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Go back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Deception by flexible alarm mimicry in an African bird Last updated: 05/11/24 It’s been found that the species Dicrurus adsimilis (fork-tailed drongos) uses deception by flexible alarm mimicry to target and carry out food-theft attempts. The deceptive tactics of the fork-tailed drongo were studied which includes the use of false alarm calls and mimicked calls. Research was done on 64 wild drongos in the Kalahari Desert and it was found that the drongos spent more than a quarter of their time watching their target species which included southern pied babblers and meerkats. The other species’ would listen to the alarm calls made by drongos and would rush to take cover as they would if it was an alarm call from their species. These alarm calls were beneficial to them as it increased the number of returns from foraging and reduced their vigilance. However, the drongos used this to their advantage and if the target species was to find a large item of food the drongos could produce a false alarm call to make the target species run to cover out of fear which allowed the observing drongo to steal the deserted food. In 42% of cases of false alarms the drongos used a mimicked cry and in another 27% it was a mixture of mimicked and drongo-specific. This could be because target species are more likely to respond to a mimicked alarm call. In the case of babblers, if they heard a mimicked alarm call they would take longer to carry on foraging than with a drongo-specific call. The results show that false alarm calls by drongos work to distract their target but the call should also be frequently changed and not overused for best results. Written by Areebah Khan Related article: Conserving the Californian condor SUMMARISED FROM Flower, T.P., Gribble, M. and Ridley, A.R. (2014) “Deception by flexible alarm mimicry in an African bird,” Science, 344(6183), pp. 513–516.

Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link What can our canine friends tell us about cancer? 05/12/24, 12:26 Comparative oncology Comparative oncology is a field of study within cancer that has been adopted to study cancer and develop new therapies. It involves studying cancer in animals to uncover similarities between human and animal cancers. By combining scientific findings across a range of species, including companion animals such as dogs and horses or non-human primates such as monkeys, comparative oncology will advance cancer research and help develop effective novel therapies. This approach not only explores cancers in both animals and humans but also aims to bridge the gap between human and veterinary medicine. By examining similarities and differences in cancer biology, progression and treatment responses across species, comparative oncology provides valuable insights that can benefit both fields. Understanding how cancer behaves in animals can offer new perspectives and potential therapies for human patients. Conversely, while findings in human oncology can inform veterinary medicine, leading to improved diagnostics and treatments for animals. ( Figure 1 summarises the aims of comparative oncology). This article aims to explore this field of oncology further by discussing what it entails, the methodologies utilised, some recent advancements, and finally, things to look out for in the future. Comparative oncology has been developed and expanded into two areas of study. This includes spontaneous oncology and experimental oncology. Spontaneous oncology focuses on naturally occurring tumours in animals by investigating aspects of carcinogenesis, epidemiology, diagnosis, and treatment. It provides unique insights by drawing comparisons with human oncology research. These results can then be extrapolated to human oncology to gain a better understanding of cancer. This is because the similarities and differences observed in naturally occurring tumours across species provide valuable insights into underlying mechanisms within tumours and treatment responses. Experimental oncology serves as a distinct discipline where there are specialisations such as studying viral, chemical, and radiation oncogenesis alongside studying environmental factors such as pollution residues and food additives. This area involves studying both spontaneous tumours in animals and lab settings, where controlled conditions are used to explore different parts of cancer biology and treatment strategies. Additionally, the primary methodology utilised in comparative oncology involves studying spontaneous tumours in animals. Unlike artificially induced tumours in lab animals, these spontaneous tumours in pets closely mimic the complexity and heterogeneity of human cancers. For example, canines will live in similar living environments and experience similar external stimuli to their owner, such as pollution. The nature of these external stimuli means that they develop cancer in similar ways caused by epigenetic alterations, metabolic, and immune changes. (Figure 2 illustrates this process). Furthermore, comparative oncology uses advanced imaging techniques, genetic analysis, and immunological studies to predict pathways that may be shared among animals and humans which, could drive cancer development. Overall, these methods will allow the identification of promising therapies which directly target cancer and expand on current treatment choices such as chemotherapy and immunotherapy. One of the recent advancements in comparative oncology relates to osteosarcomas. This refers to cancer cells which begin to grow in the bones. For this specific form of cancer, molecular signatures were identified to predict clinical outcomes for both humans and canines, which can help improve treatment outcomes. Led by Amy K. LeBlanc, scientists have identified gene activity patterns in osteosarcoma tumours in nearly 200 dogs, revealing distinct groups with varying prognoses. These findings help us understand the biology behind osteosarcomas further and can potentially help us develop targeted therapies that take advantage of the immune system to treat the disease in both species. This potentially includes a range of therapies including PD-L1 inhibitors and cancer vaccines targeting the immune system. Moreover, breakthroughs in immunotherapies such as checkpoint inhibitors and CAR-T cell therapy are effective in treating haematological malignancies in both humans and canines. Furthermore, studies in canine melanoma reveal similar gene expression changes to human melanoma, such as in the PI3K/AKT/mTOR and MAPK pathways, even when the driver mutations are different. (Figure 3 shows how the pathway contributes to cancer). Useful data was provided in trials using companion animals with spontaneous tumours, providing an insight into safety, dosage, and efficacy, which have paved the way to develop treatments for both species. To conclude, it is clear with comparative oncology, researchers will be able to identify new molecular targets, assess novel drugs, and identify patient populations which will benefit the most from these therapies. It holds great promise in helping streamline cancer diagnosis further and even plays a role in preventing cancer. While the field shows great potential, more studies still need to be conducted to understand the similarities and differences in cancers between animals and humans. Additionally, more collaboration is needed amongst oncologists, veterinarians, and researchers across these disciplines to harness collective expertise to address questions relating to cancer diagnosis, treatment, and prevention. Ultimately, this field will help us identify new avenues of treating and diagnosing cancer whilst improving healthcare outcomes for humans and animals alike. Written by Harene Elayathamby Related article: Rare zoonotic diseases REFERENCES Schiffman, J.D. and Breen, M. (2015) ‘Comparative oncology: What dogs and other species can teach us about humans with cancer’, Philosophical Transactions of the Royal Society B: Biological Sciences , 370(1673), p. 20140231. doi:10.1098/rstb.2014.0231. Oh, J.H. and Cho, J.-Y. (2023) ‘Comparative oncology: Overcoming human cancer through companion animal studies’, Experimental & Molecular Medicine , 55(4), pp. 725–734. doi:10.1038/s12276-023-00977-3. Al, B. and C., C. (2007) ‘Chapter 1 COMPARATIVE ONCOLOGY ’, in Comparative oncology . Bucharest (RO): The Publishing House of the Romanian Academy, p. 1. Vail, D.M., LeBlanc, A.K. and Jeraj, R. (2020) ‘Advanced cancer imaging applied in the comparative setting’, Frontiers in Oncology , 10. doi:10.3389/fonc.2020.00084. New findings highlight shared features of human and canine osteosarcoma (2023) Center for Cancer Research . Available at: https://ccr.cancer.gov/news/article/new-findings-highlight-shared-features-of-human-and-canine-osteosarcoma (Accessed: 02 March 2024). Mochel, J.P. et al. (2018) Car T-cell immunotherapy in human and veterinary oncology: Changing the odds against hematological malignancies [Preprint]. doi:10.20944/preprints201811.0525.v1. LeBlanc AK, Mazcko CN, Khanna C. (2016) ‘Defining the Value of a Comparative Approach to Cancer Drug Development’, Clinical cancer research : an official journal of the American Association for Cancer Research , 22(9). p. 2133-2138. doi: 10.1158/1078-0432.CCR-15-2347 FIGURE REFERENCES Boddy, A.M., Harrison, T.M. and Abegglen, L.M. (2020) ‘Comparative oncology: New insights into an ancient disease’, iScience , 23(8), p. 101373. doi:10.1016/j.isci.2020.101373. Oh, J.H. and Cho, J.-Y. (2023) ‘Comparative oncology: Overcoming human cancer through companion animal studies’, Experimental & Molecular Medicine , 55(4), pp. 725–734. doi:10.1038/s12276-023-00977-3. Rascio, F. et al. (2021) ‘The pathogenic role of PI3K/Akt pathway in cancer onset and drug resistance: An updated review’, Cancers , 13(16), p. 3949. doi:10.3390/cancers13163949. Project Gallery

Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The rising threat of antibiotic resistance 05/12/24, 12:25 Understanding the problem and solutions An overview and history of antibiotics Antibiotics are medicines that treat and prevent bacterial infections (such as skin infections, respiratory infections and more). Antibiotic resistance is the process of infection-causing bacteria becoming resistant to antibiotics. As the World Health Organisation (WHO) stated, antibiotic resistance is one of the biggest threats to global health, food security and development. In 1910, Paul Ehrlich discovered the first antibiotic, Salvarsan, used to treat syphilis at the time. His idea was to create anti-infective medication, and Salvarsan was successful. The golden age of antibiotic discovery began with the accidental discovery of penicillin by Alexander Fleming in 1928. He noticed that mould had contaminated one of the petri dishes of Staphylococcus bacteria. He observed that bacteria around the mould were dying and realised that the mould, Penicillium notatum , was causing the bacteria to die. In 1940, Howard Florey and Ernst Chain isolated penicillin and began clinical trials, showing that it effectively treated infectious animals. Penicillin was then used to treat patients by 1943 in the United States. Overall, the discovery and use of antibiotics in the 21st century was a significant scientific discovery, extending people’s lives by around 20 years. Factors contributing to antibiotic resistance Increasing levels of antibiotic resistance could mean routine surgeries and cancer treatments (which can weaken the body’s ability to respond to infections) might become too risky, and minor illnesses and injuries could become more challenging to treat. There are various factors contributing to this, including overusing and misusing antibiotics and low investment in new antibiotic research. Antibiotics are overused and misused due to misunderstanding when and how to use them. As a result, antibiotics may be used for viral infections, and an entire course may not be completed if patients start to feel better. Some patients may also use antibiotics not prescribed to them, such as those of family and friends. Moreover, there has not been enough investment to fund the research of novel antibiotics. This has resulted in a shortage of antibiotics available to treat infections that have become resistant. Therefore, more investment and research are needed to prevent antibiotic resistance from becoming a public health crisis. Combatting antibiotic resistance One of the most effective ways to combat antibiotic resistance is through raising public awareness. Children and adults can learn about when and how to use antibiotics safely. Several resources are available to help individuals and members of the public to do this. Some resources are linked below: 1. The WHO has provided a factsheet with essential information on antibiotic resistance. 2. The Antibiotic Guardian website is a platform with information and resources to help combat antibiotic resistance. It is a UK-wide campaign to improve and reduce antibiotic prescribing and use. Visit the website to learn more, and commit to a pledge to play your part in helping to solve this problem. 3. Public Health England has created resources too support Antibiotic Guardian. 4. The E-bug peer-education package is a platform that aims to educate individuals and provide them with tools to educate others. Written by Naoshin Haque Related article: Anti-fungal resistance Project Gallery

Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Rare zoonotic diseases 05/12/24, 12:23 Lesser-known illnesses Introduction From COVID-19 possibly coming from livestock in Wuhan market to HIV resulting from numerous transmissions between African primates, it seems that zoonotic diseases are difficult to control. They occur when pathogenic microorganisms are spread from animals to humans or vice-versa. Their impact on human civilization is alarming because they are responsible for 2.5 billion cases of illness and 2.7 million deaths in humans annually around the world. Although there is a lot of information regarding more familiar zoonotic diseases such as rabies and malaria, this article focuses on those that may be less discussed as they could become more problematic in the future. Crimean-Congo haemorrhagic fever (virus) To begin, Crimean-Congo haemorrhagic fever (CCHF) is a viral disease, which spreads when humans are bitten by ticks carrying the virus along with farmers killing infected livestock. It is endemic in more than 30 European, African and Asian countries with the exact factors contributing to the increased cases of CCHF being a mystery. Diagnosing the disease involves detecting the virus through Enzyme-linked immunosorbent assay (ELISA), real time polymerase chain reaction (RT-PCR) along with detecting IgM and IgG antibodies using ELISA. As for the treatment options for CCHF, they are finite as there are no available vaccines and the only antiviral drug used against the virus is ribavirin, which prevents replication of various DNA and RNA viruses in-vitro. Given all this information, it is evident that extensive research is necessary to better understand the disease holistically and design drugs that can stop more fatalities associated with CCHF. Trichinellosis (parasite) The next zoonotic disease to address is trichinellosis or trichinosis , which is caused by Trichinella spiralis and so it is a parasitic infection. It can spread by eating poorly prepared meat such as pork and mammals like horses and wild carnivores are typically the reservoirs of infection. Its epidemiology in humans seems to be limited because it has 10,000 cases and 0.2% death rate annually. Moreover, an important factor that can contribute to the spread of trichinellosis is culture because certain communities have dishes containing raw meat. For example, a review referenced more than 600 outbreaks, 38,797 infections and 336 deaths in humans between 1964 and 2011 in China. As for diagnosing trichinellosis, it is challenging because it has general signs. With this in mind, the common method to spot the disease is detecting IgG antigens that work against Trichinella spiralis . On the other hand, its major drawback is getting a false negative in early trichinellosis infection. Like CCHF, trichinellosis is not as prevalent compared to other zoonotic diseases but it can have devastating impacts on specific countries, so increasing the supply of antiparasitic drugs like albendazole and/or mebendazole would be beneficial to stop the spread of Trichinella spiralis. Brucellosis (bacteria) The next zoonotic disease which is caused by a bacterial pathogen is brucellosis and is common worldwide, though certain places have higher prevalence of the disease compared to others. The pathogen can be transmitted through various ways such as direct contact with infected animal tissue on broken skin and consuming contaminated meat or dairy. Interestingly, it has been linked to childhood pulmonary infections as 18 out of 98 brucellosis patients have experienced such symptoms, but this is rare. The graph above indicates that when brucellosis occurs in animals, it has a high likelihood of being passed onto humans. For example, the years 2004-2007 could be when brucellosis cases were most frequent. This could have been alleviated through specific antibiotics used to treat brucellosis that include rifampin, doxycycline and streptomycin. Similar to trichinellosis, brucellosis diagnosis can be difficult because the symptoms can vary and are not exclusive to one disease, suggesting that different laboratory techniques are needed to find brucellosis in patients. Conclusion It looks like there is a recurring pattern of the zoonotic diseases outlined in this article occurring in developing countries as opposed to developed countries. As such, there have to be more effective interventions to prevent their ramifications on populations living in these countries. For this to occur, there has to be sufficient information, awareness, and education of these rarer zoonotic diseases to begin with. Furthermore, the current treatments for CCHF, trichinellosis and brucellosis may be unsuccessful due to the threat of antimicrobial resistance, hence finding alternative treatments for the aforementioned zoonotic diseases is vital in the future. Written by Sam Jarada Relate articles: Rabies / Canines and cancer Project Gallery

Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link A deep dive into ovarian cancer 05/12/24, 12:22 Insight into the different stages Intro 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 / Potential treatment for prostate cancer / Immune signals and metastasis 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

Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Breast Cancer and Asbestos 05/12/24, 12:19 A collaboration with the Mesothelioma Center (Asbestos.com), USA Breast cancer is a prevalent disease characterized by abnormal cell growth in the breast. There are various types of breast cancer, including invasive ductal carcinoma, invasive lobular carcinoma, Paget's disease, medullary mucinous carcinoma, and inflammatory breast cancer. In 2022, approximately 287,850 new cases of invasive breast cancer were diagnosed, making it the most commonly diagnosed cancer in women. Natural risk factors for breast cancer include gender, age, race, early onset of menstruation, family history, and genetics. Environmental factors, such as exposure to radiation, pesticides, polycyclic aromatic hydrocarbons, and metals, may also contribute to the risk of developing breast cancer. Some studies have suggested a possible connection between asbestos exposure and breast cancer. While the link between asbestos and other health conditions like mesothelioma cancer is well-established, the exact relationship between asbestos and breast cancer remains unclear. Statistical significance refers to the level of confidence in the results of a study or experiment. In the context of studies investigating the correlation between asbestos exposure and breast cancer, Dr. Debra David points out that many studies fail to establish a conclusive link due to a lack of statistical significance. Certain factors can increase the risk of developing breast cancer, known as "partial risk factors." Some of these factors can be controlled by individuals, such as alcohol consumption. However, many other partial risk factors are not within an individual's control without compromising their overall health. For example, receiving radiation therapy to the chest or making decisions regarding childbirth can be deeply personal choices that impact breast cancer risk. Examples of partial risk factors include consuming more than two alcoholic drinks per day, having children after the age of 30, not having children, not breastfeeding, using the drug diethylstilbestrol (DES) to prevent miscarriage, recent use of birth control pills, receiving hormone replacement therapy (HRT), undergoing radiation therapy to the chest area, and exposure to toxic substances or carcinogens. According to the American Cancer Society, approximately 5 to 10% of breast cancer cases can be directly attributed to inherited gene mutations. However, many other factors, such as exposure to carcinogens, may be beyond a cancer patient's control. Summary written by the Mesothelioma Center ( Asbestos.com ) For more information, visit their website , and also read important facts breast cancer and mesothelioma survival rate . For further information, particularly the legal consequences, check out the Lanier Law Firm, which has more specific information Project Gallery

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Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Cancer on the Move 05/12/24, 12:18 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: Epitheliod hemangioendothelioma / Immune signals and metastasis 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 . Tarin, D. (2005). The Fallacy of Epithelial Mesenchymal Transition in Neoplasia. Cancer Research , 65(14), pp.5996–6001. doi: https://doi.org/10.1158/0008-5472.can-05-0699 . WANG, R.-A., LU, Y.-Y. and FAN, D.-M. (2015). Reasons for cancer metastasis: A holistic perspective. Molecular and Clinical Oncology , 3(6), pp.1199–1202. doi: https://doi.org/10.3892/mco.2015.623 . Project Gallery

Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link An end at the beginning: the tale of the Galápagos Tortoises 05/12/24, 12:15 Conservation efforts The Galápagos Islands Most who know of the name “Darwin” will be familiar with the Galápagos. These relatively uninviting islands protrude harsh, crashing waves like spears of mountainous rock, formed through millions of years of fierce volcanic activity. Even Charles Darwin himself thought life could not be sustained in such a remote and harsh environment, writing in his 1835 Journal of Researches: A broken field of basaltic lava, thrown into the most rugged waves, and crossed by great fissures, is everywhere covered by stunted, sun-burnt brushwood, which shows little signs of life. Little did the 22-year-old university graduate know at the time, these rugged islands would spark the most pivotal and influential theory in the field of modern biology. Due to the Hawaiian archipelago’s unique volcanic origins, the cluster of islands have grown jagged and fractured, with some islands showcasing altitudes as low as a few meters above sea level to others flexing spaces over 5000 feet above sea level. These extremely diverse habitats enable the observation of vastly different sub-populations of the same (or closely related) species*, exhibiting differing adaptations to their unique environments. These morphological distinctions lead to Darwin’s infamous 1859 book ‘On the Origin of Species’, detailing his evidence for the theories of evolution. *This article may refer to the Galápagos Tortoises as different subspecies or species interchanagably, as this remains a contentious area. The giant tortoises One most apparent examples of evolution that Darwin noted were the Galapagos tortoises, Chelonoidis niger , of which there were at least 15 subspecies. Darwin devoted almost four pages of his Journal of Researches to the Galapagos tortoise, more than he did to any other Galápagos species. These captivating reptiles can grow up to 5 feet in length and weigh over 220kg, making them the largest tortoises in the world. This miraculous species can survive over a year without food or water, able to store tremendous volumes of liquid in their bladders in periods of drought - one of the many adaptive characteristics that enable them to routinely live well over 150-years-old. Darwin notably observed the species’ two unique primary shell morphologies - saddleback and domed. Some subspecies, such as the Pinta Island Tortoise ( Chelonoidis niger abingdonii ), have saddle-shaped shells which raise at the front, making it easier for the neck to stretch upwards to feed on taller vegetation on hotter, more arid islands. Whereas the populations with the dome-shaped shells, including the Chelonoidis niger porteri , occupy islands where there’s an abundance of flora lower to the ground, making upward stretching of the neck unnecessary to feed. Features such as these are well documented in Darwin’s evidence for evolutionary adaptation throughout the islands. Torment and tragedy Only two centuries ago, the Galápagos Islands were rife with life, with an estimated 250,000 giant tortoises. Today, multiple species are extinct, with only around 10% of the individuals surviving. The dramatic decline of the Galápagos tortoises has been characterised by frequent human failure, and in some instances, human design. Between the 1790s and 1800s, whalers began operating around the Galápagos, routinely taking long voyages to explore the Pacific Ocean. With whaling voyages lasting about a year, the tortoises were selected as the primary source of fresh meat for the whalers, with each taking 200 to 300 tortoises aboard. Here, in a ship’s hold, the hundreds of tortoises would live without food or water for months, before being killed and consumed. Documentation regarding how many tortoises were taken aboard by whalers is scarce, however estimates place the number between 100,000 and 200,000 by 700 whaling ships between 1800 and 1870. This initial decimation via over-consumption was then followed by the introduction of harmful invasive species. In the years since, multiple foreign species have been introduced to the archipelago, mainly for farming, including pigs (a lot of which are feral), dogs, cats, rats, goats and donkeys. These non-native species are an enduring threat to the giant tortoise populations, preying on their eggs and hatchings, whilst also providing fierce and unprecedented competition for food. Furthermore, increasing temperatures attributed to climate change are thought to trigger atypical migrations. These migrations have the potential to reduce tortoise nesting success, further adding to the list of threats these species have had to endure. The Pinta giant tortoise, Chelonoidis nigra abingdonii, a species of the unique saddleback shell variety, was thought to be extinct since the early 20th century. But then, in 1971, József Vágvölgyi, a Hungarian scientist on Pinta island made a special discovery – Lonesome George. Seemingly a sole survivor of his kind, Lonesome George became an icon of the sparking conservation movement surrounding the Galápagos species. This lone Pinta individual could have been wandering the small island for decades in search for another member of his species - a search that would unfortunately never bear fruit. Despite selective breeding efforts, on June 24, 2012, at 8:00 A.M. local time, Lonesome George would pass away without producing any offspring, found by park ranger Fausto Llerena who had looked after him for forty years. Hope and the future Despite all the devastation the Galápagos tortoises have endured, not is all lost. Just like the story of Lonesome George, a microcosm of this larger crisis, there is a small light at the end of the tunnel. Just prior to George’s passing a remarkable discovery was made. During 2008, research conducted by the Ecology and Evolutionary Biology Department of Yale University on neighbouring Isabela Island, set out to genetically sequence the local giant tortoise population. Over 1,600 tortoises were tagged and sampled for their DNA, with analyses revealing an astonishing number of tortoises with mixed genetic ancestry. Within this sample, 17 individuals contained DNA from the Pinta tortoise species (and more contained DNA from the also extinct Floreana species). Retrospective study of old whaling logbooks seems to indicate that, in order to lighten the burden of their ships, whalers and pirates dropped large numbers of tortoises in Banks Bay, near Volcano Wolf, Isabela Island, likely accounting for these hybrids. This miracle discovery opens the door to selective breeding efforts, pathing a future of reintroduction of the previously-extinct Pinta Island species. While only a fraction of their original numbers remain, the Galápagos tortoises continue to personify evolution’s stunning intricacies and persist as a bright beacon of hope for the greater world of conservation. It is vital that we do our part as human beings to correct the errors of our past and to respect and nurture these gentle giants and all that they represent in this world we call home. Written by Theo Joe Andreas Emberson Related articles: Conservation of marine iguanas / 55 years of vicuna conservation / Conserving the Californian condor REFERENCES Sulloway FJ. Tantalizing tortoises and the Darwin-Galápagos legend. J Hist Biol. 2009;42(1):3-31. doi:10.1007/s10739-008-9173-9 Patrick J. Endres. AlaskaPhotoGraphics.com Project Gallery

Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The cost of coats: celebrating 55 years of vicuña conservation 05/12/24, 12:13 Vicuñas are members of the camelid family This is article no. 1 in a series on animal conservation. Next article: Conserving the California condor . Is the softest coat in the world worth the near-extinction of a species? Just ask a vicuña, the wild cousin of llamas and alpacas. After being widely hunted in South America in the mid-20th century, the vicuña population thrives. Their recovery is considered one of the earliest successes in modern wildlife conservation, setting a precedent for sustainable development. This October marks the 55th anniversary of the first international agreement to conserve these furry friends. In its honour, here is the story of vicuña conservation. What are vicuñas? Vicuñas have a unique biology. They are members of the camelid family ー which includes llamas, alpacas, and camels. Vicuñas live in high-altitude arid grasslands in South America ( Figure 1 ). Their families consist of one alpha male, multiple females, and their offspring – while bachelor males form their own groups. Unlike other camelids, vicuña families remain together for most of the year. Vicuñas are herbivores with characteristic grazing and defecating behaviours that shape the surrounding plant community. Therefore, their ecological role cannot be underestimated. How vicuñas nearly went extinct However, vicuñas are hunted by humans because their wool is the finest and softest in the world. They are difficult to domesticate, and their habitat has no hiding spots, so they are easy poaching targets. Their intricate social structure means killing one vicuña has unforeseen impacts on the rest of the population. Consequently, expensive wool comes at the expense of a fascinating species. Demand for ultra-fine vicuña wool made hunting the animals a lucrative business in South America. Although 15th-16th century Inca rulers wore high-end clothing made from vicuña wool, it was usually harvested without killing the animals. European colonisation in the 19th-20th centuries opened vicuña wool to a wealthy international market, making poaching more popular and reckless than under Inca rule. These inconsiderate hunting practices continued after South American countries gained independence. As the luxurious wool remained in demand, the vicuña population decreased by over 99% between 1940 and 1965. Conservation policies saved the vicuñas South American national governments soon realised that indiscriminate vicuña hunting had to stop. As well as being ecologically important, vicuñas should not be allowed to go extinct because of their economic value. Peru had the largest proportion of the vicuña population, so in 1966 its government set up a nature reserve called Pampa Galeras. Creating this reserve involved negotiating with rural communities so that both people and vicuñas benefitted, for example, by employing locals at the reserve. This was one of the earliest examples of what is now known as sustainable development, which provides rural communities with a way of life that works alongside ecosystems rather than damaging them. Scientists found that vicuñas changed their social structures inside Pampa Galeras to maximise reproductive success. A 1987 study suggested that because females had more time to graze without the constant threat of predators and poachers, their reproductive success was higher. The creation of this reserve was the first of many successful steps South America took in the 1960s towards vicuña recovery. In October 1969, Argentina, Chile, Ecuador, and Bolivia joined Peru in the efforts to conserve vicuñas. Their Convention for the Conservation of the Vicuña banned international trade and massively restricted hunting. Since the convention successfully led to a rise in vicuña numbers, it was modified in 1979 so that sustainable vicuña wool could be sold. Meanwhile, conservation laws were being established in the United States and European Union, the wildlife trade regulator CITES was established, and public awareness about the biodiversity crisis was rising. This international effort saved vicuñas from extinction, and today there are 350,000 to 500,000 of them ( Figure 2 ). Vicuñas were classified as ‘least concern’ for conservation by the International Union for Conservation of Nature in 2018. Climate change, mite infestations, and competition with livestock are affecting the population today – but to a much smaller extent than poaching was. Thus, vicuñas are back to freely roaming the Andes. Conclusion Conserving the vicuña relied on political willpower and community involvement. In the 55 years since, ecologists have used this charismatic and distinctive animal to galvanise wildlife conservation worldwide. The vicuña’s story should also remind us that what we wear has financial and ecological costs. Written by Simran Patel Related articles: Conservation of marine igunanas / Gal á gapos tortoises REFERENCES Acebes, P., Wheeler, J., Baldo, J.L., Tuppia, P., Lichtenstein, G., Hoces, D. & Franklin, W.L. (2018) Vicuna: Vicugna vicugna . The IUCN Red List of Threatened Species 2018 . Available from: https://ri.conicet.gov.ar/handle/11336/178499 (Accessed 12th September 2024). Bosch, P.C. & Svendsen, G.E. (1987) Behavior of Male and Female Vicuna (Vicugna vicugna Molina 1782) as It Relates to Reproductive Effort. Journal of Mammalogy . 68 (2): 425–429. Available from: https://doi.org/10.2307/1381491 (Accessed 23rd September 2024). González, B. et al. (2019) Phylogeography and Population Genetics of Vicugna vicugna : Evolution in the Arid Andean High Plateau. Frontiers in Genetics . 10. Available from: https://doi.org/10.3389/fgene.2019.00445 (Accessed 22nd September 2024). Karandikar, H., Donadio, E., Smith, J.A., Bidder, O.R. & Middleton, A.D. (2023) Spatial ecology of the Vicuña ( Lama vicugna ) in a high Andean protected area. Journal of Mammalogy . 104 (3): 509–518. Available from: https://doi.org/10.1093/jmammal/gyad018 (Accessed 11th September 2024). Lyster, S. (1985) VICUNA. In: International Wildlife Law: An Analysis of International Treaties concerned with the Conservation of Wildlife . Cambridge: Cambridge University Press: 88–94. Reider, K.E. & Schmidt, S.K. (2021) Vicuña dung gardens at the edge of the cryosphere. Ecology . 102 (2): 1–3. Available from: https://www.jstor.org/stable/26998110 (Accessed 11th September 2024). Vilá, B. & Arzamendia, Y. (2022) Weaving a vicuña shawl. Pastoralism . 12 (1): 46. Available from: https://doi.org/10.1186/s13570-022-00260-6 (Accessed 11th September 2024). Wakild, E. (2020) Saving the Vicuña: The Political, Biophysical, and Cultural History of Wild Animal Conservation in Peru, 1964–2000. The American Historical Review . 125 (1): 54–88. Available from: https://doi.org/10.1093/ahr/rhz939 (Accessed 11th September 2024). Yacobaccio, H. (2009) The Historical Relationship Between People and the Vicuña. In: Gordon, I.J., ed. The Vicuña: The Theory and Practice of Community Based Wildlife Management . Boston, MA: Springer US: 7–20. Project Gallery