Rock-wallabies are adapted to occupy specific rocky habitats, like outcrops, cliffs and caves Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Protecting rock-wallabies in Australia Last updated: 06/11/25, 11:54 Published: 29/05/25, 08:00 Rock-wallabies are adapted to occupy specific rocky habitats, like outcrops, cliffs and caves This is the final article (article no. 7) in a series on animal conservation. Previous article: Emperor penguins, kings of ice . First article: 55 years of vicuna conservation . Australia is home to many unique mammals because they have evolved in geographic isolation for millennia. Over 200 years ago, European colonists brought their own mammals to Australia, devastating this unique wildlife in ways that can still be seen today. One example is the rock-wallabies ( Petrogale spp. ), a group of 25 animal species and subspecies related to kangaroos. Australian scientists are monitoring rock-wallaby populations to ensure they remain safe from natural and human-caused threats. This article will describe those threats and how rock wallabies are being conserved. Rock-wallaby habitat As their name suggests, rock-wallabies are adapted to occupy specific rocky habitats, including outcrops, cliffs and caves. Since they are primarily nocturnal, these habitats provide shelter in the daytime. Rock-wallabies have modified foot pads to grip tricky surfaces and access places their predators cannot. Recent research found that for two rock-wallaby species, their abundance is associated with more complex and rocky habitats. Because their habitat type is so niche and they rarely migrate, one small disturbance could wipe out an entire rock-wallaby population. This is reflected by their protections under Australian law: five types of rock-wallaby are classified as ‘vulnerable’, six as ‘endangered’, and one as ‘critically endangered’. Thus, the complex habitat of rock-wallabies is both a blessing and a curse. Threats to rock-wallabies Rock-wallabies are vulnerable or endangered mainly because of invasive predators such as foxes, cats, and goats. After being introduced from Europe during colonisation, these predators have eaten many wallabies and scared the rest into foraging elsewhere. If predators live between two rock-wallaby populations, there will be less migration and interbreeding, reducing overall genetic health ( Figure 1 ). In addition, rock-wallabies will not forage if predators are in an area, so they have limited food sources under high pressure ( Figure 1 ). Combined with these indirect reasons, direct predation by invasive mammals is the biggest threat to rock-wallaby survival. Invasive predators are not the only threats to rock-wallaby populations. Wildfires kill the plants that wallabies rely on for food and shelter, such as rock figs. For example, one wildfire in the 2019/2020 season destroyed about 38% of brush-tailed rock-wallaby habitat. The already dwindling rock-wallaby populations may disappear if the climate crisis makes wildfires less predictable and more severe. Native herbivores like the euro and invasive herbivores like goats may also compete with rock-wallabies for food. There is evidence that euros out-compete rock-wallabies when food supplies are limited, but no evidence for goats yet. Thus, fires and competition combine with invasive predators to endanger rock-wallabies. Translocation and monitoring Monitoring existing rock-wallaby populations and creating new ones by translocation are reducing the threats of predation, fire, and competition. Brush-tailed rock-wallabies were translocated to Grampians National Park in 2008, but most animals died by 2013. Scientists thought manually handling wallabies might make them stressed and more vulnerable to predators. From 2014 onwards, non-invasive monitoring procedures like cameras and faecal DNA monitoring reduced predation and increased the survival rate of young rock-wallabies. Meanwhile, black-flanked rock-wallabies were being translocated from four different source populations to Kalbarri National Park, hoping they would interbreed and create a new genetically diverse population. The project was successful, as microsatellite genotyping found that the translocated population had more heterozygotes and more alleles per locus than the source populations ( Figure 2 ). This population is predicted to grow until at least 2028 because it is diverse enough to avoid the inbreeding mentioned earlier. The Grampians and Kalbarri translocations show the importance of careful monitoring and genetic considerations for conserving rock-wallabies. Conclusion After invasive mammalian predators have decimated rock-wallaby populations throughout Australia for over 200 years, wildfires and herbivore competition make survival even more difficult. Conservation efforts are made harder by the specific and limited habitats that rock-wallabies need. However, translocation efforts which consider genetic diversity and the stress of manual handling keep rock-wallaby populations afloat. Written by Simran Patel Related article: Wildlife corridors REFERENCES Campbell, I. & Woods, S. (2013) Wildlife of Australia . Princeton, UNITED STATES: Princeton University Press. Kleemann, S., Sandow, D., Stevens, M., Schultz, D.J., Taggart, D.A. & Croxford, A. (2022) Non-invasive monitoring and reintroduction biology of the brush-tailed rock-wallaby (Petrogale penicillata) in the Grampians National Park, Australia. Australian Journal of Zoology . 69 (2): 41–54. Available from: https://www.publish.csiro.au/zo/ZO21009 (Accessed 10th December 2024). Lavery, T.H., Eldridge, M., Legge, S., Pearson, D., Southwell, D., Woinarski, J.C.Z., Woolley, L.-A. & Lindenmayer, D. (2021) Threats to Australia’s rock-wallabies (Petrogale spp.) with key directions for effective monitoring. Biodiversity and Conservation . 30 (14): 4137–4161. Available from: https://doi.org/10.1007/s10531-021-02315-3 (Accessed 9th December 2024). Morris, S.D., Johnson, C.N. & Brook, B.W. (2020) Roughing it: terrain is crucial in identifying novel translocation sites for the vulnerable brush-tailed rock-wallaby (Petrogale pencillata). Royal Society Open Science . 7 (12): 201603. Available from: https://royalsocietypublishing.org/doi/full/10.1098/rsos.201603 (Accessed 10th December 2024). Nilsson, K., Pearson, D., Paxman, M., Desmond, A., Kennington, J., Byrne, M. & Ottewell, K. (2023) Translocations restore a population of a threatened rock-wallaby and bolster its genetic diversity. Conservation Genetics . 24 (5): 547–561. Available from: https://doi.org/10.1007/s10592-023-01520-7 (Accessed 9th December 2024). Silcock, J.L., Gynther, I.C., Horsup, A., Molyneux, J., Wattz, T.L., Fairfax, R.J., Healy, A.J., Murphy, D. & McRae, P.D. (2024) Half a century of survey data reveal population recovery but persistent threats for the Vulnerable yellow-footed rock-wallaby in Queensland, Australia. Oryx . 1–13. Available from: https://www.cambridge.org/core/journals/oryx/article/half-a-century-of-survey-data-reveal-population-recovery-but-persistent-threats-for-the-vulnerable-yellowfooted-rockwallaby-in-queensland-australia/D976E61ABE458B9FADA059372117382E (Accessed 10th December 2024). Project Gallery

The main difference between children and adults lies in what needs to be rebuilt Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Why brain injuries affect children and adults differently Last updated: 13/06/26, 16:54 Published: 13/11/25, 08:00 The main difference between children and adults lies in what needs to be rebuilt When we think about a brain injury, it is easy to assume that the same thing happens in everyone; a bump to the head, swelling, and hopefully a recovery. In reality, things aren’t quite that simple. A child’s brain is not a smaller version of an adult’s, it is still developing, which makes it both incredibly adaptable and, at the same time, especially vulnerable. Smaller bodies, bigger risks Although the brain’s basic reaction to injury is similar in children and adults, injuries in younger people tend to cause more widespread and severe damage. This is due to the differences in anatomical development. Children’s heads are proportionally larger compared to the rest of their bodies, and their neck muscles are much weaker than those of adults. This means that when a child falls or is knocked, their head can move suddenly and forcefully, placing extra strain on the brain. On top of that, children’s brains have a higher water content and are softer in texture, which makes them more vulnerable to rotational forces and acceleration-deceleration injuries. These types of movements can lead to diffuse axonal injury, where nerve fibres are torn across large areas, and cerebral swelling, both of which are less common in adults experiencing similar trauma. Additionally, a November 2024 study from the University of Glasgow found that while adults often have damaged medium/ large blood vessels, children suffer damage to the smallest vessels (capillaries) and more severe brain swelling. A clear example of this vulnerability is seen in abusive head trauma. When an infant is shaken, their softer skull and brain structure can lead to a combination of skull fractures, internal bleeding, and swelling. Sadly, these injuries are often linked to very poor outcomes. The double-edged sword of brain plasticity One of the most remarkable things about the young brain is its plasticity, which is its ability to reorganise itself and form new connections after injury. This flexibility often means that children recover some functions, such as movement or daily activities, more quickly than adults do in the early months after a brain injury. However, this adaptability has limits. During childhood, the brain is constantly developing new skills and abilities. If an injury occurs during one of these critical periods, it can interrupt processes essential for normal development. This means that difficulties might not appear straight away. A child could seem to recover well at first but then struggle later when their brain is expected to handle more complex tasks, such as problem-solving or emotional regulation. Over time, recovery often plateaus, and children may continue to face long-term challenges with learning, behaviour, and social interaction. Research also shows that injury severity is a major factor in long-term outcomes. Children who suffer severe traumatic brain injuries are more likely to experience lower academic performance and, later in life, face higher rates of unemployment or lower paid work compared with their peers. Behaviour, learning and life after injury Brain injuries in childhood can also affect behaviour and mental health. Conditions such as ADHD are especially common following injury, affecting between 20-50% of children. These difficulties can make returning to school and social life far more challenging. Children from lower socioeconomic backgrounds often experience extra barriers, including limited access to rehabilitation and educational support. This can increase the risk of social isolation and mental health difficulties. Children are also more likely than adults to develop secondary brain conditions, such as epilepsy, after an injury which adds further complexity to their recovery. Why recovery is not the same The main difference between children and adults lies in what needs to be rebuilt. Adults are generally trying to re-learn skills they already had, while children are still learning those skills for the first time. That makes recovery a much more delicate and unpredictable process. Moreover, most rehabilitation is concentrated in the first few months after the injury, but children’s challenges often become clearer years later, when their brains, and the demands placed on them, have developed further. In summary The developing brain is both fragile and flexible . While its biological features make it more prone to injury, its capacity for plasticity allows for impressive short-term recovery. Yet the same developmental processes that support growth also make it more vulnerable to long-term disruption. Injuries sustained during childhood can alter the course of brain development, leading to lasting effects on thinking, learning, and behaviour. These consequences can shape a person’s future long after the initial recovery period has ended. Understanding these differences is crucial, not just for doctors, but also for teachers, parents, and anyone supporting a young person recovering from a brain injury. Written by Alice Greenan Related articles: Synaptic plasticity / Brain plasticity / Traumatic Brain Injury (TBI) / Childhood intelligence REFERENCES Anderson, V. (2005). Functional Plasticity or Vulnerability After Early Brain Injury? PEDIATRICS , 116 (6), 1374–1382. https://doi.org/10.1542/peds.2004-1728 Anderson, V., Brown, S., Newitt, H., & Hoile, H. (2011). Long-term outcome from childhood traumatic brain injury: Intellectual ability, personality, and quality of life. Neuropsychology , 25 (2), 176–184. https://doi.org/10.1037/a0021217 Anderson, V., & Yeates, K. O. (2010). Pediatric Traumatic Brain Injury. In Cambridge University Press eBooks . Cambridge University Press. https://doi.org/10.1017/cbo9780511676383 ARAKI, T., YOKOTA, H., & MORITA, A. (2017). Pediatric Traumatic Brain Injury: Characteristic Features, Diagnosis, and Management. Neurologia Medico-Chirurgica , 57 (2), 82–93. https://doi.org/10.2176/nmc.ra.2016-0191 Blackwell, L. S., & Grell, R. M. (2023). Pediatric Traumatic Brain Injury: Impact on the Developing Brain. Pediatric Neurology . https://doi.org/10.1016/j.pediatrneurol.2023.06.019 Figaji, A. A. (2017). Anatomical and Physiological Differences between Children and Adults Relevant to Traumatic Brain Injury and the Implications for Clinical Assessment and Care. Frontiers in Neurology , 8 (685). https://doi.org/10.3389/fneur.2017.00685 Manfield, J., Oakley, K., Macey, J.-A., & Waugh, M.-C. (2021). Understanding the Five-Year Outcomes of Abusive Head Trauma in Children: A Retrospective Cohort Study. Developmental Neurorehabilitation , 24 (6), 1–7. https://doi.org/10.1080/17518423.2020.1869340 Narad, M. E., Kaizar, E. E., Zhang, N., Taylor, H. G., Yeates, K. O., Kurowski, B. G., & Wade, S. L. (2022). The Impact of Preinjury and Secondary Attention-Deficit/Hyperactivity Disorder on Outcomes After Pediatric Traumatic Brain Injury. Journal of Developmental & Behavioral Pediatrics , 43 (6), e361–e369. https://doi.org/10.1097/dbp.0000000000001067 Neumane, S., Câmara-Costa, H., Francillette, L., Araujo, M., Toure, H., Brugel, D., Laurent-Vannier, A., Ewing-Cobbs, L., Meyer, P., Dellatolas, G., Watier, L., & Chevignard, M. (2021). Functional outcome after severe childhood traumatic brain injury: Results of the TGE prospective longitudinal study. Annals of Physical and Rehabilitation Medicine , 64 (1), 101375. https://doi.org/10.1016/j.rehab.2020.01.008 Parker, K. N., Donovan, M. H., Smith, K., & Noble-Haeusslein, L. J. (2021). Traumatic Injury to the Developing Brain: Emerging Relationship to Early Life Stress. Frontiers in Neurology , 12 . https://doi.org/10.3389/fneur.2021.708800 Project Gallery

IT cells and their impact on public opinion Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The spread of digital disinformation 13/06/26, 16:19 Last updated: Published: 05/08/23, 11:06 IT cells and their impact on public opinion As of 2026, the internet boasts a staggering 5.66 billion estimated social media accounts, with a 4.8% year-on-year growth of +259 million users. The average person now spends 6 hours and 40 minutes daily connected to online screens, underscoring the significant role the internet plays in our lives. Consequently, it comes as no surprise that governments worldwide have recognised its potential as a critical tool to advance their agendas, policies, and achievements. Through diverse digital channels, governments aim to reach a vast audience and change public perception, striving to build transparency, trust, and legitimacy while maintaining a powerful digital presence. However, this approach also raises concerns about bias, propaganda, and information manipulation, which can impact public perceptions in questionable ways. One such phenomenon that has emerged is the presence of IT cells, organised groups typically affiliated with political parties, organizations, or interest groups. These Information Technology cells dedicate themselves to managing and amplifying their respective organisations' online presence, predominantly on social media platforms and other digital avenues. During contentious political events or national issues, IT cells deploy coordinated messaging in support of government policies and leaders, inundating social media platforms. Unfortunately, dissenting voices and critics may face orchestrated attacks from these IT cells, aimed at discrediting and silencing them. While some IT cells may operate with genuine intentions, they have faced criticism for engaging in tactics that spread misinformation, disinformation, and targeted propaganda to sway public sentiment in favour of their affiliated organisations. In such instances, IT cells strategically amplify positive news and government achievements while downplaying or deflecting negative information. Social media influencers and online campaigns have become tools to project a positive image of the government and maintain public support. One striking example of how governments can exploit IT cells for their gain was evident in the infamous Cambridge Analytica scandal. In 2018, revelations exposed how the political consulting firm, Cambridge Analytica, acquired personal data from millions of Facebook users without consent. The firm then weaponised this data to construct highly targeted and manipulative political campaigns, including during the 2016 United States presidential election and the Brexit referendum. In India, the ruling BJP party has come under scrutiny for its orchestrated online campaigns through its social media cell. The cell allegedly intimidates individuals perceived as government critics and actively disseminates misogyny, Islamophobia, and animosity. According to Sadhavi Khosla, a BJP cyber-volunteer associated with the BJP IT Cell, the organisation promotes divisive content and employs trolling tactics against users critical of the BJP. Journalists and Indian film actors have also found themselves targeted by these campaigns. As technology continues to evolve, it is imperative to strike a balance between leveraging the internet for transparency and legitimacy while safeguarding against potential misuse that could erode trust in digital governance and public discourse. Monitoring and addressing the activities of IT cells can be a significant step towards ensuring responsible and ethical use of digital platforms in the political arena. Written by Jaspreet Mann Related articles: COVID-19 misconceptions / Fake science websites Project Gallery

Life's origins Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The genesis of life 09/03/26, 14:46 Last updated: Published: 23/11/23, 11:22 Life's origins Did the egg or the chicken come first? This question is often pondered regarding life’s origin and how biological systems came into play. How did chemistry move to biology to support life? And how have we evolved into such complex organisms? The ingredients, conditions and thermodynamically favoured reactions hold the answer, but understanding the inner workings of life’s beginnings poses a challenge for us scientists. Under an empirical approach, how can we address these questions if these events occurred 3.7 billion years ago? The early atmosphere of the Earth To approach these questions, it is relevant to understand the atmospheric contents of the primordial Earth. With a lack of oxygen, the predominant make-up included CO2, NH3 and H2, creating a reducing environment for the drive of chemical reactions. When the earth cooled, and the atmosphere underwent condensation, pools of chemicals were made - this is known as “primordial soup”. It is thought that reactants could collide from this “soup” to synthesise nucleotides by forming nitrogenous bases and bonds, such as glycosidic or hydrogen bonds. Such nucleotide monomers were perhaps polymerised to create long chains for nucleic acid synthesis, that is, RNA, via this abiotic synthesis. Thus, if we have nucleic acids, genetic information could have been stored and passed later down the line, allowing for our eventual evolution. Note: there has now been a c hange in terminology from primordial soup, to focus on protocellular systems and the geochemically driven origin of life hypothesis. Conditions for nucleic acid synthesis The environment supported the formation of monomers for said polymerisation. For example, hydrothermal vents could have provided the reducing power via protons, allowing for the protonation of structures and providing the free energy for bond formation. Biology, of course, relies on protons for the proton gradient in ATP synthesis at the mitochondrial membrane and, in general, acid-base catalysis in enzymatic reactions. Therefore, it is safe to say protons played a vital role in life’s emergence. The eventual formation of structures by protonation and deprotonation provides the enzymatic theory of life’s origins. That is, some self-catalytic ability for replication in a closed system and the evolution of complex biological units. This is the “RNA World” theory, which will be discussed later. Another theory is wet and dry cycling at the edge of hydrothermal pools. This theory Is provided by David Deamer, who suggests that nucleic acid monomers placed in acidic (pH 3) and hot (70-90 degrees Celsius) pools could undergo condensation reactions for ester bond formation. It highlights the need for low water activity and a “kinetic trap” in which the condensation reaction rate exceeds the hydrolysation rate. The heat of the pool provides a high activation energy for the localised generation of polymers without the need for a membrane-like compartment. But even if this was possible and nucleic acids could be synthesised, how could we “keep them safe”? This issue is addressed by the theory of "protocells" formed from fatty acid vesicles. Jack Szostak suggests phase transition (that is pH decrease) allowed for the construction of bilayer membranes from fatty acid monomers, which is homologous to what we see now in modern cells. The fatty acids in these vesicles have the ability to “flip-flop” to allow for the exchange of nutrients or nucleotides in and out of the vesicles. It is suggested that clay encapsulated nucleotide monomers were brought into the protocell by this flip-flop action. Vesicles could grow by competing with surrounding smaller vesicles. Larger vesicles are thought to be those harbouring long polyanionic molecules - that is RNA - which creates immense osmotic pressure pushing outward on the protocell for absorption of smaller vesicles. This represents the Darwinian “survival of the fittest” theory in which cells with more RNA are favoured for survival. The RNA World Hypothesis DNA is often seen as the “Saint” of all things biology, given its ability to store and pass genetic information to mRNA and then mRNA can use this information to synthesise polypeptides. This is the central dogma, of course. However, the RNA world hypothesis suggests that RNA arose first due to its ability to form catalytic 3D structures and store genetic information that could have allowed for further synthesis of DNA. This makes sense when you think about how the primer for DNA replication is formed out of RNA. If RNA did not come first, how could DNA replication be possible? Many other scenarios suggest RNA evolution preceded that of DNA. So, if RNA arose as a simple polymer, its ability to form 3D structures could have allowed ribozymes (RNA with enzymatic function) within these protocells. Ribozymes, such as RNA ligase and polymerase, could have allowed for self-replication, and then mutation in primary structure could have allowed evolution to occur. If we have a catalyst, in a closed system, with nutrient exchange, then why would life’s formation not be possible? But how can we show that RNA can arise in this way? The answer to this is SELEX - selective evolution of ligands by exponential enrichment (5). This system was developed by Jack Szostak, who wanted to show the evolution of complex RNA, ribozymes in a test tube was possible. A pool of random, fragmented RNA molecules can be added to a chamber and run through a column with beads. These beads harbour some sequence or attraction to the RNA molecules the column is selecting for. Those that attach can be eluted, and those that do not can be disregarded. The bound RNA can be rerun through SELEX, and the conditions in the column can be more specific in that only the most complementary RNAs bind. This allowed for the development of RNA ligase and RNA polymerase - thus, self-replication of RNA is possible. SELEX helps us understand how the evolution of RNA in the primordial Earth could have been possible. This is also established by meteorites, such as carbon chondrites that burnt up in the earth’s atmosphere encapsulating the organic material in the centre. Chondrites found in Antarctica have been found to contain 80+ amino acids (some of which are not compatible with life). These chondrites also included nucleobases. So, if such monomers can be synthesised in a hostile environment in outer space/in our atmosphere, then the theory of abiotic synthesis is supported. Furthermore, it is relevant to address the abiotic synthesis of amino acids since the evolution of catalytic RNA could have some complementarity for polypeptide synthesis. Miller and Urey (1953) set up a simple experiment containing gas representing the early primordial earth (Methane, hydrogen, ammonia, water). They used a conduction rod to provide the electrical discharge (meant to simulate lightning or volcanic eruption) to the gases and then condensed them. The water in the other chamber turned pink/ brown. Following chromatography, they identified amino acids in the mixture. These simple manipulations could have been homologous to early life. There has lately been a new concept introduced of the thioester-RNA link, which unites the RNA world theory with the thioester world theory (which states that thioesters played a powerful role in the earliest stages of life). Recent findings suggest that the beginnings of life likely formed from both thioesters and RNA. Conclusion The abiotic synthesis of nucleotides and amino acids for their later polymerisation would support the theories that address chemistry moving toward biological life. Protocells containing such polymers could have been selected based on their “fitness” and these could have mutated to allow for the evolution of catalytic RNA. The experiments mentioned represent a small fragment of those carried out to answer the questions of life’s origins. The evidence provides a firm ground for the emergence of life to the complexity of what we know today. Written by Holly Kitley Project Gallery

It plays a key role in many cancers Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The Hippo signalling pathway 11/07/25, 10:59 Last updated: Published: 06/06/24, 12:35 It plays a key role in many cancers Introduction The Hippo signalling pathway controls tissue growth, and it is also a vital pathway involved in many cancers. It is a serine/threonine kinase pathway, which regulates tissue growth by the control of cell proliferation and apoptosis. It was first discovered in a Drosophila genetic screen and was named Hippo, as a loss of Hippo results in an overgrowth (or hippopotamus) phenotype. When the Hippo pathway is ‘on,’ YAP and TAZ (transcription factors/activators) are degraded in the cytoplasm. This occurs via phosphorylation: Sterile 20-related (MST) kinases are phosphorylated, which in turn phosphorylate Large tumour suppressor 1 and 2 (LATS1/2). LATS phosphorylation then causes phosphorylation of YAP/TAZ. In turn, YAP/TAZ then bind to 14-3-3 proteins in the cytoplasm and are broken down by ubiquitin-dependent degradation (see fig. 1). YAP/TAZ has also been shown to activate transcription of YAP/TAZ regulators, such as LATS1/2, in a negative feedback loop. Conversely, when Hippo is ‘off,’ YAP/TAZ are unphosphorylated and are free to move to the nucleus, where they bind to Transcriptional enhanced associate domain (TEAD). YAP/TAZ-TEAD then are able to bind DNA and be involved in transcription of genes such as Axl, c-Myc, survivin, CTGF , and Cyr61 , which are anti-apoptotic or proliferative. Hippo pathway in cancer YAP/TAZ have been shown to be crucial for cancer initiation, progression, and metastasis. They are known to be involved in many cancers, including prostate, bone, eye, brain, spinal cord, breast, and liver cancers. They are also involved in the rare blood vessel cancer epithelioid hemangioendothelioma (EHE). Interestingly, it appears YAP/TAZ act differently depending on the cell type. YAP/TAZ are oncogenic transcription factors in many solid tumours, but surprisingly, they are thought to act as tumour suppressors in some blood cancers e.g. Multiple myeloma (it is still unknown why this is). Therefore, for YAP/TAZ to behave in a regular manner (i.e. non-oncogenic), they must be tightly regulated. Regulation of the Hippo pathway Hippo signalling is regulated by tight/adherens junctions, mechanical signals, and growth factors/receptors. Tight junctions exist where there is a permeability barrier between adjoining cells, and proteins bind to these membranes for a range of different functions. A protein which binds to these adherens junctions is Merlin (encoded by the gene, NF2 ), which is another regulator of the Hippo pathway and a well-known tumour suppressor. Merlin is known to bind to adherens junction proteins in confluent cells, and loss of Merlin causes a lack of development of adherens junctions. Merlin is also an important component involved in contact inhibition during proliferation. Contact inhibition is where cell growth is inhibited upon contact with other cells. The specific mechanism by which Merlin regulates the Hippo pathway and contact inhibition is still unknown. Another regulator of the Hippo pathway is mechanical signals. Fluid shear stress is the frictional force between flowing blood and endothelial cells lining the blood vessels and is known to cause vascular growth, remodelling and maintenance. This stress can result in changes to endothelial cell shape and cause the activation of transcription factors, leading to gene expression. An additional regulator of the Hippo pathway is growth factors/receptors. Growth factors, such as Sphingosine 1-phosphate (S1P) and lysophosphatidic acid (LPA) are both part of the phospholipids growth factor family. They bind to the S1P receptor and LPA receptor, respectively, inhibiting LATS and causing activation of YAP/TAZ. Whereas molecules, such as glucagon and epinephrine have been shown to suppress YAP/TAZ. Cytokines, vascular endothelial growth factors (VEGF), epidermal growth factors (EGF), Wnt, bone morphogenic protein (Bmp), insulin, and transforming growth factor β (TGF-β) have also been shown to regulate the Hippo pathway, which suggests that regulation of the Hippo pathway is complex and linked to several different other pathways. Conclusion The Hippo pathway is a vitally important pathway regulating tissue growth. YAP/TAZ, which are part of the Hippo pathway, are oncogenic factors in many solid tumours but can act as tumour suppressors in some blood cancers. As YAP/TAZ are involved in transcription in this pathway, they are crucial for cancer initiation, growth and metastasis. Hence, targeting of this pathway could lead to further cancer treatments. For example, TEAD inhibitors may offer a therapeutic avenue of treatment and are currently being investigated. In the future, further research on targeting the Hippo pathway may improve on the current targeted therapeutic landscape, realising the need for diverse treatment options for such a complex disease as cancer. Written by Eleanor R. Markham Related articles: MAPK/ ERK signalling pathway / Epitheliod hemnagioendothelioma Project Gallery

The different models of health and disease Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Beyond medicine: understanding health through various stances 16/10/25, 11:21 Last updated: Published: 22/04/24, 11:24 The different models of health and disease Introduction Various models can show what factors produce health outcomes between individuals and populations. This article looks at the biomedical, social, humanistic and biopsychosocial models, reviewing each through examples and its applications to the real world. With this said, every model has advantages and disadvantages because they are imperfect. Each one is essential as it provides a way to treat patients, so they need to be used alongside one another to address the different aspects involved in a person’s health. Biomedical model- figure 1 To start with the most familiar, the biomedical model looks at finding the cause of illness through a physiological perspective, i.e. finding malfunctions in organs and cells. For example, infections are caused by microorganisms, or metabolic disorders usually occur due to at least one critical genetic mutation. This model has some advantages, such as using evidence-based strategies to treat patients, and it has contributed to medical breakthroughs that have improved overall health. Also, it can lead to effective treatment plans through medical interventions to handle specific diseases. However, the biomedical model does not consider external factors involved in illness. Moreover, it focuses on curing diseases instead of preventative plans that may be more successful, and its recommendation of pharmaceutical drugs for certain conditions may cause addiction, which is another health problem. Social-ecological model- figure 2 Now, the social-ecological model considers societal factors, ranging from economic to political, that are influential in population health. It helps investigate non-communicable and infectious diseases. An advantage of this model is it emphasises preventative strategies, which can lead to long-term advancements in health. Moreover, it encourages cooperation within communities in shaping initiatives that benefit everyone and regards collaboration between multiple work sectors like education and law enforcement as vital to progressing society. A significant downside of the social model is that it is complicated, suggesting it is difficult to tackle all of these determinants of health effectively. In turn, allocating resources to resolve specific issues would take much work. Lastly, some detractors of this model believe it absolves people’s responsibility for their health. Humanistic model- figure 3 Subsequently, the humanistic model is about an individual’s wellbeing, experiences, and self-exploration. Its applications are mainly in psychology, though it can manifest in other areas of life through a person making decisions they are satisfied with. A few advantages of this model include prioritising a person’s autonomy, encouraging their psychological well-being, and facilitating collaboration between clinicians and patients in treatment. On the other hand, only some can think for themselves or their experiences; the model relies on subjectivity, so it can be challenging to measure parts of well-being, and it is more beneficial for chronic conditions than acute ailments. Biopyschosocial model- figure 4 The biopsychosocial (BPS) model includes biological, psychological and social factors related to a patient’s health. Therefore, it can be used for any individual with chronic or acute disease(s) and is used broadly in psychology between the psychiatrist/ counsellor and the patient. One advantage is that it aids primary care doctors in comprehending the interrelations between an illness's biological and psychosocial parts. In turn, this strengthens the patient-clinician relationship. Similar to the social model, this can promote preventative measures against diseases. However, the addition of biological and psychosocial factors makes the model complicated to implement in clinical contexts. Moreover, there needs to be more distinct guidelines for its use in treating patients compared to the biomedical model. Lastly, applying the biopsychosocial can change between healthcare practices, possibly leading to different standards of care. Conclusion Reflecting on the models outlined, the biopsychosocial model seems to be the perfect one compared to the others because it includes all of the models above or others not mentioned in this article. In turn, it succeeds in providing a balanced view of health. On the other hand, as iterated before, the BPS model has its disadvantages. Thus, it may require more refinements to be widely implemented across healthcare settings. Written by Sam Jarada Related articles: Key discoveries in public health / Healthcare challenges in Sudan / Conflicted Kashmir / Colonialism, geopolitics and health REFERENCES Leeper HE. Survivorship and Caregiver Issues in Neuro-oncology. Current Treatment Options in Oncology. 2019 Nov;20(11). Rocca E, Anjum RL. Complexity, Reductionism and the Biomedical Model. Rethinking Causality, Complexity and Evidence for the Unique Patient. 2020 Jun 3;1(1):75–94. Williams H. What Is the Biomedical Model? The Health Board. 2011. Golden TL, Wendel ML. Public Health’s Next Step in Advancing Equity: Re-evaluating Epistemological Assumptions to Move Social Determinants From Theory to Practice. Frontiers in Public Health. 2020 May 7;8. Isaacs P. A Humanistic Psychological Approach To Autism. Paul Isaacs’ Blog. 2017. Flow Psychology. 10 Humanistic Approach Strengths and Weaknesses | Flow Psychology. Flowpsychology.com . 2016. Hardie M. Three Aspects of Health and Healing: The Biopsychosocial Model in Medicine. Department of Surgery. 2021. Kusnanto H, Agustian D, Hilmanto D. Biopsychosocial model of illnesses in primary care: A hermeneutic literature review. Journal of Family Medicine and Primary Care. 2018 May;7(3):497–500. Project Gallery

A short exploration of the genetic predisposition behind human behaviours Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Can we blame our genes for excessive smoking and drinking? 07/05/26, 19:37 Last updated: Published: 13/01/24, 15:33 A short exploration of the genetic predisposition behind human behaviours The advancing research on how tobacco, alcohol addictions, and other detrimental behaviors are consequences of complex interplays between genetic and environmental factors has gradually developed and gained credibility. A collaborative effort involving over 100 international scientists, including researchers from the National Institutes of Health (NIH) and the National Institute on Drug Abuse (NIDA), embarked on a genome-wide association study (GWAS) to explore the heritable traits associated with tobacco and alcohol addiction. The study analyzed data from a sample size of 1.2 million biobanks, epidemiological research, and genetic testing companies, shedding light on the relationship between genetics and addiction behaviors. Researchers discovered that phenotypes related to smoking, such as when individuals began smoking habits, are genetically correlated with various diseases. In contrast, increased genetic risk for alcohol consumption is linked to reduced risk of many diseases. Previous studies pinpointed 10 genes involved in the risk of tobacco and alcohol addiction. In addition, this study further contributed to genetic links by identifying more than 400 locations in the genomes with over 500 variants associated with critical functions involving dopamine regulation, glutamate transmission and acetylcholine activation in the brain. Another study involving 3.4 million people with diverse ancestries suggested that approximately 3,823 genetic variants may impact addiction behaviors, with specific variants associated with the age at which individuals start smoking and the number of cigarettes or alcoholic drinks consumed. These studies could indicate a future where genetic screening for genes relevant to addiction behaviors is available, and this could be especially useful for those with relatives involved in certain addictions. Furthermore, it also provides perspective on whether certain genes can increase the likelihood of addiction to illegal drugs like cocaine, heroin or MDMA. However, increasing people’s awareness of whether they are at risk of developing addictions may be insufficient in deterring them from pursuing risky behaviors, which suggests that genetic screening for these genes would be beneficial as an optional screening assessment for individuals. While the influence of environmental and social factors on tobacco and alcohol addictions has long been acknowledged and explored, these studies underscore the significant role genetics plays in determining an individual’s susceptibility to nicotine and alcohol dependence. The prospect of predicting a person’s risk of addiction can lead to early interventions. Furthermore, it prevents countless health-related fatalities associated with smoking and alcoholic beverages. This primary prevention provides a different aspect to risk factors for smoking and alcohol addiction while also reducing the burden of these highly prevalent public health concerns. Written by Maya El Toukhy Related articles: Smoking cessation / Smoking and trigeminal neuralgia References: New Scientist (n.d.). Thousands of genetic variants may influence smoking and alcohol use. [online] New Scientist. Available at: https://www.newscientist.com/article/2350516thousandsofgenetic-variants-may-influence-smoking-and-alcohol-use/ [Accessed 23 Oct. 2023]. Today’s Clinical Lab. (n.d.). Do Your Genes Predispose You to Smoking and Drinking? [online] Available at: https://www.clinicallab.com/do-your-genes-predispose-you-tosmokinganddrinking-26963 [Accessed 23 Oct. 2023]. University of Minnesota. (2019). Hundreds of genes affecting tobacco and alcohol use discovered. [online] Available at: https://twin-cities.umn.edu/newsevents/hundredsgenesaffecting-tobacco-and-alcohol-use-discovered [Accessed 23 Oct. 2023]. Schlaepfer, I., Hoft, N. and Ehringer, M. (2008). The Genetic Components of Alcohol and Nicotine Co-Addiction: From Genes to Behavior. Current Drug Abuse Reviewse, 1(2), pp.124– 134. doi: https://doi.org/10.2174/1874473710801020124 . Project Gallery

How can patients with metastasised cancer be treated? Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Cancer on the Move 09/07/25, 14:31 Last updated: Published: 30/01/24, 19:57 How can patients with metastasised cancer be treated? Introducing and Defining Metastasis Around 90% of patients with cancer die due to their cancer spreading (metastasis). Despite its prevalence, many critical questions remain in the field of cancer research about how and why cancers metastasise. The metastatic cascade has three main steps: dissemination, dormancy, and colonisation. Most cells that disseminate die once they leave the primary tumour, thus, posing an evolutionary bottleneck. However, the few that survive will face another challenge of entering a foreign microenvironment. Those circulating tumour cells (CTCs) acquire a set of functional abilities through genetic alterations, enabling them to survive the hostile environment. CTCs can travel as single cells or as clusters. If they travel in clusters, CTCs can be coated with platelets, neutrophils, and other tumour-associated cells, protecting CTCs from immune surveillance. As these CTCs travel further, they are named disseminated tumour cells (DTCs). These cells are undetectable by clinical imaging and can enter a state of dormancy. The metastatic cascade represents ongoing cellular reprogramming and clonal selection of cancer cells that can withstand the hostile external environment. How does metastasis occur, and what properties allow these cancer cells to survive? How & Why Does Cancer Metastasise? The Epithelial-to-Mesenchymal Transition (EMT) is a theory that explains how cancer cells can metastasise. In this theory, tumour cells lose their epithelial cell-to-cell adhesion and gain mesenchymal migratory markers. Tumour cells that express a mixture of epithelial and mesenchymal properties were found to be the most effective in dissemination and colonisation to the secondary site. It is important to note that evidence for the EMT has been acquired predominantly in vitro , where additional in vivo research is necessary to confirm this phenomenon. Nevertheless, although EMT does not accurately address why cancers metastasise, it provides a framework for how a cancer cell develops the properties to metastasise. Many factors contribute to why cancers metastasise. For example, a lack of blood supply, which occurs when a cancer grows too large, causes the cells in the centre to lack access to the oxygen carried by red blood cells. Thus, to evade cell death, cancer cells detach from the primary tumour to regain access to oxygen and nutrients. In addition, cancer cells exhibit a high rate of glycolysis to supply sufficient energy for its uncontrollable proliferation. However, this generates lactic acid as a by-product, resulting in a low pH environment. This acidic pH environment stimulates cancer invasion and metastasis as cancer cells move away from this hostile environment to evade cell death once again, an effect referred to as the ‘Warburg Effect’. In Figure 2, you can see that multiple interplaying factors that contribute to metastasis. So, how can patients with metastasised cancer be treated? Current Treatments and Biggest Challenges? Depending on what stage the patient presents at and what cancer type, the treatment options differ. Figure 3 shows an example of these treatment plans. For early stages I and II, chemotherapy and targeted treatments are offered, and in specific cases, local surgery is done. These therapies are done to slow the growth of the cancer or lessen the side effects of treatments. An example of treating metastasised prostate cancer includes hormone therapy, as the cancer relies on the hormone testosterone to grow. Currently, cytotoxic chemotherapy remains the backbone of metastatic therapy. However, there are emerging immunotherapeutic treatments under trial. These aim to boost the ability of the immune system to detect and kill cancer cells. Hopefully, these new therapies may improve the prognosis of metastatic cancers when used in complement with conventional therapies, shining a new light into the therapeutic landscape of advanced cancers. Future Directions Recent developments have opened new avenues to discovering potential treatment targets for metastatic cancer. The first is to target the dormancy of DTCs, where the role of the immune system plays an important part. Neoadjuvant ICI (immune checkpoint inhibitor) studies are anticipated to provide insight into novel biomarkers and can eliminate micro-metastatic cancer cells. Also, using novel technology such as single-cell RNA sequencing reveals complex information about the plasticity of metastatic cancer cells, allowing researchers to understand how cancer cells adapt in stressful conditions. Finally, in vivo models, such as patient-derived models, could provide crucial insight into future treatments as they reproduce the patients’ reactions to different drug treatments. There are many limitations and challenges to the research and treatment of cancer metastasis. It is clear, however, that with more studies into the properties of metastatic cancers and the different avenues of novel targets and therapeutics, there is a promising outcome in the field of cancer research. Written by Saharla Wasame Related articles: Immune signals and metastasis / Cancer magnets for tumour metastasis / Brain metastasis / Novel neuroblastoma driver for therapeutics REFERENCES Fares, J., Fares, M.Y., Khachfe, H.H., Salhab, H.A. and Fares, Y. (2020). Molecular principles of metastasis: a hallmark of cancer revisited. Signal Transduction and Targeted Therapy , 5(1). doi: https://doi.org/10.1038/s41392-020-0134-x . Ganesh, K. and Massagué, J. (2021). Targeting metastatic cancer. Nature Medicine , 27(1), pp.34–44. doi: https://doi.org/10.1038/s41591-020-01195-4 . Gerstberger, S., Jiang, Q. and Ganesh, K. (2023). Metastasis. Cell , [online] 186(8), pp.1564–1579. doi: https://doi.org/10.1016/j.cell.2023.03.003 . Li, Y. and Laterra, J. (2012). Cancer Stem Cells: Distinct Entities or Dynamically Regulated Phenotypes? Cancer Research , [online] 72(3), pp.576–580. doi: https://doi.org/10.1158/0008-5472.CAN-11-3070 . Liberti, M.V. and Locasale, J.W. (2016). The Warburg Effect: How Does it Benefit Cancer Cells? Trends in Biochemical Sciences , [online] 41(3), pp.211–218. doi: https://doi.org/10.1016/j.tibs.2015.12.001 . Mlecnik, B., Bindea, G., Kirilovsky, A., Angell, H.K., Obenauf, A.C., Tosolini, M., Church, S.E., Maby, P., Vasaturo, A., Angelova, M., Fredriksen, T., Mauger, S., Waldner, M., Berger, A., Speicher, M.R., Pagès, F., Valge-Archer, V. and Galon, J. (2016). The tumor microenvironment and Immunoscore are critical determinants of dissemination to distant metastasis. Science Translational Medicine , 8(327). doi: https://doi.org/10.1126/scitranslmed.aad6352 . Oscar Hernandez Dominguez, Yilmaz, S. and Steele, S.R. (2023). Stage IV Colorectal Cancer Management and Treatment. Journal of Clinical Medicine , 12(5), pp.2072–2072. doi: https://doi.org/10.3390/jcm12052072 . Steeg, P.S. (2006). Tumor metastasis: mechanistic insights and clinical challenges. Nature Medicine , [online] 12(8), pp.895–904. doi: https://doi.org/10.1038/nm1469 . Project Gallery

Resources to help you prepare for university admission. Entrance Exam Preparation Resources to help you with university admission for: medicine , dentistry, natural sciences , physics , maths , engineering . Do note these entrance exams are mainly for UK universities, but can be used for international unis too. It is advised to check with the university when applying. You may also like: Personal statements , A-level resources, IB resources and Extra resources MEDICINE: University Clinical Aptitude Test (UCAT) UCAT resources: UCAT website / The Medic Portal / 6med UCAT Books: 1300 UCAT Practice Questions / 1250 UKCAT Practice Questions / UCAT 700+ UCAT online course: Medify Help with medical exams DENTISTRY: UCAT and BioMedical Admissions Test (BMAT; for University of Leeds only) Dentistry application preparation BMAT: online mastery course / Medify guide / Past papers / 700 BMAT Practice Questions / BMAT ebook For UCAT resources, see above OTHER ADMISSION TESTS Engineering: STEP / PAT University of Cambridge: natural sciences (NSAA) / engineering (ENGAA) / maths (STEP) / physics (PAT)

Insight into the different stages Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link A deep dive into ovarian cancer 03/07/25, 11:24 Last updated: Published: 04/04/24, 15:41 Insight into the different stages Introduction Ovarian cancer occurs when abnormal cells in the ovary begin to grow and divide uncontrollably ; this may lead to tumour formation. According to Cancer Research UK , there are around 7,500 new cases of ovarian cancer each year - that is around 21 a day. This makes ovarian cancer the 6th most common cancer in females in the UK, as it makes up around 4% of all cancer cases. Nevertheless, a total of around 11% of all ovarian cancer cases are thought to be preventable. This article aims to provide a comprehensive overview of ovarian cancer including the risk factors, prevention, diagnosis, and treatment. Diagnostics At present, there is no screening test specific for ovarian cancer. Hence, this often leads to late-stage diagnosis, which results in death or high rates of recurrence within ten years of initial diagnosis, should remission be reached. Initial diagnostic testing includes transvaginal ultrasonography and serum cancer antigen 125 (CA 125) level testing. Transvaginal Ultrasonography This type of imaging is used to assess the overall architecture and vascularity of the ovaries as well as to differentiate cystic from solid masses and detect ascites (a collection of fluid within abdominal spaces). The sensitivity (a tests ability to correctly identify if an individual has a disease) and specificity (a tests ability to correct identify individuals who do not have a disease) for distinguishing malignant lesions using this type of imaging is 86% - 94%. Blood Testing Complete blood count, as well as liver function tests, calcium, and serum biomarkers, are often obtained if ovarian cancer is suspected. CA 125 is the most commonly tested biomarker. However, its usefulness in the diagnosis of ovarian cancer depends on the stage of the disease at the time of testing. CA 125 is elevated in around 80% of epithelial ovarian cancers overall. However, it is only elevated in around 50% of early-stage epithelial ovarian cancers. This biomarker may also rise in conditions such as fibroids and endometriosis. Other biomarkers involved include human epididymis protein 4 (HE4), a glycoprotein expressed in about 1/3rd of ovarian cancers that lack elevated CA125. Biomarkers for non-epithelial cancers include inhibin A/B for sex-cord stromal tumours and serum α-fetoprotein and quantitative human chorionic gonadotropin for germ cell tumours. Staging Ovarian cancer is often categorised using the FIGO (1 – 4 staging) system, named after the International Federation of Gynaecological Oncologists. Stage 1 Stage one ovarian cancer means that the cancer is only located in the ovaries and is further divided into three groups. According to the CRUK website the three groups are: Stage 1A : the cancer is entirely confined within a singular ovary Stage 1B : the cancer is entirely confined within both ovaries Stage 1C is split into 3 subgroups: Stage 1C1 : the cancer is present in one or both ovaries and the ovary ruptures during a surgical procedure Stage 1C2 : the cancer is present in one or both ovaries and the ovary ruptures before a surgical procedure or there is evidence of cancer on the surface of the ovary Stage 1C3 : the cancer is present in one or both ovaries and cancer cells are detected in the fluid collected from the abdominal cavity during surgery These groups can be further illustrated in Figure 1 at the end of the text. Stage 2 Stage 2 ovarian cancer means the cancer has grown outside the ovaries and is growing within the pelvis. It is divided into two groups. According to the CRUK website the two groups are. Stage 2A : the cancer has extended its growth into either the fallopian tubes or the womb Stage 2B : the cancer has infiltrated surrounding tissues within the pelvic region such as the bladder or the bowel These groups can be further illustrated in Figure 2 at the end of the text. Stage 3 Stage 3 ovarian cancer means the cancer has grown outside the pelvis into the abdominal cavity or lymph nodes. It is divided into three groups. According to the CRUK website the three groups are: Stage 3A is divided into two subgroups: Stage 3A1 : the cancer has infiltrated lymph nodes in the rear of the abdomen Stage 3A2 : there are cancer cells detected in tissue samples taken from the peritoneum, cancer may also be present within the lymph nodes Stage 3B : Cancerous growths are present on the peritoneum that measure up to 2 cm in size, cancer may also be present within the lymph nodes Stage 3C : Cancerous growths are present on the peritoneum that measure over 2 cm in size, cancer may also be present within the lymph nodes These groups can be further illustrated in Figure 3 and Figure 4 at the end of the text. Stage 4 Stage 4 ovarian cancer means the cancer has metastatic and has spread to organs some distance away from the ovaries. It is divided into two groups. According to the CRUK website, the two groups are: Stage 4A : the cancer has induced a build-up of fluid in the pleura Stage 4B : the cancer has infiltrated various locations throughout the body including the interior of the liver or spleen, lymph nodes outside the abdominal region and any other organ within the body These groups can be further illustrated in Figure 5 and Figure 6 at the end of the text. Types of Ovarian Cancers There are three known types of ovarian cancer: epithelial, germ cell ovarian tumours and sex cord-stromal tumours. Epithelial Ovarian Cancer Epithelial ovarian cancer is the most common type of cancer. According to Cancer Research UK , about 90% of all ovarian tumours are epithelial. In this type of ovarian cancer, cancer starts in the surface layer covering the ovary. There are four stages of epithelial ovarian cancer - stages 1 to 4. Type Summary High-grade serous tumours ● 90% of all tumour tumours ● 10-year mortality rate of roughly 70% Low-grade serous tumours ● 10% of all tumour types ● Diagnosed at a younger age; better prognosis than high-grade serous tumours Endometrioid carcinomas ● Origins linked to endometriosis ● Good prognosis; mostly diagnosed at an early stage and are low-grade Clear cell carcinomas ● Origins linked to endometriosis ● 10% of epithelial ovarian cancers; rare form ● Often diagnosed in early stages. Late diagnosis has a poor prognosis. Mucinous carcinoma ● Least common form of epithelial ovarian cancer ● Origins linked with metastasis from gastrointestinal tract Table 1. Types of epithelial ovarian cancers. Germ Cell Ovarian Cancers Germ cell ovarian tumours are rare as they make up only 3% of ovarian cancer cases. They have a younger age of diagnosis with the average age being between 10 and 30 years old. Germ cell ovarian tumours can be benign (non-cancerous) or malignant (cancerous) Sex Cord-Stromal Tumours Sex cord-stromal tumours (SCSTs) are rare tumours of the ovary that originate in tissues that support the ovaries, known as the stroma or the sex cords. SCSTs account for around 5% of all ovarian cancer cases and are often diagnosed early. There are three main groups of SCSTs: Pure stromal tumours such as fibromas and thecomas. These are mainly benign. Pure sex cord tumours such as adult and juvenile granulosa cell tumours. These are the most common types of SCSTs and are malignant. Mixed sex cord-stromal tumours such as Sertoli-Leydig cell tumours. These can be either malignant or benign. Symptoms Historically, the signs and symptoms of ovarian cancer are non-specific and vague. The most common presenting symptoms in women are: Swelling or bloating of the abdomen Feel full quickly when eating Unexplained weight loss Pelvic and or abdominal pain or discomfort Unexplained fatigue A frequent need to urinate Changes in bowel habits or IBS symptoms The most common presenting symptom in children and adolescents is persistent abdominal pain. However, precocious puberty, irregular periods or hirsutism (excessive hair growth) may also be present. Due to the non-specific nature of these symptoms, many women will not get them checked by a doctor. It is still vitally important for a person to get any non-typical symptoms checked out by a doctor. Early diagnosis will lead to better outcomes. Treatment There are a variety of different treatment options for ovarian cancer. The treatment an individual undergoes is dependent on the size and location of the cancer as well as if it is metastatic. Debulking Surgery Debulking is a type of cytoreductive surgery that aims to remove as much cancer as possible if it has spread to areas within the pelvis and abdomen. This type of surgery is a mainstay of ovarian cancer treatment as most cases are more advanced in staging when initially diagnosed. Generally, debulking surgery is used on cancer that has spread widely throughout the abdomen and its goal is to do ‘optimal cytoreduction’, meaning no visible cancer is left behind or, if removing all visible disease is not possible, lesions less than 1cm in size are left. Hysterectomy For most women, a hysterectomy is the first-line treatment for ovarian cancer. The surgery removes the womb (including the cervix) as well as both ovaries and fallopian tubes and is known as a total abdominal hysterectomy (TAH) and bilateral salpingo-oophorectomy (BSO) . This procedure is further illustrated by Figure 7 at the end of the text. Chemotherapy Chemotherapy is the use of anti-cancer drugs to destroy cancer. These drugs circulate throughout the body via the bloodstream. In the treatment of ovarian cancer, chemotherapy can be given before, during or after surgery. The most commonly used drugs are carboplatin and paclitaxel. However, these are not the only options. Chemotherapy is typically used in the treatment of ovarian cancer if the cancer is: ● Stage 1C or above ● Stage 1A or 1B but is high grade ● Has come back (recurrence) Medication Route of administration Stage treated Duration Paclitaxel and carboplatin Intravenous I 21 days Paclitaxel and carboplatin Intravenous I 7 days Docetaxel and carboplatin Intravenous I 21 days Paclitaxel and cisplatin Intravenous or intraperitoneal II, III, IV 21 days Paclitaxel and carboplatin Intravenous or intraperitoneal II, III, IV 21 days Dose-dense paclitaxel and carboplatin Intravenous II, III, IV 21 days Paclitaxel and carboplatin Intravenous II, III, IV 7 days Docetaxel and carboplatin Intravenous II, III, IV 21 days Carboplatin and liposomal doxorubicin Intravenous II, III, IV 28 days Bevacizumab with paclitaxel and carboplatin Intravenous II, III, IV 21 days Table 2. Commonly used chemotherapy drugs for ovarian cancer Radiotherapy Radiotherapy involves the use of high-energy X-rays to destroy ovarian cancer cells. It is not the main treatment of ovarian cancer and is often used to try and shrink the size of tumours or to reduce the symptoms of advanced ovarian cancer. This is known as palliative radiotherapy . Targeted Therapies Cancer-targeting drugs change how a cell works by acting on cellular processes or by modifying cell signalling. They stimulate the body to attack or control cancer cell growth. These drugs are a form of palliative treatment. The two most common drugs are olaparib and bevacizumab. Olparib Olaparib (Lynparza) belongs to a drug type known as cancer growth blockers. It acts on PARP (poly ADP-ribose polymerase); a protein that helps damaged cells repair and regenerate themselves. Olaparib inhibits PARP from working. Bevacizumab Bevacizumab (Avastin) belongs to a drug type known as anti-angiogenesis treatments. It targets VEGF (vascular endothelial growth factor) proteins. VEGFs aid in cancer cell growth as they help cancers develop their blood supplies, meaning they can become self-sufficient. Bevacizumab blocks VEGF proteins from working, which cuts off the blood supply that feeds the cancer, ultimately starving it and preventing its growth. Risk Factors Modifiable Nonmodifiable Smoking BRCA1 and/ord BRCA2 mutation carrier Hormone Replacement Therapy (particularly for more than five years) Family predisposition/history Obesity Lynch syndrome Endometriosis Uninterrupted ovulation cycles Ethnicity/race Table 3. Ovarian cancer risk factors Genetic Syndromes Familial genetic syndromes are the strongest known risk factor for the development of ovarian cancers, as they account for around 10% - 12% of all cases. Table 4 which is taken from the paper ‘Diagnosis and Management of Ovarian Cancer’ by Doubeni et al (2016) illustrates genetic syndromes known to have an increased risk of ovarian cancer. Hereditary Breast and Ovarian Cancer Syndrome (HBOC) Mutations of the BRCA1 and BRCA2 genes are primarily associated with a genetic risk of developing ovarian cancer and can increase the risk from 1.6% to 40% ( BRCA1 ) and 1.6% to 18% ( BRCA2 ). This syndrome should be considered if a woman has close blood relative with a diagnosis of ovarian or breast cancer by the age of 50. Lynch Syndrome Although less common, Lynch syndrome is also linked to the development of ovarian cancer as it is involved in 2% - 3% of cases. Lynch syndrome is an autosomal dominant genetic disorder in which there is a mutation that increases the risk for certain cancers, specifically colorectal cancer, as well as increases the risk for other malignancies. Ovulation Ovulation is directly linked to the risk of ovarian cancer. Studies have shown that the more ovulatory cycles a woman has, the higher her risk of developing ovarian cancer. This may be due to the pro-inflammatory response from the distal fallopian tube during ovulation, which is known to promote malignant ovarian tendencies. Assuming this is true, factors that interrupt or prevent ovulation, such as contraception, early onset menses, pregnancy, breastfeeding and early menopause, could decrease a woman’s risk of developing ovarian cancer. Endometriosis Endometriosis, a disease in which tissue similar to the uterine lining grows outside the uterus, is known to be linked to some types of epithelial ovarian cancers. Endometriosis-associated epithelial ovarian cancers tend to develop in younger women and have an overall better prognosis. -- Where to seek help if affected by this article... F or support and more information regarding ovarian cancer: Macmillan Cancer Research If you or somebody you know have been affected by this article, help is always available: Mind and Samaritans -- Written by Lily Manns Related articles: A breakthrough drug discovery process in cancer treatment / Immune signals and metastasis / Novel neuroblastoma driver for therapeutics Reference guide Cancer Research. Ovarian Cancer Statistics: https://www.cancerresearchuk.org/health-professional/cancer-statistics/statistics-by-cancer-type/ovarian-c ancer Cancer Research. Epithelial Ovarian Cancer: https://about-cancer.cancerresearchuk.org/about-cancer/ovarian-cancer/types/epithelial-ovarian-cancers/ep ithelial Cancer Research. Stages and grades of ovarian cancer: https://www.cancerresearchuk.org/about-cancer/ovarian-cancer/stages-grades Elsevier. Ovarian Cancer: An integrated review: https://www.sciencedirect.com/science/article/pii/S0749208119300129?via%3Dihub American Family Physician. Diagnosis and Management of Ovarian Cancer: https://www.aafp.org/pubs/afp/issues/2016/0601/p937.html Cancer Research. Treatment for Ovarian Cancer: https://www.cancerresearchuk.org/about-cancer/ovarian-cancer/treatment Project Gallery