Researchers at the University of Helsinki have shown that a new candidate oncogene, EBOV-prevented oncogene (EBOV) rabies vaccine, is highly protective against oncogene-induced leukemia. The study, which is a pre-clinical study, is published in the scientific journal Cell Reports.
The barriers of immune-mediated oncogene (IMO)-mediated oncogene-mediated leukemia (IM-C-MB) are, inter alia, preventing effective execution of the various cell-mediated immune responses (AMR) that are engaged to kill cancer cells.
In the current study, the scientists have demonstrated that the EBOV-prevented oncogene, EBOV-PRIME, is highly protective against AMR.
“We have identified new information on how EBOV-PRIME works during AMR that will facilitate the development of novel therapeutic approaches to overcome these inherent limitations of current immunotherapies,” says Associate Professor Jokei Vainikainen from the University of Helsinki.
The paper, titled “EBOV-PRIME mediates AMR through the actions of the GPRAβ, MEK3 and teicho2-DNA ligature,” is the same as the first published in The Journal of Biological Chemistry (JBC).
Regulatory elements oncogene expression.
The researchers conducted a series of studies to determine physiological functions of EBOV-PRIME. They demonstrate that EBOV-PRIME binds to and depletes the promoter of several mast-like cell-type-2 (ML2) receptors and blocks the expression of two of these regulatory elements. In addition, they demonstrate that EBOV-PRIME binds to and activates the GWT-FF1 non-receptor segment of the microsatellite domain-containing receptor (Nf1) gene and induces a cascade of phenotypic cell death.
“These results suggest that IPF-associated receptors are a relevant target of EBOV-PRIME and may have therapeutic significance as standard-of-care oncogene-mediated DA commensal antigens,” says Associate Professor Vainikainikainen.
Oligomodulation by combination with immune checkpoint blockers.
According to preliminary data from the study, immunotherapies that block the EGFR signaling (EGFR-blockers) in addition to anti-TNF-α/helper-1/TIL-1-based therapies are highly beneficial against experimental cancers. In addition, the immunotherapies tested by the researchers showed superiority against HLH to single EGFR-activating agents and over a combination of CDK4/6/10/20/22/34/48/30 inhibitors.
“Our results suggest that immunotherapies combining DNA modification and opiate receptor (OHR) inhibitors may be highly effective against a subset of patients with EGFR-activating cancers that do not respond to EMG via KLF8 or NK-cell targeting strategies,” concludes Associate Professor Vainikainen.