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Genetic engineering in non-human primates has long been limited by the need for virus-based gene delivery methods. Recently, researchers in Japan successfully used a nonviral system to introduce a transgene—that is, a gene that has been artificially inserted into an organism—into cynomolgus monkeys, which is a species of primate closely related to humans. The paper is published in the journal Nature Communications.

Small animal models such as mice do not fully replicate the complexity of human diseases, particularly in areas like infectious disease and neuropsychiatric disorders. This limitation has made non-human primates an essential model for .

However, genetic modification of these primates has been challenging. For example, conventional virus-based methods require specialized containment facilities and are limited in terms of the size of transgenes that the viruses can carry. Also, these methods do not allow for precise selection of modified embryos before implantation.

A joint team of professors—Hajun Kim, Taejoon Kwon, and Joo Hun Kang—from the Department of Biomedical Engineering at UNIST has unveiled a novel diagnostic technique that utilizes artificially designed polymers known as peptide nucleic acid (PNA) as probes. The research is published in the journal Biosensors and Bioelectronics.

The fluorescence in situ hybridization (FISH) technique works by detecting fluorescent signals generated when probe molecules bind to specific genetic sequences in bacteria. This innovative FISH method employs two PNA molecules simultaneously. By analyzing the of 20,000 bacterial species, the research team designed PNA sequences that specifically target the ribosomal RNA of particular species.

The method is significantly faster and more accurate than traditional bacterial culture and (PCR) analysis, and it holds promise for reducing mortality rates in critical conditions such as sepsis, where timely administration of antibiotics is crucial.

Sporotrichosis, a neglected tropical disease caused by Sporothrix species, is a growing concern, particularly due to the emergence of highly virulent, cat-transmitted S. brasiliensis. Rapid diagnosis and surveillance are crucial for controlling sporotrichosis. This study investigated the 3-carboxymuconate cyclase (CMC) gene, which encodes the major Sporothrix antigen (Gp60–70), as a molecular marker to understand the genetic diversity and evolution of these fungi. Analysis of 104 isolates (S. brasiliensis, S. schenckii, S. globosa, and S. luriei) revealed 79 unique haplotypes, demonstrating superior discriminatory power over traditional molecular markers. High–CMC polymorphisms, especially in S. brasiliensis and S. schenckii, suggest recent population expansion or positive selection, potentially driven by environmental pressures such as polyaromatic hydrocarbon pollutants. The conserved chromosomal location of CMC in pathogenic Sporothrix and its absence in less virulent species suggest a role in virulence. Identifying conserved residues within predicted B-cell epitopes provides targets for diagnostics and therapeutics. Additionally, we identified N-linked glycosylation sequons (e.g. NGS at 62, NNT at 225, and NGT at 373/374) conserved in pathogenic Sporothrix but absent in environmental Sordariomycetes, possibly contributing to pathogenicity and niche adaptation. This study establishes CMC as a valuable marker for understanding Sporothrix evolution and virulence, aiding in sporotrichosis management.

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Sunburns and aging skin are obvious effects of exposure to harmful UV rays, tobacco smoke and other carcinogens. But the effects aren’t just skin deep. Inside the body, DNA is literally being torn apart.

Understanding how the body heals and protects itself from DNA damage is vital for treating genetic disorders and life-threatening diseases such as cancer. But despite numerous studies and medical advances, much about the molecular mechanisms of DNA repair remains a mystery.

For the past several years, researchers at Georgia State University tapped into the Summit supercomputer at the Department of Energy’s Oak Ridge National Laboratory to study an elaborate molecular pathway called nucleotide excision repair, or NER relies on an array of highly dynamic protein complexes to cut out, or excise, damaged DNA with surgical precision.

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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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.

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.

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.