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Promising therapeutic approach identified for multiple myeloma

by Dr. Michael Lee – Health Editor
written by Dr. Michael Lee – Health Editor

New Drug Combo Targets Myeloma Growth

Uppsala University Study Uncovers Promising Dual-Action Therapy for Blood Cancer

A significant stride in combating the persistent blood cancer, multiple myeloma, has been made by researchers at Uppsala University. Their recent preclinical findings reveal a dual-drug approach that effectively curbs tumor expansion and triggers cancer cell demise.

Targeting Epigenetic Regulators

Multiple myeloma, a challenging bone marrow malignancy, remains incurable despite advancements in treatment. The disease is marked by significant genetic and clinical variability, often seen as rapid proliferation of antibody-producing immune cells. Crucial to its progression are epigenetic alterations—changes to the genome not caused by direct mutations, which influence gene activity and cell growth.

The Uppsala University team zeroed in on two proteins, G9a and DNMTs, known to play a role in multiple myeloma’s development and linked to poorer patient prognoses. Inhibiting these specific proteins in laboratory settings, using cultivated cancer cells and actual patient samples, yielded substantial reductions in cell viability and promoted programmed cell death, also known as apoptosis.

“The proteins we focused on are called G9a and DNMTs. We treated cultivated both cancer cells and primary patient samples with two different drug substances that inhibit these proteins. We found that this significantly reduced cell viability and induced apoptosis – programmed cell death. The combination therapy also led to a notable decrease in the levels of critical oncoproteins.”

—Patrick Nylund, Postdoctoral Researcher, Department of Immunology, Genetics and Pathology

Synergistic Effect in Preclinical Models

Further investigations using a mouse model demonstrated a synergistic impact when both G9a and DNMT inhibitors were administered together. This combined treatment resulted in greater tumor growth reduction than would be expected from the sum of individual treatments.

This dual inhibition strategy also activated tumor suppressor genes and a range of genes associated with apoptosis, amplifying the anti-tumor effects observed. The research, a collaboration involving institutions in Sweden, Belgium, and Spain, provides the first preclinical backing for simultaneously targeting both DNMTs and G9a as a therapeutic avenue.

This breakthrough is particularly encouraging given that multiple myeloma affects approximately 30,000 individuals in the United States annually, with about 12,600 new cases expected in 2024, according to the American Cancer Society (American Cancer Society 2024).

Professor Helena Jernberg Wiklund, who spearheaded the study, noted, “Our research offers important insights into how G9a and DNMTs cooperate to mediate gene silencing through epigenetic mechanisms in multiple myeloma. This study is the first preclinical evidence to support the therapeutic potential of simultaneously targeting both DNMTs and G9a. This is exciting for the development of new therapeutic strategies for this challenging disease.”

Source: Nylund, PW, et al. (2025). Dual targeting of G9a and DNMTs induces anti-tumour effects in multiple myeloma. Blood Advances. doi.org/10.1182/bloodadvances.2023010571.

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Health

Immune System Defends Against Parasitic Worms: NSAIDs Could Offer New Treatment

by Dr. Michael Lee – Health Editor
written by Dr. Michael Lee – Health Editor

Here’s a breakdown of the key takeaways from the provided text about type 2 immune responses and Gasdermin C:

Understanding Type 2 Immunity:

Purpose: Primarily a defense against external threats like parasites.
 Mechanism: Works by driving inflammation and accelerating cell turnover and differentiation, making the environment inhospitable to parasites and expelling them.
association: Erroneous activation is linked to food and environmental allergies.

The Role of Gasdermin C:

Revelation: Researchers identified Gasdermin C as a protein that increases in response to parasitic infection.
Activation: It’s activated by an enzyme called Cathepsin S, which chops it in half.
 Essential for Immunity: Both Gasdermin C and Cathepsin S are crucial for type 2 immune responses against helminth parasites, as demonstrated in mouse studies.

How Gasdermin C Works (Uniquely):

Different from other Gasdermins: Unlike most gasdermins that trigger cell death, Gasdermin C’s active fragment has a different function.
 targets Vesicles: It targets and penetrates Rab7-positive vesicles (cellular transport structures).
Reduces Prostaglandin D2: This action leads to a reduction in prostaglandin d2, a chemical messenger.
 boosts Immunity: By lowering prostaglandin d2 (which normally dampens type 2 responses), Gasdermin C enhances immunity and helps clear parasitic infections.

Therapeutic Implications:

New perspectives: The findings offer new avenues for anti-parasitic therapies.
 COX Inhibitors: Cyclooxygenase (COX) inhibitors, like NSAIDs (e.g., ibuprofen), are a promising approach because prostaglandin d2 synthesis relies on COX. These are widely available and generally safe.
Caution: Clinical trials are needed to confirm effectiveness in humans, and medical advice should be sought before using new medications.Connection to Gut Microbiome and Allergies:

Commensal Microbes: Certain harmless gut microbes can trigger type 2 immunity in mice.
Disease Contribution: This suggests that commensal microbes might contribute to symptoms in conditions like food allergies and inflammatory bowel disease (IBD) when type 2 immune responses are involved.
 Potential Biomarker: Identifying microbes that induce Gasdermin C could potentially serve as a marker or predictor for food allergy risk.

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Health

New approach doubles chemotherapy effectiveness by targeting cancer cell memory

by Dr. Michael Lee – Health Editor
written by Dr. Michael Lee – Health Editor

Scientists Disrupt Cancer’s Defense Mechanism, Boosting Chemo Efficacy

Novel Approach Targets Cellular Adaptability, Not Just Tumors

A groundbreaking strategy from Northwestern University engineers has demonstrated the potential to significantly enhance chemotherapy’s power by preventing cancer cells from adapting and resisting treatment, a key factor in treatment failure.

Unlocking Chemo’s Full Potential

Researchers have discovered a way to neutralize cancer’s remarkable ability to evolve and withstand therapies. This new method focuses on the internal scaffolding of cancer cells, known as chromatin, which governs gene expression and cellular responses to stress. By subtly altering chromatin’s physical structure, scientists believe they can disarm cancer’s adaptive superpowers, making existing chemotherapy drugs far more effective.

This innovative approach achieved near-complete eradication of cancer in laboratory cell cultures. In animal trials involving human ovarian cancer models, the combination therapy dramatically improved the outcomes compared to chemotherapy alone.

“Cancer cells are great adapters. They can adapt to almost anything that’s thrown at them… We did not set out to directly kill cancer cells. We wanted to take away their superpower—removing their inherent abilities to adapt, to change and to evade.”

—Vadim Backman, Lead Study Author and Professor at Northwestern University

The findings, published in the Proceedings of the National Academy of Sciences, suggest that rather than developing new, potent drugs, the focus can shift to optimizing the delivery and efficacy of current treatments by inhibiting cancer’s resilience. This could lead to less toxic treatment regimens and improved patient quality of life.

Chromatin: The Key to Cancer’s Tenacity

Cancer’s persistent survival, even when faced with aggressive treatments, has long puzzled scientists. While genetic mutations play a role, they don’t fully explain the rapid adaptive responses observed. Researchers led by **Vadim Backman** identified the intricate organization of DNA and proteins within the cell nucleus, known as chromatin, as the critical factor. This complex structure not only controls gene activity but also acts as a cellular memory system, enabling cells to adapt to changing environments and stresses.

When this chromatin architecture becomes disordered, cancer cells gain increased “plasticity,” allowing them to quickly develop resistance to therapies like chemotherapy. The precise 3D arrangement of chromatin stores “transcriptional memory,” guiding cellular function and adaptation.

Reprogramming Cell Memory to Enhance Treatment

The Northwestern team developed a computational model to analyze how chromatin packing influences cancer cell survival. Their research pinpointed celecoxib, an existing anti-inflammatory medication, as a compound capable of modulating chromatin structure and reducing cellular plasticity. By combining celecoxib with standard chemotherapy agents, the researchers observed a significant increase in cancer cell death.

In preclinical trials, the combination of paclitaxel (a common chemotherapy) with celecoxib in mice with ovarian cancer significantly slowed tumor growth compared to paclitaxel alone. “It doubled the efficacy,” **Backman** stated, highlighting the substantial benefit of this combined approach.

The ability to make chemotherapy more effective could also allow for lower, more tolerable doses, potentially alleviating the severe side effects that often lead patients to discontinue treatment. For instance, in 2023, the American Cancer Society reported that over 1.9 million new cancer cases were diagnosed in the U.S. alone, underscoring the immense need for more effective and less burdensome treatments (American Cancer Society).

Future Applications Beyond Cancer

While initially focused on cancer, **Backman** believes that modulating chromatin conformation could offer therapeutic benefits for a range of complex diseases, including neurodegenerative conditions and heart disease. Many debilitating illnesses may stem from cells losing their correct functional “memories,” leading to loss of function or disease development. Restoring these cellular memories through chromatin reprogramming could offer a pathway to recovery.

“In many diseases, cells forget what they should be doing,” **Backman** explained. “Many impactful diseases of the 21st century are, to a large extent, related to cell memory.” He likens the computational processes within each cell’s chromatin to an early computer, emphasizing its capacity for storing and potentially altering cellular memory. This discovery could unlock a new era of “source code” manipulation for treating a variety of human ailments.

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Health

Dual cancer drugs restore memory and rewire brain cells in Alzheimer’s mouse models

by Dr. Michael Lee – Health Editor
written by Dr. Michael Lee – Health Editor

Alzheimer’s Breakthrough: Cancer Drugs Reverse Memory Loss in Mice

A pioneering study reveals that a combination of two repurposed cancer drugs shows remarkable promise in restoring memory and correcting brain cell dysfunction in mice models of Alzheimer’s disease, hinting at a new era of multi-targeted therapies.

Targeting Brain Cell Networks

Researchers explored combining letrozole, an aromatase inhibitor, with irinotecan, a topoisomerase I inhibitor. Their goal was to reverse specific transcriptomic disturbances identified in various brain cell types affected by Alzheimer’s disease (AD), ultimately aiming to improve cognition and reduce disease pathology.

A Complex Challenge

Dementia affects millions globally, with Alzheimer’s disease projected to triple its prevalence by 2050. Current treatments, primarily monoclonal antibodies targeting amyloid-beta, offer limited cognitive benefits, underscoring the need to address the intricate dysfunctions across neurons and glial cells, which are intricately linked in AD progression.

Repurposing for Faster Intervention

The strategy of repurposing existing, approved drugs offers a potentially faster and safer path to new treatments. However, many existing therapies focus on single targets, failing to address the broad cellular heterogeneity observed in AD. This study specifically sought to correct multi-cell-type network imbalances.

Identifying Promising Candidates

The research team identified 25 drugs with predicted multi-cell-type effects. Further analysis of human clinical records revealed that only five correlated with a reduced risk of AD. Among these, letrozole and irinotecan were chosen for their complementary potential in targeting both neuronal and glial cells, offering hope for a dual-action approach.

Preclinical Validation

To test their hypothesis, scientists utilized mouse models genetically engineered to mimic key aspects of Alzheimer’s disease. Mice received either a placebo, letrozole, irinotecan, or the combination therapy over three months. Cognitive function was assessed using the Morris water maze, and brain tissue was analyzed for key pathological markers and transcriptomic changes.

Cognitive Recovery and Reduced Pathology

The study’s results were striking. While individual drugs showed some benefits, the combination therapy significantly restored both short- and long-term spatial memory in the mice. This dual treatment also demonstrated superior effects in preserving hippocampal volume, reducing both amyloid-beta plaques and, crucially, phosphorylated tau, a hallmark of AD progression. Furthermore, the combination therapy modulated glial inflammation and preserved neuronal loss, with synergistic effects observed.

Rewiring Gene Networks

At the molecular level, parallel hippocampal single-nucleus RNA sequencing confirmed that the combined regimen effectively rewired disease-specific gene networks across multiple cell types. The treatment normalized gene expression, including APOE in microglia, astrocytes, and oligodendrocyte precursor cells, and reversed neuronal gene expression associated with estrogen signaling and synaptic plasticity, while glial gene expression changes pointed to reduced oxidative stress and improved cholesterol transport.

Future Directions

The findings suggest that this repurposed combination therapy offers a powerful, cell-type-directed strategy for Alzheimer’s disease. While promising, further research is needed to confirm these results in human clinical trials, with a particular focus on understanding and addressing any sex-specific efficacy differences observed in the preclinical models. According to the Alzheimer’s Association, over 6 million Americans are currently living with Alzheimer’s disease, a number projected to nearly double by 2060 (Alzheimer’s Association, 2024).

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Health

Pancreatic Cancer: STAT3 Link & Early Detection Strategy

by Dr. Michael Lee – Health Editor
written by Dr. Michael Lee – Health Editor

Here’s a rewritten version of the article, focusing on clarity and conciseness while retaining the key details:

New Gene Signature Could Predict aggressive Pancreatic Cancer

San Diego, CA – Researchers at the University of California San Diego School of Medicine have identified a crucial link between cellular stress, inflammation, and the progression of pancreatic ductal adenocarcinoma (PDAC), one of the deadliest forms of cancer. This revelation could lead to an early warning system for the disease, potentially allowing for detection before it becomes life-threatening.

Previous research indicated that inflammation and cellular stress activate a protein called STAT3 in pancreatic cells, contributing to tumor growth and treatment resistance. The new study sheds light on how STAT3 achieves this.

The UC San Diego team found that in the face of inflammatory signals and low oxygen levels (a common stressor), STAT3 activates specific genes essential for cell adaptation. Notably, they discovered that STAT3 turns on the gene integrin β3 (ITGB3) in both mouse and human pancreatic cells.

Key findings from the study include:

ITGB3’s Role: Increased expression of ITGB3 was found to promote the initial advancement and accelerate the progression of PDAC tumors.
 Chemotherapy’s Impact: Inflammation and stress caused by chemotherapy also activated STAT3, leading to higher ITGB3 levels in PDAC cells.
Blocking the Pathway: Inhibiting the STAT3 pathway that controls ITGB3 expression slowed down tumor initiation.
 The “STRESS” Signature: STAT3 activates a group of 10 genes, including ITGB3, which the researchers have named the “STRESS” gene signature. This signature proved to be a more accurate predictor of pancreatic cancer development and tumor aggressiveness compared to existing gene signatures.

These findings hold significant promise for precision medicine. The “STRESS” signature could be used to develop early screening tools for precancerous cells. Furthermore,it may help clinicians identify patients at higher risk of aggressive disease and predict their response to traditional treatments as the cancer progresses.

The researchers are now investigating molecules that can block the inflammation-driven activation of ITGB3. This approach could potentially be applied to other cancers that affect tissue surfaces,such as lung,breast,and skin cancers,to prevent tumor progression,spread,and drug resistance.

Source: University of California – San Diego
Journal Reference: Campos,A. D., et al. (2025). A STAT3/integrin axis accelerates pancreatic cancer initiation and progression. Cell Reports. doi.org/10.1016/j.celrep.2025.116010

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Health

Australian study uncovers first potential prophylactic treatment against HTLV-1

by Dr. Michael Lee – Health Editor
written by Dr. Michael Lee – Health Editor

HIV Drugs Offer Hope for Neglected HTLV-1 Virus

Breakthrough Study Identifies Potential Treatments to Halt Transmission and Clear Infection

A major scientific advance may soon provide the first preventative treatments for the human T-cell leukaemia virus type 1 (HTLV-1), a widespread and dangerous infection that currently lacks effective therapies. The research also points toward a future cure.

Promising Suppression Found

New research, co-led by Australian scientists, has discovered that existing HIV medications can significantly reduce the transmission of the HTLV-1 virus in laboratory mice. This groundbreaking work, published in the journal Cell, could pave the way for crucial interventions, particularly for First Nations communities where the virus is endemic.

The study by WEHI and the Peter Doherty Institute for Infection and Immunity also pinpointed a novel drug target. This could lead to strategies for eradicating HTLV-1 from infected individuals, thereby preventing the progression of associated diseases.

Key Findings Unveiled

Researchers found that two specific HIV antivirals, already approved for human use, effectively suppressed HTLV-1 transmission in mice. This marks the first identification of a prophylactic treatment against HTLV-1. Furthermore, when combined with a compound that triggers cell death, these HIV drugs eliminated infected cells, suggesting a potential curative approach.

These unprecedented results may allow these existing drugs to be tested in clinical trials, aiming to prevent the establishment of pathogenic levels of HTLV-1 infection.

Understanding HTLV-1

HTLV-1 infects T cells, a vital component of the immune system responsible for fighting off infections, much like HIV. While most infected individuals remain asymptomatic, a small percentage develop severe conditions such as adult T-cell leukemia and inflammatory conditions affecting the spinal cord.

Dr Marcel Doerflinger, a study co-lead author and WEHI laboratory head, stated the findings offer much-needed hope. Our study marks the first time any research group has been able to suppress this virus in a living organism, he commented. As HTLV-1 symptoms can take decades to appear, by the time a person knows they have the infection the immune damage is already in full swing. He added that stopping the virus at transmission could prevent irreversible immune damage.

Developing a New Model

Over a decade, the research team developed a world-first humanized mouse model for HTLV-1. This innovative model allowed them to observe the virus’s behavior within a human-like immune system. The mice, engrafted with human immune cells susceptible to HTLV-1, developed leukemia and lung disease when infected with both international and Australian strains of the virus.

Treatment with tenofovir and dolutegravir, both HIV antivirals, demonstrated powerful suppression of HTLV-1. What’s most exciting is that these antivirals are already in use for millions of HIV patients, meaning there’s a direct path for the clinical translation of our findings, said Dr Doerflinger. We won’t have to start from scratch because we already know these drugs are safe and effective. And now we’ve shown that their use can very likely be extended to HTLV-1.

A Dual Approach to Treatment

Remarkably, the study also revealed that combining HIV drugs with a therapy targeting the MCL-1 protein, which helps rogue cells survive, could selectively destroy HTLV-1-infected human cells. The team is now exploring precision RNA therapies to target MCL-1, aiming to create combination treatments for clinical testing and a potential cure.

Crucial Insights into Viral Strains

The development of the crucial humanized mouse models was led by first author Dr James Cooney and study lead author, WEHI Honourary Fellow and Executive Director at Centenary Institute, Professor Marc Pellegrini. Professor Pellegrini highlighted the models’ importance not only for identifying therapeutic targets but also for understanding how different HTLV-1 strains influence disease outcomes, particularly the unique Australian variant, HTLV-1c.

It’s long been hypothesised that differences in viral subtype may influence disease outcomes, but a lack of research into HTLV-1 has made it difficult for us to find the evidence needed to support this claim – until now, stated Professor Pellegrini. Our study provides critical insights that enable us to better understand the consequences of the distinct molecular make-up of the virus affecting our First Nations communities.

Advocacy and Future Directions

Associate Professor Lloyd Einsiedel, a Clinician Scientist at the Doherty Institute, played a key role in obtaining human HTLV-1 samples for the mouse models through his extensive clinical work in Central Australia. This research, co-led by Professor Damian Purcell from the University of Melbourne, identified significant genetic differences in the HTLV-1c strain compared to international strains, with the Australian variant showing more aggressive disease characteristics in the mice. Notably, the identified drug therapies proved equally effective against both strains.

Professor Purcell and Associate Professor Einsiedel, in collaboration with the National Aboriginal Community Controlled Health Organisation (NACCHO) and the Australian Department of Health, successfully advocated for the World Health Organization (WHO) to classify HTLV-1 as a Threatening Pathogen to Humans in 2021. This led to global policies aimed at reducing transmission and the development of clinical guidelines for HTLV-1c in Central Australia.

Despite Australia’s high burden of HTLV-1, the virus and its associated diseases are still not notifiable in most states and true infection rates in the nation remain unknown, observed Professor Purcell. People at risk from HTLV-1 deserve biomedical tools like those that provide game-changing therapeutic and prevention options for other blood-borne persistent viral infections, such as HIV. He emphasized the significant opportunity to prevent HTLV-1 transmission and end its associated diseases.

The research team is currently in discussions with pharmaceutical companies to include HTLV-1 patients in ongoing HIV antiviral clinical trials. Success in these discussions could establish these drugs as the first approved pre-exposure prophylaxis for HTLV-1 acquisition.

The research was supported by The Australian Centre for HIV and Hepatitis Virology Research, The Phyllis Connor Memorial Trust, Drakensberg Trust, and the National Health and Medical Research Council (NHMRC).

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