Tag: Medication

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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.

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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.

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From peripheral initiation to central integration: a narrative review of the antihypertensive mechanisms of acupuncture in regulating autonomic nervous system homeostasis

Essential Hypertension (EH) is one of the most prevalent chronic cardiovascular diseases, imposing a significant burden on healthcare systems worldwide due to its high rates of disability and mortality. Long-term elevation of blood pressure leads to multi-organ damage in the heart, brain, and kidneys, resulting in severe complications such as coronary heart disease, stroke, and chronic kidney disease. Current treatment for hypertension primarily relies on pharmacological interventions. Although antihypertensive drugs have achieved notable success in controlling blood pressure, challenges remain, including poor long-term medication adherence, side effects, and inadequate blood pressure control in some patients with resistant hypertension. In parallel, acupuncture, a key modality of traditional Chinese medicine, has demonstrated unique advantages in hypertension management in recent years. Characterized by its holistic regulatory effects and minimal side effects, acupuncture is recognized by the World Health Organization as a recommended complementary and alternative therapy for hypertension, although its precise mechanisms remain incompletely understood. This review aims to summarize the “peripheral-central synergy” antihypertensive mechanism of acupuncture in regulating autonomic nervous system (ANS) homeostasis. Studies indicate that acupuncture primarily modulates autonomic homeostasis through the following pathways: (1) activating peripheral nerve fibers to convert physical stimulation into complex bioelectrical signals; (2) regulating synaptic neurotransmitter release and the expression of related membrane receptors; (3) modulating the synaptic microenvironment; (4) regulating the NTS-CVLM-RVLM neural circuit; and (5) modulating the HPA axis neuro-endocrine circuit. Through in-depth analysis, this review elucidates the multi-level and multi-dimensional impact of acupuncture therapy on primary hypertension, providing stronger evidence and a theoretical foundation for its clinical application.
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Acute liver failure and hemolytic anemia induced by quetiapine and aripiprazole overdose in a patient with schizophrenia and metastatic breast cancer: a unique case report

This case report describes a rare situation in which a patient with schizophrenia and metastatic breast cancer experienced acute liver failure and hemolytic anemia caused by an overdose of quetiapine and aripiprazole. On the day of admission, the patient received lipid emulsion infusion, continuous renal replacement therapy (CRRT), and blood perfusion. After these treatments, the patient’s consciousness improved from mild coma to full awareness. However, 48 hours after admission, the patient developed hemolytic anemia and acute liver failure. Following supportive treatments like plasma exchange, bilirubin adsorption, washed red blood cell transfusion, and low-dose dexamethasone for inflammation, the patient recovered and was discharged. This is the first reported case of hemolytic anemia and acute liver failure caused by mixed toxicity of quetiapine and aripiprazole in an adult patient. We analyze the characteristics of this case to enhance awareness of toxicity from atypical antipsychotics like quetiapine and aripiprazole, and to heighten vigilance regarding the potential risks of combined medication in patients with underlying liver disease, thereby improving the success rate of treatment.
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Plasma proteomic signature of the human menstrual cycle

Nature Medicine, Published online: 13 April 2026; doi:10.1038/s41591-026-04326-5

This Resource presents a large-scale analysis of nearly 3,000 circulating plasma proteins across the menstrual cycle in over 2,700 women from the UK Biobank, revealing distinct proteomic patterns across menstrual phases. This work sheds light on female reproductive biology and gynecological disorders, and provides a proteomic signature for accurate prediction of the menstrual cycle phase.

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STAT+: Revolution Medicines touts ‘unprecedented’ data for pancreatic cancer pill

Metastatic pancreatic cancer patients who received a targeted pill from Revolution Medicines lived nearly twice as long as patients who received chemotherapy, a striking result in a notoriously deadly and intractable malignancy. 

Patients who took the daily pill, called daraxonrasib, lived a median of 13.2 months, compared to 6.7 months for patients who received chemotherapy.

It’s “very impressive,” said Benjamin Weinberg, an associate professor of medicine at Georgetown University who was not involved in the study, in an email.

Continue to STAT+ to read the full story…

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Health Issues Linked to Obesity Differ Between Men and Women

A study of middle-aged adults carried out by researchers at Dokuz Eylul University in Turkey shows that health and metabolic profiles differ between men and women with obesity.

The results, which will be presented at the European Congress on Obesity in Istanbul in May, show men with obesity are more likely to develop abdominal fat and have high levels of liver enzymes and triglycerides in the blood than women.

In contrast, women with obesity had higher levels of total and low-density lipoprotein cholesterol and increased inflammatory markers such as C-reactive protein compared with men.

“Our findings reveal intriguing differences in the way men and women respond to obesity,” said presenting author Zeynep Pekel, from Dokuz Eylul University, Izmir, Turkey, in a press statement.

“They show just how important gender-specific research is. Not only are sex differences a powerful player in the pathology and course of obesity, but our results indicate that such differences could be a stepping stone toward finding targeted, sex-based therapies to help in the management of people living with obesity.”

Although it is known that men and women with obesity have different adipose tissue distribution and have differences in metabolism more generally, this knowledge is not widely applied in obesity care.

In this study, Pekel and colleagues carried out an analysis of 1134 adults living with obesity attending a tertiary obesity clinic, including 886 women and 248 men. They measured standard factors like age, body mass index (BMI), waist and hip circumference and blood pressure as well as blood-based biomarkers like lipids, liver enzymes and inflammatory markers such as C-reactive protein, erythrocyte sedimentation rate, and white blood cell count.

The results showed that women were slightly older at 45 years on average. Men had significantly greater waist circumference and systolic blood pressure than women, as well as higher levels of the liver enzymes alanine aminotransferase and gamma‑glutamyl transferase and the kidney health biomarker creatinine. Men also had higher levels of triglycerides than women in the study.

Women with obesity had significantly higher total and low-density lipoprotein cholesterol than men in the study. They also had greater erythrocyte sedimentation rate, C-reactive protein, and platelet count, than the men.

“It’s still early days and these findings need to be confirmed in other patient groups, but they offer important insight into how obesity may affect men and women differently,” said Pekel.

“These differences are likely influenced by biological factors such as hormones, immune responses, and fat distribution. Our next steps are to validate these findings in larger populations, better understand the biological processes behind these differences, and explore how these patterns relate to clinical risk.”

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FDA Clears First AI Algorithm to Diagnose Cardiac Amyloidosis

Anumana has received FDA approval for its ECG-AI algorithm designed to support the diagnosis of cardiac amyloidosis at the point of care. This makes it the first and only AI algorithm cleared by the FDA for this severe heart condition, which is often missed by the human eye when looking at electrocardiogram (ECG) data.  

“Cardiac amyloidosis can be challenging to detect early, especially when its signs overlap with more common heart conditions,” said Martha Grogan, MD, consultant in cardiovascular medicine at Mayo Clinic and co-principal investigator of the clinical study that supported the approval. “A tool that helps clinicians recognize suspicion of amyloidosis from a routine ECG could support earlier diagnosis and more timely next steps in care.”

Caused by abnormal protein deposits in the heart, cardiac amyloidosis is a life-threatening condition that can lead to heart failure if missed. Early diagnosis is critical to ensure a timely intervention, which can significantly improve patient outcomes, but the condition is often underdiagnosed due to unspecific symptoms that can be easily mistaken for other, more common heart conditions. 

Symptoms of cardiac amyloidosis are evaluated using a routine ECG. However, diagnosis requires identifying a combination of subtle features found in ECG data, meaning human interpretation can often miss the condition. 

Anumana’s ECG-AI algorithm can analyze ECG waveform to detect these subtle patterns in the data and support the diagnosis process. In a validation study involving more than 15,000 adults presenting signs, symptoms, or comorbidities of cardiac amyloidosis, the AI model detected the condition with 78.9% sensitivity and 91.2% specificity. 

“What makes this work especially meaningful is the rigor of the validation,” said Angela Dispenzieri, MD, hematologist at Mayo Clinic and co-principal investigator of the clinical study. “This ECG-AI algorithm was validated in a large multicenter study that included both ATTR and AL cardiac amyloidosis at major referral centers with deep expertise in amyloidosis diagnosis, supporting its potential to help identify patients earlier.”

Because the algorithm leverages ECGs obtained in routine clinical practice, it can be directly integrated into existing workflows without requiring clinicians to conduct any additional testing, helping them identify patients at risk and informing treatment decisions. 

Anumana previously received FDA clearance for two other ECG-AI algorithms, one for the diagnosis of low ejection fraction and another for pulmonary hypertension. All of these heart conditions are characterized by complex diagnoses that are often delayed or missed; for these patients, early diagnosis and treatment can significantly increase their outcomes and life expectancy.

“Each of our FDA-cleared algorithms addresses a specific and frequently missed cardiovascular condition, and cardiac amyloidosis represents an important addition to that portfolio,” said Maulik Nanavaty, CEO of Anumana. “The more conditions we can identify from a single ECG, the more valuable the test becomes in clinical practice. That’s what Anumana is working toward with each new clearance as we continue to advance our rigorous clinical evidence approach.”

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Metabolic Driver of Radiation Resistance in Lung Cancer Identified

Radiation therapy remains a cornerstone of lung cancer treatment, yet its long-term effectiveness is often undermined by a persistent challenge: tumors adapt and become resistant. Understanding, and overcoming, this resistance is a major priority in oncology.

A new study from researchers at The University of Texas MD Anderson Cancer Center, published in Cancer Research, identifies a metabolic mechanism that allows lung cancer cells to evade radiation-induced death and proposes a clinically actionable strategy to counter it.

A hidden driver of resistance

Radiotherapy works by damaging cancer cells in multiple ways, including triggering ferroptosis—an iron-dependent form of cell death driven by oxidative stress. However, many tumors develop the ability to suppress this process, allowing them to survive treatment.

The new study pinpoints a key player in this resistance: the mitochondrial enzyme dihydroorotate dehydrogenase (DHODH). Researchers found that radiation exposure increases DHODH activity in lung cancer cells, enabling them to withstand ferroptosis and continue growing.

“This is an important finding because of the immediate translational opportunity,” said Boyi Gan, PhD, senior author of the study. “By understanding how DHODH is preventing cell death in radioresistant cancer cells, we were able to develop a strategy to overcome radiation therapy resistance in tumor models.”

A metabolic shield against cell death

DHODH is best known for its role in nucleotide synthesis, helping cells produce the building blocks needed for DNA repair and replication. But the study highlights an additional function that is particularly relevant in cancer.

The enzyme also supports the production of ubiquinol, a molecule that protects cells from oxidative damage. In the context of radiation therapy, this acts as a shield, preventing the lipid damage required to trigger ferroptosis.

By simultaneously promoting DNA repair and suppressing ferroptosis, DHODH enables cancer cells to survive what would otherwise be lethal radiation-induced stress.

Repurposing an existing drug

Rather than developing a new inhibitor from scratch, the researchers turned to leflunomide—an FDA-approved drug currently used to treat rheumatoid arthritis, which is known to inhibit DHODH.

In preclinical models, blocking DHODH alone modestly increased sensitivity to radiation. However, the most striking results emerged when the team combined three treatment modalities: radiation therapy, immune checkpoint blockade, and DHODH inhibition.

Radiation plus immunotherapy alone was insufficient to control tumor growth. But when leflunomide was added, the combination restored ferroptosis and led to a marked reduction in tumor progression.

“DHODH inhibition alone had some effect on sensitization to radiation therapy, but it was really this triple combination that had a marked effect,” Gan said.

Leveraging the immune response

A key aspect of the strategy lies in its interaction with the immune system. Immunotherapy, specifically anti–PD-1 checkpoint blockade, stimulates the production of interferon-gamma (IFN-γ), a signaling molecule that can enhance ferroptosis.

However, in resistant tumors, this signal alone is not enough to overcome the protective effects of DHODH. By inhibiting the enzyme, the researchers effectively remove this metabolic barrier, allowing IFN-γ–driven ferroptosis to proceed.

The result is a coordinated therapeutic effect in which radiation induces stress, immunotherapy amplifies cell death signals, and DHODH inhibition prevents tumor cells from escaping.

Toward clinical translation

One of the most compelling aspects of the study is its translational potential. Leflunomide is already widely used in clinical practice, with a well-characterized safety profile, potentially accelerating its evaluation in oncology settings.

“These findings provide a good rationale for testing this combination in clinical studies,” Gan said in a press release.

If validated in patients, this approach could offer a new strategy for overcoming resistance not only in lung cancer but potentially in other solid tumors treated with radiotherapy.

A broader shift in cancer therapy

The findings also reflect a broader trend in cancer research: targeting metabolic pathways that enable tumor survival under stress. While traditional therapies focus on directly damaging cancer cells, emerging approaches aim to disrupt the adaptive mechanisms that allow tumors to recover.

By linking metabolism, immune signaling, and cell death pathways, the study provides a more integrated view of how resistance develops—and how it can be reversed.

Although the results are based on preclinical models, they offer a clear path forward. Future clinical trials will be needed to determine whether the triple combination strategy can improve outcomes in patients with radioresistant lung cancer.

More broadly, the work highlights the importance of identifying “druggable” vulnerabilities within resistance pathways, especially those that can be targeted with existing therapies.

In this case, a drug originally developed for autoimmune disease may help solve one of the most persistent challenges in cancer treatment: restoring the effectiveness of radiation therapy when it begins to fail.

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Therapeutic Potential of GLP-1 Receptor Agonists for Smoking Cessation

Glucagon-like peptide-1 (GLP-1) therapies are under investigation for a growing number of neuropsychiatric conditions, including substance use disorders. Cigarette smoking accounts for the largest proportion of substance use-related morbidity and mortality, in part reflecting increased risk for cardiometabolic disease among people who smoke. Given modest quit rates with approved smoking cessation therapies, medications with novel mechanisms of action are needed to expand the available monotherapy and combination treatment options.