Pancreatic ductal adenocarcinoma, the most common form of pancreatic cancer, is particularly deadly and hard to treat.
Most tumors of this type are driven by one or more mutations in the KRAS gene, pushing rapid cell division that’s difficult to stop.
They’ve long been considered so challenging to treat that KRAS has been labeled “undruggable” across decades of prior research.
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A new study by researchers at The University of Texas MD Anderson Cancer Center has identified genetic factors that determine whether prostate cancers are susceptible to a type of cell death known as ferroptosis. These findings, published in Nature Communications, could help guide treatment strategies for patients whose tumors do not respond to current treatment options.
The study was led by Di Zhao, Ph.D., associate professor, and Boyi Gan, Ph.D., professor, both of Experimental Radiation Oncology.
“Prostate cancer is such a genetically diverse cancer that there are many possible treatment options, so getting patients on the right treatment as quickly as possible is crucially important,” Zhao said. “The two genetic findings in this study could help identify some patients who are more likely to respond, as well as some patients who are significantly less likely.”
A new study from researchers at The University of Texas MD Anderson Cancer Center has uncovered how one of the most common genetic alterations in glioma rewires the cancer cell genome to fuel tumor progression, suggesting a potential new therapeutic strategy for patients with ATRX-mutant gliomas.
The findings show that mutations in the ATRX gene fundamentally reprogram the epigenome and change the three-dimensional structure of chromatin, creating new interactions that activate developmental programs that tumors exploit to grow and spread. Targeting one of the genes downstream of ATRX in preclinical models—particularly in the HOXA family—slowed cancer progression.
The study, published in Nucleic Acids Research, was co-led by Jason Huse, M.D., Ph.D., professor of Anatomic Pathology, and Kunal Rai, Ph.D., professor of Genomic Medicine, with major contributions from Prit Benny Malgulwar, Ph.D., instructor of Translational Molecular Pathology, Anand Singh, Ph.D., senior research scientist in Genomic Medicine, and Ajay Saw, Ph.D., previous postdoctoral fellow in Genomic Medicine.
Adelaide University researchers have carried out the first in-human trial of a new type of treatment for a leading cause of blindness in working age adults, with promising results.
Retinitis pigmentosa is a genetic condition in which the retinal cells responsible for detecting light don’t work properly, resulting in progressive blindness. Current treatment options for later stages of the disease are limited, and there’s no cure. Now, a new approach to treating the disease is providing fresh hope. Working with researchers from the University of Washington, University of Adelaide experts carried out a small pilot trial to see whether a potential therapy based on a molecule could be safely tolerated by humans.
They found that when the small molecule was injected into the eye, it revived some of the damaged retinal cells, making them sensitive to light again. This happened even after the normal light-sensing cells had been lost.
Researchers led by Universitätsmedizin Frankfurt and Goethe University Frankfurt have identified how particularly aggressive forms of lymphoma can be recognized. By combining genetic and proteomic analyses, the scientists identified biological characteristics of tumors, particularly in high-risk patients for whom standard therapy offers little chance of cure. In the future, such patients could receive alternative, more effective therapies directly. In addition, experimental laboratory research provided initial clues to potential therapeutic targets. The study is published in Cancer Cell.
With more than 150,000 new cases worldwide each year, diffuse large B-cell lymphoma (DLBCL) is the most common aggressive form of lymphoma. Following diagnosis, patients typically receive a standard treatment regimen consisting of a therapeutic antibody and chemotherapy (R-CHOP or Pola-R-CHP), and nearly two-thirds of patients have a good chance of being cured. However, more than one-third of patients experience a relapse after treatment, or their tumors fail to respond to therapy, requiring alternative treatments such as CAR T-cell therapy.
The varying effectiveness of standard therapy is due to the considerable molecular heterogeneity of the disease. Researchers have therefore long been searching for molecular tumor characteristics that would allow them to distinguish among different DLBCL subtypes and treat them more specifically.
Damage to the body’s peripheral nerves can cause pain and movement disorders. Researchers at Leipzig University have recently investigated how damaged nerves can regenerate better. They found that fat tissue strongly supports the Schwann cells needed for repair during the healing process. The results were published in the renowned journal “Cell Metabolism”
Our bodies are transversed by millions of nerve fibres that transmit information. This allows us to do things like control muscles and perceive sensory impressions. Peripheral nerves, like those in our arms and legs, are often damaged by acute injuries, for example, in accidents. As a result, those affected suffer from loss of muscle strength and sensory problems such as numbness. Peripheral nerves do have a strong regenerative potential, but complete recovery of nerve function is still rare for reasons that are not yet fully understood.
When a nerve is crushed or severed, the individual nerve fibres affected by the damage initially die. In principle, they have the ability to grow back and regenerate completely. This depends on the Schwann cells that surround the nerve fibres. These cells do not die after nerve damage, but instead are responsible for coordinating the breakdown and regrowth of nerve fibres in their original areas. Schwann cells therefore play a key role in the repair process. It was previously unknown how these cells cope with the enormous metabolic load associated with the breakdown and rebuilding of nerve tissue. Researchers at the University of Leipzig Medical Center have now discovered that Schwann cells receive crucial support with nerve repair from the fat tissue that surrounds nerves in the body. Using genetically modified mice, they have shown that the chemical messenger leptin plays a key role in this process.
