In “proof of concept” experiments with mouse and human cells and tissues, Johns Hopkins Medicine researchers say they have designed tiny proteins, called nanobodies, derived from llama antibodies, that could potentially be used to deliver targeted me
In "proof of concept" experiments with mouse and human cells and tissues, Johns Hopkins Medicine researchers say they have designed tiny proteins, called nanobodies, derived from llama antibodies, that could potentially be used to deliver targeted medicines to human muscle cells.
Nanobodies from Llamas Could Yield Cell-Specific Medications for Humans miragenews.com - get the latest breaking news, showbiz & celebrity photos, sport news & rumours, viral videos and top stories from miragenews.com Daily Mail and Mail on Sunday newspapers.
share:
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.
Two of the three research studies led by Jacqueline Douglass, M.D., Ph.D. candidate at the Johns Hopkins University School of Medicine and Emily Han-Chung Hsiue, M.D., Ph.D., postdoctoral fellow at Johns Hopkins report on a precision medicine immunotherapy approach that specifically kills cancer cells by targeting mutant protein fragments presented as antigens on the cancer cell surface.
Although common across cancer types, p53 mutations have not been successfully targeted with drugs. Genetic alterations in tumor suppressor genes often resulted in their functional inactivation. Traditional drugs are aimed at inhibiting proteins. Inhibiting an already inactivated tumor suppressor gene protein in cancer cells, therefore, is not a feasible approach, says Hsiue, lead author on the