Lifeboat Foundation

Glioblastoma is a fast-growing and aggressive brain tumor. As one of the most common malignant brain tumors, life expectancy after diagnosis is between 14 and 16 months. Roughly 1% of patients survive more than ten years with the longest patients living over 20 years. Symptoms include headaches, double vision, vomiting, loss of appetite, changes in mood and personality, inability to accurately think and learn, seizures, and difficulty speaking. Unfortunately, there is no cure, and treatment options include radiation and chemotherapy with limited efficacy. Glioblastoma is difficult to treat due to its location in the brain, its resistance to common treatment, the brains limited ability to heal itself, disrupted blood supply, blood vessel leakage, seizures, and neurotoxicity from treatments. Due to limited treatment and the life expectancy of this devastating disease, researchers at the SALK Institute in La Jolla, California have set out to find better ways to treat glioblastoma and prolong survival in patients.

Immune checkpoint inhibitors (ICIs) are a form of immunotherapy that block receptors on immune cells which activate them to kill tumor cells. The ICI using by the SALK group is known as anti-CTLA-4, which binds to the CTLA-4 protein on the T immune cells responsible for killing infected cells. This therapy was generated by Dr. James Allison at the MD Anderson Comprehensive Cancer Center in Houston, Texas. For his work, he was awarded the Nobel Prize in Physiology or Medicine in 2018. While this therapy proved effective in other cancers such as melanoma, it was unclear its effect in glioblastoma. The researchers at SALK recently published their findings on the effect of anti-CTLA-4 on glioblastoma.

The study published in Immunity by Dr. Susan Kaech and colleagues at SALK demonstrated prolonged survival of mice with glioblastoma after treatment with anti-CTLA-4. They also discovered that the treatment was largely dependent on CD4+ T cells, which aid in activating other cells, and not CD8+ T cells, which directly kill the tumor. More specifically, CD4+ T cells were found to infiltrate the brain and trigger other immune cells, like microglia to destroy cancerous cells. In Kaech’s work, the lab significantly shrunk the glioblastoma in mice and in some cases completely eradicated it.

Benjamin Oakes’ Scribe Therapeutics is developing specialized Crispr proteins to tackle a wide range of diseases–and it’s garnered deals with Big Pharma potentially worth over $4 billion.

Pigs might help solve the organ transplant crisis if researchers can make the process safe enough. Preventing rejection in brain-dead subjects is a step toward that goal.

GTB-3550 is the company’s first TriKE® product candidate that was evaluated in Phase 1 clinical trials for the treatment of acute myeloid leukemia (AML), myelodysplastic syndrome (MDS), and other CD33+ hematopoietic malignancies. Phase 1 clinical trials were shown to be both safe and well-tolerated, as well as proving the molecule’s clinical concept and providing a framework for future product candidates.

GTB-3650 is a second-generation protein developed to treat AML and MDS. It has replaced GTB-3550 and utilizes camelid nanobody technology. GTB3650 has successfully completed pre-clinical trials and is in the good manufacturing process (GMP) stage, which is usually the last developmental milestone before progressing into phase 1 clinical trials.

DURHAM – A big licensing deal potentially worth hundreds of millions of dollars with an Austrlia-based company at the same time also has triggered what Precision Biosciences calls a “right-sized” organization of the company.

“Prior to the announcement, we had 190 employees, with 110 going forward with Precision. Most of the 80 employees went with Imugene, with the remainder parting ways with a reduction in force,” Mei Burris, director of investor relations and finance for the company,” told WRAL TechWire.

What “right-sized” means was not immediately explained in the company’s announcement Tuesday night after the markets closed. The company’s stock is trading at under $1 and it lost $12 million in its most recent quarter ending June 30.

A study that peered into live mouse brains suggests for nearly 70 years we’ve been targeting the wrong neurons in our design of antipsychotic drugs.

Untangling the vast web of brain cells and determining how drugs work upon them is a tough task. Using a miniature microscope and fluorescent tags, a team of researchers led by Northwestern University neuroscientist Seongsik Yun discovered that effective antipsychotic drugs cling to a different type of brain cell than scientists originally thought.

Just like research suggesting depression might not be a chemical imbalance in serotonin levels, our understanding of schizophrenia treatments may need a rethink if widely-used antipsychotics are targeting different neurons than expected.

Canadian researchers at the University of Montreal have successfully recreated and mathematically confirmed two molecular languages at the origin of life.

Their groundbreaking findings, recently published in the Journal of American Chemical Society, pave the way for advancements in nanotechnologies, offering potential in areas like biosensing, drug delivery, and molecular imaging.

Living organisms are made up of billions of nanomachines and nanostructures that communicate to create higher-order entities able to do many essential things, such as moving, thinking, surviving, and reproducing.

Genome-wide association analyses of magnetic resonance imaging data describe the genetic architecture of 13 cortical phenotypes at both global and regional levels, implicating neurodevelopmental and constrained genes.

A new method allows large quantities of muscle stem cells to be safely obtained in cell culture. This provides a potential for treating patients with muscle diseases – and for those who would like to eat meat, but don’t want to kill animals.