London, June 15 (ANI): A gene called eIF4G1 has been found to be over expressed in many cases of inflammatory breast cancer (IBC), and is believed to trigger the proliferation of the disease, according to a study.
Inflammatory breast cancer (IBC) is the most lethal form of primary breast cancer, often striking women in their prime and causing death within 18 to 24 months.
Scientists from The Cancer Institute at NYU Langone Medical Center have now found that eIF4G1, allows the cells to form highly mobile clusters that are responsible for the rapid metastasis that makes IBC such an effective killer.
The finding could lead to the identification of new approaches, therapies and a new class of drugs to target and treat IBC.
Lead researcher Dr. Robert Schneider, associate director for translational research at The Cancer Institute, said that the finding were a critical development in the fight against IBC, which respond poorly to chemotherapy, radiation or any other current treatments for breast cancer.
"The tragedy of IBC is that it is often misdiagnosed and misclassified. Rather than presenting as a 'typical' lump, IBC looks like an inflammation of the breast and is frequently mistaken for an infection. Physicians often prescribe antibiotics, losing valuable time for treating this fast-moving killer," Nature quoted Schneider as saying.
"In fact, IBC has only recently been recognized as a unique, genetically distinct form of breast cancer," he said.
The researchers found that the over-expression of eIF4G1 reprograms how the IBC tumour cells make proteins.
This is the first gene that has been shown to orchestrate how IBC tumour cells form special structures-unique to this disease-known as "tumour emboli".
These small clusters of highly mobile tumour cells are responsible for the rapid metastasis of IBC.
"The good news is that we're beginning to understand IBC at both a molecular and genetic level. 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," said Schneider.
The findings will be published on Nature Cell Biology's website. (ANI)