According to a new American study, a molecule that turns off a particular gene in triple-negative breast cancers could represent a promising therapeutic alternative.
Breast cancer is the most common cancer in women worldwide. It also represents 16% of all female cancers. According to the World Health Organization (WHO), it would have killed 519,000 the number of women worldwide in 2004. Of all breast cancers, the most dreaded is called triple negative (up to a fifth of cases). Unlike the majority of breast cancers, estrogen and progesterone do not fuel the growth of triple negative tumors. That’s why drugs that block these hormones don’t work. According to a new finding reported in the journal Nature Scientific Reportsa molecule that turns off a particular gene in these tumors could serve as a promising therapeutic alternative.
Usuallyent, hormone therapy is proposed in case of breast cancer with positive hormone receptors (ER+, PR+ or both) at an early stage and whose risk of recurrence is low or locally advanced, advanced or recurrent. The type of hormone therapy offered depends on the menopause. Anti-CDK 4/6 are molecules that bring new hope in HER2+ metastasized breast cancer.
This time, during their study, researchers from Tulane University School of Medicine in New Orleans (USA) worked with cultures of a triple-negative cancer cell line from a patient treated in 1973 in Houston, Texas. They then deactivated two known breast cancer genes, Rab27a and TRAF3IP2. Result: stopping TRAF3IP2 would further disrupt cancer-associated metabolic pathways in cells. The scientists were then able to confirm this discovery in a mouse model with breast cancer.
While stopping Rab27a did slow tumor growth in rodents, very few cancer cells did spread, or “micrometastasize.” However, when the researchers turned off TRAF3IP2, it not only suppressed the growth of new tumors, but also prevented the formation of metastases for up to a year. Even better, the treatment shrank existing tumors until they became undetectable, the study authors describe.
Pending FDA approval to begin clinical trials
“This exciting discovery revealed that TRAF3IP2 may play a role as a new therapeutic target in the treatment of breast cancer.”welcomes Dr. Reza Izadpanah, assistant professor of medicine at Tulane University School of Medicine, in charge of the research.
“A limitation of the present study is that we used a single breast cancer cell line to investigate the potential roles of Rab27a and TRAF3IP2 silencing on tumor growth. Our future studies will involve the use of patient-derived xenotransplants to further validate these early fundamental findings. live and in vitro”, however admits Eckhard U. Alt, of Tulane University. Also, scientists are now awaiting approval from the Food and Drug Administration (FDA), the American drug agency, to begin clinical trials as soon as possible.
Another promising avenue in the treatment of triple-negative tumors
Recently, another interesting discovery was made regarding the treatment of triple negative breast cancer and presented at the ASCO in early June.
“The combination of pembrolizumab with chemotherapy significantly improves progression-free survival compared to chemotherapy alone in triple-negative, locally recurrent, inoperable or metastatic breast cancer: median survival of 9.7 months vs 5.6 months in tumors expressing PDL-1 with a CPS score greater than or equal to 10. These data from the Keynote 355 essay presented at the ASCO congress were collected after a median follow-up of 17.5 months for the 566 patients in the immunochemotherapy arm and 15.5 months for the 281 women who received chemotherapy aloneexplains Doctor Isabelle Hoppenot to Why doctor. In women with a CPS score greater than or equal to 1, the median progression-free survival was 7.6 months vs. 5.6 months in the chemotherapy alone armshe continues. The study is continuing, but these initial data are very encouraging for this particularly aggressive type of breast cancer, which often affects young women.”
Silencing TRAF3IP2 to treat heart failure?
Besides treating healthy cancer, silencing TRAF3IP2, as tested in the present study, could work against several cancers as well as to support heart failure. Indeed, this gene is known to activate various cellular pathways that promote inflammation.
As part of its breast cancer research, the Tulane School of Medicine team collaborated with Dr. Chandrasekar Bysani of the University of Missouri School of Medicine in Columbia. The latter identified the role played by TRAF3IP2 in the role of inflammation in heart failure. He was also involved in research that recently revealed that stopping TRAF3IP2 could be used to treat glioblastoma, a type of malignant brain cancer.
Below, the Q&A program on metastatic breast cancer with Dr. Mahasti Saghatchian:
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