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Genetic Variant linked to Increased Risk of Leukemia in Hispanic/Latino Children

The AHA! Team — Fri, 17 May 2024 08:07:50 +0000

Keck School of Medicine of USC via News-Medical – Acute lymphoblastic leukemia (ALL), the most common childhood cancer, disproportionately affects children of Hispanic/Latino origin in the United States. They are 30-40% more likely to get ALL than non-Hispanic white children, but the exact genetic basis and cause of that increased risk are unknown. (ALL) disproportionately affects children of Hispanic/Latino origin in the United States Now, a study from the Keck School of Medicine of USC has revealed a key genetic variant contributing towards the increased risk, as well as details about the biological basis of ALL. The team used genetic fine-mapping analysis, a statistical method that allows researchers to disentangle the separate effects of genetic variants in a region of the genome. They identified a variant found at a relatively high frequency in people of Hispanic/Latino origin that increases ALL risk by around 1.4 times. The study, funded in part by the National Institutes of Health, was just published in the journal Cell Genomics. “Combined with the fact that around 30% of Hispanic/Latino people in the United States carry this gene variant, but it’s basically absent in people of predominantly European ancestry, we think it’s an important contributor to the increased ALL risk among this group,” said the study’s lead author, Adam de Smith, PhD, an assistant professor of population and public health sciences and a member of the USC Norris Comprehensive Cancer Center at the Keck School of Medicine, as well as a scholar of the Leukemia & Lymphoma Society. The researchers also performed tests to better understand how the variant, located on the IKZF1 gene, which underlies B-cell development, relates to ALL through its influence on the development of B-cells, a type of white blood cell known to be disrupted by the disease. “Together, the analyses in our study provide the statistical, biological and evolutionary insights behind this increased risk, and may ultimately aid scientists working to develop screening tools and therapies for ALL.” -Charleston Chiang, PhD, associate professor of population and public health sciences and associate director of the Center of Genetic Epidemiology at the Keck School of Medicine and study’s co-senior author The genetic basis of leukemia risk To pinpoint the genetic basis of the elevated ALL risk Hispanic/Latino children face, the researchers analyzed genetic data from the California Cancer Records Linkage Project. Their dataset included 1,878 Hispanic/Latino children in California with ALL and 8,411 without the condition; 1,162 non-Hispanic white children with ALL and 57,341 without; and 318 East Asian children with ALL and 5,017 without. The research team focused on the IKZF1 gene, known to relate to ALL but never before linked with ethnic risk disparities. Using genetic fine-mapping analysis, they independently analyzed each position along the gene-;known as a single nucleotide polymorphism (SNP)-;to determine whether having a certain variant increased ALL risk. They found three independent SNPs linked to higher ALL incidence, one of which was present in about 30% of people of Hispanic/Latino origin in the U.S. and less than 1% of people of primarily European origin. Although overall risk for the disease is low across all racial/ethnic groups, children with that gene variant, located at SNP rs76880433, were 1.44 times as likely to develop ALL as children without the variant. The genetic ancestry of most Hispanics/Latinos can be traced to Europe, Africa, and Indigenous America. Further investigation revealed that the risk variant was specifically linked with Indigenous American ancestry and may have become more common in this group because it conferred a selective advantage at some point in human history. Next, the Keck School of Medicine team partnered with co-senior author Vijay Sankaran, MD, PhD, an associate professor of pediatrics at Harvard Medical School and attending physician at the Dana-Farber/Boston Children’s Cancer and Blood Disorders Center, to conduct a series of experiments to better understand how the genetic variant at IKZF1 increases risk for ALL. One experiment analyzed chromatin accessibility, a test which indicates how fully a given gene can be expressed. The researchers found that the risk variant reduced chromatin accessibility, preventing IKZF1 proteins from being fully expressed. Sankaran and his team also conducted experiments with stem cells, finding that “knocking out” the IKZF1 gene caused B-cell development to stall in its early stages. “Looking at all of this together, we think that the risk variant is reducing IKZF1 expression,” de Smith said. “By doing so, it’s keeping B-cells in a more immature state, which would increase ALL risk by giving the cells more chance to develop mutations that could eventually lead to overt leukemia.” Leukemia screening and treatment The new insights about IKZF1 bring researchers one step closer to developing effective screening tools to predict who may develop ALL, but more research is needed. In addition, the findings provide important clues about potential ways to treat the disease, for instance by progressing B-cell development after it stalls. “We also need to understand whether this variant is associated with different patient outcomes, such as the risk of relapse or chances of survival, and why that might be,” de Smith said. He and his colleagues also hope to explore whether the newly identified risk variant helps explain the even higher risk of ALL among Hispanic/Latino adolescents and young adults, who are more than twice as likely to get the disease than people who are non-Hispanic white. About this research In addition to de Smith, Chiang and Sankaran, the study’s other authors are Soyoung Jeon, Jalen Langie, Tsz-Fung Chan, Steven Gazal, Nicholas Mancuso and Joseph Wiemels from the Center for Genetic Epidemiology and the USC Norris Comprehensive Cancer Center, Keck School of Medicine of USC; Lara Wahlster, Susan Black, Liam Cato, Soumyaa Mazumder and Fulong Yu from Boston Children’s Hospital and Department of Pediatric Oncology, Dana-Farber Cancer Institute; Linda Kachuri from the Stanford University School of Medicine; Nathan Nakatsuka from the New York Genome Center; Guangze Xia from the Guangzhou National Laboratory, Guangzhoi, China; Wenjian Yang and Jun Yang from St. Jude Children’s Research Hospital, Memphis; Celeste Eng, Donglei Hu, Esteban Gonzalez Burchard and Elad Ziv from the Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco; Catherine Metayer from the School of Public Health, University of California, Berkeley; and Xiaomei Ma from the Yale School of Public Health. This work was supported by the National Institutes of Health [R01CA262263, R01CA155461, R00CA246076, R35GM142783, R01DK103794, R01CA265726]; the New York Stem Cell Foundation; and the Dana-Farber Cancer Institute Presidential Priorities Initiative. Source: Keck School of Medicine of USC Journal reference: de Smith, A. J., et al. (2024) A noncoding regulatory variant in IKZF1 increases acute lymphoblastic leukemia risk in Hispanic/Latino children. Cell Genomics. doi.org/10.1016/j.xgen.2024.100526. To read the original article click here.

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Childhood Brain Tumors Linked to Mother’s Exposure to Pesticides

AHA Publisher — Mon, 12 Apr 2021 07:00:03 +0000

UCLA Fielding School of Public Health via Newswise – LOS ANGELES (April 2, 2021) – Research published in the peer-reviewed journal Environmental Research suggests that exposure during pregnancy to a wide variety of pesticides may lead to the development of central nervous system tumors during childhood. And the increased risk of these tumors – estimated as much as twice to 2.5 times higher for some pesticides – occurs even if the mother is not a farmworker, but lived as much as 2.5 miles (4000 meters) away from the field where the pesticides are sprayed, researchers found. “Exposure to certain pesticides, simply through residential proximity to agricultural applications during pregnancy, may increase the risk of childhood central nervous system tumors,” said Dr. Beate Ritz, UCLA Fielding School of Public Health (FSPH) professor of epidemiology and of environmental health sciences, one of the co-authors. “Policy interventions to reduce pesticide exposure in individuals residing near agricultural fields should be considered to protect the health of children.” The research – “Residential Proximity to Pesticide Application as a Risk Factor for Childhood Central Nervous System Tumors” – is being published in an upcoming edition of the peer-reviewed journal Environment Research, and is available on-line. Pesticides have been investigated as possible risk factors for childhood cancer since the 1970s, and the U.S. Environmental Protection Agency has classified more than 100 as possible or probable carcinogens, based on toxicological and epidemiological data. “Many pesticides are neurotoxicants, and have even been found in cord blood, indicating placental transfer of these toxins to the developing fetus,” said co-author Shiraya Thompson, an epidemiology MS candidate at FSPH. “This, in turn, suggests prenatal pesticide exposure may increase childhood brain cancer risk.” This latest work, however, is the first study to track exposure and estimate risks of 77 separate and specific pesticides, said co-author Dr. Julia Heck, associate dean for research at the University of North Texas College of Health and Public Service and an associate professor of epidemiology at FSPH. “This study is the first, to our knowledge, to estimate effects for a large number of specific pesticides in relation to CNS tumor subtypes,” Heck said. “Our results suggest that exposure to specific pesticides may best explain the results of previous studies that reported relationships between broader pesticide types and central nervous system tumors.” The research team, from UCLA, Cedars-Sinai Medical Center, and the University of Southern California, all in Los Angeles, and the University of North Texas, analyzed cases of childhood central nervous system tumors in California between 1998 and 2013, with a focus on those living near agricultural fields. “California’s agricultural work force numbers more than 800,000, according to state estimates,” said Dr. Christina Lombardi, a co-author and epidemiologist with the Samuel Oschin Comprehensive Cancer Institute at Cedars-Sinai Medical Center in Los Angeles. “In addition to the negative health effects of pesticides on workers there are large numbers of pregnant women and young children living adjacent to treated fields who may experience detrimental health effects as well.” Their findings include that three types of cancers – medulloblastoma, ependymoma, and astrocytoma – are associated with specific pesticides, and the pesticides inuron, thiophanate-methyl, and triforine are possibly carcinogenic, among others. Because pesticides are often applied to fields and orchards from the air, the study makes clear that while California’s agricultural workforce are the most at risk, any expectant mother who lives in a community adjacent to agricultural land is as well, said co-author Dr. Myles Cockburn, with the University of Southern California’s Keck School of Medicine. “This transition from farmland to residential neighborhoods is abrupt across California, and, of course, constantly changing as farmland is developed,” Cockburn said. “The simplest way to mitigate these risks are by reductions in exposure to pesticides, through restrictions as aerial spraying and air blast that lead to increased drift, and by farming methods that decrease reliance on pesticides.” Methods: Cancer cases in children ages 0 to 5 years were drawn from California Cancer Registry records for 1988-2013 and matched to their birth certificates using name, date of birth, and social security number when available. The team achieved 89% matching success; most of the remaining 11% were likely born out of state. Researchers also excluded birth addresses outside of California; exposure information was not available for these locations, since most states do not require pesticide use reporting. The team limited analyses to the time period when full residential addresses were available on the electronic dataset of birth certificates (1998-2011). Because of the focus on rural areas, the present study was restricted to those mothers living during pregnancy within 2.5 miles (4000 meters) of an agricultural field to which at least one pesticide was applied. The final study population consisted of 387 cases of all astrocytoma (combined), 119 cases of diffuse astrocytoma, 256 cases of pilocytic astrocytoma, 123 cases of ependymoma, 157 cases of medulloblastoma, and 123,158 controls. Possible carcinogens were selected per the U.S. EPA’s classifications, and prenatal exposure was assessed according to pesticides reported by the California Department of Pesticide Regulation’s Pesticide Use Reporting system. To read the original article click here.

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Study Opens the Way for a Potential New Cure for Children with Hard-to-Treat Neuroblastoma

AHA Publisher — Mon, 11 Jan 2021 08:00:58 +0000

University of Gothenburg via News-Medical Net – Researchers at the University of Gothenburg now suggest a possible cure for children with hard-to-treat forms of neuroblastoma using a new combination of drugs. In a new study in the journal Cancer Research, they describe how a two small molecule-based drug combination likely inhibit the tumor’s growth. Neuroblastoma is the most common form of childhood cancer, derived from the peripheral nervous system, i.e., the part of the nervous system that is not the brain or spinal cord. The disease can occur in the chest, neck, abdomen and adrenal glands and can also spread to the spine. Symptoms include general aches, anemia and skeletal pain. The average age of children at diagnosis is 17 months, and it is rarely diagnosed over the age of five. The milder form of neuroblastoma can, in some cases, self-heal, while the more aggressive form is the deadliest form of childhood cancer. Treatment is successful in less than half of these cases. A Long Noncoding RNA Molecule Influences Tumor Suppressor Gene Expression Central molecule in the study is the p53 gene. The p53 gene is often mutated in other cancer forms but rarely in neuroblastoma. When it is not mutated, p53 codes for a protein that inhibit the growth of cancer. This study shows that how the expression levels of a long non-coding RNA molecule influences the function of p53 protein. Interestingly, this long non-coding RNA increases p53 function in the nucleus to make tumor cells more susceptible to cytostatic treatment.” (Chandrasekhar Kanduri, Professor, Medical genetics specialized in RNA epigenetics, University of Gothenburg) Two Small Molecule-Based Drug Combination for Neuroblastoma The RNA molecule NBAT1 changes the function of the protein CRM1, which transports p53 from nucleus to cytoplasm. NBAT1 also helps in keeping the p53 protein in the nucleus to increase p53 controlled gene expression. Based on these findings, the research group tested a new treatment that combines the drugs Selinexor and Nutlin-3a. Both drugs are currently undergoing clinical trials for cancer treatments but not for neuroblastoma. Selinexor restores p53’s ability to inhibit cancer growth and Nutlin-3a inhibits the breakdown of p53. “The combination treatment blocks the protein export function of CRM1, which leads to p53 accumulation in the cell nucleus. This treatment increases p53 dependent functions, such as DNA damage and cell death. We think that combining these two drugs with current treatment strategies may allow us to cure hard-to-treat neuroblastomas.” The results are promising, but they are based on preclinical studies of cancer cell lines and mouse models (xenografts) and more research is needed before the findings can be translated into treatment. These laboratory results have been partly validated with the neuroblastoma patient data, obtained in collaboration with the researchers at Karolinska Institutet. Thus, this study has clearly opened the way for a potential new treatment strategy for high-risk neuroblastoma patients. To read the original article click here.

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New Immunotherapy Shows Promise Against Rare Childhood Cancer

AHA Publisher — Mon, 30 Nov 2020 08:00:55 +0000

University College London via EurekAlert – A novel CAR T-cell therapy developed by researchers at UCL and designed to target cancerous tumours, has shown promising early results in children with neuroblastoma, a rare form of childhood cancer. For this proof-of-principle study, researchers at the UCL Great Ormond Street Institute for Child Health (GOS ICH) and the UCL Cancer Institute modified the patient’s own T-cells (a type of immune cell), equipping them to recognise and kill neuroblastoma tumour cells. Twelve children with relapsed or refractory (where the disease does not respond to treatment) neuroblastoma were treated as part of the Cancer Research UK-funded phase I clinical trial. The research, published in Science Translational Medicine, is one of the first studies to demonstrate CAR T-cells achieving rapid regression against a solid cancer (non-blood cancer). Although the beneficial effects only lasted a short while, the study provides important evidence that this specific CAR T-cell treatment could be used as a future treatment for children with solid cancers. Neuroblastoma is a rare type of cancer that mostly affects babies and young children and develops from specialised nerve cells (neuroblasts) left behind from a baby’s development in the womb. Up to 100 children in the UK are diagnosed with neuroblastoma each year. Current treatment for children with an aggressive type of neuroblastoma includes surgical removal, chemotherapy with stem-cell transplant, radiotherapy and antibody therapy. Despite this intensive treatment long-term survival is between 50-60 per cent. In CAR T-cell therapy, a type of immunotherapy, T-cells are engineered to contain a molecule called a chimeric antigen receptor (CAR) on their surface which can specifically recognise cancerous cells. For this study the patients’ own T-cells were modified with a CAR to target the GD2 surface protein, which is highly abundant on almost all neuroblastoma cells, but found at very low levels in healthy cells. Researchers found that when using a sufficient dose* of the modified CAR T-cells, this treatment induced rapid reduction in tumour size in some of the patients treated. These effects were transient. Importantly, in all patients the CAR T-cells did not cause any harmful side effects in healthy tissues that express the GD2 molecule. Lead author, Dr Karin Straathof, Research group leader at UCL GOS ICH and Consultant Paediatric Oncologist at Great Ormond Street Hospital NHS Trust said: “It’s encouraging to see the anti-tumour activity induced by these modified T-cells in some of the patients on this study. “While the anti-tumour activity seen was only transient, it provides an important proof-of-principle that CAR T-cells directed at the GD2 molecule could be used against solid cancers in children. “New treatments are needed for high-risk neuroblastoma and with more research we hope to develop this further into a treatment that results in lasting responses and increases the number of patients that can be cured.” Senior author, Dr Martin Pule (UCL Cancer Institute) said: “Targeting of solid cancers by CAR T-cells is dependent on their infiltration and expansion within the tumour microenvironment, and thus far fewer clinical responses have been reported. “The rapid regression in neuroblastoma cells is promising, particularly as this activity was observed in the absence of neurotoxicity which occurs with antibody-based approaches that target GD2.” Dr Pule added: “Targeting neuroblastoma with GD2 CAR T-cells appears to be a valid and safe strategy but requires further modification to promote CAR T-cell longevity.” Dr Sue Brook, medical advisor at Cancer Research UK, said: “Children who have hard to treat cancers like neuroblastoma have limited treatment options open to them, especially when the cancer returns. “The early results for the GD2 CAR-T treatment look promising, especially due to the initial safety data. However more work is needed on making the response last longer, and we are looking forward to seeing the next steps in its development.” The research team are preparing for their next clinical study in collaboration with Autolus, a clinical-stage biopharmaceutical company developing next-generation, programmed T-cell therapies for the treatment of cancer. This study will evaluate AUTO6NG, which builds on this approach utilising the same GD2 CAR alongside additional programming modules designed to enhance efficacy and persistence. To read the original article click here.

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Scientists Discover a Way to Stop the Spread of Devastating Childhood Cancer

AHA Publisher — Thu, 16 Jul 2020 07:00:55 +0000

University of East Anglia via EurekAlert – Researchers at the University of East Anglia and University of Manchester have made an important breakthrough that could lead to ‘kinder’ treatments for children with bone cancer, and save lives. Current treatment is gruelling, with outdated chemotherapy cocktails and limb amputation. But despite all of this, the five-year survival rate is poor at just 42 per cent – largely because of how rapidly bone cancer spreads to the lungs. New research published today identifies a set of key genes that drive bone cancer spread to the lungs in patients. In further experiments in mice with engineered human bone cancer cells that lack these key genes, the cancer cannot spread to the lungs. The research was led by Dr Darrell Green, from UEA’s Norwich Medical School and Dr Katie Finegan from the University of Manchester. Darrell was inspired to study childhood bone cancer after his best friend died from the disease as a teenager. Now, the team has made what could be the most important discovery in the field for more than 40 years. Dr Green said: “Primary bone cancer is a type of cancer that begins in the bones. It’s the third most common solid childhood cancer, after brain and kidney, with around 52,000 new cases every year worldwide. “It can rapidly spread to other parts of the body, and this is the most problematic aspect of this type of cancer. Once the cancer has spread it is very difficult to treat. “Around a quarter of patients have cancer that has already spread by the time they are diagnosed. Around half of patients with apparent localised disease relapse, with cancer spread detected later on. These figures have remained stagnant, with no significant breakthroughs in treatment, for more than four decades. “In high school, my best friend Ben Morley became ill with primary bone cancer. His illness inspired me to do something about it myself because during my studies I realised that this cancer has been all but left behind others in terms of research and treatment progress. So I studied and went through university and obtained my PhD to eventually work in primary bone cancer. “I want to understand the underlying biology of cancer spread so that we can intervene at the clinical level and develop new treatments so that patients won’t have to go through the things my friend Ben went through. Ultimately we want to save lives and reduce the amount of disability caused by surgery.” The research team investigated the most common type of primary bone cancer called osteosarcoma. The genetic drivers that cause osteosarcoma are well known (TP53 and RB1 structural variants) but much less is known about what drives its spread to other parts of the body. Dr Green said: “Because primary bone cancer spreads so fast to other parts of the body, it’s very important to solve exactly why this happens. “We developed new technology to isolate circulating tumour cells in the blood of patients. These cells are critical for scientific study because they effectively carry out the metastatic process. This was extremely challenging because there is only one such cell per billion normal blood cells – it took over a year to develop but we cracked it. “It was also challenging because most studies investigating circulating tumour cells are performed in common adult cancers where the methods significantly differ because the cancer biology is so different. “Osteosarcoma is a less common sarcoma cancer so we had to start from scratch to not only find these cells in the first place, but to keep them alive so we could profile their gene expression.” After profiling tumours, circulating tumour cells (CTCs) and metastatic tumours from patient donors, they were able to identify a potential driver for metastasis – known as MMP9. Dr Green said: “This driver that we identified is well known in cancer, but it is also considered ‘un-druggable’ because the cancer quickly becomes resistant to treatment, or it finds a way to escape being targeted. “So we thought we would try something a bit clever and find the ‘master regulator’ of MMP9 so that we could ‘action’ the ‘un-actionable’.” The team began collaborating with researchers at the University of Manchester who were working on the proposed master regulator of MMP9 – MAPK7 – in several cancers using mouse models including osteosarcoma. Together, they engineered human osteosarcoma cells to contain a silenced version of MAPK7. They found that when these cells were put into mice, the primary tumour grew much more slowly. Importantly, it didn’t spread to the lungs – even when the tumours were left to grow for a long time. “Getting even deeper, our study shows that silencing MAPK7 stopped metastasis because that gene pathway was hijacking a particular part of the immune system that caused the spread,” said Dr Green. “This is really important because not only do we now have a gene pathway associated with metastasis, we know that removing this gene pathway actually stops cancer spread in a live animal. And we also know how and why this is happening – through hijacking the immune system. “The next step already gearing up to take place is to silence this pathway in treatment form, now that we have shown how critical this pathway is. “If these findings are effective in clinical trials, it would no doubt save lives and improve quality of life because the treatment should be much kinder, compared to the gruelling chemotherapy and life changing limb amputation that patients receive today.” Senior author Dr Katherine Finegan from the University of Manchester said: “It has been great to work together with Darrell and the team at UEA. This is the first output from a new co-operative we have set up to tackle the significant unmet need that is finding an effective treatment once osteosarcoma has spread. This co-operative called OMeNet brings together researchers from across the UK to cohesively study the spread of osteosarcoma and expedite the discovery of new treatments. “Using Darrell’s genetic insights from patient material, we were able to validate their work in models of primary bone cancer. As a result, we have highlighted a potential new way to treat metastatic bone cancer by targeting a key protein that promotes metastases: MAPK7. This work has uncovered a novel treatment option for osteosarcoma, something we have not had for the last 40 years. “In the Finegan lab we are already in the process of developing new drugs against MAPK7, which we hope to implement for the benefit of primary bone cancer patients in the future. “We would also like to thank the charity Friends of Rosie who funded the work in the Manchester lab and support childhood cancer research here in the North West.” Super Strong Sophie One of the patients who donated tissue to the study was five-year-old ‘Super Strong’ Sophie Taylor from Norwich. She was first diagnosed with osteosarcoma in January 2018, and underwent surgery to amputate part of her leg, as well as chemotherapy. Sadly Sophie was taken to hospital with breathing difficulties a year after diagnosis at the beginning of January 2019, where her family were told there was extensive cancer in her lungs. She passed away on January 18, 2019. Sophie’s dad Alex Taylor said: “Sophie was diagnosed with Osteosarcoma in January 2018. Unfortunately it was in her lungs at the time it was found. “When we were informed necrosis from chemotherapy was low we embarked on finding additional options and were fortunate to come into contact with Dr Darrell Green. “We did not hesitate in offering Sophie’s tumour for research and to also have her DNA and RNA analysed to link it to additional drugs to pursue. It gave us hope and it was amazing to have Darrell fighting in our corner. “Unfortunately the way Sophie’s journey panned out we didn’t get to try the options we put on the table but we are extremely pleased that Sophie has been able to help in the way she did. “We will continue to support Darrell and the work he does and Sophie’s future charity will aim to support the continuation of bone cancer research so future Sophies get a better outcome. “We are delighted Darrell’s work is being recognised, he is a remarkable man and we are really grateful for his support during treatment, after treatment and since Sophie’s passing. He truly deserves the credit and recognition he receives. “Sophie was simply a child from out of this world, she demonstrated strength and courage beyond comprehension and deserved a much better outcome. She had her leg amputated, months of hard chemotherapy, nursed an awful wound from surgery and just got on with it, fulfilling a range of achievements including going to the top of Snowdon, playing football with and becoming close friends Leicester City’s James Maddison, and she inspired many people around the world. We are so proud of how she fought and even more so that she has contributed to research which will be lifesaving for future children. “We will add this to her legacy and share it with pride and will continue to ‘takeasophie’ and stick our tongue out at cancer just like Sophie did. Thank you Darrell and well done that your immense hard work is paying off, we are very proud of you.” To read the original article click here.

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Controlling the Immune System’s Brakes to Treat Cancer, Autoimmune Disorders

AHA Publisher — Sun, 03 Nov 2019 07:00:36 +0000

St. Jude Children’s Research Hospital via EurekAlert – The findings may also influence cancer treatment by supercharging immunotherapy–in which the patient’s own immune system is activated to target a tumor. Immunologists at St. Jude Children’s Research Hospital have discovered key biological switches that control regulatory T cells–specialized white blood cells that keep the immune system in check. A paper detailing this work was published today in Immunity. “Understanding the mechanisms that govern regulatory T cells opens up an array of options for drug development,” said corresponding author Hongbo Chi, Ph.D., of the St. Jude Department of Immunology. “By boosting or suppressing the activity at the right time, you could develop treatments for cancer or autoimmune disorders.” In their studies, the researchers traced the molecular machinery controlling a biological switch called mTORC1 that activates regulatory T cells. Until this work, that machinery had been a mystery. The immunologists’ studies revealed that two central mTORC1 regulators are enzymes called Rag and Rheb. The enzymes’ crucial role in activating the protective regulatory T cells was revealed when the scientists discovered that mice lacking Rag or Rheb developed lethal autoimmune disease. Regulatory T cells are critical to preventing the immune system from attacking the body’s own tissues in autoimmune diseases such as lupus and rheumatoid arthritis. The discovery of the roles of Rag and Rheb is important because drugs that activate those enzymes could prove useful as treatments for autoimmune diseases. The drugs would enhance the regulatory T cells’ function as immune safety brakes. The findings may also influence cancer treatment by supercharging immunotherapy–in which the patient’s own immune system is activated to target a tumor. A significant barrier to such therapies has been the immune-damping activity of regulatory T cells. Drugs that inhibit Rag or Rheb could aid immunotherapies against cancers by suppressing the regulatory T cells. The researchers found that amino acids play a major role in activating mTORC1 in regulatory T cells, functions that were mediated by Rag and Rheb. Amino acids are the building blocks of proteins, which means that “nutrient-sensing” by the immune system, for example of the food a person eats, could influence that individual’s immune response–not only to cancers, but also to organ transplants and infections. To read the original article click here.

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