Author: admin

Posted on

Quantum Mechanics Principles Help Researchers Build Cancer Prediction Model

A team of researchers at the University of Utah has developed a quantum mechanics-based artificial intelligence and machine learning method, which they say can improve the prediction of cancer outcomes and identify treatment targets using the comprehensive molecular background of individual patients. The approach, described in APL Quantum, addresses a major roadblock to leveraging conventional AI for predicting patient outcomes in clinical trials, namely the vast amounts of data needed to train large language models and to account for the complexity of disease drivers.

“It’s much more than just one gene—everything that’s happening in the cells of the patient matters,” said Orly Alter, PhD, associate professor of biomedical engineering at the University of Utah’s Scientific Computing & Imaging Institute. To take this into account, the team developed a method that is capable of analyzing multiple layers of molecular information simultaneously, including tumor DNA, blood DNA, and tumor RNA.

Clinical trials can enroll as few as 20 to 100 patients, while existing genomic datasets often contain data detailing millions to billions of molecular features. According to the researchers, many existing AI and machine-learning methods need more patient samples than genetic features to properly train the model. For instance, they pointed to a recent large language model of the 30,000-nucleotide genome of the COVID-19 virus, which needed 110 million samples. Extrapolating from this, the Utah team said that a complete modeling of the three billion nucleotides in the human genome would require 33 trillion patient samples.

To overcome this constraint, the investigators used a collection of algorithms known as multitensor comparative spectral decompositions, which Alter developed based on the quantum mechanical concepts of entanglement and superposition. The result, the team said, is analogous to a prism splitting light into its individual color components, providing data on multiple layers of a patient’s molecular makeup, including tumor and blood genomes and RNA transcriptomics, able to demonstrate linked patterns in cancer that can predict individual patient outcomes.

“The model rewrites a set of multiple omic profiles from one patient as a superposition of phenotypes, each represented by a set of multiple entangled patterns,” the researchers wrote. Importantly, data from one molecular profile can approximate an analysis from other profiles, which allows predictions to remain consistent among different types of biological data.

The researchers tested their model using an open-source dataset of the childhood cancer neuroblastoma. Their analysis found two previously unrecognized predictors of survival and treatment response, with each predictive element found in three separate, but interconnected data types: tumor genomes, blood genomes, and tumor transcriptomes. The study found that these predictors outperformed the currently used biomarker, the MYCN gene, for predicting treatment response and outcomes.

The new method builds on the substantial body of work by Alter and colleagues. Earlier research in this area had used related comparative spectral decomposition methods to analyze genomic and transcriptomic data in other tumor types, including glioblastoma.

The team will continue its work as it looks to develop an approach that can be used in the clinic. “That’s the ultimate precision medicine,” Alter said. “You have a single person. Can you take the data from just that one person and come up with a treatment for them? I think we can get there.”

The post Quantum Mechanics Principles Help Researchers Build Cancer Prediction Model appeared first on Inside Precision Medicine.

Posted on

STAT+: Exclusive: Mystery man gets experimental GLP-1

You’re reading the web edition of D.C. Diagnosis, STAT’s twice-weekly newsletter about the politics and policy of health and medicine. Sign up here to receive it in your inbox on Tuesdays and Thursdays.

Let’s jump right in with Lizzy’s super interesting scoop about the one-and-only person granted compassionate-use access to an experimental GLP-1. Send news tips and best guesses to John.Wilkerson@statnews.com or John_Wilkerson.07 on Signal.

Why did one man get special access to an experimental GLP-1?

Here’s what we know about the sole person granted special access to Eli Lilly’s experimental obesity drug, thanks to Lizzy Lawrence’s reporting.

Continue to STAT+ to read the full story…

Posted on

Solid Tumor CAR-T Therapy Approved in China, a World First

In a landmark advance for cellular immunotherapy, CARsgen Therapeutics has received regulatory approval in China for satricabtagene autoleucel (satri-cel; CT041), the first CAR-T cell therapy globally approved for the treatment of a solid tumor.

The National Medical Products Administration (NMPA) of China approved satri-cel for Claudin18.2 (CLDN18.2)-positive, HER2-negative advanced gastric or gastroesophageal junction adenocarcinoma (G/GEJA) patients who have progressed after two prior lines of therapy. The decision is a turning point for the CAR-T field, which has improved hematologic malignancies but has struggled to overcome solid tumor biological barriers.

The approval addresses a major unmet need in gastric cancer, the fifth most commonly diagnosed cancer and the fifth leading cause of cancer-related death worldwide, with more than one million new cases and over 750,000 deaths annually. East Asia, particularly China, accounts for 40% of global cases due to risk factors like Helicobacter pylori infection, dietary exposures, and an aging population.

Despite advances in chemotherapy, targeted therapy, and immune checkpoint inhibitors, advanced gastric cancer patients have poor outcomes, especially after multiple treatment lines fail. CAR-T therapy first entered clinical testing for solid tumors in the late 1990s and early 2000s, with pioneering studies targeting ovarian cancer and later neuroblastoma and colorectal cancer, laying the groundwork for today’s next-generation cell therapies.

Satri-cel is an autologous CAR-T therapy that targets CLDN18.2, a stomach-specific tight-junction protein that is highly expressed in gastric and pancreatic cancers but has limited expression in normal tissues. The therapy uses a humanized anti-CLDN18.2 CAR construct that is linked to CD28 and CD3ζ signaling domains, which allows for targeted elimination of tumor cells.

The program’s CARsgen preconditioning strategy boosts CAR-T activity in the immunosuppressive solid tumor microenvironment. Patients receive low-dose nab-paclitaxel to increase CAR-T cell infiltration and antitumor efficacy in addition to cyclophosphamide and fludarabine lymphodepletion.

Clinical evidence supporting approval comes from a randomized confirmatory study published in The Lancet in 2025. In heavily pretreated patients with advanced G/GEJA, satri-cel demonstrated clinically meaningful efficacy and a manageable safety profile compared with available treatment options. The results provide one of the strongest demonstrations to date that CAR-T therapy can generate meaningful clinical benefit in solid tumors.

Importantly, CARsgen is already aggressively pursuing a development strategy beyond late-line gastric cancer. Currently, there are Phase Ib studies in advanced gastric, gastroesophageal junction, and pancreatic cancers, a confirmatory Phase II study in advanced G/GEJA, a Phase Ib study evaluating satri-cel as adjuvant therapy in pancreatic cancer, and investigator-initiated studies evaluating adjuvant and first-line sequential therapy. Satri-cel is being tested in a Phase Ib/II trial for advanced gastric and pancreatic adenocarcinoma outside China, demonstrating its global development goals.

The program has also been the subject of considerable regulatory attention. The FDA has designated satri-cel for CLDN18.2-positive gastric and gastroesophageal junction cancers as an RMAT and Orphan Drug. In Europe, the therapy has been awarded Orphan Medicinal Product designation and PRIME status by the European Medicines Agency. In China, the NMPA designated this product a Breakthrough Therapy for advanced gastric or gastroesophageal junction cancer patients who had failed at least two lines of treatment.

Satri-cel may be the first CAR-T therapy to clear the regulatory finish line in solid tumors, but the competition is heating up. Several companies are developing CLDN18.2-targeted CAR-T, T-cell engager, and antibody programs. AstraZeneca’s zolbetuximab franchise validated CLDN18.2 as a gastric cancer therapeutic target, and Chinese and U.S. biotech companies are developing cell therapy programs to replicate or improve on satri-cel’s results.

For cancer specialists and cell therapy specialists, satri-cel’s approval is not just a new treatment option but a proof-of-concept that engineered cellular therapies can successfully address the challenges of solid tumors. Whether this breakthrough can be applied to other tumor types remains to be seen, but the field has crossed a milestone that has eluded oncology for decades.

The post Solid Tumor CAR-T Therapy Approved in China, a World First appeared first on Inside Precision Medicine.

Posted on
<![CDATA[Clinicians empower schizophrenia patients with shared decisions and flexible treatment options—oral, long-acting injectable, or transdermal—to improve adherence, trust, and remission potential.]]>
Posted on

Manchester Met wins funding to boost AI health innovation

Manchester Metropolitan University will promote AI for business and the development of wearable health technologies through funding awarded by UK Research and Innovation’s Local Innovation Partnership Fund (LIPF). The funding will support two initiatives: Grow AI, which aims to accelerate AI adoption among businesses, and GM-WIC, which will bring together the NHS, universities, businesses and […]
Posted on
<![CDATA[Explore how the asenapine transdermal patch helps schizophrenia care with steadier dosing, fewer side effects, and new options beyond sublingual pills.]]>
Posted on

Dynamic changes of gut microbiota during progression of three Alzheimer’s disease mice models

IntroductionAlzheimer’s disease (AD) is an age-related and progressive neurodegenerative disorder characterized by cognitive impairment and irreversible neuronal degeneration, affecting approximately 55 million individuals worldwide. Despite extensive research efforts, the underlying pathogenic mechanisms of AD remain incompletely understood, and effective therapeutic strategies for preventing or delaying disease progression are still lacking. Increasing evidence suggests that the microbiota-gut-brain axis plays an important role in neurodegenerative diseases, including AD. However, the dynamic alterations of gut microbiota during AD progression across different transgenic mouse models remain poorly characterized.MethodsIn the present study, we investigated age-dependent changes in gut microbiota composition in three commonly used AD mouse models, including APP/PS1, 3xTg, and 5xFAD mice, using 16S rRNA gene sequencing. Fecal samples were collected longitudinally at 2, 4, 6, and 8 months of age to evaluate microbial diversity, community structure, and differential bacterial taxa during aging and disease progression.ResultsOur results demonstrated distinct and model-dependent alterations in gut microbiota composition across different stages of AD progression. Significant changes in microbial diversity and bacterial community structure were observed among the three AD mouse models and wild-type controls. In particular, dynamic alterations in Verrucomicrobiota, Proteobacteria, and Actinobacteriota were consistently identified during aging in AD mice. In addition, β-diversity, Linear discriminant analysis effect size (LEfSe), and correlation network analyses further revealed differential microbial signatures associated with different AD mouse models and age stages.DiscussionOverall, our findings provide additional evidence that gut microbiota composition undergoes dynamic alterations during aging in multiple AD mouse models and may be associated with AD-related progression. This study may contribute to a better understanding of microbiota-associated changes during AD development and provide a basis for future mechanistic studies targeting the microbiota-gutbrain axis in AD.
Posted on

Contemporary pharmacological strategies for acute peripheral facial palsy: a narrative review with clinical decision considerations

Acute peripheral facial palsy (APFP) sometimes known as Bell’s palsy is a common neurological condition and is marked by the acute onset of lower motor weakness on one side of the face. Whereas spontaneous recovery is widespread, there is a significant rate of incomplete recovery, synkinesis, or enduring functional and psychosocial disability of patients. The past decades witnessed the improvement of the diagnostic and therapeutic plans, particularly the pharmacological and adjunctive ones, due to the developments in pathophysiological and clinical trials and the creation of guidelines. This narrative review summarizes the existing evidence on the classification, diagnosis, and treatment of APFP, particularly corticosteroid disease treatment, antiviral medication, combination therapy, adjunct, and rehabilitative therapies, and the future of precision medicine. Randomised controlled trials and high-quality systematic reviews have shown evidence in support of the early initiation of systemic corticosteroids within 72 h of symptom onset as the foundation of treatment practice, improving the likelihood of achieving full facial nerve recovery and less morbidity in the long run. Conversely, antiviral monotherapy has not demonstrated significant clinical benefit with combination therapy with antivirals potentially presenting some benefit to older patients and with severe cases of paralysis. New data highlight the significance of risk stratification, electrophysiological testing, and focal rehabilitation to maximize the results and reduce the sequelae. The developments in artificial intelligence, the work on biomarkers and adaptive clinical trial designs will likely enable more personalized prognostication and treatment choice. In general, a shift towards precision risk-based approaches to the management of acute peripheral facial palsy is also being considered and emerging diagnostic strategies, promotion of the use of corticosteroids as early as possible and focused adjunctive operations that are tailored to a child are becoming the key to improving functional outcomes in the long term.
Posted on

Physical bacteria–neuron proximity and early cellular responses: a conceptual perspective

Recent experimental observations obtained in reduced in vitro systems have reported direct proximity between bacteria and neuronal cells associated with intracellular Ca2+ dynamics and transcriptomic alterations. In particular, studies involving Lactiplantibacillus plantarum and primary cortical neuronal cultures have described bacterial adhesion to neuronal surfaces together with modulation of neuroplasticity-associated proteins and gene networks related to cellular signaling and neuronal regulation. Current models of the microbiota–gut–brain axis primarily emphasize indirect communication mediated through metabolites, immune pathways, neuroendocrine signaling, vagal pathways, extracellular vesicles, and soluble mediators. Although these mechanisms possess substantial explanatory value, certain early cellular responses observed under conditions of direct bacteria–neuron proximity may not be fully interpretable exclusively through soluble signaling mechanisms. This manuscript proposes a conceptual perspective in which the neuronal membrane is considered a dynamic cellular interface potentially sensitive to localized mechanical, physicochemical, or membrane-associated perturbations generated under conditions of direct biological proximity. Within this context, intracellular Ca2+ dynamics are interpreted as possible early cellular responses that may emerge in association with membrane-associated perturbation. Potential candidate mechanisms including mechanosensitive ion channels, localized membrane perturbation, adhesion-associated signaling, cytoskeletal remodeling, membrane reorganization, and local physicochemical microenvironmental alterations are discussed together with alternative explanations involving soluble mediators, immune activation, extracellular vesicles, osmotic or ionic perturbations, and generalized cellular stress responses. Importantly, the currently available evidence derives exclusively from reduced experimental systems and does not establish physiological relevance or demonstrated neuromodulation in vivo. Rather than proposing an alternative model of microbiota–brain communication, this perspective aims to refine interpretation of emerging neurobacterial interface observations by defining experimentally testable hypotheses and mechanistically plausible questions for future investigation.