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IMAGE: Research from UVA s Jogender Tushir-Singh, PhD, explains why the antibody approaches effectively killed cancer tumors in lab tests but proved ineffective in people. view more
Credit: Dan Addison | UVA Communications
New research from UVA Cancer Center could rescue once-promising immunotherapies for treating solid cancer tumors, such as ovarian, colon and triple-negative breast cancer, that ultimately failed in human clinical trials.
The research from Jogender Tushir-Singh, PhD, explains why the antibody approaches effectively killed cancer tumors in lab tests but proved ineffective in people. He found that the approaches had an unintended effect on the human immune system that potentially disabled the immune response they sought to enhance.
Researchers say theyâve made a discovery in a cancer treatment originally thought not to work Cancer Center (FILE) By Daniel Grimes | April 6, 2021 at 2:22 PM EDT - Updated April 6 at 2:22 PM
CHARLOTTESVILLE, Va. (WVIR) - Researchers at the University of Virginia Cancer Center say theyâve made a discovery that could revive a cancer treatment originally thought not to work.
It is an antibody treatment for solid cancer tumors like ovarian, colon, and triple negative breast cancers. Originally the treatment had an unintended effect, suppressing a personâs immune system in clinical trials.
Now researchers say theyâve figured out a way to make it work.
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This news release, issued by Johns Hopkins Medicine, describes a novel targeted immunotherapy approach. This new approach employs bispecific antibodies to treat cancer by eliciting a Tcell response against mutated p53. The researchers used the Highly Automated Macromolecular Crystallography (AMX) and Frontier Microfocusing Macromolecular Crystallography (FMX) beamlines to characterize the molecular structure of the proteins. AMX and FMX are beamlines at the National Synchrotron Light Source II (NSLS-II) a U.S. Department of Energy (DOE) Office of Science User Facility at Brookhaven National Laboratory. NSLS-II offers a comprehensive suite of life science research capabilities. Johns Hopkins media contacts: Amy Mone, 410-614-2915, amone@jhmi.edu, or Valerie Mehl, 410-614-2916, mehlva@jhmi.edu. Brookhaven Lab media contacts: Cara Laasch, 631-344-8458, laasch@bnl.gov or Peter Genzer, 631-344-3174, genzer@bnl.gov.
Credit: The Wistar Institute
PHILADELPHIA (April 1, 2021 Scientists at The Wistar Institute identified a new mechanism of transcriptional control of cellular senescence that drives the release of inflammatory molecules that influence tumor development through altering the surrounding microenvironment. The study, published in
Nature Cell Biology, reports that methyltransferase-like 3 (METTL3) and 14 (METTL14) proteins moonlight as transcriptional regulators that allow for establishment of the senescence-associated secretory phenotype (SASP).
Cellular senescence is a stable state of growth arrest in which cells stop dividing but remain viable and produce an array of inflammatory and growth-promoting molecules collectively defined as SASP. These molecules account for the complex crosstalk between senescent cells and neighboring cells and the effect of cellular senescence in various physiological processes and diseases. Although senescence is regarded as a potent barrier for tum