Credit: The Wistar Institute
PHILADELPHIA (March 12, 2021) Scientists at The Wistar Institute identified a new function of ADAR1, a protein responsible for RNA editing, discovering that the ADAR1p110 isoform regulates genome stability at chromosome ends and is required for continued proliferation of cancer cells. These findings, reported in
Nature Communications, reveal an additional oncogenic function of ADAR1 and reaffirm its potential as a therapeutic target in cancer.
The lab of Kazuko Nishikura, Ph.D., professor in the Gene Expression & Regulation Program of The Wistar Institute Cancer Center, was one of the first to discover ADAR1 in mammalian cells and to characterize the process of RNA editing and its multiple functions in the cell.
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Dana-Farber research leads to better understanding of immune system in kidney cancer
Two research papers highlight single-cell dissection of kidney tumors to identify new immunotherapy treatments and targets
In the last two decades, immunotherapy has emerged as a leading treatment for advanced renal carcinoma cancer (more commonly known as kidney cancer). This therapy is now part of the standard of care, but it doesn’t work for all patients, and almost all patients, no matter how they respond initially, become more resistant to treatment over time. The immune system plays a critical role in kidney cancer disease progression and in response to therapies, and so a fundamental challenge in the field is to understand the underlying “immune circuitry” of this disease.
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A study led by researchers at Baylor College of Medicine reveals a novel role of the steroid receptor coactivator 3 (SRC-3/NCOA3), a protein crucial for steroid hormone function and a prognostic marker for aggressive human breast and other cancers.
The team discovered that SRC-3 also regulates human immune T regulatory cells (Tregs), which contribute to the regulation of the body s immunological activity by suppressing the function of other immune cells, including those involved in fighting cancer. The study, which appears in the journal
Scientific Reports, shows that Tregs whose SRC-3 function was eliminated failed to suppress the activity of other immune cells in the lab. The authors anticipate that their findings may help in the fight against cancer in the future by leading to new approaches to inhibit Tregs activity which consequently would release immune attack in tumors.
Diabodies see the unseeable
RAS oncogene mutations are common in various cancers, controlling their growth and survival. Targeting mutant RAS proteins with antibodies has been unsuccessful due to low surface expression, even when targeting mutant RAS peptides presented via HLA on the surface of cancer cells. Douglass
et al. used phage display to generate single-chain variable fragments (scFvs) specific for mutant RAS peptide-HLA complexes. The authors tested various bispecific, T cell–engaging antibody formulations, finding that single-chain diabodies (scDbs) combining the aforementioned scFv with an anti-CD3 scFv were able to induce T cell activation and subsequent killing of tumor cells expressing mutant RAS peptide-HLA complexes. This scDb approach opens the door for antibody-based therapies against mutant neoantigens expressed at very low levels on the surface of cancer cells.