An analysis of cervical cancers in Ugandan women has uncovered significant genomic differences between tumors caused by different strains of human papillomavirus (HPV), signifying HPV type may impact cervical cancer characteristics and prognosis.
Scientists may have discovered a new way of identifying and targeting hidden HIV viral reservoirs during treatment with antiretroviral therapy (ART). These findings may have translational implications for improving the long-term care of HIV positive people.
Researchers have successfully determined the characteristics of electron emission when high-velocity ions collide with adenine – one of the four key nucleobases of DNA.
Scientists have developed a synthetic peptide that can make multidrug-resistant bacteria sensitive to antibiotics again when used together with traditional antibiotics, offering hope for the prospect of a combination treatment strategy to tackle certain antibiotic-tolerant infections. On its own, the synthetic antimicrobial peptide can also kill bacteria that have grown resistant to antibiotics.
Creative chemists employ enzymes to build a complex but promising natural anti-cancer agent called cepafungin I in a lean nine steps.
Researchers found a single genetic mutation that leads to reduced growth of a transmissible cancer in Tasmanian devils in the wild. The finding gives hope for the animals‘ survival and could lead to new treatment for human cancers.
Researchers have now identified a protein called histone deacetylase 3 (HDAC3) as the orchestrator of the immune system’s inflammation response to infection. By using both specially cultured cells and small animal models, HDAC3 was found to be directly involved in the production of agents that help kill off harmful pathogens as well as the restoration of homeostasis, the body’s state of equilibrium. This work shows that some of the methods being tested to fight cancer and harmful inflammation, such as sepsis, that target molecules like HDAC3 could actually have unintended and deadly consequences.
Scientists are increasingly trying to use the body’s own immune system to fight cancer. A new study now shows the strategies tumor cells use to evade this attack. The method developed for this work contributes to a better understanding of the “arms race“ between immune defense and disease. The results could help to improve modern therapeutic approaches.
Specific antibodies protect us against viral infections – or do they not? Researchers studied the immune response to papillomaviruses in mice and discovered a hitherto unknown mechanism by which the pathogens outwit the immune system: At the beginning of the infection cycle, they produce a longer version of a protein that surrounds the viral genome. The body produces antibodies against this protein, but they are not effective in fighting the pathogen.
The mechanism unveiled triggers a mutation fog, causing hundreds of mutations in each tumor, which spread through the genome of lung, head-and-neck and breast cancers. Researchers have identified the antiviral APOBEC3A enzyme as the major cause of this new type of hypermutation. Published in Nature Genetics, the study shows how the mutation fog process generates many oncogenic “cancer driver“ mutations, thus accelerating tumour development.
Targeted protein degradation (TPD) represents a novel paradigm in drug discovery that could lead to more efficient medicines to treat diseases such as cancer. ‚Molecular glue degrader’are an emerging but understudied class of small molecules that have been shown to induce degradation of proteins commonly considered ‚undruggable‘. Researchers have described a strategy that, for the first time, enables the rational and highly scalable discovery of novel molecular glue degraders.
Researchers have revealed the multiple, intertwined cell death systems that prevent the spread of the ‚intracellular‘ bacterium Salmonella, an important cause of typhoid fever which kills more than 100,000 people annually.
More than 200 genes with novel and known roles in glioblastoma – the most aggressive type of brain cancer – offer promising new drug targets. Researchers engineered a new mouse model to show for the first time how a mutation in the well-known cancer gene, EGFR initiates glioblastoma, and works with a selection from more than 200 other genes to drive the cancer.
Researchers have uncovered a new mechanism by which cancer cells adapt to the stresses they encounter as they grow and respond to therapies.
Researchers have shown that an approach called federated learning is successful in the context of brain imaging, by being able to analyze magnetic resonance imaging (MRI) scans of brain tumor patients and distinguish healthy brain tissue from cancerous regions.
Researchers have identified the process by which stem cells in the airways of the lungs switch between two distinct phases — creating more of themselves and producing mature airway cells — to regenerate lung tissue after an injury.
Researchers report that inhibiting a key enzyme caused human cancer cells associated with two major types of breast and ovarian cancer to die and in mouse studies reduced tumor growth.
Tiny finger-like projections called filopodia drive invasive behavior in a rare subset of lung cancer cells. Analysis of molecular features distinguishing leader from follower cells focuses on filopodia and the MYO10 gene.
A new imaging method uses the natural autofluorescence within cells to assess T cell activity. The technique could help assess T cell involvement in immunotherapies.
Researchers suggest that community-based genetic screening has the potential to efficiently identify individuals who may be at increased risk for three common inherited (CDC Tier 1) genetic conditions known to cause several forms of cancer and increased risk for heart disease or stroke.
Researchers have discovered a new method to treat human herpes viruses. The new broad-spectrum method targets physical properties in the genome of the virus rather than viral proteins, which have previously been targeted. The treatment consists of new molecules that penetrate the protein shell of the virus and prevent genes from leaving the virus to infect the cell. It does not lead to resistance and acts independently of mutations in the genome of the virus.
The novel coronavirus changes the appearance of its messenger RNA cap to trick the host cell into not recognizing it is foreign, according to a new study.
Researchers identified a discordant phenomenon in which a subset of patients displayed profoundly decreased expression of the transgenic TCR over time, despite the transgenic TCR being present at the DNA level.