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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.
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IMAGE: Novel cancer immunotherapy approach inverts a missing gene copy into an immune cell-activating signal. view more
Credit: Elizabeth Cook
Researchers developed a prototype for a new cancer immunotherapy that uses engineered T cells to target a genetic alteration common among all cancers. The approach, which stimulates an immune response against cells that are missing one gene copy, called loss of heterozygosity (LOH), was developed by researchers at the Ludwig Center, Lustgarten Laboratory and the Bloomberg~Kimmel Institute for Cancer Immunotherapy at the Johns Hopkins Kimmel Cancer Center.
Genes have two alleles, or copies, with one copy inherited from each parent. Cancer-related genetic alterations commonly involve the loss of one of these gene copies.
Targeting a neoantigen derived from a common TP53 mutation sciencemag.org - get the latest breaking news, showbiz & celebrity photos, sport news & rumours, viral videos and top stories from sciencemag.org Daily Mail and Mail on Sunday newspapers.
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.