Copper binding drives MYH9 polymerization, triggering cytoskeletal collapse and cuproptosis. HThPA releases intracellular copper through glutathione depletion, exposing a therapeutic vulnerability in drug-resistant tumors.
Two patients receive the same immunotherapy for the same cancer. In one, the tumor retreats and stays gone for years. In the other, the treatment does nothing. Oncologists still have no reliable way to tell these patients apart before therapy begins. Why does immunotherapy succeed for some and fail for others?
A new study led by Professor Dvir Aran of the Technion Faculty of Biology and the Henry and Marilyn Taub Faculty of Computer Science, together with first author Dr. Zhongyang Lin and collaborators including Professor Jürgen C. Becker of the German Cancer Consortium (DKTK), offers a new way to think about that question. Its central message: The answer may depend less on how a tumor looks before treatment begins than on how it changes during the first weeks of therapy. The findings are published in the journal Cancer Cell.
At the center of the study is the tumor microenvironment, the complex ecosystem of immune cells, blood vessels and structural cells that surround and interact with the tumor. This environment can either support the immune system’s attack or suppress it, and researchers have long suspected it plays a major role in whether immunotherapy succeeds or fails.
It was mid-2020, and Patrick Varilly, a software engineer and data scientist, was stuck at home, eager to help the world navigate the ongoing COVID-19 pandemic. He reconnected with Pardis Sabeti, a core institute member of the Broad Institute who was at the forefront of analyzing how the SARS-CoV-2 virus was spreading, and with Ben Fry, her longstanding collaborator and principal at Fathom Information Design, a software firm known for tackling complex data problems. Varilly had worked closely with Sabeti and Fry at MIT more than 20 years earlier.
At the time, Sabeti, Fry and their teams were studying thousands of SARS-CoV-2 genomes from COVID-19 patients to reconstruct the path of viral transmission and identify which viral variants were emerging. Normally, retracing that path—by mapping how different variants are genetically related to each other in what’s called a phylogenetic tree—takes a lot of time and computing power.
Varilly, Sabeti and Fry saw an opportunity to accelerate the process while making data more accessible and easier to interpret. The result is Delphy, a new platform for rapid, interactive phylogenetic analysis. In a paper published in Nature, the researchers report how they rebuilt state-of-the-art phylogenetic tree models to make them faster, more efficient and scalable while maintaining the models’ accuracy. Because Delphy runs entirely within a web browser, anyone with a laptop can perform these analyses without specialized training, software or computing infrastructure.
The biologic drug interferon-alpha can benefit patients with blood cancers called myeloproliferative neoplasms by forcing mutant blood stem cells to become shorter-lived white blood cells, according to a study by Weill Cornell Medicine investigators. Because the broad activity of interferon-alpha can induce significant side effects, developing more focused strategies based on these mechanistic findings could meet an important need in cancer therapy.
Myeloproliferative neoplasms arise when DNA mutations in blood stem cells lead to the excess production of specific types of blood cells, such as megakaryocytes, which make platelets. Interferon-alpha often helps patients by reducing these imbalances and depleting the pool of mutant blood cells.
In the study, published in Nature Genetics, the investigators used advanced single-cell profiling tools to discover how interferon-alpha exerts these effects.
Somewhere in the world, a woman over 50 will have fractured a bone by the time you finish reading this sentence due to osteoporosis, a silent bone disease that can weaken the structural integrity of the skeletal system and a person’s quality of life. The disease weakens bones and makes them more likely to break because of reduced bone mineral density and bone mass, and it affects an estimated 75 million people across Europe, the USA, and Japan.
Menopause-associated estrogen loss makes the burden of this disease higher in women globally, as 1 in 3 women over age 50 is at risk of suffering an osteoporosis-related fracture.
A recent study published in Cell explored a novel stem cell therapy for advanced osteoporosis that cleverly uses a patient’s own stem cells as a biological targeting tag, binding to blood vessels in the bone marrow and guiding the infused stem cells directly to damaged bone tissue.
MIT researchers have created a new computing platform that could be used to develop intelligent and adaptive next-generation electronics that can simultaneously perform multiple functions, like computing and memory, all within one extremely compact, energy-efficient device.
Such a platform opens opportunities for low-power edge computing applications, interactive medical and environmental monitoring systems, and smart robots.
The researchers accomplished this by leveraging the unique mechanical response of soft polymers at the nanoscale. A mechanical response is how a structure changes when a force is applied to it.
Researchers have created mice with half-human brains in an effort to understand and develop new treatments for disorders such as schizophrenia, epilepsy, cerebral palsy, intellectual disability and rare forms of dementia.
The scientists transplanted lab-grown human brain cells into animals that were engineered to be born without a cortex or hippocampus. This made space for the human tissue to grow inside the rodents’ skulls.
The procedure means scientists can now take cells from patients with brain disorders, turn them into brain tissue in the laboratory, and grow that tissue in living animals. The animals can then be studied to see how the disorder takes hold in human brain tissue, and how drugs might treat the conditions.