New Inflammatory Breast Cancer Research Offers Promise
"Oh, yes. I've heard of IBC. It's that new type of breast cancer," people sometimes say to me. I can understand their reaction. When I was diagnosed in 1998, I had never heard of inflammatory breast cancer. Lately this most deadly form of breast cancer is getting more media attention, so people tend to assume if they have just now heard of IBC, it must be new.
The IBC Research Foundation website documents just how long doctors have recognized the specific characteristics of IBC and provides the following information. Surgeon Sir Charles Bell described the disease in his medical textbook in 1814, "When a purple colour is on the skin over the tumor, accompanied by shooting pains, it is a very unpropitious beginning." It wasn't until 1924 that Burton J. Lee and Norman E. Tannenbaum introduced the term "inflammatory breast cancer (IBC)."
While doctors have long recognized the IBC the deadly nature of IBC, they haven't been in agreement about whether it is a separate type of breast cancer and why it is so likely to spread. My doctor told me that IBC cells are the same as other breast cancer cells. What makes them different, he said, is that they form in the lymph vessels of the skin of the breast and because they are in the lymph vessels, they get a free ride to the rest of the body.
Since 1998, however, researchers have been investigating the molecular structure of IBC cells and have learned some important ways they tend to differ from other forms of breast cancer. One important question has been, "Why don't IBC cells clump together like other breast cancer cells and form hard lumps easily felt or seen on a mammogram?"
A study by researchers at New York University's Cancer Institute at Langone Medical Center released June 14 in Nature may be the breakthrough researchers have been looking for. Scientists "have identified a key gene-eIF4G1-that is overexpressed in the majority of cases of IBC, allowing cells to form highly mobile clusters that are responsible for the rapid metastasis that makes IBC such an effective killer."
Eurekalert reports that Dr. Robert Schneider and his colleagues found that "the overexpression of the gene eIF4G1 reprograms how the IBC tumor cells make proteins. Other researchers have identified genes associated with IBC, but this is the first gene shown to orchestrate how IBC tumor cells form special structures-unique to this disease-known as "tumor emboli." These small clusters of highly mobile tumor cells are responsible for the rapid metastasis of IBC. Because these cell clumps are not stationary or fixed, they can quickly travel to other areas of the body."
Dr. Schneider says, "We believe this gene is a target for new drug discovery, and we also believe it is possible to silence the gene without hurting normal cells. Our next step will be to focus on the genetic basis of this disease and look at the genetic changes underlying IBC to reveal more targets at the genetic level."
Of course, it will take time to learn how to turn off the gene, and more time to test that such drugs are safe and effective. It may be years before this breakthrough yields practical results, but each new piece of information offers hope that someday IBC will no longer be the deadliest form of breast cancer.