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Category: genetics – Page 2

A deadly fungal epidemic in Brazil is evolving fast: pollution, cats, and genetics may be fueling its unstoppable spread.

Brazil is facing the world’s largest and most persistent sporotrichosis epidemic, a fungal infection spread primarily through cats. A new study reveals an alarming genetic diversity in the fungus, suggesting that urban pollutants may be accelerating its evolution. Researchers identified molecular markers that could enhance diagnostics and treatments, while also highlighting the rapid adaptation and virulence of Sporothrix brasiliensis.

Unraveling the Largest Sporotrichosis Epidemic.

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Continue reading “Cortisol Increases During Aging: A Sign Of Low NAD?” | >

Genome sequencing of cancer and normal tissues, alongside single-cell transcriptomics, continues to produce findings that challenge the idea that cancer is a ‘genetic disease’, as posited by the somatic mutation theory (SMT). In this prevailing paradigm, tumorigenesis is caused by cancer-driving somatic mutations and clonal expansion. However, results from tumor sequencing, motivated by the genetic paradigm itself, create apparent ‘paradoxes’ that are not conducive to a pure SMT. But beyond genetic causation, the new results lend credence to old ideas from organismal biology. To resolve inconsistencies between the genetic paradigm of cancer and biological reality, we must complement deep sequencing with deep thinking: embrace formal theory and historicity of biological entities, and (re)consider non-genetic plasticity of cells and tissues. In this Essay, we discuss the concepts of cell state dynamics and tissue fields that emerge from the collective action of genes and of cells in their morphogenetic context, respectively, and how they help explain inconsistencies in the data in the context of SMT.

Citation: Huang S, Soto AM, Sonnenschein C (2025) The end of the genetic paradigm of cancer. PLoS Biol 23: e3003052. https://doi.org/10.1371/journal.pbio.

Copyright: © 2025 Huang et al. This is an open access distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Professor Kwang-Hyun Cho’s research team has recently been highlighted for their work on developing an original technology for cancer reversal treatment that does not kill cancer cells but only changes their characteristics to reverse them to a state similar to normal cells. This time, they have succeeded in revealing for the first time that a molecular switch that can induce cancer reversal at the moment when normal cells change into cancer cells is hidden in the genetic network.

KAIST (President Kwang-Hyung Lee) announced on the 5th of February that Professor Kwang-Hyun Cho’s research team of the Department of Bio and Brain Engineering has succeeded in developing a fundamental technology to capture the critical transition phenomenon at the moment when normal cells change into cancer cells and analyze it to discover a molecular switch that can revert cancer cells back into normal cells.

A critical transition is a phenomenon in which a sudden change in state occurs at a specific point in time, like water changing into steam at 100℃. This critical transition phenomenon also occurs in the process in which normal cells change into cancer cells at a specific point in time due to the accumulation of genetic and epigenetic changes.

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Ten years ago, nobody knew that Asgard archaea even existed. In 2015, however, researchers examining deep-sea sediments discovered gene fragments that indicated a new and previously undiscovered form of microbes.

With computer assistance, the researchers assembled these fragments like puzzle pieces to compile the entire genome. It was only then that they realized they were dealing with a previously unknown group of archaea.

Like bacteria, archaea are . Genetically, however, there are significant differences between the two domains, especially regarding their cell envelopes and metabolic processes.

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The researchers turned to a group of molecules called acylcarnitines, which are associated with declining cognition and breaking down or metabolizing fats and proteins for energy. To test if high acylcarnitine levels in the blood could predict who’s at risk of developing Alzheimer’s, the researchers used data from a large-scale study called the Alzheimer’s Disease Neuroimaging Initiative.

“It was fascinating,” the author said. “Dividing research participants into groups based on their specific acylcarnitine levels highlighted people with more severe Alzheimer’s disease and others with fewer symptoms.” This led the researchers to define a bioenergetic clock based on acylcarnitines—how old a person’s metabolism acts, compared to actual age. Higher bioenergetic age is linked to higher acylcarnitine levels, worsened Alzheimer’s pathology, cognitive decline and brain atrophy.

The researchers also quantified cognitive decline using a common test called the mini-mental state examination, on which a score below 24 out of 30 points indicates impairment. They found that people with low acylcarnitine levels to begin with declined more slowly, losing about 0.5 points less per year than people with high acylcarnitine levels. The benefit is on par with the Alzheimer’s drug lecanemab.

To some degree, a person’s bioenergetic clock ticks forward at a rate determined by their genetics, but having a healthy lifestyle—for example, eating a plant-based diet and exercising —can help keep acylcarnitine levels low, which means a younger bioenergetic age, the author explained.

They went on to identify a subgroup of participants, about 30% of the Alzheimer’s Disease Neuroimaging Initiative, with older bioenergetic age but favorable genetic background. These individuals may benefit more from early lifestyle interventions designed to decrease their bioenergetic age and potentially delay or prevent the onset of Alzheimer’s.

Moving forward, the senior author hopes to home in on the lifestyle interventions most effective for lowering bioenergetic age. For example, eating a low-carb diet may help maintain metabolic health, but just how low would carbohydrate consumption have to be for a person to see benefits?

Continue reading “Lowering bioenergetic age may help fend off Alzheimer’s” | >

Like people, bacteria get invaded by viruses. In bacteria, the viral invaders are called bacteriophages, derived from the Greek word for bacteria-eaters, or in shortened form, “phages.” Scientists have sought to learn how the single-cell organisms survive phage infection in a bid to further understand human immunity and develop ways to combat diseases.

Now, Johns Hopkins Medicine scientists say they have shed new light on how bacteria protect themselves from certain phage invaders—by seizing genetic material from weakened, dormant phages and using it to “vaccinate” themselves to elicit an immune response.

In their experiments, the scientists say Streptococcus pyogenes bacteria (which cause ) take advantage of a class of phages known as temperate phages, which can either kill cells or become dormant. The bacteria steal from temperate phages during this dormant period and form a biological “memory” of the invader that their offspring inherit as the bacteria multiply. Equipped with these memories, the new population can recognize these viruses and fight them off.

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A drug-resistant type of bacteria that has adapted to health care settings evolved in the past several years to weaponize an antimicrobial genetic tool, eliminating its cousins and replacing them as the dominant strain. University of Pittsburgh School of Medicine scientists made the discovery when combing through local hospital data—and then confirmed that it was a global phenomenon.

The finding, published in Nature Microbiology, may be the impetus for new approaches in developing therapeutics against some of the world’s deadliest . It also validates a new use for a system developed at Pitt and UPMC that couples genomic sequencing with computer algorithms to rapidly detect infectious disease outbreaks.

“Our lab has a front row seat to the parade of pathogens that move through the ,” said senior author Daria Van Tyne, Ph.D., associate professor of medicine in Pitt’s Division of Infectious Diseases. “And when we took a step back and zoomed out, it quickly became apparent that big changes were afoot with one of the world’s more difficult-to-treat bacteria.”

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