Category: Uncategorized

Posted on

STAT+: FDA pushes drugmakers to report missing clinical trial results

In a bid toward greater transparency, the Food and Drug Administration sent reminder letters to more than 2,200 companies and researchers that they are required to report clinical trial results to a federal government database or they may face fines.

FDA officials disclosed that an internal analysis found results were not submitted for nearly 30% of studies that were “highly likely” to fall under mandatory reporting requirements. The agency also noted that the letters were sent to companies and researchers associated with more than 3,000 registered trials, some of which were publicly funded.

In explaining its move, the regulator acknowledged a long-standing complaint from researchers who have argued that without access to specific data, trial results cannot be easily duplicated, which inhibits greater understanding of how medicines might work. They also contend this can adversely affect treatment decisions and health care costs.

Continue to STAT+ to read the full story…

Posted on

STAT+: Federal judge tosses California No Surprises Act lawsuit against HaloMD

A federal judge has tossed one of the four pending civil lawsuits against HaloMD, a company that represents providers in No Surprises Act arbitration cases. 

The ruling, which grants HaloMD’s motion to dismiss, represents a major win for the Texas-based middleman, which quickly rose to become the number one user of the federal arbitration process in the first half of 2025. The judge found that Anthem Blue Cross of California’s lawsuit failed to establish a legal basis for invalidating HaloMD’s arbitration wins against the company. 

Lawsuits from four Blue Cross Blue Shield plans alleged that many of the disputes in which HaloMD prevailed weren’t actually eligible for arbitration. The lawsuits claimed to reveal a costly side effect of the process: Providers could potentially game the system to extract more money from health insurers for out-of-network services than they got before the surprise billing law passed. 

Continue to STAT+ to read the full story…

Posted on
<![CDATA[New youth-focused substance use guidelines spotlight prevention, brain development, and coordinated mental health support to improve outcomes early.]]>
Posted on

Advancing Fully Walkaway Automation in Genomics Workflows

SPT Labtech and the European Molecular Biology Laboratory’s Genomics Core Facility (EMBL GeneCore) in Heidelberg, Germany, agreed to collaborate to advance fully walkaway automated genomics workflows. As part of the collaboration, SPT Labtech’s firefly®+ all-in-one liquid handling platform has been installed at EMBL GeneCore.

Officials at EMBL GeneCore say they will expand the facility’s capacity to develop new protocols and further validate and optimize existing workflows for challenging applications such as low-input and metagenomics samples to support the broader genomics community. The SPT platform is designed to simplify complex genomics workflows, combining pipetting, dispensing, incubating, and shaking technologies into a single instrument.

The automated protocols use New England Biolabs (NEB) library preparation kits, NEBNext®, to generate libraries from a wide input range. According to a SPT spokesperson, the installation of the company’s firefly+ platform at EMBL GeneCore, combined with NEB kits, creates strong foundation for fully walkaway automation, enabling more streamlined, end-to-end workflows and supporting labs to scale automation more easily.

“The installation of SPT Labtech’s firefly+ platform as part of our collaboration underscores our commitment to remain at the forefront of scientific innovation. Fully walkaway automation will address key bottlenecks in genomics workflows, helping us develop high-quality, scalable NGS protocols,” says Vladimir Benes, head of EMBL GeneCore.

“Our latest collaboration with EMBL GeneCore marks a significant step towards advancing fully walkaway automation, providing end-to-end genomics workflows for a much wider range of applications, including environmental and rare species research,” adds Morten Frost, CCO, SPT Labtech.

“Integration of our library prep kits with SPT Labtech’s firefly+ platform at EMBL GeneCore creates a compelling opportunity for faster, scalable DNA and RNA-Seq workflows,” notes Bjoern Textor, PhD, sales and senior applications manager, New England Biolabs.

The post Advancing Fully Walkaway Automation in Genomics Workflows appeared first on GEN – Genetic Engineering and Biotechnology News.

Posted on

Why Leukemia Cells Escape Immune Attack—and How to Stop Them

Immunotherapy strategies that harness the body’s innate immune system have long focused on a central concept: cancer cells evade destruction by displaying “don’t eat me” signals that inhibit macrophages. Blocking these signals, most notably CD47, has been a major therapeutic goal. Yet in acute myeloid leukemia (AML), clinical responses to CD47-targeting therapies have been inconsistent, raising questions about whether additional immune evasion mechanisms are at play.

A new study published in Science by researchers at Mass General Brigham, Dana-Farber Cancer Institute, and the Broad Institute suggests that the field may have been overlooking a more dominant signal. The team identifies CD43, a heavily glycosylated surface protein, as a key regulator of macrophage evasion in AML.

Revisiting macrophage immune evasion

Macrophages are critical components of the innate immune system, capable of recognizing and engulfing tumor cells through phagocytosis. This process is regulated by a balance between pro-phagocytic “eat me” signals and inhibitory “don’t eat me” signals expressed on the surface of cancer cells.

Therapeutic efforts have largely focused on CD47, a well-characterized inhibitory signal that binds to SIRPα on macrophages to suppress phagocytosis. However, the limited success of CD47 inhibitors in AML has suggested that this pathway may not fully account for immune evasion in these cancers.

To systematically explore alternative mechanisms, the researchers performed a genome-scale loss-of-function screen in AML cell lines, turning off genes one by one and assessing their impact on macrophage recognition.

CD43 emerges as a dominant signal

The results were unexpected. While CD47 had only a modest effect, CD43 stood out as a major determinant of whether leukemia cells were engulfed by macrophages.

The study reveals that CD43 functions not simply as a surface marker, but as part of a broader protective structure. Specifically, its sialylated form creates a dense, glycosylation-based barrier that interferes with immune recognition.

As described by the authors, “Sialylated CD43 forms a glyco-immune barrier that restrains anti-leukemic immunity.”

This finding introduces a new conceptual framework for immune evasion in AML—one that emphasizes the role of glycosylation and surface architecture, rather than individual receptor–ligand interactions alone.

Explaining limits of current therapies

The identification of CD43 helps clarify why targeting CD47 alone has not produced the expected therapeutic outcomes in AML. If CD43-mediated shielding plays a dominant role, then blocking CD47 may be insufficient to restore effective macrophage activity.

The study suggests that immune evasion in AML is more complex than previously appreciated, involving multiple overlapping mechanisms that together suppress phagocytosis.

By uncovering this additional layer, the work highlights the need for combination strategies or alternative targets in macrophage-based immunotherapy.

A new therapeutic opportunity

From a translational perspective, CD43 represents a promising new target. Interventions that disrupt its glycosylation or block its function could weaken the protective barrier surrounding leukemia cells, making them more susceptible to immune clearance.

Because CD43 operates through a distinct mechanism, targeting it could complement existing therapies rather than replace them. Combining CD43 inhibition with CD47 blockade or other immunotherapies may enhance overall efficacy.

The findings also point to the broader relevance of glyco-immune interactions in cancer. Similar glycosylation-dependent barriers may exist in other tumor types, suggesting that the implications of this work could extend beyond AML.

A shift toward glyco-immunology

The study reflects a growing recognition of the role of glycobiology in cancer and immunology. While protein-based signaling pathways have dominated the field, complex carbohydrate structures on the cell surface are increasingly understood to play critical roles in immune recognition.

By identifying CD43 as a key mediator of immune evasion, the research highlights how these glycosylated molecules can shape interactions between cancer cells and the immune system.

Looking ahead

Although the findings are based on preclinical models, the researchers believe that they provide a strong rationale for further investigation in patient samples and clinical settings. Future studies will be needed to determine how CD43 expression varies across AML subtypes and whether it correlates with treatment response.

If validated, targeting CD43 could represent a new direction for immunotherapy in AML—one that addresses a fundamental mechanism of immune escape.

More broadly, the work highlights the importance of revisiting established paradigms in cancer biology. By moving beyond well-studied targets like CD47 and systematically exploring the full landscape of immune interactions, researchers are uncovering new vulnerabilities that could be exploited therapeutically.

The post Why Leukemia Cells Escape Immune Attack—and How to Stop Them appeared first on Inside Precision Medicine.

Posted on

Sex-Related Differences in Immune System Aging May Impact Disease Susceptibility

Immune system aging, known as immunosenescence, is associated with changes in immune cell composition and function that increase susceptibility to disease. The results of a study by researchers at the Barcelona Supercomputing Center – Centro Nacional de Supercomputación (BSC–CNS) have now shown that immunological aging follows different dynamics between men and women.

The team analyzed single-cell RNA sequencing data from the peripheral blood mononuclear cells (PBMCs) of 982 female and male donors across adulthood, to identify cells and genes involved in immunosenescence, and potentially provide a molecular explanation for the differences that had previously only been observed globally in the population.

“Until now, most studies analyzed the immune system based on the average of many cells at once, which makes it difficult to capture the progressive effects of aging,” said Maria Sopena-Rios, PhD. “With cell-by-cell analysis and a much larger sample, we were able to detect these patterns and compare them robustly between biological sexes.” Their strategy identified sex-related differences in immunological aging may help to explain why women have an 80% higher incidence of autoimmune diseases than do men, and why men are more likely than women to develop hematological cancers and chronic infections.

Sopena-Rios is co-first author of the team’s published paper in Nature Aging, titled “Single-cell analysis of the human immune system reveals sex-specific dynamics of immunosenescence,” in which the investigators concluded “Together, our findings provide a high-resolution map of sex-specific immune aging and lay the groundwork for tailored sex-specific strategies to monitor and improve immune health across the lifespan.”

Statistics show clear differences in the population’s immune system according to sex: men are more susceptible to infections and cancers, while women have stronger immune responses, which translate, for example, into better responses to vaccines. Even so, with a more reactive immune system, the probability of the body attacking itself also increases, causing 80% of autoimmune disease development to occur in women. In this context, understanding the aging of the immune system is key since, with age, the composition of immune cells changes and their protective functions deteriorate, causing a greater susceptibility to diseases.

Aging of the immune system, or immunosenescence, refers to “… the gradual decline of the immune system, which predisposes to multiple diseases, including infection, cancer, and autoimmune and vascular diseases,” the authors wrote. “Importantly, the age-related decline of the immune system involves both changes in the composition of immune cell populations and molecular alterations.” However, understanding how sex influences this profound transformation was not possible until now. “…how biological sex shapes immune aging at the cellular level remains poorly understood,” the investigators stated.

For their reported study, the team analyzed blood samples from nearly 1,000 people of different ages covering the entire adult life, and carried out single-cell RNA sequencing to analyze the activity of 20,000 genes in more than one million blood cells. This approach allowed them to identify how the immune system changes over the years and detect clear differences between sexes. Although evidence existed that the immune system ages differently according to sex, women have been traditionally underrepresented in studies, the authors comment. This is the first time that large quantities of samples were analyzed with a balance between men and women, a fact that was decisive in obtaining these results.

“Many studies still do not take sex into account in their analyses, or directly only use data from men, so they leave key questions unanswered,” said study director Marta Melé, PhD, leader of the Transcriptomics and Functional Genomics group at BSC. “Our research was born precisely from this need and combines a scientific outlook with a sex perspective, inclusive data, and great computational power.”

BSC researchers Aida Ripoll-Cladelles (left), Marta Melé (center) and Maria Sopena-Rios (right) in front of MareNostrum 5 supercomputer. [Mario Ejarque / BSC-CNS]
BSC researchers Aida Ripoll-Cladelles (left), Marta Melé (center) and Maria Sopena-Rios (right) in front of MareNostrum 5 supercomputer. [Mario Ejarque / BSC–CNS]

The results revealed that women present more pronounced changes in the immune system with age, with an increase in inflammatory immune cells. This finding could help explain why autoimmune diseases are mainly developed by women, especially at advanced ages, as well as the worsening of certain inflammatory pathologies after menopause.

“Female individuals typically mount stronger immune responses, enhancing resistance to infections and vaccine efficacy, but also contributing to an 80% higher incidence of autoimmune diseases,” the authors noted. “Aging further increases autoimmune risk, and we showed that this is accompanied by the female expansion of cell subpopulations with pivotal roles in autoimmunity.”

On the other hand, the study found that changes associated with immune system aging observed in men are globally less extensive, but an increase in certain blood cells presenting pre-leukemia alterations was observed, a fact that could explain why some blood cancers are more frequent in older men. “Male immune aging is less transcriptionally pronounced, with fewer sex-specific signatures and subtler shifts in immune cell abundance,” the investigators wrote. “.… a subset of male participants shows an age-associated expansion of a B cell population linked to an asymptomatic precursor state of chronic lymphocytic leukemia … Our findings suggest that male immune remodeling may contribute to increased vulnerability to hematological malignancies and chronic infections.”

To manage, process, and analyze a volume of data of this magnitude, the scientific team required the use of advanced computational methods that had never been applied to such complex data sets, with the MareNostrum 5 supercomputer as a key piece to make possible a study that would not have been viable without high-performance computing infrastructure.

With these discoveries, the study establishes the bases for incorporating biological sex as a key variable in precision medicine for aging. The identification of sex-specific aging cells and biomarkers opens the door to the development of preventive, diagnostic, and therapeutic strategies better adapted to women and men, contributing to more individualized and equitable healthcare in an increasingly aging population.

“The immune system plays a fundamental role throughout the organism; therefore, the differences we observed have a very important generalized impact on the entire body. Better understanding the aging of the immune system can help us understand processes that go beyond the blood and affect multiple tissues,” noted co-first author Aida Ripoll-Cladellas, PhD.

Treating aging as a homogeneous process in the entire population hides key biological differences, and understanding how it varies between women and men, the authors concluded, will be essential to improve immune health and promote healthy aging within everyone’s reach. “Stratifying analyses according to sex uncovers key sex-specific features of immunosenescence that may otherwise be misinterpreted as shared effects,” they stated. “This underscores the importance of considering sex as a biological variable to ensure biologically accurate conclusions. Ultimately, our findings lay the foundation for sex-tailored strategies to monitor immune aging and mitigate the burden of age-related immune dysfunction.”

The post Sex-Related Differences in Immune System Aging May Impact Disease Susceptibility appeared first on GEN – Genetic Engineering and Biotechnology News.

Posted on

Salk to Lead $41.3M ARPA-H Effort to Advance Sonogenetics Therapies

The scientists responsible for developing sonogenetics, which refers to the application of low-intensity ultrasound to noninvasively achieve precise control of cellular proteins, have secured an influx of federal funding that will allow them and their collaborators transform the technology into a potential therapy for various conditions starting with peripheral neuropathies.

Late last week, Salk Institute for Biological Studies announced that Sreekanth Chalasani, PhD, an associate professor in Salk’s molecular neurobiology laboratory, and his partners in collaborating laboratories elsewhere, were awarded $41.3 million from the Advanced Research Projects Agency for Health (ARPA-H), an agency within the United States Department of Health and Human Services. Working on multiple fronts over the next five years, the partners will develop core biological tools and ultrasound delivery systems while generating the preclinical evidence needed to move sonogenetics into human clinical trials. 

“This award is a major step toward a long-held goal—a drug-free way to deliver therapy exactly where it’s needed and only when it’s needed,” said Chalasani, who serves as the principal investigator for the grant and is also the co-founder of SonoNeu, a startup launched to commercialize therapies based on the technology. Key to accomplishing that goal is “a platform that pairs engineered ultrasound-sensitive proteins with wearable ultrasound technology, which, unlike conventional pharmaceutical treatments, could let us treat conditions with cellular and temporal control.” 

Reaching cells through sound

In 2011, armed with support from Salk’s Innovation and Collaboration Grants program, Chalasani and his team pioneered sonogenetics, a technique for sensitizing specific cell types to ultrasound by equipping them with ultrasound-responsive proteins. In 2015, his group first identified a particular protein in the roundworm Caenorhabditis elegans (C. elegans) that makes cells sensitive to low-frequency ultrasound. When they added this protein to C. elegans neurons that did not usually have it, they were able to activate these cells using ultrasound waves. 

Since that initial discovery, Chalasani’s team and others have shown that they can use sonogenetics to manipulate mammalian cells. Some of their work was published in a 2022 Nature Communications paper which describes efforts to engineer a human channel protein in cultured mammalian cells and living animal models to confer cell-specific sensitivity to ultrasound stimulation.

Chalasani noted in an interview with GEN that the pace of their progress from an idea to potential clinical translation in the span of about 15 years is remarkable, compared to the typical multi-decade timeline for most new therapies. “In terms of how quickly this has gone from a [research] idea to what patients should we look at [and] how are we going to help them? The pace has been overwhelming,” he said. He attributed much of that progress to the work of the trainees, post-doctoral students, and collaborators through the years who were willing to take on “this crazy idea and work on this project, even though there was no guarantee it would get anywhere.” He also highlighted the early investment from Salk and other entities including the National Institutes of Health’s Brain Initiative as key to project’s success.  

Though Chalasani and his lab pioneered sonogenetics, the next phase of its development is not a solo effort. It involves a multiple institutions and teams all of whom are contributing essential and specialized expertise. The list of collaborators includes Scripps Research, where a team led by 2021 Nobel Laureate Ardem Patapoutian, PhD, will support the discovery and engineering of ultrasound-sensitive proteins. Then a team at St. Boniface Hospital Research and the University of Manitoba led by Paul Fernyhough, PhD, will help define how ultrasound-triggered signals move through cellular machinery and drive nerve repair pathways.

Another team, led by Aravind Asokan, PhD, at Duke University will work on targeted vectors for delivering ultrasound-sensitive proteins to specific cell types. Separately, a team led by Xuanhe Zhao, PhD, at Massachusetts Institute of Technology will work on targeted mechanisms for delivering ultrasound to animal and human targets. Then scientists at the University of California, San Diego, led by Nigel Calcutt, PhD, will validate the efficacy of sonogenetics across established paradigms and in mammalian systems. Finally, Ghassan Kassab, PhD, and his team at California Medical Innovations Institute, will support advanced translational validation and clinically relevant assessment in preclinical systems. 

For their part, Chalasani and his team at Salk will work on finding additional actuators or sensors for ultrasound that will be optimized for targeted delivery. “What we have are proteins that can respond to that small amount of mechanical deflection that ultrasound can cause,” Chalasani explained. “These proteins are channels [that] sit on the membrane of the cell and when the cell experiences ultrasound, the protein gets activated, it opens up, and allows calcium [for example] into the cell. Because these proteins can actuate an effect, they are called ultrasound actuators.” 

Currently, the group has identified proteins that can move things like calcium and chloride into cells in response to ultrasound but they are hunting for other proteins that can activate various signaling pathways. Besides new actuators, the Salk scientists will work on validation studies in mouse models, and lay the groundwork for experiments in larger animal models, specifically pigs, Chalasani told GEN. 

There is a plan in place to commercialize therapies developed using sonogenetics technology. Salk spinout SonoNeu will receive a portion of the ARPA-H funding to help  move potential therapies through the regulatory process and commercialization. Chalasani is listed as a co-founder as is Venkat Reddy, chief scientific officer of General Inception, a firm that partners with scientific founders to build their companies. The target, Chalasani said, is to have something ready for the U.S. Food and Drug Administration in the next five years. 

The initial treatment target condition is peripheral neuropathies and in that context, “there are a lot of interesting places for us to evaluate,” he said. “But I think the real question is going to be what pathway are we targeting? We can do calcium and chloride [but] is that enough to get a therapeutic benefit in a patient or should we have to activate something else other than that? Do we have to activate an enzyme [or] a kinase? And how would we do that? Can we link these proteins to those signals? So there are some unknowns here.”  

If all goes well, other patient populations could benefit from sonogenetics-based therapies besides peripheral neuropathies including people with diabetes, heart conditions or it could help with bladder control, Chalasani said. There are even possible applications in the context of brain-computer interfaces. 

The post Salk to Lead $41.3M ARPA-H Effort to Advance Sonogenetics Therapies appeared first on GEN – Genetic Engineering and Biotechnology News.

Posted on

AACR 2026: Professional Awards Acknowledge Community’s Contributions to Cancer Research

The American Association for Cancer Research (AACR) has released the names of the recipients of several annual professional awards. These awards recognize outstanding accomplishments and achievements in cancer research, therapy development, education, mentorship, and more. The honorees, listed below, will give lectures during this year’s meeting, which is being held in San Diego, CA. This year’s meeting runs from April 17-22.

 

AACR Lifetime Achievement in Cancer Research Award 

James P. Allison, PhD, FAACR

This award honors individuals who have made fundamental contributions to cancer research through a single scientific discovery or a body of work. Allison is being recognized for his contributions to cancer research and patient care. Most notably, he is being celebrated for his identification of CTLA-4 as a negative regulator of T-cell activation, an insight that has since been translated into a first-in-class therapy that revitalized the field of cancer immunology and led to a revolution in cancer immunotherapies. Allison is a fellow of the AACR Academy, a professor and chair of the department of immunology, vice president for immunobiology, and the founding director of the James P. Allison Institute at the University of Texas MD Anderson Cancer Center.

 

AACR Outstanding Achievement in Basic Cancer Research Award 

Housheng Hansen He, PhD

This award recognizes early-career investigators for meritorious achievements in basic cancer research. He is a professor in the department of medical biophysics at the University of Toronto and a senior scientist in the Princess Margaret Cancer Center. He is recognized for contributions to cancer epigenetics and RNA medicine, particularly in revealing how chromatin accessibility and epigenomic landscapes govern oncogenic transcription. His studies of FOXA1-androgen receptor networks, noncoding RNAs, and RNA modifications have improved scientists’ understanding of tumor progression, plasticity, and therapeutic resistance.  

 

AACR Outstanding Achievement in Blood Cancer Research Award 

John F. DiPersio, MD, PhD

This award recognizes individuals with meritorious achievements and contributions to blood cancer research. DiPersio is this year’s recipient for his work in leukemia and stem cell biology, including essential contributions to the development of the hematopoietic stem cell mobilizing agents plerixafor and motixafortide. DiPersio identified AK1/2 signaling in graft-versus-host disease, which led to the identification and approval of JAK inhibitors, including ruxolitinib (Jakafi). DiPersio is the Virginia E. and Sam J. Golman professor of medicine and a professor of medicine, immunology, and pathology at Washington University School of Medicine in St. Louis. He is also director of the Center for Gene and Cellular Immunotherapy at Siteman Cancer Center at Barnes-Jewish Hospital and WashU Medicine.

 

AACR Outstanding Achievement in Chemistry in Cancer Research Award 

Cheryl H. Arrowsmith, PhD

This award honors individuals who have done novel and significant chemistry research that has led to important contributions in basic and translational cancer research, cancer diagnosis, prevention, and treatment. Arrowsmith is being recognized for foundational studies defining the structure and function of chromatin-associated proteins that regulate gene expression in cancer. Her work enabled the development of chemical probes that target epigenetic regulators. She is a senior scientist at the Princess Margaret Cancer Centre, University Health Network and chief scientist of the Structural Genomics Consortium. She is also a professor in the department of medical biophysics at the University of Toronto.

 

AACR Daniel D. Von Hoff Award for Outstanding Contributions to Education and Training in Cancer Research

Charles W.M. Roberts, MD, PhD, FAACR

This award recognizes significant contributions to education and training for cancer scientists and physicians at any career level. Roberts is a fellow of the AACR Academy and the executive vice president and director of the St. Jude Comprehensive Cancer Center. He is also a member in the department of oncology and the Lillian R. Cannon Comprehensive Cancer Center Director Endowed Chair at the St. Jude Children’s Research Hospital. This award recognizes his leadership and dedication to the education and training of cancer researchers across the spectrum of childhood cancer research, including basic, translational, clinical, and population science. 

 

AACR James S. Ewing-Thelma B. Dunn Award for Outstanding Achievement in Pathology in Cancer Research 

David L. Rimm, MD, PhD

The award celebrates pathologists who have contributed to advancing cancer research, diagnosis, treatment, and prevention. Rimm is recognized this year for innovations in quantitative biomarker science that transformed cancer diagnostics and treatment. His invention of the fluorescence-based Automated Quantitative Analysis platform improved immunohistochemistry by enabling precise, reproducible protein quantification in tissue specimens. Rimm is the Anthony N. Brady professor of pathology, a professor of medicine in oncology, director of quantitative diagnostics in the anatomic pathology lab, director of Yale Pathology Tissues Services, and director of the physician scientist training program in pathology at Yale University School of Medicine. He is also a member of Yale Cancer Center and director of the Yale Cancer Center Tissue Microarray Facility.

 

AACR Margaret Foti Award for Leadership and Extraordinary Achievements in Cancer Research

Antoni Ribas, MD, PhD, FAACR

This award recognizes individuals whose leadership and achievements contributed to the acceleration of progress against cancer, raising national or international awareness of the importance of cancer research, among other achievements. Ribas is being recognized for contributions to melanoma biology and cancer immunotherapy that were instrumental to the clinical development of pembrolizumab (Keytruda) and other transformative therapies. His research helped define mechanisms of immunotherapy response and resistance, which guided the design of innovative combination therapy approaches. Ribas is a fellow of the AACR Academy and AACR Past President. He is also a professor of medicine, surgery, and molecular and medical pharmacology at the University of California Los Angeles (UCLA), as well as director of the tumor immunology program at the UCLA Jonsson Comprehensive Cancer Center. He also serves as the director of the Parker Institute for Cancer Immunotherapy Center at UCLA. 

 

AACR Team Science Award

The Cancer Dependency Map (DepMap) team

This award recognizes interdisciplinary research teams for science that advances or is likely to advance our fundamental knowledge of cancer, or a team that has applied existing knowledge to advance the detection, diagnosis, prevention, or treatment of cancer. The Broad Institute Cancer Dependency Map (DepMap) team is recognized this year for systematically mapping genetic dependencies across cancer cells and creating a comprehensive resource that reveals genes and pathways essential for tumor survival. By combining large-scale CRISPR functional genomic screens, drug response data, and multiomic profiling, the team uncovered lineage- and genotype-specific cancer vulnerabilities, including synthetic lethal dependencies such as WRN in microsatellite instability cancers and PRMT5 dependencies in cancers with MTAP deletions. 

 

AACR American Cancer Society Award for Research Excellence in Cancer Epidemiology and Prevention

Elizabeth A. Platz, ScD, MPH 

This award recognizes research accomplishments in cancer epidemiology, biomarkers, and prevention. Platz is the Martin D. Abeloff, MD Scholar in Cancer Prevention in the epidemiology department at the Johns Hopkins Bloomberg School of Public Health. She is also the associate director of population sciences at the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins. This award recognizes her contributions to scientists’ understanding of prostate cancer development, progression, and prevention. Her research linked intraprostatic inflammation to prostate cancer risk, identified telomere length patterns as prognostic biomarkers, and demonstrated protective associations between statin use, cholesterol, and disease lethality. 

 

AACR Cancer Research Institute Lloyd J. Old Award in Cancer Immunology 

Kenneth M. Murphy, MD, PhD 

This award recognizes scientists whose research has had a major impact on the cancer field and has the potential to stimulate new directions in cancer immunology.  Murphy is the Eugene Opie First Centennial Professor in pathology and immunology at the Washington University School of Medicine in St. Louis. This award recognizes his work on discoveries related to the development and functional specialization of dendritic cell subsets that regulate adaptive immune responses. His work elucidated the transcriptional programs that control dendritic cell lineage commitment, including the role of transcription factors such as BATF3 in the development of cross-presenting dendritic cells required to prime cytotoxic T-cell responses. 

 

AACR G.H.A. Clowes Award for Outstanding Basic Cancer Research 

Andrew P. Feinberg, MD, MPH

This award, which has the distinction of being AACR’s oldest award, recognizes individuals who have made outstanding recent accomplishments in basic cancer research. Feinberg is recognized this year for discoveries about the fundamental role of epigenetic alterations in cancer, including the identification of early, widespread DNA methylation abnormalities and the role of genomic imprinting in tumor development. His research demonstrated that large-scale epigenomic alterations contribute to tumor initiation, progression, and cellular heterogeneity, leading to the concept of epigenetic plasticity as a driver of cancer evolution. Feinberg is the Bloomberg Distinguished Professor at the Johns Hopkins University Schools of Medicine, Engineering, and Public Health. He also serves as director of the Center for Epigenetics of the Institute for Basic Biomedical Sciences.

 

AACR Irving Weinstein Foundation Distinguished Lectureship Award

Dennis Lo, DM, DPhil

The recipient for this award is selected by the AACR president, and acknowledges individuals whose personal innovation in science and whose position as a thought leader in fields relevant to cancer research have the potential to inspire creative thinking and new directions in cancer research. Lo is the vice-chancellor and president of the Chinese University of Hong Kong, where he also serves as the Li Ka Shing Professor of Medicine and professor of chemical pathology. He is being recognized for his discovery of fetal DNA in maternal plasma. Lo was the first to identify cell-free fetal DNA and fetal epigenetic markers in maternal plasma, enabling safer and earlier prenatal diagnostics. He also demonstrated that DNA released by tumors may be used for cancer screening, an insight that led to the development of circulating DNA-based tools for early cancer detection and screening. 

 

AACR Joseph H. Burchenal Award for Outstanding Achievement in Clinical Cancer Research 

Luis A. Diaz Jr., MD, FAACR

This award recognizes outstanding achievements in clinical cancer research. Diaz, a fellow of the AACR Academy, heads the division of solid tumor oncology and is the Grayer Family Chair at the Memorial Sloan Kettering Cancer Center. This award recognizes his pioneering discoveries such as biomarker-driven immunotherapies and for demonstrating that tumors with mismatch repair deficiencies and microsatellite instability are highly responsive to immune checkpoint blockade. Diaz has also advanced the use of circulating tumor DNA to detect minimal residual disease and led clinical trials of PD-1 blockade in mismatch repair-deficient cancers. 

 

AACR Minorities in Cancer Research Jane Cooke Wright Lectureship

Ahmedin M. Jemal, DVM, PhD

This lectureship recognizes scientists with meritorious contributions to the field of cancer research and who have furthered the advancement of minority investigators in cancer research. This year’s awardee is recognized for research that quantified temporal and geographic trends in cancer burden using large-scale analysis of cancer registries, mortality rates, and risk factor data, and identified population-level determinants of cancer incidence, survival, and stage at diagnosis across demographic groups. Jemal’s work linked changes in risk factor exposure, screening uptake, and treatment advances to declines in cancer mortality and informed strategies for cancer prevention, early detection, and population-level cancer control. He is the senior vice president of the Surveillance, Prevention, & Health Services Research department at the American Cancer Society. He is also an adjunct professor in the department of epidemiology at the Rollins School of Public Health at Emory University. 

 

AACR Princess Takamatsu Memorial Lectureship 

David C. Lyden, MD, PhD

This award recognizes individual scientists whose work has had or may have a far-reaching impact on the detection, diagnosis, treatment, or prevention of cancer. Lyden is the Stavros S. Niarchos Professor in pediatric cardiology and professor of pediatrics at Weill Cornell Medicine. He is also director of the physician-scientist training program in pediatrics, a founding member of the Drukier Institute for Children’s Health  and a member of the Sandra and Edward Meyer Cancer Center. He is being recognized for describing how primary tumors systemically promote metastasis by forming pre-metastatic niches in distant organs. Lyden’s research demonstrated that tumor-derived extracellular vesicles and exomeres, together with bone marrow-derived progenitor cells, remodel distant microenvironments and determine organ-specific metastatic tropism.

 

AACR St. Baldrick’s Foundation Award for Outstanding Achievement in Pediatric Cancer Research

Kimberly Stegmaier, MD, FAACR

This award recognizes individuals who have contributed to pediatric cancer research, resulting in the fundamental improvement of the understanding and/or treatment of pediatric cancer. Stegmaier serves as chair in the department of pediatric oncology at Dana-Farber Cancer Institute and the David G. Nathan professor of pediatrics at Harvard Medical School. She is also the associate chief of the division of hematology/oncology at Boston Children’s Hospital and an institute member at the Broad Institute. This award recognizes her genomic discoveries that defined the molecular landscape of childhood cancers and led to the identification of key drivers of fusion oncoprotein positive malignancies. Her research used systematic functional genomic screening and chemical biology strategies to identify critical dependencies in high-risk acute leukemias and pediatric solid tumors. 

 

AACR Waun Ki Hong Award for Outstanding Achievement in Translational and Clinical Cancer Research

Eliezer M. Van Allen, MD

This award recognizes cancer researchers under the age of 51 who have conducted meritorious translational and clinical cancer research anywhere in the world. Van Allen is the Chandra Nohria Family Chair for AI in Cancer Research and chief of the division of population sciences at Dana-Farber Cancer Institute. He is also a professor of medicine at Harvard Medical School and an institute member at the Broad Institute. Through large-scale tumor sequencing and integrative genomic analyses, Van Allen’s research defined genomic mechanisms underlying resistance to targeted therapies, including BRAF inhibition in melanoma, and identified genomic features associated with response to immune checkpoint blockade. His work has advanced biomarker discovery and the use of genomic data to guide personalized cancer treatments, as well as bridged advances in artificial intelligence with translational cancer research.

 

AACR Women in Cancer Research Charlotte Friend Lectureship 

Maryellen L. Giger, PhD

This award recognizes scientists’ contributions to the cancer research field and those who have furthered the advancement of women in science through leadership or by example. Giger is the A.N. Pritzker Distinguished Service Professor of Radiology at the University of Chicago. Giger’s research has established quantitative imaging and radiomics approaches that extract high-dimensional features from radiologic images to characterize tumor phenotype and predict cancer risk, diagnosis, and treatment response. She has also guided more than 120 trainees and consistently championed the careers of women scientists and clinicians.

 

Pezcoller Foundation-AACR International Award for Extraordinary Achievement in Cancer Research

Douglas R. Lowy, MD, FAACR and John T. Schiller, PhD, FAACR

This award is presented to international scientists who have made a scientific discovery in basic cancer research or who have made significant contributions to translational cancer research. Lowy is principal deputy director of the National Cancer Institute (NCI) and chief of the Laboratory of Cellular Oncology at NCI. Schiller is deputy chief of the Laboratory of Cellular Oncology at NCI and chief of the lab’s neoplastic disease section. Both awardees are also fellows of the AACR Academy and NIH Distinguished Investigators. They are being recognized for pioneering the molecular and immunologic foundations of human papillomavirus vaccines, engineering virus-like particles for safe and effective immunization, and driving their translation into global cancer prevention strategies that have dramatically reduced cervical and other HPV-related cancer incidence.  

The post AACR 2026: Professional Awards Acknowledge Community’s Contributions to Cancer Research appeared first on GEN – Genetic Engineering and Biotechnology News.

Posted on

Acute Physiological and Emotional Responses to a Brief 24-Minute Yoga Session: Randomized Exploratory Pilot Study With Waitlist Comparison

Background: Wellness tourism increasingly incorporates short yoga sessions for stress management, yet evidence on their immediate physiological and emotional responses remains limited. Objective: This exploratory pilot study aimed to generate preliminary data on acute physiological and emotional responses to a single 24-minute yoga session (breathing, postures, and meditation) compared with quiet sitting in novice practitioners. Methods: In this single-center, randomized waitlist-controlled exploratory pilot study (1:1 allocation), 19 university-affiliated adults with self-reported daily stress and no prior guided yoga experience were allocated to an immediate 24-minute yoga session (n=10) or quiet sitting (n=9). The primary outcome was change in salivary cortisol from baseline to postintervention. Secondary outcomes included salivary alpha-amylase, heart rate (Apple Watch [Apple Inc], subset n=12), and real-time emotional indices (stress, calmness, and concentration) measured by a commercial single-channel electroencephalogram (EEG) device (Kansei Analyzer [Dentsu ScienceJAM], subset n=8). Data were analyzed using change scores relative to the breathing phase, with between-group comparison performed by independent tests or multivariable linear regression adjusted for age, sex, and baseline values as appropriate. Results: No significant between-group differences were observed for salivary cortisol or alpha-amylase. In the yoga group, heart rate increased during postures and remained mildly elevated during meditation relative to the breathing phase, consistent with mild physical exertion. Exploratory individual EEG analyses suggested reduced stress and increased concentration during breathing and meditation phases in some participants. Conclusions: In this small exploratory pilot study, a single 24-minute yoga session did not significantly alter salivary stress biomarkers at the group level. However, it induced measurable cardiovascular activation and heterogeneous EEG-derived emotional responses. These hypothesis-generating findings demonstrate marked interindividual variability, suggesting the need for larger validation studies with improved control conditions.
<img src="https://jmir-production.s3.us-east-2.amazonaws.com/thumbs/4888ec268eb7bb97167592e681af43d2" />

Posted on

Combined Small-Cell Lung Cancer Evolution Insights May Improve Diagnosis, Treatment

A spatial multi-omics study of the rare lung cancer subtype known as combined small-cell lung cancer (cSCLC) has shown that these mixed tumors, which contain features of both small-cell and non-small-cell lung cancer (NSCLC), arise from a single ancestral cell that evolves and transitions between the two cancer types over time.

The results “provide a foundation for understanding cSCLC evolution and advancing innovative diagnostics and therapeutics,” write the authors in Cell Reports Medicine.

cSCLC represents approximately 2–5% of all SCLC cases, with diagnosis primarily based on pathologic evaluation of surgically resected tumor specimens. This can lead to underdiagnosis because small biopsies may not capture the full histological diversity of the tumor. Although cSCLC is more diverse and has a worse prognosis than typical SCLC, it is usually treated the same way because its underlying biology and tumor environment are not well understood.

Traditionally, the mixed histologies within cSCLC were thought to arise from independent tumor populations, but recent studies have revealed that the different histological components share common genetic mutations.

To investigate further, Zhuo Wang, from Fudan University in Shanghai, China, and colleagues applied spatially resolved genomic and transcriptomic sequencing, alongside single-cell RNA sequencing, to 19 treatment-naive cSCLC tumors.

“We found that these tumors are not simply mixtures of different cancer types,” said Wei Wei, PhD, associate professor at the Institute for Systems Biology in Seattle and co-corresponding author of the study. “They are dynamic systems, with cancer cells actively changing their identity. That flexibility may help explain why they are so difficult to treat.”

The team reports that the different tumor components originate from a single clone but later diverge as they acquire different mutations and copy-number changes.

The study also revealed that tumor cells can exist in intermediate or hybrid states, carrying features of multiple cancer types at once. About one-third of the SCLC-like tumor cells analyzed showed these mixed identities, suggesting that cancer progression is not a simple on-off switch, but a continuum.

In addition, the researchers found that different regions within the same tumor create distinct microenvironments. Some areas were rich in immune cells, while others were largely immune-excluded. Dense bands of fibroblasts often separated these regions. Those fibroblast-rich boundaries may help wall off parts of the tumor from immune attack.

“By combining spatial genomics, single-cell analysis, and multi-region sequencing, we were able to trace how these tumors evolve across both space and time,” said Fudan University’s Qihui Shi, PhD, co-corresponding author of the study. “This approach allowed us to capture transitional cell states that are not visible using conventional methods.”

Finally, the researchers developed “cSCLC Detector,” a four-gene diagnostic tool that may help identify these mixed tumors more accurately. The tool was built on a key insight from the study: although the small-cell and non-small-cell parts of cSCLC can look very different under the microscope, they come from the same ancestral tumor and share early trunk mutations.

In independent biopsy and blood samples, the assay, which detects mutations in the NSCLC-specific driver genes EGFR, KRAS, BRAF, and PIK3CA, identified cSCLC-like cases in 14% of samples, compared with a prevalence of 2%–5% estimated from surgically resected specimens.

The findings highlight the importance of understanding not just the genetic mutations in cancer, but also how cancer cells change state and interact with their environment.

“Cancer is not static,” Wei said. “To treat it effectively, we need to understand how it evolves—not just what it is at a single point in time.”

The post Combined Small-Cell Lung Cancer Evolution Insights May Improve Diagnosis, Treatment appeared first on Inside Precision Medicine.