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Dysregulation of this pathway occurs in many different types of cancers Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The MAPK/ERK signalling pathway in cancer Last updated: 24/02/25, 11:29 Published: 20/02/25, 08:00 Dysregulation of this pathway occurs in many different types of cancers Introduction The mitogen-activated protein kinase (MAPK) signalling pathway is an important pathway in apoptosis, proliferation, differentiation, angiogenesis and metastasis. It is a protein kinase pathway (causes phosphorylation) with between 3-5 sets of kinases and is known to be activated via Ras, KC-mediated (Kupffer cells/liver macrophages), Ca2+, or G protein-coupled receptors. The MAPK/ERK pathway, also known as the Ras-Raf-MEK-ERK pathway, is conserved in mammals, and dysregulation of this pathway occurs in many different types of cancers. MAPK/ERK function Ras (GTPase) activates Raf (serine/threonine kinase), which activates MEK1/2 (tyrosine & serine/threonine kinases) and ERK1/2 (serine/threonine kinases), which controls certain transcription factors. ERK1/2 also phosphorylates various substrates in the cytoplasm (not shown). This results in gene expression, which can cause apoptosis, cell cycle regulation, differentiation, proliferation, etc. (Fig. 1). It is estimated that there are more than 150 target substrates of ERK1/2, either directly or indirectly. Furthermore, Ras and RAF have several different subtypes which have different functions. Ras has four different subtypes, which are the GTPases: HRAS, KRAS4A/4B, and NRAS, with KRAS being the common form found in human cancers. RAF has subtypes, which are the kinases: ARAF, BRAF, and CRAF (in humans). Ras is activated when GRB2 (growth-factor-receptor bound protein 2) binds to SOS (son of sevenless). This occurs via the complex moving to the cell membrane upon activation of a transmembrane receptor, such as EGFR (epidermal growth factor receptor). SOS transports the signal from the receptor to RAS and aids in the conversion of RAS-GDP to RAS-GTP. This switches ‘on’ RAF, which leads to the phosphorylation of MEK and ERK (Fig. 1). ERK is then able to move into the nucleus and alter gene expression, of genes such as CREB, MYC, FOS, MSK, ELK, JUN, etc., which are involved in processes such as metabolism, proliferation, angiogenesis (formation of blood vessels), haematopoiesis (formation of blood cells), wound healing, differentiation, inflammation, and cancer. However, ERK is also able to activate other substrates in the cytoplasm, such as BIM, RSK, MNK, and MCL, which are involved in processes such as apoptosis and blood pressure regulation. A regular level of ERK expression is needed for activation of genes involved in the cell cycle and to inhibit negative cell cycle control. ERK phosphorylates Cyclin D and Cdk4/6, which are bound together and aid the cell in the movement from G1 (gap) to the S phase (DNA synthesis/repair) of the cell cycle. MAPK/ERK pathway in cancer The MAPK/ERK pathway has been linked with many cancers, such as colon, thyroid, melanoma, pancreatic, lung, and glioblastoma. Mutations in epidermal growth factor receptor (EGFR), Ras, and Raf are well-known to cause cancer, with an estimated 33% of cancers containing Ras mutations, and an estimated 8% being caused by Raf mutations. It is also estimated that 85% of cancers have elevated activity of MEK. The MAPK/ERK pathway has also been shown to interact with the PI3K/Akt pathway, which controls the cell cycle and causes increased cell proliferation, which is obviously an important factor in tumourigenesis (tumour initiation). Regulation of the MAPK/ERK pathway There is a negative feedback mechanism of ERK1/2 on RAS/RAF/MEK, by ERK1/2 phosphorylating SOS, which causes the RAF-RAS link to be disrupted. ERK also inhibits MEK via the phosphorylation of BRAF and CRAF. There are inhibitors for Ras/Raf/MEK/ERK, but not all of these inhibitors work well/are without issues. ERK is problematic, in that their ATP-binding sites are very like cell cycle proteins, so are more difficult to inhibit. Also, it is difficult to target Ras due to its high GTP binding affinity, profuse cellular GTP, and lack of appropriate binding pockets. Therefore, the main focus currently appears to be on Raf/MEK inhibition. Raf inhibitors include drugs such as sorafenib, vemurafenib, encorafenib, and dabrafenib (these drugs are used on specific BRAF mutations). On the other hand, MEK inhibitors include drugs such as trametinib, cobimetinib, binimetinib, and selumetinib (these drugs can be used on specific mutations in Ras and Ras/Raf). Negative feedback mechanisms tightly control the MEK/ERK pathway and therefore great care is taken with inhibitor drug doses. To illustrate, if the doses are too low, the negative feedback loops are activated, which can lead to drug resistance/ poor therapeutic outcome. Conclusion The MAPK/ERK pathway is essential for several cellular processes, such as apoptosis, cell cycle regulation, differentiation, and proliferation. Therefore, it has a critical role in tumourigenesis. Raf and MEK in particular are susceptible to inhibition, which has led to the production of several different drugs for use in various types of cancer. There are currently other clinical trials in progress, and these will hopefully lead to further therapies for other cancers involved in this pathway. Written by Eleanor R Markham Related articles: HIPPO signalling pathway / Thyroid cancer REFERENCES Lake, D., Corrêa, S.A.L. & Müller, J. Negative feedback regulation of the ERK1/2 MAPK pathway. Cell. Mol. Life Sci. 73 , 4397–4413 (2016). https://doi.org/10.1007/s00018-016-2297-8 Song Y, Bi Z, Liu Y, Qin F, Wei Y, Wei X. Targeting RAS-RAF-MEK-ERK signaling pathway in human cancer: Current status in clinical trials. Genes Dis. 2022 May 20;10(1):76-88. doi: 10.1016/j.gendis.2022.05.006. PMID: 37013062; PMCID: PMC10066287 Ullah R, Yin Q, Snell AH, Wan L. RAF-MEK-ERK pathway in cancer evolution and treatment. Semin Cancer Biol. 2022 Oct;85:123-154. doi: 10.1016/j.semcancer.2021.05.010. Epub 2021 May 13. PMID: 33992782. Project Gallery

The future of precision healthcare: nanocarriers Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Nanomedicine and targeted drug delivery Last updated: 17/07/25, 10:53 Published: 17/07/25, 07:00 The future of precision healthcare: nanocarriers In recent years, nanomedicine - the application of nanotechnology in healthcare - has emerged as a powerful and versatile area of research and is rapidly developing with many promising opportunities in the medical sciences. Nanocarriers are being developed for pharmaceuticals for example, with uses in cancer treatment and in particular targeted drug delivery. In nanomedicine, the materials are engineered at the nanoscale, with sizes ranging from 100 to 1000 nm, and can be used to perform specific biomedical tasks. These nanomaterials, such as nanoparticles, are often made from crosslinked polymer chains and can encapsulate therapeutic molecules for delivery within the body. Their small sizes give them unique properties, as they can interact with cells at a molecular level, and be designed to respond at specific times and locations, which can be directed to specific tissues or environments. Since the coronavirus disease (COVID-19) pandemic, nanoparticle-based drug delivery platforms have been widely studied - lipid nanoparticles were used in the vaccine to combat the virus. Being highly successful, and looking ahead, research and development in nanomedicine-based drug delivery is expected to keep growing, as the interest in more precise and effective treatments continues to rise. How can nanoparticles be used for drug delivery? A significant challenge in conventional drug therapies lies in their limited solubility, which can reduce the effectiveness of a drug and cause harmful side effects. Nanoparticles offer a solution to this: they can encapsulate poorly soluble drugs, protecting them from degradation in the body, and this allows them to be carried safely to the targeted tissues. This localised delivery improves the drugs’ biodistribution, and reduces systemic toxicity, which is a common concern in treatments such as chemotherapy, where healthy tissues in the body are damaged. Nanoparticles in particular are exciting as they have tuneable surface properties and a high surface to area volume ratio. This means their physical and chemical behaviours can be adjusted - for example through changing their sizes, shapes, or surface chemistries - to match a specific medical application or target. In addition to this, nanoparticles undergo the enhanced permeability and retention (EPR) effect; a phenomenon where they naturally accumulate in tumour tissues due to the leaky nature of tumour blood vessels. This effect improves the targeting precision, and drugs can be delivered more efficiently to cancer cells, while sparing healthy ones one, avoiding unnecessary damage and side effects to the patient. While drug delivery is a major focus, nanomedicine research also plays a role in diagnostics. Nanoparticles can be engineered to function as contrast agents in medical imaging, helping doctors detect diseases earlier and monitor treatments more accurately. There is also a growing interest in using nanomaterials for tissue regeneration, by creating scaffolds that support the repair and regrowth of damaged tissues. As research continues, nanomedicine holds promise for tacking some of the most pressing challenges in modern healthcare - from treating cancer more safely to developing new vaccines and personalised therapies. Though there are some hurdles, particularly around large-scale manufacturing and regularly approval, the path ahead for nanomedicine has huge potential. As the field of nanomedicine continues to grow, it shows great promise in reshaping healthcare with treatments that are smarter, safer, and more effective - ultimately improving patient outcomes and transforming the way we fight disease. Written by Saanchi Agarwal Related articles: Nanomedicine / Nanoparticles and diabetes treatment / Nanoparticles and health / Nanogels Project Gallery

Global warming can lead to higher transmission rates of dengue fever Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The impacts of global warming on dengue fever Last updated: 08/10/25, 16:42 Published: 19/06/25, 07:00 Global warming can lead to higher transmission rates of dengue fever Introduction Dengue fever is a viral disease transmitted by two mosquitoes: Aedes aegypti and Aedes albopictus . These mosquitoes are called ‘vectors’. Symptoms of dengue fever include a sudden high fever and severe headaches, making it hard to diagnose. Transmission suitability is endemic, meaning the virus spreads where the conditions are suitable for the vectors to survive and reproduce for 10-12 months. This disease is endemic in the tropics, including much of Sub-Saharan Africa and Central Africa, Northern South America, Brazil, South and Southeast Asia, and parts of Northern Australia. The World Health Organisation (WHO) has stated that it is “the most important mosquito-borne viral disease in the world”. Dengue fever does not currently have a vaccine. There are many areas of transmission, and dengue fever impacts communities worse if they have weaker health systems. Severe dengue can be fatal, especially in children, who have a weaker immune system. Due to climate change and increasing temperatures, more areas will be habitable for the vectors in the future. This could lead to higher transmission rates of dengue fever. Researchers used a modelling approach using different datasets to make projections of the impact of changing temperatures and predict the future spread of dengue fever. They specifically looked at locations and months suitable for dengue transmission if conditions were suitable for both vectors. Method The researchers used temperature data from the Berkeley Earth Surface Temperatures dataset for the present day (2001-2020). They also used projected temperature data for 2050 based on the Coupled Model Intercomparison Project Phase 6 (CMIP6) projections for the socio-economic pathway (SSP) 1-2.6 scenario and SSP5-8.5 scenario, as used in the Intergovernmental Panel on Climate Change Sixth Assessment Report. The SSP1-2.6 scenario is the best-case scenario and assumes international policy agreements and emissions reductions will be followed, limiting the average global temperature to 1.5 °C above pre-industrial levels. The SSP5-8.5 scenario is the “business as usual” scenario and assumes that continued fossil fuel use and development will occur. Researchers used the most recent climate projections from the CMIP6, which gave an up-to-date, holistic view of the impact of potential differences between climate change trajectories on vulnerable populations. This information can be used to support climate change mitigation strategies and disease prevention and control. Thermal limits for the mosquito vectors used in this study were 19.9 - 29.4 °C for Aedes aegypti and 21.3 - 34 °C for Aedes albopictus , since the vectors can only survive and reproduce within these temperatures. Modelling the thermal limits of both vectors, instead of just one, made the analysis more comprehensive. The researchers also applied an aridity mask using the Normalised Difference Vegetation Index (NDVI), which excluded areas too dry for mosquito survival and reproduction. They then applied the thermal limits and aridity mask to the climate data to predict areas with suitable conditions for the vectors and estimate the number of months suitable for transmission. Using aridity masks (previously only done with malaria) enhanced the model's accuracy because moisture is an important factor for mosquito breeding. Results Figure 1 shows that under the SSP1-2.6 (best-case) scenario, there will be new suitability for dengue transmission in temperate regions by 2050, lasting about 1 to 2 months. In addition, northwestern South America could see increases of up to 5 months of new suitability, and Eastern Africa up to 6 months of new suitability. In addition, eastern and southern Central America, central and northwestern South America, northern Australia, and parts of Southeast Asia are also becoming suitable for year-round transmission. Figure 2 shows that under the SSP5-8.5 (“business as usual”) scenario, areas will become suitable for year-round transmission in similar locations as under the SSP1-2.6 scenario by 2050. Dengue transmission suitability could increase by up to 6 months in Eastern Africa, and up to 10 months in parts of northwestern South America. Areas as far north as the Arctic Circle also have new suitability under this scenario. This demonstrates that climate change could result in the expansion of areas and the length of time during which dengue fever transmission is possible. Evaluation It’s essential to also acknowledge the study's limitations. For example, the model did not account for other variables impacting disease transmission, such as mosquito adaptation and extreme weather. The potential adaptation of mosquitoes and parasites to changing environmental conditions could alter transmission dynamics. In addition, extreme weather events, such as heavy rain, could eliminate breeding sites. Furthermore, the method of using modelling and projections is unreliable, because many things could change between now and 2050. For example, there could be temperature fluctuations, or temperatures could fall between SSP1-2.6 and SSP5-8.5, rather than being fixed in either scenario. This could affect the reliability of predicting future dengue fever transmission suitability. The study also did not include aridity projections under climate change scenarios. As future projections of NDVI are not currently available, NDVI values for 2020 were held constant for the 2050 projections. There will likely be changes in aridity by 2050, which will affect mosquito reproduction and dengue transmission. Nevertheless, this study's results are still important because they suggest that with increasing climate change, dengue fever transmission could increase, which would be a public health issue. Further listening and reading If you would like to know more about dengue fever, consider listening to this short 5-minute podcast from the World Health Organisation. If you would like to know more about the impacts of climate change on health, consider listening to this podcast , also from the World Health Organisation. If you would like to know more about the impacts of climate change on neglected tropical diseases (NTDs), consider reading the full open-access paper mentioned in this article . Written by Naoshin Haque Related articles: Potential vaccine for malaria / Correlation between HDI and mortality rate / Healthcare challenges during civil war in Sudan / Rising temperatures impacts Project Gallery

Understanding the cause of bullying can provide effective prevention and intervention Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The brain of a bully Last updated: 13/05/25, 14:22 Published: 29/05/25, 07:00 Understanding the cause of bullying can provide effective prevention and intervention Introduction Bullying is a global social issue affecting any individual regardless of sex, age, or gender, particularly in childhood and adolescence. Approximately one-third of the youth is bullied worldwide; the range could be as low as 7% in Tajikistan to 74% in Samoa. While much neuroscientific research focuses on bullying victimisation and social exclusion, there is a growing field to understand the brain mechanisms behind bullying behaviour. Why does bullying occur? Is there a neurological basis for such behaviour? This article will answer these questions with insights into prevention and intervention strategies. The neural basis of bullying As per Johnna R. Swartz, an assistant professor at the University of California, Davis : Bullying is fairly common during adolescence, with about 25-50% of teenagers in the U.S. reporting that they have bullied or been a victim of bullying. The Swartz team focused on the amygdala, a small almond-shaped structure deep within the brain. The amygdala is critical for processing emotions, particularly fear and aggression. Swartz and her colleagues conducted a functional resonance imaging (fMRI) study on 49 adolescents, examining how their amygdala responded to different emotional expressions during a face-matching task. The findings indicated that the adolescents who engaged in bullying behaviour exhibited a heightened amygdala response to angry faces and a diminished amygdala response to fearful faces. This pattern suggests that bullies may struggle to recognise fear in others, potentially making them less likely to empathise with their victims. Moreover, a study revealed that adolescents who reported higher rates of bullying showed increased activation of the ventral striatum (the area that responds to rewarded feelings), amygdala (emotion processing), medial prefrontal cortex (involved with social cognition, decision-making), and insula (salience detection) while observing social exclusion scenarios. The findings suggest that bullying is not just about aggression but also about maintaining social dominance and hierarchy. Another study by the University of Chicago conceded that bullies might enjoy others in pain by observing a robust activation of the amygdala and ventral striatum when watching pain inflicted on others. Why is knowing the neural basis of bullying useful? Understanding the root cause of bullying can provide effective prevention and intervention strategies: Social-emotional training (SET) to improve emotional regulation and empathy, which can help reshape neural pathways. For example, programmes like the ‘Roots of Empathy’ initiative have shown that training children to recognise emotions can reduce bullying behaviours in schools. Cognitive-behavioural therapy (CBT) allows bullies to reframe negative thoughts and develop a healthier response to social interactions. For instance, the CBT techniques, like role-playing social situations, have been successfully used in school-based interventions. Mindfulness and cognitive training strengthen the prefrontal cortex by meditation and improve decision-making skills and impulse control. School-based interventions (like anti-bullying programs) create supportive environments that reward prosocial behaviour rather than only punishing aggressive behaviour. Conclusion The neuroscience of bullying helps us understand the root cause of bullying scientifically. Bullying is not simply a matter of choice; there is a deeper scientific basis to consider. This knowledge can help to develop comprehensive solutions to prevent bullying and create a healthier social environment. Future studies should focus on longitudinal studies that track brain development in children and adolescents involved in bullying, thereby informing how early interventions can reshape them for positive change. Written by Prabha Rana Related articles: Aggression / Depression in childhood / Forensic neurology REFERENCES Assistant Secretary for Public Affairs (ASPA). “Facts about Bullying.” StopBullying.Gov , 9 Oct. 2024, www.stopbullying.gov/resources/facts . “Bullies May Enjoy Seeing Others in Pain: Brain Scans Show Disruption in Natural Empathetic Response.” University of Chicago News , news.uchicago.edu/story/bullies-may-enjoy-seeing-others-pain-brain-scans-show-disruption-natural-empathetic-response . Accessed 15 Feb. 2025. Dolan, Eric W. “Neuroscience Study Finds Amygdala Activity Is Related to Bullying Behaviors in Adolescents.” PsyPost , 7 Dec. 2019, www.psypost.org/neuroscience-study-finds-amygdala-activity-is-related-to-bullying-behaviors-in-adolescents/ . Perino, Michael T., et al. “Links between adolescent bullying and neural activation to viewing social exclusion.” Cognitive, Affective, & Behavioral Neuroscience , vol. 19, no. 6, 10 July 2019, pp. 1467–1478, https://doi.org/10.3758/s13415-019-00739-7 . Project Gallery

Richard Dawkins's work and the Modern Evolutionary Synthesis Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Is the immune system ‘selfish’? – a Dawkins perspective Last updated: 22/09/25, 10:59 Published: 25/09/25, 07:00 Richard Dawkins's work and the Modern Evolutionary Synthesis Evolution and Dawkins’ perspective Charles Darwin introduced the unprecedented theory of evolution by natural selection in his famous work ‘On the Origin of Species’, published in 1859. Gregor Mendel, who explained the concept of Mendelian genetics (the inheritance of genes), was a contemporary of Darwin, but his research was recognised much later on, beyond his time. In the 20 th century, the Modern Evolutionary Synthesis was formed and gave a foundation for how biological life has formed as we see it today. The Modern Evolutionary Synthesis is widely accepted and strongly supported by experimental and observational evidence across an array of life. Human beings have even leveraged these concepts for hundreds of years through artificial selection, imposing our own sometimes superficial selective pressures on organisms to express characteristics that we desire (such as the case of the Belgian Blue cattle, with a mutation in the myostatin gene making it a muscular, lean beef, or perhaps artificial selection in dog breeding). Richard Dawkins’ breakout book, ‘The Selfish Gene’, published in 1976, took him from an unknown voice at the University of Oxford passionate about the works of evolution across all animals, to a lauded voice in the scientific community. His concept of genes being selfish is the idea that natural selection works at the gene level, whereby genes over time become better at replication, with the organism acting as a ‘survival machine’ built to help genes propagate. It is important to note that the term ‘selfish’ is not meant metaphysically or philosophically. Figure 1 explains what ‘selfish’ means. Taking this further, it can be argued that genes helping organisms resist pathogenic attack are more likely to survive and propagate. This means the immune system does not exist to protect the body holistically but rather to protect its genes individually. The immune system evolved through the gene-centric lens As previously mentioned, the immune system has become integral to all complex organisms responding to pathogens as a selective pressure. Those genes that have conferred a greater ability to combat or resist a particular pathogen allow the organism an improved survival chance until reproductive age has been achieved. The window whereby the organism has reached reproductive maturity and is reproducing is what the genes have been selected to get, which is why many genetic pathways end up becoming detrimental to an organism in old age (explained by the antagonistic pleiotropy hypothesis- APT- and the disposable soma theory). This remains especially true for the immune system. One must also understand that only vertebrates are biologically equipped with an adaptive immune system (allowing for memory and effective response to previous pathogens), with Figure 2 explaining this difference. This supports that the immune system is a ‘selfish system’, as while many organisms survive without adaptive immunity, more complex organisms have evolved to include it because of our prolonged individual survival and delay in reproductive maturity (indicating that survivability until our reproductive window is an intense selective pressure). Immune imperfection through the ‘Selfish System’ lens We now understand there is a compelling point to be made that the immune system has evolved with the reproductive window in mind and to allow as much gene propagation in a population as possible. If we accept this point of view, it explains many of the trade-offs and imperfections of the immune system when we look at the potential harm caused by immunity. Allergies are one such example, whereby hypersensitivity causes an immune response to harmless substances, which, through the gene-centric lens, may have evolved to detect pathogens such as parasites. This further supports the ‘selfish system’ idea as reproductive success on a population scale is not impaired by a significant amount by allergies. One such study showed that women with allergies and asthma, despite having systemic inflammation, did not have a reduced fertility rate when analysing the relationship between an increase in allergic diseases in the 20 th century and a decrease in fertility globally. Chronic inflammation through persistent immune activation in old age (a concept termed inflammaging) is another such example. We previously mentioned that past reproductive age natural selection weakens, meaning that our genes are selected for early life immune optimisation, even if that means they cause problems later in old age. Processes such as cellular senescence, inflammasome activation, oxidative stress, immune cell dysregulation and so on begin to occur, leading to an increased risk of age-related diseases such as cardiovascular disease, cancer, dementia, sarcopenia and so on. Immune evolution is therefore a ‘selfish system’ because it seems to care more about gene propagation in the young to middle-aged years in comparison to long-term organism health, as many immune systems rapidly decline and become detrimental. Conclusion This perspective of the immune system as a ‘selfish system’ allows us to understand that it is not a protector of the organism throughout its life span, as we may perceive it to be, but rather that it is a mechanism evolved and optimised to propagate genetic material during the organism’s reproductive window (expanding beyond humans). This analysis of the immune system through Richard Dawkins' lens of the “selfish gene” helps us to understand many of the limitations of the immune system. Working on treatments to preserve and maintain the immune system’s healthy state, which reflects young adult life, appears to be a promising approach for future clinical prevention plans for old age diseases. There are many currently being researched and emerging treatments with this principle in mind, such as senotherapeutics and mTOR inhibitors (such as rapamycin and other rapalogs), making this an interesting field to keep up to date with. Written by Yaseen Ahmad Related article: Darwin and Galápagos Tortoises Project Gallery

Impact of war and geopolitics on health in Palestine Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Life under occupation: the health and well-being of Palestinians Last updated: 27/11/25, 15:13 Published: 13/03/25, 08:00 Impact of war and geopolitics on health in Palestine This is article no. 1 in a series about global health injustices. Next article: Civil war in Sudan . Introduction Welcome to the Global Health Injustices Series, which will focus on critically examining the health inequalities and inequities faced by vulnerable populations within different countries and regions worldwide and even put forward actionable steps to improve their health and wellbeing. This series will begin with Palestine, as it has been an enduring crisis that should be addressed to include long-lasting benefits and outcomes for the Palestinians. Palestine: from a rich history to current occupation Palestine is a country in the Middle East (West Asia) mainly bordered by Israel. Palestine is unique in its various cultures and knowledge, moulded by multifaceted events and geopolitical shifts over centuries. The multidimensional cultural landscape of Palestine illustrates the impact of civilisations, such as the Romans, Byzantines, and Ottomans, who each had their religions, languages, and cultures, which still exist in various forms today. The resilience of the Palestinians is evident through their distinct traditions, art, food and environment, which are essential to their identity. With these testaments in mind, Palestinians are facing consistent strife because they are under constant occupation, blockade and cutting off of needed supplies carried out by Israel, as noted by several humanitarian and human rights non-governmental organisations (NGOs) like Amnesty International and Save the Children. These actions are facilitated by nations, notably the United States and the United Kingdom, through arms and weapons trade. Hence, the struggle for the Palestinians to have autonomy and freedom, among other human rights within their own homeland, is a consistent fight that requires ongoing international cooperation and solidarity. Geopolitics: its detrimental impacts on the Palestinians Given the currently divisive geopolitical landscape, it is essential to bring attention to the health outcomes of the Palestinian population, especially since at least half of them are children. A report from the Global Nutrition Cluster called “Nutrition Vulnerability and Situation Analysis / Gaza” had several key findings and tables (see Tables 1 and 2 ). Firstly, more than 90% of children less than a year old, along with pregnant and breastfeeding women, encounter high under-nutrition due to poverty. Another finding was that approximately 90% of children under five are impacted by at least one infectious disease, and 81% of households in Gaza lack clean and safe water. However, the authors noted limitations in their analysis, such as limited data sources because collecting it is difficult within the context of Gaza, and this was true for screening. Another report from the organisation Medical Aid For Palestinians (MAP), titled “Health Under Occupation” from 2017, discussed healthcare access and outcomes more broadly. For example, they noted that in 2016, up to one-third of patients’ permits to exit Gaza for healthcare access were either denied or delayed. Moreover, they stated that 40% of people in Gaza live below the poverty line. Given the recent geopolitical shifts in power, these findings from both reports will likely be higher now. This brings forthcoming uncertainty about whether the health outcomes of Palestinians will improve. In a recent qualitative study involving the views of Palestinian physicians in the West Bank, they shared their experiences of violence, threats of violence, issues with healthcare access for themselves and patients, financial difficulties to support their families, struggle to help their patients and limited access to education due to harsher life under occupation. Thinking more largely about emergency care in Palestine, one scoping review reported the depletion of healthcare resources such as medical equipment and medications. The authors even related how human rights violations and the destruction of the Palestinian healthcare system, including emergencies, have exacerbated outcomes; the most notable were stroke, myocardial infarction and traumatic injury, among other non-infectious diseases. Although the authors included this information from a human rights standpoint, they called for additional interventions and research to fill in and learn gaps within emergency care to enhance health outcomes for Palestinians. This review was published in 2022, and again, many geopolitical shifts in power have taken place within a few years. Therefore, it can be deduced that emergency care is drastically needed for the Palestinians; this is primarily compelled by the blockade in Gaza and occupation in the West Bank. Focusing on the mental health outcomes among Palestinians, they have become worse. In another scoping review, researchers focused on trauma among young Palestinian people in Gaza; the authors noted that events, such as exposure to devastation and violence, as well as the death or loss of friends and family, have contributed to mental health outcomes ranging from post-traumatic stress disorder (PTSD) to depression. Nevertheless, the authors stated that further qualitative research is vital to addressing gaps in knowledge and enhancing mental health outcomes among the Palestinian youth and the wider population. Connecting back to how the modern geopolitical landscape is very dynamic, the poorer mental health outcomes among Palestinians have conceivably increased. Urgent calls to action: recommendations from NGOs to upholding human rights Given all of these detrimental impacts on the health and wellbeing of Palestinians, there are recommendations from organisations, notably the United Nations (UN), for ways forward towards upholding the human rights of Palestinians: Immediately end all practices of collective punishment, including lifting its blockade and closures – and the “complete siege”- of Gaza, and urgently ensure immediate access to humanitarian and commercial goods throughout Gaza, commensurate with the immense humanitarian needs. Ensure that all Palestinians forcibly displaced from Gaza are allowed to return to their homes creating safe conditions and fulfil its responsibilities as an occupying Power in this regard. End the 56-year occupation of the Occupied Palestinian Territory, including East Jerusalem as part of a broader process towards achieving equality, justice, democracy, non-discrimination, and the fulfilment of all human rights for all Palestinians. These recommendations, among others mentioned in the report from the United Nations (UN) High Commissioner for Human Rights, were divulged in 2024; the year had been a challenging time, particularly in Gaza, due to the complete blockade of food, water and essentials like medical supplies; in addition to this, many explosives were dropped on Gaza, killing thousands of men, women and children. Finally, buildings, such as hospitals and homes, were destroyed. Conclusion: moving forward towards a equitable and equal future for Palestinians Reflecting on everything discussed in this article, the numerous injustices happening to Palestinians must not go on; they have been suppressed for nearly 75 years by governments and the mainstream media before receiving closer attention, examination and debate within Western society recently. Therefore, we need to take actionable steps by initiating more open discussions of justice and advocacy involving the voices of Palestinians, such as myself and others. Furthermore, it is crucial always to nudge those in positions of power worldwide to fulfil their responsibilities as civil servants and defend human rights for everyone. Both of these actions uphold the health and wellbeing of Palestinians living in Gaza and the West Bank, especially as enabling the recommendations from the UN and other NGOs. As for the wider international community, we must continue upholding human rights to maintain our health and wellbeing. In my next article, I will discuss Sudan because this population has also encountered many injustices, primarily the civil war that has been occurring since 2023. This has impacted the health and wellbeing of the Sudanese population, which requires thorough attention and discussion. Written by Sam Jarada Related articles: A perspective on well-being / Gentrification and well-being / Understanding health through different stances / Impacts of global warming on NTDs / Global health injustices- Bangladesh , Sri Lankan Tamils REFERENCES Human rights in Israel and the Occupied Palestinian Territory. Amnesty International. 2022. Available from: https://www.amnesty.org/en/location/middle-east-and-north-africa/middle-east/israel-and-the-occupied-palestinian-territory/report-israel-and-the-occupied-palestinian-territory/ Occupied Palestinian Territory. Save the Children International. 2024. Available from: https://www.savethechildren.net/occupied-palestinian-territory Nutrition Vulnerability and Situation Analysis / Gaza. 2024. Available from: https://www.nutritioncluster.net/sites/nutritioncluster.com/files/2024-02/GAZA-Nutrition-vulnerability-and-SitAn-v7.pdf HEALTH UNDER OCCUPATION. Medical Aid For Palestinians. 2017. Available from: https://www.map.org.uk/downloads/health-under-occupation---map-report-2017.pdf Husam Dweik, Hadwan AA, Beesan Maraqa, Taher A, Zink T. Perspectives of Palestinian physicians on the impact of the Gaza War in the West Bank. SSM - Qualitative Research in Health. 2024 Nov 14;6:100504–4. Available from: https://www.sciencedirect.com/science/article/pii/S2667321524001136 Rosenbloom R, Leff R. Emergency Care in the Occupied Palestinian Territory: A Scoping Review. Health and Human Rights. 2022 Dec;24(2):255. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC9790939/ Abdallah Abudayya, Fugleberg T, Nyhus HB, Radwan Aburukba, Tofthagen R. Consequences of war-related traumatic stress among Palestinian young people in the Gaza Strip: A scoping review. Mental Health & Prevention. 2023 Nov 25;32:200305–5. Available from: https://www.sciencedirect.com/science/article/pii/S2212657023000478 M.I. Human rights situation in the Occupied Palestinian Territory, including East Jerusalem, and the obligation to ensure accountability and justice - Report of the United Nations High Commissioner for Human Rights - Advance unedited version (A/HRC/55/28) - Question of Palestine. United Nations. Available from: https://www.un.org/unispal/document/human-rights-situation-in-opt-unohchr-23feb-2024/ Project Gallery

Nanogels are tiny, water swollen polymer networks and encapsulate therapeutic agents Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Nanogels: the future of smart drug delivery Last updated: 17/07/25, 10:54 Published: 17/07/25, 07:00 Nanogels are tiny, water swollen polymer networks and encapsulate therapeutic agents Nanomedicine is a rapidly advancing field, with nanogels emerging as promising innovations for drug delivery applications. Nanogels are soft nanoscale hydrogels that are transforming how we deliver drugs and treat diseases. Whilst hydrogels themselves have long been used in biomedical applications such as tissue engineering and wound healing, their relatively larger sizes (above 100 micrometres) limits their ability to interact with cells and cross biological barriers. Nanogels, however, are thousands of times smaller, and offer unique advantages as a result. What are nanogels? Nanogels are tiny, water swollen polymer networks and are made up of crosslinked polymer chains to form a 3D matrix. Nanogels can encapsulate therapeutic agents inside their porous core shell structure. This swelling allowing nanogels to carry payloads, such as drugs, proteins, nucleic acids and these cargo materials are protected from degradation in the body whilst enabling controlled and targeted delivery. Due to their small sizes, nanogels can penetrate tissues and even enter cells, which overcomes the limitations faced with hydrogels. The surface of nanogels can also be engineered for specificity, to allow for precise targeting of drugs to receptors on diseased cells or inflamed tissues. Advantages over other nanocarriers Compared to liposomes and polymeric micelles, nanogels have a larger inner surface, which means they can carry more payload. The higher loading capacity improves the therapeutic efficiency whilst reducing the risks of side effects cause by off-target drug release. Nanogels also undergo the enhanced permeability and retention (EPR) effect - a phenomenon where the nanoparticles naturally accumulate in tumour or inflamed tissues due to leaky blood vessel, and as a result this improves drug delivery to targeted disease sites. Stimuli responsive ‘smart’ nanogels A key feature of nanogels is their stimuli responsiveness, or ability to act as ‘smart’ materials. The nanogels can be designed to respond to environmental triggers such as changes in pH, temperature, light, redox conditions, pressure and more. This responsiveness enables controlled release of drugs exactly when and where they are needed12. For example, thermoresponsive nanogels can change their structure at body temperature or when exposed to localised heating, making them ideal for applications like wound healing and cancer therapy. This controlled release prevents premature drug leakage, reduces systemic toxicity and overall improves the precision of the treatment. The future of nanogels in medicine Nanogels have huge potential as customisable drug delivery systems to target specific disease systems. They are biocompatible, stable, and have high drug loading capacities and are stimuli responsive; these properties combined make them a powerful tool in applications such as targeted drug delivery and gene therapy. As nanomedicine research progresses, nanogels are set to revolutionise healthcare with smarter, safer and more targeted therapies. Written by Saanchi Agarwal Related articles: Nanomedicine / Nanoparticles and diabetes treatment / Nanoparticles and health / Nanocarriers / Silicon hydrogel REFERENCES L. Blagojevic and N. Kamaly, Nanogels: A chemically versatile drug delivery platform, Nano Today, 2025, 61, 102645. F. Carton, M. Rizzi, E. Canciani, G. Sieve, D. Di Francesco, S. Casarella, L. Di Nunno and F. Boccafoschi, Use of Hydrogels in Regenerative Medicine: Focus on Mechanical Properties, Int. J. Mol. Sci. , 2024, 25 , 11426. N. Rabiee, S. Hajebi, M. Bagherzadeh, S. Ahmadi, M. Rabiee, H. Roghani-Mamaqani, M. Tahriri, L. Tayebi and M. R. Hamblin, Stimulus-Responsive Polymeric Nanogels as Smart Drug Delivery Systems, Acta Biomater. , 2019, 92 , 1–18. N. Rabiee, S. Hajebi, M. Bagherzadeh, S. Ahmadi, M. Rabiee, H. Roghani-Mamaqani, M. Tahriri, L. Tayebi and M. R. Hamblin, Stimulus-Responsive Polymeric Nanogels as Smart Drug Delivery Systems, Acta Biomater. , 2019, 92 , 1–18. A. Vashist, G. P. Alvarez, V. A. Camargo, A. D. Raymond, A. Y. Arias, N. Kolishetti, A. Vashist, P. Manickam, S. Aggarwal and M. Nair, Recent advances in nanogels for drug delivery and biomedical applications, Biomater. Sci. , 2024, 12 , 6006–6018. K. S. Soni, S. S. Desale and T. K. Bronich, Nanogels: an overview of properties, biomedical applications and obstacles to clinical translation, J. Control. Release Off. J. Control. Release Soc. , 2016, 240 , 109–126. A. Bordat, T. Boissenot, J. Nicolas and N. Tsapis, Thermoresponsive polymer nanocarriers for biomedical applications, Adv. Drug Deliv. Rev. , 2019, 138 , 167–192. K. S. Soni, S. S. Desale and T. K. Bronich, Nanogels: an overview of properties, biomedical applications and obstacles to clinical translation, J. Control. Release Off. J. Control. Release Soc. , 2016, 240 , 109–126. T. Alejo, L. Uson, G. Landa, M. Prieto, C. Yus Argón, S. Garcia-Salinas, R. de Miguel, A. Rodríguez-Largo, S. Irusta, V. Sebastian, G. Mendoza and M. Arruebo, Nanogels with High Loading of Anesthetic Nanocrystals for Extended Duration of Sciatic Nerve Block, ACS Appl. Mater. Interfaces , 2021, 13 , 17220–17235. S. V. Vinogradov, Nanogels in The Race for Drug Delivery, Nanomed. , 2010, 5 , 165–168. Project Gallery

Immunosenescence and related therapies Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Ageing and its association with immune decline Last updated: 24/02/25, 11:28 Published: 20/02/25, 08:00 Immunosenescence and related therapies Introduction Ageing is a profoundly complex and integral part of human life. As pharmaceutical developments have occurred, introducing new medicines and therapies such as biologics and antibiotics within the last 100 years, research has begun to look at malignancy at a more macro scale. To be clear, while it has become easier to combat infectious diseases in recent times, the combating of diseases tied to our genetic composition is far more complicated, whether it be autoimmune diseases or onset conditions such as cases of dementia. Ageing is one such case of a process that is hard to combat because the mechanisms that cause it are diverse and currently not fully understood. Strides have been made under a concept known as senescence, which continues to enlighten researchers and the anti-ageing pharmaceutical industry. This article provides a short summary of what immunosenescence is and how we can utilise our understanding to develop therapies for human immunity. What is immunosenescence? Immunosenescence is the change from a healthy, active immune cell phenotype to one that is no longer conventionally active and begins to secrete inflammatory chemical messengers known as the senescence-associated secretory phenotype (SASP) ( Figure 1 ). A most important aspect of senescence is that a cell undergoes cell cycle arrest, meaning it cannot proliferate. You may now question why cells are programmed to senesce if the outcomes are detrimental to the host? It prevents the continued proliferation of old or damaged cells, including cells with uncontrolled proliferation (such as cancer cells). If we stop senescence altogether, we run the risk of accumulating damaged and/or mutated cells, increasing the chances of disease progression, such as through fibrosis and tumorigenesis, so specific targeting and dosage of drug interventions have to be considered. The immune system in particular, displays biological changes that are indicative of senescent progression. These include thymic involution (shrinking of the thymus associated with a decrease in T cell production), inflammaging (chronic inflammation associated with SASP), an increase in mitochondrial stress through metabolic changes, and an increase in differentiated memory T cells (EMRA T cells). Knowledge of these changes can give insight into potential mechanisms to target for therapeutics. Current and developing therapies for immunosenescence Given our expanding understanding of senescence, as of the time of writing, there are no clinically approved drugs for senescence specifically. The development of therapies for diseases such as cancer, heart disease and diabetes (diabetic patients tend to exhibit increased levels of cellular senescence owing to “accelerated ageing”) have been implicated with suppressing senescence. These drugs would be mTOR inhibitors such as Rapamycin, statins, P13K inhibitors, as well as immune checkpoint inhibitors for T cells, such as anti CTLA-4 PD-L1 and PD-L2, and the anti-diabetic metformin, which have all shown in vitro to be effective against high levels of senescent cells. There was also the development of the recent first senolytic drugs dasatinib and quercetin in 2015 that kill senescent cells selectively against non-senescent cells and stand to provide a proof of concept for targeting disease through senescent mechanisms. Conclusion The field of senescence is certainly one to keep an eye on, with a bibliometric analysis in 2023 showing an increase every year in the number of published papers ( Figure 2 ). It may be sooner rather than later that we see this become a trending topic of discussion for treating an array of disease states. Continuous research into specific immune cell subtypes (B, T and NK cells) and their relation to a decline in immunity in response to age can tell us more about potential therapeutic pathways or lifestyle choices that can improve the health of the immunocompromised elderly. One such example of this is Treg-mediated increased glucose consumption in the tumour microenvironment leading to an increase in cell senescence in effector T cells, suggesting that high sugar diets can accelerate tumorigenesis. Our understanding of ageing through senescence will help reduce the mortality rates of elderly groups in decades to come through knowing that mechanisms such as the SASP and altered immune cell function, which can promote disease states. Written by Yaseen Ahmad Related articles: Genetics of ageing and longevity / Accelerated ageing REFERENCES Henson, S.M. and Aksentijevic, D. (2021) ‘Senescence and type 2 diabetic cardiomyopathy: How young can you die of old age?’, Frontiers in Pharmacology , 12. doi:10.3389/fphar.2021.716517. Wang, R. et al. (2017) ‘Rapamycin inhibits the secretory phenotype of senescent cells by a NRF2-independent mechanism’, Aging Cell , 16(3), pp. 564–574. doi:10.1111/acel.12587. Henson, S.M. et al. (2012) ‘Reversal of functional defects in highly differentiated young and old CD8 T cells by PDL blockade’, Immunology , 135(4), pp. 355–363. doi:10.1111/j.1365-2567.2011.03550.x. Islam, M.T. et al. (2023) ‘Senolytic drugs, dasatinib and quercetin, attenuate adipose tissue inflammation, and ameliorate metabolic function in old age’, Aging Cell , 22(2). doi:10.1111/acel.13767. Li, C., Liu, Z. and Shi, R. (2023) ‘A comprehensive overview of cellular senescence from 1990 to 2021: A machine learning-based bibliometric analysis’, Frontiers in Medicine , 10. doi:10.3389/fmed.2023.1072359. Herranz, N. and Gil, J. (2018) ‘Mechanisms and functions of cellular senescence’, Journal of Clinical Investigation , 128(4), pp. 1238–1246. doi:10.1172/jci95148. Li, L. et al. (2019) ‘TLR8-mediated metabolic control of human Treg function: A mechanistic target for cancer immunotherapy’, Cell Metabolism , 29(1). doi:10.1016/j.cmet.2018.09.020. Project Gallery

Arginine, the key to metabolic reprogramming in liver cancer Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Linking arginine and tumour growth: a breakthrough in cancer research Last updated: 20/02/25, 15:29 Published: 27/02/25, 08:00 Arginine, the key to metabolic reprogramming in liver cancer Unpicking the secrets of tumour growth: arginine, the key to metabolic reprogramming in liver cancer. We will look at how unleashing the power of arginine and elevating levels of this amino acid drive metabolic reprogramming and fuel tumour growth. Introduction In recent years, the field of cancer research has made significant progress in unravelling the complexities of this devastating disease. Scientists at the University of Basel have made a groundbreaking discovery regarding the role of the amino acid arginine in promoting tumour growth. Their findings shed light on the mechanisms underlying metabolic reprogramming in cancer cells and present new avenues for improving liver cancer treatment. Elevated levels of arginine: a surprising revelation An intriguing aspect of the study conducted by the researchers is the observation that tumour cells accumulate high levels of arginine despite producing less or none of this amino acid. Through careful analysis of liver tumour samples from both mice and patients, the team discovered that the tumour cells achieve this accumulation by increasing the uptake of arginine and suppressing its consumption. The role of arginine in tumorigenicity Upon further investigation, the scientists at the University of Basel found that high concentrations of arginine bind to a specific factor, triggering metabolic reprogramming in the tumour cells. This reprogramming, in turn, promotes tumour growth by regulating the expression of metabolic genes. The tumour cells revert to an undifferentiated embryonic cell state, enabling them to divide indefinitely. Immune system escape: a beneficial effect for tumour cells Another fascinating discovery made by the researchers is the role of arginine in aiding tumour cells in evading the immune system. Immune cells rely on arginine to function properly. By depleting arginine in the tumour environment, the tumour cells can escape immune surveillance. This finding opens up new possibilities for targeted therapies. Targeting the arginine-binding factor: a novel approach Instead of depleting arginine levels overall, which can have unwanted side effects, the scientists propose targeting the specific arginine-binding factor responsible for promoting metabolic reprogramming. By inducing the degradation of this factor, the researchers were able to prevent metabolic reprogramming in liver tumours. This approach offers a promising alternative to liver cancer treatment. Metabolic changes as biomarkers for early cancer detection Furthermore, the study suggests that metabolic changes, such as increased arginine levels, may serve as biomarkers for the early detection of cancer. Early detection is crucial for successful cancer treatment and patient survival. This finding provides hope for the development of non-invasive diagnostic methods that can detect elevated arginine levels. By measuring arginine levels in patients, these diagnostic methods can potentially identify liver cancer at an early stage. By identifying the elevated levels of arginine in liver tumour cells, these diagnostic methods could potentially use metabolic changes, such as increased arginine levels, as biomarkers for detecting cancer. Therefore, this would be crucial for successful cancer treatment and patient survival, as early detection allows for prompt intervention and improved outcomes. Conclusion The discovery of the role of arginine in driving metabolic reprogramming and promoting tumour growth opens up new avenues for liver cancer treatment. Additionally, the elevated levels of arginine observed in liver cancer patients suggest the potential for using arginine as a biomarker for non-invasive cancer detection. Further research is needed to explore the full potential of arginine as a diagnostic marker and to develop targeted therapies that exploit the metabolic vulnerabilities of cancer cells. With continued advancements in our understanding of cancer metabolism and the role of arginine in tumour growth, further research is needed to explore the full potential of arginine as a diagnostic marker and to develop targeted therapies that exploit the metabolic vulnerabilities of cancer cells. By studying the specific arginine-binding factor and its role in promoting metabolic reprogramming, scientists may be able to develop new treatments that selectively target tumour cells while minimising harm to immune cells that rely on arginine. Additionally, investigating the metabolic changes associated with increased arginine levels may lead to new biomarker designs for early cancer detection, which is crucial for successful treatment and patient survival. Written by Sara Maria Majernikova Related articles: Immune signals and metastasis / Cancer research treatment / Prostatate cancer treatment REFERENCE MOSSMANN, D., MÜLLER, C., PARK, S., RYBACK, B., COLOMBI, M., RITTER, N., WEISSENBERGE, D., DAZERT, E., COTO-LLERENA, M., NUCIFORO, S., BLUKACZ, L., ERCAN, C., JIMENEZ, V., PISCUOGLIO, S., BOSCH, F., TERRACCIANO, L. M., SAUER, U., HEIM, M. H. & HALL, M. N. Arginine reprograms metabolism in liver cancer via RBM39. Cell . DOI: https://doi.org/10.1016/j.cell.2023.09.011 Project Gallery

Unlocking the mystery of spinal disorders and paving the way for targeted therapies Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Unveiling the cancer magnet: vertebral stem cells and spinal tumour metastasis Last updated: 29/05/25, 10:46 Published: 24/04/25, 07:00 Unlocking the mystery of spinal disorders and paving the way for targeted therapies Introduction Researchers at Weill Cornell Medicine have discovered that the vertebral bones in the spine contain a unique type of stem cell that secretes a protein-promoting tumour metastasis. This protein, called MFGE8, plays a significant role in attracting tumours to the spine, making it more susceptible to metastasis when compared to other bones in the body. A new line of research on spinal disorders This groundbreaking study , published in the journal Nature, sheds light on the mechanisms behind the preference for solid tumours to spread to the spine. The findings open up a new line of research on spinal disorders, potentially leading to a better understanding and treatment of bone diseases involving the spine. Identifying vertebral stem cells The researchers began their study by isolating skeletal stem cells, which are responsible for bone and cartilage formation, from various bones in lab mice. Through gene activity analysis, they identified a distinct set of markers for vertebral stem cells. Further experiments in mice and lab-dish cell culture systems confirmed the functional roles of these stem cells in forming spinal bone. Unravelling the mystery of spinal tropism Previous theories attributed the spine's susceptibility to metastasis to patterns of blood flow. However, the study's findings challenged this long-standing belief. Animal models reproduced the phenomenon of spinal tropism, but the researchers discovered that blood flow was not the sole explanation. Instead, they found evidence pointing towards vertebral stem cells as the possible culprits. The role of MFGE8 The researchers discovered that spinal tropism is largely a result of the protein MFGE8, which vertebral stem cells secrete in greater quantities than other bone stem cells. Removing vertebral stem cells eliminated the difference in metastasis rates between spine bones and other long bones. Implications for cancer patients These findings have significant implications for cancer patients, particularly those at risk of spinal metastasis. The researchers are now exploring methods to block the activity of MFGE8, aiming to reduce the risk of tumour spread to the spine. By understanding the distinctive properties of vertebral stem cells, researchers hope to develop targeted treatments for spinal disorders. A new frontier in orthopaedics According to study senior author Matthew Greenblatt, the identification of these unique stem cells opens up a new subdiscipline in orthopaedics called spinal orthopaedics. Many conditions in this clinical category may be attributed to the properties of vertebral stem cells. Further research in spinal orthopaedics is needed to understand how these distinct properties of vertebral stem cells contribute to spinal disorders. The discovery of MFGE8, a protein secreted in higher amounts by vertebral stem cells, has shed light on the mechanism behind the preferential spread of tumours to the spine. By investigating methods to block MFGE8, researchers hope to reduce the risk of spinal metastasis in cancer patients. Additionally, the study findings highlight the importance of understanding the role of vertebral stem cells in bone diseases that primarily affect the spine. This new line of research may provide insights into the development of novel treatments for spinal disorders. Conclusion In conclusion, the study by researchers at Weill Cornell Medicine has shown that vertebral bones, which make up the spine, contain a particular type of stem cell that secretes a protein known as MFGE8. This protein plays a significant role in promoting tumour metastases, explaining why solid tumours often spread to the spine. The findings have opened up new avenues of research in understanding spinal disorders and may lead to the development of strategies for reducing the risk of spinal metastasis in cancer patients. Overall, this study highlights the importance of vertebral stem cells in contributing to spinal disorders and emphasises the need for further investigation in this field. Written by Sara Maria Majernikova Related articles: Cancer metastasis / Brain metastasis / Stem cells REFERENCE Sun, J., Hu, L., Bok, S. et al. A vertebral skeletal stem cell lineage driving metastasis. Nature 621, 602–609 (2023). https://doi.org/10.1038/s41586-023-06519-1 Project Gallery