Researchers have identified a gene that drives one of the most aggressive forms of breast cancer.

The hope is that by finding a way to block the gene, it will be possible to make the cancer less aggressive.

The gene known as “inhibitor of differentiation4” (ID4) not only indicates a highly aggressive form of triple-negative breast cancer, but also appears to control it.

Triple negative breast cancers are cancers that lack estrogen, progesterone and HER2 receptors. Breast cancers that have these receptors can be targeted by drugs.


Some patients succumb to the disease within 3-5 years while other can survive disease-free for much longer than many non-triple-negative breast cancer patients. Researchers attribute the difference in survival prospects to two distinct forms of triple-negative breast cancer which originate from different cell types.


ID4 is produced at high levels in about half of all triple-negative breast cancer, these cancers tend to have a particularly poor prognosis.


Researchers also found that when the ID4 gene is blocked in experimental models of triple-negative breast cancer, the tumor cells stop dividing.


About 15% of all breast cancer cases are triple negative breast cancers. Patients that develop this type of breast cancer usually have a higher risk of recurrence and shorter survival than patients with other forms of breast cancer.


Researchers believe that by blocking ID4, it might be possible to turn stem-cell breast cancers into less aggressive breast cancers that may even respond to tamoxifen.


When ID4 is blocked n a stem cell, other genes that drive cell specialization are activated. The estrogen receptor and a number of other genes expressed by forms of breast cancer with better prognoses are also activated.


The team will not investigate ID4 in order to work out the best strategy for blocking it in humans. They are also planning a mouse study to assess whether blocking ID4 can make tumors vulnerable to tamoxifen.


The team will be working in collaboration with a world expert on estrogen receptor function.



Gerry Oginski
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