starts seven years ago with a search for cancer biomarkers in a fluid far removed from the breast: urine. Over the years, Moses, the program’s director, has collected a large biorepository of human urine and other samples, as well as associated clinical data, which she and her lab use to search for proteins whose presence is associated with different cancers.