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Comment by Dr. Krishna Kumari Challa on January 25, 2025 at 11:30am

Immune checkpoint inhibitors have revolutionized cancer treatment. But not everyone responds well to these drugs. This study found that patients whose tumors had more mitochondrial mutations were less likely to benefit from checkpoint inhibitors, likely because the mitochondrial hack already compromised their T-cells.

Researchers blocked extracellular vesicle release from cancer cells using a compound called GW4869, which inhibits the production of small extracellular vesicle-like exosomes. Applying this inhibitor in their models showed a significant reduction in mitochondrial transfer from cancer cells to T-cells. This intervention helped prevent the T-cells from taking up damaged mitochondria, reducing their dysfunction.

As a result, T-cells showed improved energy production, reduced markers of exhaustion, and a better ability to perform their immune functions. The blocking strategy restored the effectiveness of immune checkpoint inhibitors, particularly in tumors with high levels of mitochondrial transfer. These findings suggest that targeting extracellular vesicles could be a promising strategy to counteract cancer's immune-evasion tactic.
Typically, science works in small, iterative steps toward discovery, with each new element of knowledge putting a piece of the larger puzzle into place. This discovery helps explain why some treatments are ineffective and discovers the mechanism behind their ineffectiveness. Remarkably, it also found a potential solution, representing a significant leap for future research to build from.

Hideki Ikeda et al, Immune evasion through mitochondrial transfer in the tumour microenvironment, Nature (2025). DOI: 10.1038/s41586-024-08439-0

Jonathan R. Brestoff, Mitochondrial swap from cancer to immune cells thwarts anti-tumour defences, Nature (2025). DOI: 10.1038/d41586-025-00077-4

Part 2

Comment by Dr. Krishna Kumari Challa on January 25, 2025 at 11:29am

Scientists uncover how cancer cells hijack T-cells, making it harder for the body to fight back

Researchers have discovered a surprising way cancer evades the immune system. It essentially hacks the immune cells, transferring its own faulty mitochondrial DNA (mtDNA) into the T-cells meant to attack it.

This sneaky move weakens the immune cells, making them less effective at stopping the tumor. The findings could help explain why some cancer treatments, like immunotherapy, are effective for some patients but not others.

In the study, "Immune evasion through mitochondrial transfer in the tumour microenvironment," published in Nature, the multi-group collaboration looked at how cancer cells interact with tumor-infiltrating lymphocytes, a type of T-cell that typically fights tumors. The research is also featured in a News and Views piece.

Clinical specimens from melanoma and non-small-cell lung cancer patients were analyzed for mtDNA mutations. Mitochondrial transfer was studied using mitochondrial-specific fluorescent reporters and multiple in vitro and in vivo models. Tumor-infiltrating lymphocyte functions, metabolic profiles, and responses to immune checkpoint inhibitors were evaluated.

Melanoma and lung sample analysis showed that mitochondria, the energy-making engines of cells, could jump from cancer cells into T-cells. These transferred mitochondria carried functional errors in their DNA that interfered with the T-cells' energy production and function processes.

Mitochondria are essential for powering cells, including T-cells, which depend heavily on energy production to fight cancer. But when cancer cells pass on their defective mitochondria, they lose their ability to function properly, throttling the energy of the T-cells and causing them to become exhausted.

Transfer was observed in two main ways: tunneling nanotubes and extracellular vesicles. The nanotubes extend out and tunnel into the T-cell, creating tiny passages between cells that deliver mitochondria directly. Extracellular vesicles form as bubbles released by the cancer cells, encapsulating mtDNA and other molecules.

Once inside the T-cells, the damaged mitochondria replace the healthy ones through a mechanism that would normally operate in reverse, where healthy mitochondria would migrate to replace damaged ones. The study found that cancer cells protect their transferred mitochondria by attaching molecules that prevent the T-cells from breaking them down.

Part 1

Comment by Dr. Krishna Kumari Challa on January 24, 2025 at 11:56am

Record-Shattering 20,000 Mph Winds Detected on Wild Alien Planet
Winds circling a gas giant more than 500 light years from Earth have been detected flowing at supersonic speeds approaching 33,000 kilometers (20,000 miles) per hour, making them the fastest air currents on any known planet by a wide margin.
Researchers from Europe cleaned and analyzed the spectrum of light reflected from the planet WASP-127b, uncovering two contrasting peaks in water and carbon dioxide signals suggestive of supersonic flows disturbing the planet's cloud tops.

Part of the atmosphere of this planet is moving towards us at a high velocity while another part is moving away from us at the same speed.
This signal shows us that there is a very fast, supersonic, jet wind around the planet's equator.

Fast is an understatement. At an incredible 7.5 to 7.9 kilometers per second, they outstrip any hurricane or jetstream known to science.
Here on Earth, the fastest puff of wind on record was a blustery 407 kilometers (253 miles) per hour, measured on Australia's Barrow Island in 1996. Neptune has the highest wind speeds in our Solar System, but even its 1,770 kilometer-per-hour high-altitude currents feel more like a mild breeze by comparison.

It's also believed to be tidally locked, rotating in step with every 4.2-Earth-day lap around its star, so one side is perpetually baked to temperatures exceeding 1,000 degrees Celsius (1832 degrees Fahrenheit), and the other never turns from the cold night sky.

https://www.aanda.org/articles/aa/full_html/2025/01/aa50438-24/aa50...

Comment by Dr. Krishna Kumari Challa on January 24, 2025 at 11:40am

Cancer cells ‘poison’ the immune system with tainted mitochondria

Immune cells lose their cancer-fighting prowess after taking tumours’ organelles on board.

Cancer cells can sabotage immune cells that try to attack them by filling them with ..., the organelles that cells rely on to make energy. In samples from three people with cancer, researchers noticed that mitochondria in both the tumour cells and immune cells called tumour-infiltrating lymphocytes (TILs) shared the same mutations. When they grew cancer cells with fluorescent-tagged mitochondria alongside TILs, the TILs had taken on some faulty mitochondria after only 24 hours. By 15 days, their native mitochondria had been replaced almost entirely. Tainted TILs were less able to divide and more likely to commit cell ‘suicide’.

https://www.nature.com/articles/s41586-024-08439-0?utm_source=Live+...

https://www.nature.com/articles/d41586-025-00176-2?utm_source=Live+...

Comment by Dr. Krishna Kumari Challa on January 24, 2025 at 11:36am

Microplastics block blood flow in the brain, mice study reveals

Real-time imaging shows how plastic-stuffed cells form clumps that affect mouse movement.

In mice, immune cells carry microplastics — specks of plastic less than 5 millimetres long — through the bloodstream, where they eventually become lodged in blood vessels in the brain. The plastic-packed cells appeared in the mice’s brains just hours after they were given polystyrene-laced water and piled up “like a car crash in the blood vessels”, says biomedical researcher and study author Haipeng Huang. The obstructions sometimes cleared eventually, but others stayed stuck for the entire month-long observation period and had effects including impairing the mice’s mobility. It’s not clear whether such blockages occur in people.

https://www.nature.com/articles/d41586-025-00178-0?utm_source=Live+...

https://www.science.org/doi/10.1126/sciadv.adr8243

Comment by Dr. Krishna Kumari Challa on January 24, 2025 at 9:55am

Researchers first took all 17,841 genetic variants from the 136 "hot spots" and inserted them into human neural cells to see how they acted in a living system. After putting the variants through the massively parallel reporter assay, researchers found that 683 of the 17,841 genetic variants had a measurable effect on gene regulation.
The researchers then categorized the 683 variants into two groups: those shared across multiple disorders (pleiotropic variants) and those specific to a single disorder (disorder-specific variants). After dividing them into categories, researchers performed a tried-and-true scientific method: compare and contrast.

Pleiotropic variants were found to be more active and more sensitive to change compared to disorder-specific variants. Researchers noted that pleotropic variants were active for much longer during brain development, compared to disease-specific ones. This extended activity suggests that pleiotropic variants may be influencing multiple stages of neurodevelopment and potentially contributing to various observable traits and disorders.

Additionally, the genes affected by these pleiotropic variants appear to be more sensitive to changes, meaning disruptions in these genes could have a bigger impact on human health.

The proteins produced by these genes are also highly connected to other proteins. Changes to these proteins in particular could ripple through the network, potentially causing widespread effects on the brain.
These findings mark an important step toward understanding how genetics contributes to shared symptoms across psychiatric disorders. Targeting these variants, their associated genes, and pathways could pave the way for treatments that address multiple conditions at once.

Sool Lee et al, Massively parallel reporter assay investigates shared genetic variants of eight psychiatric disorders, Cell (2025). DOI: 10.1016/j.cell.2024.12.022

Part 2

Comment by Dr. Krishna Kumari Challa on January 24, 2025 at 9:53am

Eight psychiatric disorders share the same genetic causes, study says

Psychiatric disorders often overlap and can make diagnosis difficult. Depression and anxiety, for example, can coexist and share symptoms. Schizophrenia and anorexia nervosa. Autism and attention deficit/hyperactivity disorder, too. But, why?

Life experiences, environment, and genetics can all influence psychiatric disorders, but much of it comes down to variations in our genetics. Over the past few years, scientists in the field of psychiatric genetics have found that there are common genetic threads that may be linking and causing coexisting psychiatric disorders.

In 2019, researchers at the Psychiatric Genomics Consortium, Harvard University, and the UNC School of Medicine identified 136 "hot spots" within the genome that are associated with eight psychiatric disorders. Among them, 109 hot spots were shared among multiple disorders, or "pleiotropic."

A new genetic study has successfully delineated the functional consequences of genetic variants into two groups. Their findings, which were published in Cell, suggest that pleiotropic variants may be optimal targets for treatment, due to their extended roles in development and sensitivity to change.

Pleiotropy was traditionally viewed as a challenge because it complicates the classification of psychiatric disorders. However, if we can understand the genetic basis of pleiotropy, it might allow us to develop treatments targeting these shared genetic factors, which could then help treat multiple psychiatric disorders with a common therapy.

The human genome acts as the body's operating manual, containing the instructions that helped us develop from a single cell into a whole person. However, everyone's genetic foundation is unique. There are specific regions of the genome that are prone to genetic variations.

Specific genetic variants can impact biological processes, like protein overproduction or altered synapse formation, affecting brain development and contributing to psychiatric disorder. But researchers are armed with tools to track these variants and learn more about the origins of disease.

In 2019, an international team of researchers at the UNC School of Medicine and the Psychiatric Genomics Consortium conducted genome-wide association studies (GWAS) on eight disorders: autism spectrum disorder, attention deficit/hyperactivity disorder (ADD), schizophrenia, bipolar disorder, major depressive disorder, Tourette syndrome, obsessive-compulsive disorder (OCD), and anorexia nervosa, to better understand the shared genetic underpinnings between psychiatric disorders. The analysis previously revealed 136 "hot spots" on the genome that have a causal effect on one or more of the eight psychiatric disorders. Of those, 109 of these locations were identical across more than one disorder.

As part of their latest study, researchers wanted to pry more information from the genetic variants embedded within these 136 "hot spots." Using a powerful technology, called a massively parallel reporter assay, they sought to determine which causal variants could be interfering with gene regulation.

Gene regulation controls how and when proteins are produced in the body, allowing the tiny machines to carry out a wide array of functions in the body. If certain variants are interfering with this important process, researchers can use that information to home in on the variants of interest and use them as new targets for treatment.

Part 1

Comment by Dr. Krishna Kumari Challa on January 24, 2025 at 9:41am

Mitochondria may be a promising therapeutic target for inflammatory diseases

Scientists have discovered how mitochondria influence the body's immune response through modulating specific cell signaling pathways, according to a study published in Science Advances.

The findings highlight the potential of targeting mitochondrial function specifically in immune cells to treat a range of inflammation-related diseases.

Therapies aimed at improving mitochondrial activity could benefit inflammatory diseases such as inflammatory bowel disease, sepsis, and chronic infections by enhancing the immune system's ability to regulate inflammation.

Mitochondria contain the mitochondrial electron transport chain (ETC), or a series of protein complexes in which electrons pass through and produce ATP, or energy, for the cell. Mitochondrial ETC function also controls macrophages, or specialized immune cells that are essential for fighting infections and regulating inflammation in the body.

Macrophages also release an anti-inflammatory protein called IL-10, which reduces inflammation and prevents excess immune responses that can harm the body. The underlying mechanisms that allow mitochondrial ETC to control macrophage immune responses, however, have remained poorly understood.

Using bulk-RNA sequencing to study mice with macrophages deficient in mitochondria ETC complex III, the scientists discovered that a type of reactive oxygen species (ROS), or unstable molecules that contain oxygen and easily react with other molecules in a cell, that is produced by mitochondrial complex III, called superoxide, is critical for macrophages to release IL-10.

The scientists also discovered those mice with the defective mitochondrial complex also struggled to recover from infection and inflammation because their cells released less IL-10. However, activating a specific ROS dependent signaling pathway in the cells restored IL-10 release, according to the study.

This finding highlights a previously unknown connection between mitochondrial activity, inflammation control and the signaling pathways that regulate it.

Overall, the findings underscore mitochondria's essential role beyond energy production and suggest that mitochondria may be a promising therapeutic target for treating a range of inflammatory diseases and enhancing current therapies, according to the researchers.

Boosting IL-10 levels through mitochondrial pathways offers promise for managing autoimmune disorders like rheumatoid arthritis and lupus, where the immune system mistakenly attacks the body. Enhancing the function of mitochondrial complex III, or mimicking its effects, may also improve recovery from severe infections. Additionally, inhibiting mitochondrial complex III would decrease IL-10 suppression of inflammation, and could cooperate with existing immunotherapies.

 Joshua S. Stoolman et al, Mitochondria complex III–generated superoxide is essential for IL-10 secretion in macrophages, Science Advances (2025). DOI: 10.1126/sciadv.adu4369

Comment by Dr. Krishna Kumari Challa on January 24, 2025 at 9:18am

Mane attraction: Molecular 'switch' may control long scalp hair

Treating hair loss may be as simple as developing therapies to flip a molecular "switch," according to a new study by researchers .

The researchers reviewed the biological and social evolution of human scalp hair. Based on their analysis, they proposed a novel theory that points to a molecular basis underlying the ability to grow long scalp hair. In short, human ancestors may have always had the ability to grow long scalp hair, but the trait remained dormant until certain environmental and biological conditions—like walking upright on two legs—turned on the molecular program.

The team published their findings, which they said could serve as the basis for future experimental work, in the British Journal of Dermatology.

Humans grow extremely long scalp hair.

Likewise, attributes of scalp hair—its length, shape, color and loss of hair—play an essential role in social communication. They signify our ancestry, age, health, sexual maturity and social status, to name but a few. And yet, despite the importance of having long scalp hair, we know very little about how this feature of human skin came about and how it is regulated.

Previous research had shown that tightly curled hair, in particular, served as an effective shield against the sun, reducing the need for excessive sweating that can cause dangerous dehydration. 

Building on this work, the researchers proposed that long scalp hair initially evolved to protect early human ancestors in equatorial Africa from the intense heat and solar radiation of their environment, and then it came to have meaning in many other spheres of life, such as signaling age, health, maturity and social status.

Long, tightly curled hair was a crucial adaptation that allowed our ancestors to thrive in hot, open environments. Understanding when long scalp hair evolved will help to better appreciate when it acquired its essential non-biological purposes.

While long hair is rare among mammals, it is not entirely unique to humans. Animals like male lions, orangutans and even now-extinct wooly mammoths also grew remarkably long hair, albeit for different reasons, according to the researchers.

What these examples tell us is that the molecular blueprint for growing very long hair has always existed, albeit often in a 'silenced' state. When human ancestors evolved their ability to grow extremely long scalp hair, it was likely accomplished by just a few genetic tweaks that reactivated a dormant program rather than via the evolution of an entirely new molecular mechanism.

The findings have broader implications for medical research, particularly in addressing hair loss, a condition that impacts millions worldwide. Understanding how human scalp hair follicles normally grow very long hair will naturally result in novel molecular targets for more efficacious therapies for hair loss.

This knowledge could lead to treatments that help restore hair growth and alleviate the emotional distress that often accompanies hair loss.

Lo-Yu Chang et al, Evolution of long scalp hair in humans, British Journal of Dermatology (2025). DOI: 10.1093/bjd/ljae456

Comment by Dr. Krishna Kumari Challa on January 24, 2025 at 9:06am

In addition to fieldwork, laboratory experiments revealed that methanotrophic microbes are remarkably adaptable. They thrive in a range of environmental conditions, including shifts in temperature, salinity, and methane levels.
As ecosystems change, methane-eating microbes adapt. When one group struggles, another takes over, keeping nature's methane filter running even in a warming world.

Tim de Groot. Environmental controls on microbial methane oxidation in the coasta... ( PhD Dissertation)

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