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Category: biotech/medical – Page 74

Synthetic tumor data helps AI improve long-read cancer mutation detection

A research team at The University of Hong Kong (HKU), has developed ClairS—a deep-learning algorithm that significantly improves the detection of cancer mutations using long-read sequencing. Tested on breast cancer, lung cancer and melanoma cell line datasets, ClairS has demonstrated high accuracy across various cancer types and sequencing conditions.

The team was led by Professor Ruibang Luo, assistant director of Learning Experience & Student Enrichment and associate head of the Department of AI & Data Science at the School of Computing and Data Science (CDS) at HKU. The findings are published in the journal Nature Methods. ClairS is open source and available on GitHub.

Inherited gene variants may shape CAR-T therapy benefits and toxic side effects

Chimeric antigen receptor (CAR)-T cell therapy, which reprograms an individual’s immune cells to seek out and destroy certain cancer cells, has revolutionized treatment for blood cancers such as lymphoma. But in some patients, the treatment can cause serious side effects. New research led by investigators at the Mass General Brigham Cancer Institute, the Broad Institute of MIT and Harvard, and Dana-Farber Cancer Institute has shown that patients’ inherited genetic makeup can influence whether they benefit from CAR-T cell therapy or experience toxicity from the treatment. The results are published in Science Immunology.

“These findings have important implications for understanding how CAR-T cells behave in patients since each CAR-T cell product is unique to the person from whom it is manufactured, unlike all prior forms of therapy, which are identical across patients,” said lead author Mark B. Leick, M.D., an oncologist at the Mass General Brigham Cancer Institute.

For the study, Leick and his colleagues sequenced the entire genomes of more than 200 patients with aggressive lymphoma from two major clinical trials of CAR-T cell therapy. In one of the trials, patients with T cells with variants that silenced the STXBP2 gene tended to experience toxicity related to CAR-T cell therapy. Also, donor T cells engineered to lack STXBP2 and/or express these STXBP2-silencing variants triggered inflammation.

Low-Frequency Ultrasound Attacks Oral Cancer Cells

When Ajay Tijore was a postdoctoral researcher in mechanobiologist Michael Sheetz’s lab at the National University of Singapore, he and his team studied how mechanical strain affected cancer cells. A few years ago, the researchers found that low-frequency ultrasound waves triggered mechanical stress that killed several invasive cancer cell types.1 “That was kind of a big revelation… Eureka moment,” said Tijore.

When he started his own lab at the Indian Institute of Science in 2021, Tijore hoped to contribute to Indian society. With India accounting for one-third of the oral cancer cases worldwide, Tijore sought to investigate whether low-frequency ultrasound could also target oral cancer cells.2

Now, Tijore and his team found that patient-derived oral cancer cells are susceptible to low-frequency ultrasound due to their distinct biomechanical properties compared to healthy cells.3 The team’s findings, published in Materials Today Bio, highlight the potential of the non-invasive approach in oral cancer therapy.

Gene therapy reverses complete congenital night blindness in mice, improving vision

A new preclinical study suggests that gene augmentation therapy may restore sight in a severe form of inherited night blindness. The work, reported in Gene Therapy, targets complete congenital stationary night blindness (cCSNB), a disorder in which the retinal circuitry fails to generate reliable visual responses from birth. In mouse models, treatment improved both retinal function and visual performance, offering a promising blueprint for future human therapies.

The researchers focused on augmenting gene activity to compensate for the underlying molecular defect driving defective photoreceptor signaling. Rather than attempting to edit the genome directly, the approach delivers functional genetic instructions to retinal cells, aiming to re-establish healthier visual transduction. This strategy is designed for conditions where disease-causing pathways can be partially rescued by restoring protein expression levels.

Using viral delivery, the team administered a therapeutic vector into the eyes of affected mice. After treatment, they monitored retinal function with electrophysiological assays that quantify how well retinal neurons respond to light. The results showed a measurable shift toward more normal response patterns, indicating that the treated retinas regained function rather than merely delaying degeneration.

Kevin Warwick: Be/Come the Cy/Borg

In February 2011, IBM’s Watson had just beaten two human champions at Jeopardy, and most people filed it under party trick.

A few days later, I sat down with Prof. Kevin Warwick for the second time. He had already run a wire into the median nerve of his own left arm and sent a signal from his nervous system straight into his wife’s. The press called him an eccentric. A few of his colleagues used a less generous word.

So I asked him where the line between genius and madness actually sits. We also got into the magnetic implants and sensory substitution devices his students were building, the trouble his rat-brain-cell robot kept running into, and why Alan Turing was owed far more than Britain ever gave him.

Fifteen years on, #BCI implants have moved from stunt to clinical trial, #AI writes the code that writes the code, and the open question is no longer whether we merge with our machines. It is on whose terms, and who gets a vote.

Kevin’s answer back in 2011 was three words: be/come the #cyborg.

Prophecy or warning? Watch it and tell me which one you hear.

Continue reading “Kevin Warwick: Be/Come the Cy/Borg” | >

Chemotherapy leaves detectable DNA fingerprints in childhood tumors within 18 months

Nearly half of childhood tumors treated with common types of chemotherapy showed detectable DNA changes linked to treatment within 18 months, according to a new international study led by The Hospital for Sick Children (SickKids). Researchers say these changes could eventually help clinicians spot treatment resistance earlier, before cancer returns or spreads, opening the door to more precise use of chemotherapy.

For their study published in Nature, researchers analyzed more than 600 tumors from 544 patients in Canada, Australia and the United States. By combining whole-genome sequencing with detailed medical records and advanced computational methods developed at SickKids, the team found distinct genomic signatures of DNA changes left behind by different chemotherapies. Some of these patterns appeared as early as 91 days after treatment began.

“There’s a long-standing belief that pediatric cancers are genetically quiet because they haven’t had much time to mutate,” says lead author Dr. Adam Shlien, senior scientist, Genetics & Genome Biology, and a lab director in Genome Diagnostics at SickKids. “Instead, it was mind-blowing to see how many mutations found in tumors that had relapsed or spread were linked to the chemotherapy used to treat the cancer in the first place.”

3D-printable material can heal the body, build better robots and recover critical minerals

A new type of 3D-printable material developed by researchers at The University of Texas at Austin mimics human tissue’s ability to sort and filter, allowing certain molecules to pass through while keeping others out. This broad functionality means the material can be used in a variety of applications across medicine, water and robotics.

Current methods for building small tissue-like materials don’t scale to sizes that can make applications possible, the researchers say. The team overcame these issues of speed and scalability by jamming billions of tiny water droplets tightly together using simple mixing and centrifuge techniques to form large, tissue-like materials in just a few minutes. Each droplet is separated by a thin membrane, allowing the membranes to link up, similar to cell organization in human tissue.

“Tissues can separate and transport ions and molecules; that’s how our kidneys or intestines work, taking only what they need and leaving the rest behind,” said Manish Kumar, professor in the Cockrell School of Engineering’s Fariborz Maseeh Department of Civil, Architectural and Environmental Engineering and the McKetta Department of Chemical Engineering. This work was recently published in Nature Materials.

Viagra may reduce cancer metastasis, study shows

Viagra was originally developed to treat high blood pressure and chest pain caused by reduced blood flow to the heart, but over the past three decades it has become the world’s best-known therapy for erectile dysfunction. In the future, this blockbuster drug may find yet another use. In a study published recently in Cancer Research, scientists in the lab of professor Ayelet Erez at the Weizmann Institute of Science found that sildenafil, Viagra’s active ingredient, may restrict cancer metastasis through a newly discovered biological mechanism.

The researchers, led by Dr. Yarden Ariav in Erez’s lab, showed that sildenafil limits cancer cells’ ability to use cholesterol, an essential component of cellular membranes. Cholesterol is particularly important for cancer cells seeking to break away from the primary tumor, migrate throughout the body and invade distant organs. When their access to cholesterol is disrupted, these cells have a harder time forming metastases.

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