Chinese investigators have reported that high levels of triggering receptor expressed on myeloid cells 2 (TREM2) expression, which are immunosuppressive in multiple solid tumors, were protective in glioblastoma multiforme (GBM). The findings were published May 23, 2024, in Cancer Cell.
Treatment with indoleamine dioxygenase-1 (IDO1) inhibitors reduced both viremia and B cell transformation in animal models of post-transplant lymphoproliferative disorder (PTLD), while IDO1 up-regulation occurred in patients who would go on to develop PTLD. The findings, which were reported in the May 24, 2024, issue of Science by researchers from the University of Basel and the University Hospital Basel, point to new ways to predict, prevent and treat complications of Epstein-Barr virus (EBV) infection.
Treatment with indoleamine dioxygenase-1 (IDO1) inhibitors reduced both viremia and B cell transformation in animal models of post-transplant lymphoproliferative disorder (PTLD), while IDO1 up-regulation occurred in patients who would go on to develop PTLD. The findings, which were reported in the May 24, 2024, issue of Science by researchers from the University of Basel and the University Hospital Basel, point to new ways to predict, prevent and treat complications of Epstein-Barr virus (EBV) infection.
In a paper published in the May 17, 2024, online issue of Cell, investigators from the Duke Human Vaccine Institute reported that a sequence of three immunizations in the HVTN-133 trial was sufficient for the development of heterologous or broadly neutralizing antibodies that protected against several strains of HIV.
In a paper published in the May 17, 2024, online issue of Cell, investigators from the Duke Human Vaccine Institute reported that a sequence of three immunizations in the HVTN-133 trial was sufficient for the development of heterologous or broadly neutralizing antibodies (bnAbs) that protected against several strains of HIV. The findings are “a real beachhead,” Barton Haynes told BioWorld. Haynes is the director of the Duke Human Vaccine Institute and the senior author of the paper.
Based on its analysis of a large cohort of individuals homozygous for the ε4 variant of apolipoprotein E (APOE4), a multinational team of researchers is arguing that homozygosity for APOE4 should be considered a genetic form of Alzheimer’s disease. However, not everyone agrees that the findings warrant reclassifying APOE from risk factor to causal gene. Currently, APOE4 is classified as the strongest risk factor for developing AD. Another variant, the APOE2 variant, is protective, while APOE3 is neutral.
Based on its analysis of a large cohort of individuals homozygous for the ε4 variant of apolipoprotein E (ApoE4), a multinational team of researchers is arguing that homozygosity for ApoE4 should be considered a genetic form of Alzheimer’s disease (AD).
Females have a much greater risk of developing an autoimmune disease than males do. Eighty percent of autoimmune disease patients are female, and specific disorders can have an even more lopsided ratio – 90% of systemic lupus erythematosus (lupus) and almost 95% of Sjögren’s disease patients are female.
The existence of two approved therapies, Lumakras (sotorasib, Amgen Inc.) and Karzati (adagrasib, Mirati Therapeutics Inc.), has been a triumphant success against KRAS, a protein that was once considered undruggable.
The existence of two approved therapies, Lumakras (sotorasib, Amgen Inc.) and Karzati (adagrasib, Mirati Therapeutics Inc.), has been a triumphant success against KRAS, a protein that was once considered undruggable. KRAS is the most frequently mutated oncogene in solid tumors. KRAS driver mutations are found in about 30% of non-small-cell lung cancers (NSCLC), about half of colorectal cancers, and more than 90% of pancreatic cancers. Lumakras and Karzati both target the G12C mutation. Inhibitors that target other mutations, like G12D, are now making their way through preclinical and clinical development, while some companies are developing therapies that would target mutated KRAS more broadly, irrespective of the specific mutation that is activating the protein.