A new study by researchers at Tulane University, located in the city of New Orleans, United States, revealed the discovery of the gene behind the most aggressive form of breast cancer, as well as how to disable it to curb tumor growth and cancer spread.

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The report published in the Scientific Report of the journal Nature, explains that the research focused on triple negative breast cancer (TNBC), the most aggressive form of this type of cancer. It is a difficult disease to treat and where the chances of survival are lower than in other types of this cancer.

The researchers looked at the role two specific genes play in TNBC called Rab27a and TRAF31P2. Subsequently, they suppressed these two genes causing them to stop working and found positive impacts in the fight against breast cancer.

Doctor Reza Izadpanah, team leader, explains:

Our findings show that both genes play a role in the growth and metastasis of breast cancer. Although the Rab27a target slows the progression of tumor growth, it does not affect the spread of small numbers of cancer cells or micrometastases. Conversely, attacking TRAF3IP2 suppresses tumor growth and spread, and interfering with it reduces preformed tumors and prevents further spread. This exciting discovery has revealed that TRAF3IP2 may play a role as a novel therapeutic target in the treatment of breast cancer.

And it is that the scientists of the University of Tulane discovered that when they turned off the TRAF3IP2 gene, the metastasis of the cancer, that is, its spread, did not take place for a full year after treatment. Furthermore, deletion of this gene was also related to stagnant tumor growth and shrinking the tumor to undetectable levels.

So far, these positive effects have been seen in animals, meaning that gene deletion therapy has yet to be tested in humans. However, Izadpanah and his team are quite positive about it and have already turned to the FDA. to speed up the path and be able to carry out clinical trials.

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They discover how to stop tumor growth in breast cancer - Explica

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