Atossa Therapeutics Inc (NASDAQ:ATOS), which is developing medicines aimed at oncology and breast cancer, announced a sponsored research agreement with Weill Cornell Medicine to address treatment challenges in triple negative breast cancer (TNBC).
The Seattle-based clinical-stage biopharma company said the aim is to determine if treating TNBC with extracellular vesicles carrying the estrogen receptor (ER) will convert the tumor to ER+ and render it sensitive to treatment with Selective Estrogen Receptor Modulators (SERM), including Atossa’s own (Z)-endoxifen.
The research project will be led by Dr David Lyden, the Stavros S Niarchos Professor in pediatric cardiology and director of the Department of Pediatrics’ Physician Scientist Training program at Weill Cornell. Dr Lyden’s lab looks at the molecular pathways activated by tumor extracellular vesicle at the metastatic site and identifies potential therapeutic targets to foil metastasis.
Dr Lyden’s work has led to a new understanding of how primary tumor cells dictate their own metastases. He has recently identified specific extracellular vesicle subpopulations and discovered a new subset of particles known as exomeres which have distinct functional roles in the systemic effects of cancer.
“We look forward to working with Atossa and think this project could provide proof of principle for novel approaches to estrogen receptor reinduction in triple negative breast cancer,” said Dr Lyden.
“If we are able to change the cancer phenotype and turn on the estrogen receptor, we could then treat these patients with hormone therapy, which is more effective than currently approved treatments for triple-negative breast cancer.”
Atossa CEO Steven Quay noted that triple-negative breast cancer spreads faster than other forms of breast cancer, and disproportionately affects Black and Hispanic women and has a higher risk of recurrence.
“It’s called TNBC because it does not have any of the receptors that are commonly found in most breast cancers. This makes TNBC particularly difficult to treat because drugs that target estrogen, progesterone, or the human epidermal growth factor protein are ineffective,” Quay noted in a statement.
“Activating the estrogen receptor and converting the tumor to ER+ would fundamentally transform the treatment paradigm for these patients.”
Triple negative breast cancer accounts for about 10-to-15% of all breast cancers, which amounts to almost 200,000 cases worldwide every year.
Atossa said (Z)-endoxifen is the most active metabolite of the FDA-approved selective estrogen receptor modulator tamoxifen. Studies have shown that the therapeutic effects of tamoxifen are driven in a concentration-dependent manner by (Z)-endoxifen.
Contact the author Uttara Choudhury at uttara@proactiveinvestors.com
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