Phagocytosis – eliminating millions of dead cells every day – requires specialized cells such as macrophages, the true professionals, which migrate to engulf waste and dying cells.

“There are hundreds of strains of bird flu, and most of them don’t infect humans, or even mammals,” Stephen Cusack told BioWorld. “There are two main reasons for that.” To be able to cause an infection, a virus “has to be able to get into the cell, and for that it needs a receptor,” Cusack said. For influenza viruses, those receptors are hemagglutinin receptors, and they differ in subtle but important ways between birds and mammals.

After decades of being woefully under-diagnosed and all but ignored by the biotech and pharma industry, recent advances in understanding its complex etiology could be opening the way to new treatments for endometriosis. Impetus is coming from (modest) increases in funding for basic research, such as the Biden administration’s $200 million for women’s health research and NIH grants under an ‘Advancing cures and therapies and ending endometriosis diagnostic delays’ call announced in March of this year.

Cross-talk between macrophages and tumor cells could modulate cachexia in pancreatic cancer patients. A group of scientists from the University of Oklahoma has discovered a new pathway that promoted muscle wasting after the recruitment of this immune cell in the tumor microenvironment, activating cachexia-inducing factors.

As with most common diseases of the developed world, aging is the major risk factor for developing cancer. Most of the half-dozen hallmarks of precancer that were published last week by investigators from Vanderbilt University and the Fred Hutchinson Cancer Research Center are also hallmarks of aging. Unfortunately, scientists reported at the American Association for Cancer Research’s (AACR) 2024 annual meeting this week that accelerated aging is increasing, and may be driving an increase in early-onset cancers.

At a recent meeting on “Research priorities for preventing and treating Alzheimer’s disease and related dementias” (ADRD), convened by the National Academies, one consensus priority on ADRD research was that there needs to be more of it at every stage. Several speakers presented stark numbers on the relative volume of research in cancer and neurodegeneration. Research output, measured in peer-reviewed papers, for dementia is estimated to be around 10,000 papers annually, compared to 150,000 for cancer, while AD clinical trials are also few and far between compared to cancer trials. This final installment of BioWorld’s series on Alzheimer’s explores some of the reasons for this discrepancy along with the latest advances and ongoing efforts to accelerate research and drug development in the field.

Scientists from the Australian National University have discovered the gene mutation responsible for causing psoriasis, and the findings could lead to improved diagnosis and treatment for patients with psoriasis and psoriatic arthritis, a chronic inflammatory skin disease. “We were able to identify the gene that could be important in enabling this progression from a skin-only condition to a skin-and-joint condition,” lead study author Chelisa Cardinez told BioWorld.

Eledon Pharmaceuticals Inc.’s tegoprubart, an investigational anti-CD40 ligand antibody, was used as part of the immunosuppressive regimen after the first-ever transplant of a kidney from a genetically modified pig to a human. The tegoprubart procedure was done March 16 at Massachusetts General Hospital on a 62-year-old man with end-stage renal disease.

Organoids are 3D models created from human stem cells and resemble fetal tissues. In an article published in Nature Medicine on March 4, 2024, researchers from University College London provided details on the possibility of generating organoids from epithelial cells collected from amniotic fluid without terminating the pregnancy.

Researchers at ETH Zurich have identified a proteomic signature that could recognize long COVID six months after acute infection. Biologically, the signature indicated that the complement system remained active in patients with long COVID six months after infection. Translationally, it could lead to a diagnostic test for long COVID, and suggests that targeting the complement system could be a therapeutic approach to prevent or treat the disorder.