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Early changes in the tumor environment may explain why immunotherapy works for some patients but not others
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.
Software rapidly tracks viral variants with high accuracy to aid outbreak responses
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.
Palantir CTO Warns AI Safety ‘Effective Altruists’ Are Attempting a ‘Coup’ — Says ‘Tiny Group of Technocrats’ Shouldn’t Decide for Everyone
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Shyam Sankar, CTO of Palantir Technologies Inc., expressed his concern over the politicization of AI safety.
In a post on X on Monday, Sankar criticized the “Effective Altruists,” accusing them of attempting a coup by deciding the pace of technological progress for everyone else.
Cancer drug pushes mutant blood stem cells to become short-lived immune cells
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.