A trailblazer in medical research, Dr Damane is spearheading the development of a cancer immunology research programme focused on addressing questions that are particularly relevant to African populations. Her research spans immuno-oncology, immunogenomics and molecular biomarkers, with a growing focus on understanding cancer within the African context and contributing to more precise, inclusive and equitable approaches to cancer research.

For Dr Damane, the journey into cancer research carries a deeply personal dimension. She lost her mother to leukaemia, an experience that strengthened her desire to understand the biology of diseases that had touched her family and contributed to her decision to pursue Haematology and Cell Biology. Years later, the loss of her father to mesothelioma broadened her scientific interests towards solid cancers and surgical oncology.

These experiences did not define her career. Rather, they gave personal meaning to a scientific path she had already chosen and strengthened her commitment to understanding cancer and improving outcomes for those affected by it.

Behind those qualifications lies a journey that demanded persistence, sacrifice and resilience. As Dr Damane reflects:

Her research programme also presents opportunities for multidisciplinary collaboration across immunogenomics, oncobiome, biomarker discovery, molecular oncology and clinical cancer research. By bringing these areas together, Dr Damane is helping build research programmes around questions that matter directly to cancer prevention, diagnosis and treatment in Africa.

But Dr Damane’s contribution extends beyond the laboratory.

She is committed to making science accessible and meaningful to wider communities through newspaper features, radio interviews and educational outreach initiatives. She also actively encourages young people particularly from underserved communities to consider careers in medical science.

Her work therefore represents more than the advancement of a scientific field. It reflects the importance of building research capacity on the continent, asking questions that arise from African populations and creating opportunities for the next generation of African scientists to participate in shaping the future of medicine.

Researchers working through the African Microbiome Project analysed wastewater from several treatment plants in the City of Tshwane. They found that extracellular DNA carrying antimicrobial resistance genes remained in water released into the environment after standard treatment. Extracellular DNA is genetic material released when bacterial cells break apart. Some microorganisms can incorporate this material into their own DNA, allowing resistance to spread even when the original bacteria are no longer present.

Some of the genes detected were linked to resistance against antibiotics of last resort. The findings do not mean that treated wastewater directly causes disease, but they identify a pathway through which resistance may survive treatment and potentially re-enter communities through drinking water, food production or recreational exposure.

The researchers argue that antibiotic resistance must be understood as both a medical and environmental issue. Monitoring systems should include genetic material, wastewater technologies may need to incorporate treatments, and stronger collaboration is needed among policymakers, engineers, microbiologists and public health practitioners. _________________________________________________________________________________________________________

By Thulani P. Makhalanyane, John Paul Makumbi, The Conversation

The article can be accessed on: Phys.org

Image Credit: Pixabay/CC0 Public Domain

Ekaterina V. Vinogradova and Kivanç Birsoy are combining expertise in cancer metabolism, organelle biology, chemical proteomics and mass spectrometry to investigate these processes. Their teams are creating tools that measure functional changes across thousands of proteins, including changes in chemically sensitive amino acids caused by oxidation, altered protein structures and interactions with metabolites. The researchers are building an atlas of how individual metabolites affect cysteine reactivity across the proteome. This reference could help distinguish whether protein changes in cancer cells are caused by oxidation, metabolite binding or other mechanisms.

Their work has already identified a role for the protein SLC33A1 in maintaining redox balance in the endoplasmic reticulum. SLC33A1 exports oxidised glutathione when levels become too high, suggesting that increasing its activity could restore balance in cancers where redox metabolites accumulate.

The team is now applying its tools to pancreatic cancer models and expanding the mapping of protein-metabolite interactions across organelles and whole cells. By identifying cancer-specific metabolic signatures, the researchers hope to uncover overlooked protein vulnerabilities and potential therapeutic targets.

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By Katherine Fenz, Rockefeller University

The article can be accessed on: Medicalxpress

Image Credit: bioRxiv (2026). DOI: 10.64898/2026.03.04.709614

The method, called mCHIRA, allows scientists to insert hundreds or thousands of regulatory DNA sequences, including enhancers and promoters, into a specific location in the genome. Researchers can then test how sequences influence transcription factor binding, enhancer accessibility and transcription while controlling for the effects of the surrounding genomic environment. Enhancers are DNA sequences that help regulate gene expression. Proteins known as transcription factors bind to them and increase the likelihood that associated genes become active. The researchers found that when several transcription factors bind to an enhancer, its probability of becoming accessible rises more strongly than when individual transcription factors bind alone. The study combined mCHIRA with single-molecule footprinting, which measures DNA sequence variation and epigenetic marks in individual cells. Analysis was supported by FootprintCharter, a computational framework developed by co-first author Guido Barzaghi with Judith Zaugg’s computational biology group.

First author Valentina Baderna said mCHIRA separates the effects of a regulatory sequence from those of its genomic environment. Group leader Arnaud Krebs said combining synthetic biology and quantitative genomics can break genome complexity into manageable components and reveal the principles connecting DNA sequence to gene regulation. Future integration with artificial intelligence could extend this work to a larger scale.

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By Shreya Ghosh, European Molecular Biology Laboratory

The article can be accessed on: Phys.org

Image Credit: Daniela Velasco/EMBL

Most people drive through Kruger National Park hoping to spot the Big Five. Few notice the small metallic insects racing across the road beneath their tyres. Yet one of South Africa’s greatest ecological engineers is not a lion or an elephant, but it’s a dazzling bronze dung beetle called Kheper nigroaeneus, better known as the Large Copper Dung Beetle.

Growing to an impressive 25–30 mm in length, K. nigroaeneus is one of South Africa’s largest metallic copper dung beetles and among the heavyweight members of the genus Kheper. It occurs throughout the wooded savannas of South Africa, particularly in protected areas such as Kruger National Park, where healthy populations of elephants, buffalo and antelope provide the fresh dung on which it depends.

What makes this beetle extraordinary isn’t its size or its shimmer, but its sense of direction.

Instead of wandering randomly, the Large Copper Dung Beetle rolls its perfectly sculpted dung ball in a remarkably straight line by reading the position of the Sun and the pattern of polarized light in the sky. This celestial compass helps it escape crowded dung piles before competitors steal its prize. Scientists have even discovered that larger individuals roll larger dung balls faster, giving them a competitive advantage in the race for survival.

But these glittering recyclers do far more than tidy the landscape. Every dung ball they bury fertilises the soil, returns nutrients to the ground, improves water infiltration, reduces parasites and flies, and disperses seeds across the African savanna. Without dung beetles, animal waste would accumulate, grazing lands would deteriorate, and nutrient cycling would slow dramatically.

Although Kheper nigroaeneus is not currently considered threatened, many dung beetle species across southern Africa are under increasing pressure. Expanding agriculture, urban development, pesticide use, fencing, and the decline of large wild mammals reduce both habitat and the steady supply of dung these insects require. Climate change is adding further stress by altering rainfall patterns that trigger breeding and emergence. Conserving wildlife therefore also protects the remarkable insects working quietly beneath them.

Their importance extends well beyond the field and into modern genetics laboratories. Researchers are  interested in sequencing dung beetle genomes to understand evolution, behaviour and adaptation. At the High Molecular Weight (HMW) DNA Jamboree last week  obtaining long, intact DNA needed for long-read sequencing technologies such as Oxford Nanopore and PacBio was surprisingly difficult.

The challenge began when preparing the sample material used for extraction. Because dung beetles feed on dung packed with bacteria, fungi and environmental microbes, accidentally puncturing the gut can release its contents over the surrounding tissues. This resulting in contamination with microbial DNA that can complicate data analysis. For this reason, researchers carefully cleaned the exterior of the beetles and used a leg or part of a leg while carefully avoiding the digestive tract to obtain tissue for genomic DNA extraction.

The HMW DNA extraction Jamboree provided an opportunity to test different extraction methods designed to minimise mechanical damage and preserve ultra- very long DNA molecules which are ideal long read DNA sequencing. This data can then be used for modern genome assembly. While further work is still needed before the genomes can be sequenced, the Jamboree was a good start on this journey.

So, the next time you see a bronze beetle rolling what appears to be nothing more than a ball of dung, remember that you’re watching one of nature’s master navigators, an essential ecosystem engineer, and perhaps the next species to unlock new discoveries in genetics. In South Africa’s wild places, the future of the savanna may depend as much on these shimmering copper giants as it does on the animals that leave their precious cargo behind.

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By Mpho Makgabutlane

Edited by : Prof Catherine Sole & Renate Zipfel

Cancer genomicist Jenny Yang became interested in the microbiome while studying cancer genetics and personalised medicine. Drawing on her experience developing translational artificial intelligence tools, she joined Alex Merwin to establish Outpost Bio, an AI-centred biotechnology company focused on studying microbial interactions in the human body. The team is developing an in vitro human microbiome model to investigate how drugs and dietary changes affect microbial communities and how differences between people’s microbiomes influence drug metabolism. Using stool samples, the researchers culture microbial communities to create “gut in a tube” models. They apply genomic and metabolomic analyses to characterise community composition and interactions before using artificial intelligence to identify patterns.

Outpost Bio is building a biobank using samples from geographically diverse populations to capture individual variation. The researchers aim to collect thousands of samples while maintaining consistent methods for collection, storage, culturing and analysis. Their first artificial intelligence model used published human microbiome genomic data and contained more than 500,000 data points. The team is refining the model with data and has worked with external groups to validate the system.

The researchers are now obtaining clinical samples to test their in vitro and computational models. Their longer-term goal is to support the development of drugs that work across more people and improve patient-drug matching.

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By Shelby Bradford, PhD

The article can be accessed on: The Scientist

Image Credit: The Scientist ©iStock.com, sorbetto

SPOP forms part of an E3 ubiquitin ligase complex that controls the levels of selected cellular proteins, including the gene regulators BRD2, BRD3 and BRD4. When these proteins are not properly regulated, they can contribute to cancer development. Although some SPOP mutations interfere directly with substrate binding, mutations found elsewhere in the protein have been more difficult to understand. Using structural studies, the researchers found that SPOP can switch between two distinct assemblies. In its inactive state, between 22 and 30 SPOP molecules form two stacked rings described as a “double donut”. When activated by its binding partner Cullin-3, SPOP instead favours a linear filament.

The study showed that cancer mutations can disrupt the normal balance between these states. Gain-of-function mutations, which increase SPOP activity, favour the active filament form. Loss-of-function mutations, which reduce its activity, favour the inactive double-donut structure. These mutations may therefore prevent SPOP from responding normally to cellular signals. The researchers also linked SPOP structure to its location within nuclear speckles, which are membraneless compartments inside the nucleus. The inactive form was strongly associated with these speckles, while activating mutations moved SPOP into the surrounding environment.

The findings provide a structural framework for understanding previously unexplained SPOP mutations and may support future efforts to control SPOP activity therapeutically. However, several common cancer mutations remain unexplained, indicating that further research is needed.

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By St. Jude Children’s Research Hospital

The article can be accessed on: Medicalxpress

Image Credit: Molecular Cell (2026). DOI:10.1016/j.molcel.2026.06.030

MASLD ranges from metabolic dysfunction-associated steatosis (MASL), characterised by fat accumulation, to metabolic dysfunction-associated steatohepatitis (MASH), which involves chronic inflammation and fibrosis. MASH can progress to cirrhosis and liver cancer and may ultimately require a liver transplant. To examine how liver macrophages change as MASL progresses to MASH, researchers at KU Leuven, UZ Leuven and Newcastle University analysed human liver samples using spatial multi-omics, single-nucleus RNA sequencing and functional assays. The study was published in Nature Genetics.

The researchers identified eight transcriptionally distinct macrophage groups, including metabolically active macrophages, or MetMacs. As disease progressed, Kupffer cell numbers declined while MetMacs increased. In MASH samples, MetMacs showed increased expression of genes linked to inflammation and interactions with other liver cells. Spatial transcriptomics showed that macrophages near fat-accumulating liver cells had high expression of glycoprotein NMB (GPNMB). Most GPNMB-positive cells belonged to the MetMac group, and their proportion increased between MASL and MASH. Proteomic analysis of independent samples supported these findings.

The team also observed that interleukin-32 expression in liver cells increased alongside GPNMB-positive macrophages as MASLD progressed. Analysis of independent omics datasets identified macrophage and serum protein markers associated with disease stage. These markers could help classify patients and improve patient selection for clinical trials. The findings reveal greater spatial and metabolic diversity among liver macrophages than earlier models suggested.

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By Stephanie DeMarco, PhD

The article can be accessed on: The Scientist

Image Credit: The Scientist © iStock.com, Rasi Bhadramani

Noelle D. Dwyer and her team, led by graduate researcher Kaela S. Lettieri, studied these errors in the developing brains of mice. When cells failed to complete abscission, they merged back into enlarged cells containing two nuclei. Their outer membranes became larger, while the cilia that help cells receive signals became longer. Some cells also developed two cilia. The researchers found that the p53 protein normally protects the developing brain by identifying these abnormal cells and triggering their death. When the team blocked p53, the cells survived and attempted to divide again. These further divisions also failed, producing increasingly abnormal cells with multiple nuclei and cilia and disrupting the regular arrangement of the developing tissue.

The findings suggest that repeated cell-division errors may contribute to tumour formation and developmental disorders when protective mechanisms fail. The researchers believe that understanding how the developing brain maintains tight control over cell division could eventually support new approaches to preventing or treating certain cancers and birth defects.

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By  University of Virginia

The article can be accessed on: Medicalxpress

Image Credit: Medicalxpress Pixabay/CC0 Public Domain

To test this, researchers from Dr. Qian Wenfeng’s lab at the Institute of Genetics and Developmental Biology (IGDB) of the Chinese Academy of Sciences studied Arabidopsis. Using a dynamic editing-based lineage tracing system, the researchers tracked cell trajectories. During division, the base editor AID (acting as a “writer”) continuously introduced heritable mutations into a synthetic DNA “readout” sequence, allowing lineage information to accumulate.

Through deep sequencing, the team identified somatic mutations in parental leaves and germline mutations transmitted to the progeny. These were used to reconstruct a cell lineage tree connecting somatic and germline cells. The results revealed two distinct patterns: some germline cells segregated during inflorescence meristem formation (late segregation), while others segregated earlier than branch formation (early segregation).

This early segregation provides a plant counterpart to Weismann’s theory, showing that germline segregation in Arabidopsis occurs earlier than previously believed. Ultimately, the study illustrates how plants balance developmental plasticity with safeguarding the genetic integrity of their offspring.

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By Liu Jia Chinese Academy of Sciences

The article can be accessed on: Phys.org

Image credit: Current Biology (2026)