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  • richardmitnick 5:12 am on October 19, 2017 Permalink | Reply
    Tags: , Cancer, , ESA incubator start-up companies,   

    From ESA: “Speeding up cancer screening” 

    ESA Space For Europe Banner

    European Space Agency

    18 October 2017
    No writer credit

    1
    Radiology scan being examined. ESA.

    Delivering breast cancer screening results in a day instead of today’s standard two weeks is being proposed by an ESA incubator start-up company using paperless technology and online image transfers. Screening vans are already on the streets.

    “By applying online connectivity to mobile scanning units we have the potential to radically overhaul mobile breast screening in the UK,” notes Viv Barrett of DEOS Consultancy, a start-up from ESA’s business incubator in Harwell, UK.

    With one in eight British women developing breast cancer at least once in their lifetime, mobile screening vans are used in the UK to bring the service closer to people, such as offering scanning near supermarkets.

    When set up 28 years ago, X-ray film cassettes were physically carried to hospitals for developing. Today, hard drives with digital images are taken by courier, taxi or mammography staff themselves to a hospital for interpretation. In addition to pushing up the cost and adding delay, it is not an efficient use of the medical staff’s time.

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    Breast cancer screening. ESA.

    Viv, a qualified mammographer herself with extensive experience of mobile screening, found this unacceptable. Having seen the benefits of working in a connected environment, she founded DEOS Consultancy in 2015 to develop a more efficient scheme.

    “When we started four years ago, we used satellite communication technology to develop our system. It enabled us to develop an automatic system and modernise the breast screening units.

    “Now we mostly transport images via 3G/4G networks, still fully automatically without involving medical staff. We use satellites if the local mobile networks are too slow.

    “We have halved today’s 42 steps, and cut out paper documentation. Our solution is all online. In addition to cutting costs and saving time, it has improved the accuracy and made the work a lot simpler. And it is quicker and much more customer-friendly.”

    Currently, bookings are closed several days in advance and the screenings then follow paper diaries printed and delivered to the vans daily, making last-minute changes difficult to handle.

    3
    DEOS Consultancy has built a demonstration van to present their paperless breast cancer screening system. Copyright DEOS Consultancy.

    “Our appointment system is now live so we can handle the breast scanning on the vans better. If a woman turns up on the wrong day, her record can quickly be accessed and if she is eligible she can be screened anyway.

    “Having direct access to the patient data, we can add clinical notes directly into the system at the time of screening. It is much safer than today’s practice of adding sticky notes to the paper documents, and occasionally losing them on the way to the hospital.

    “Our focus has been on developing a prototype for our technology that could be used in all screening vans.”

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    DEOS Consultancy demonstration van holds a screening room and a separate waiting area. Copyright DEOS Consultancy.

    Several have already been fitted with the DEOS online system and are being used, and a demonstration vehicle has been built.

    “From these, we can see that images are typically transferred back to the hospital in just 4–10 minutes. That’s impressive because it normally takes at least 24 hours, and sometimes even up to 2 days.

    “With our approach, the women could get their results within a day.”

    5
    The 50th company to graduate from the ESA Business Incubation Centre at Harwell is DEOS Consultancy which is gearing up to overhaul mobile breast screening in the UK. From left: David Osmond (DEOS co-founder) and Viv Barrett (DEOS Co-founder and CEO), with Sue O’Hare (Operations Manager at ESA BIC Harwell), and Anne Green (UK Science and Technology Facilities Council, STFC ). Copyright STFC

    “Being hosted at the ESA Business Incubation Centre Harwell puts us in the perfect position to access the specialist technology and expertise we needed to complete our prototype and network with the right audiences and markets,” notes Viv.

    “This has been a critical phase in the development of our business, completed well and quickly thanks to the support we have received.”

    DEOS became the 50th start-up company to ‘graduate’ from the Harwell centre since it opened in 2011. To date, 61 companies have joined the centre for typically two years, all exploiting space and satellite technology to develop new products and services for terrestrial applications.

    The centre is part of the European-wide network of business incubators run by the ESA’s Technology Transfer Programme.

    “Turning a brilliant idea into a viable commercial offering is a huge challenge. We help the start-ups to complete this process and become viable businesses,” said Sue O’Hare, Manager of the Harwell incubator.

    “DEOS is a good example of how satellite technology can improve a service that could be life-changing for many.”

    See the full article here .

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    The European Space Agency (ESA), established in 1975, is an intergovernmental organization dedicated to the exploration of space, currently with 19 member states. Headquartered in Paris, ESA has a staff of more than 2,000. ESA’s space flight program includes human spaceflight, mainly through the participation in the International Space Station program, the launch and operations of unmanned exploration missions to other planets and the Moon, Earth observation, science, telecommunication as well as maintaining a major spaceport, the Guiana Space Centre at Kourou, French Guiana, and designing launch vehicles. ESA science missions are based at ESTEC in Noordwijk, Netherlands, Earth Observation missions at ESRIN in Frascati, Italy, ESA Mission Control (ESOC) is in Darmstadt, Germany, the European Astronaut Centre (EAC) that trains astronauts for future missions is situated in Cologne, Germany, and the European Space Astronomy Centre is located in Villanueva de la Cañada, Spain.

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  • richardmitnick 7:47 am on October 9, 2017 Permalink | Reply
    Tags: , Cancer, , Primary Care Unable to Adequately Care for Cancer Survivors,   

    From Rutgers: “Primary Care Unable to Adequately Care for Cancer Survivors” 

    Rutgers University
    Rutgers University

    Oct 6 2017
    Carla Cantor
    848-932-0555
    ccantor@rutgers.edu

    1
    Seventy-five percent of cancer survivors are seen in primary care practices, but more must be done to meet their health care needs, says a new study. No image credit.

    Primary care medicine is currently not able to meet the health care needs of cancer survivors, despite a decade-long effort by the medical establishment to move long-term survivorship care out of the specialists’ realm, according to a new Rutgers study.

    The study, published recently in JAMA Internal Medicine, examined 12 advanced primary care practices selected from a national registry of workforce innovators. Not one had a comprehensive survivorship care program in place.

    “This is troubling because these are highly innovative practices that have a national reputation,” said study co-author Benjamin Crabtree, a medical anthropologist who is a professor in the Department of Family Medicine and Community Health, Rutgers Robert Wood Johnson Medical School (RWJMS) and a member of the Rutgers Cancer Institute of New Jersey. “As more and more people survive cancer, there will not be enough oncologists to follow these patients and meet their health care needs.”

    According to the National Cancer Institute, there are 15.5 million cancer survivors in the United States, a number expected to increase by 31 percent to 20.3 million, by 2026. The vast majority of these patients are seen in primary care practices.

    A decade ago the Institute of Medicine released a seminal report, From Cancer Patient to Survivor: Lost in Translation, outlining the need for well-informed primary care survivorship physicians and identifying the components of care. Survivorship care includes checking for cancer re-occurrence, monitoring long-term effects of radiation and chemotherapy treatment and assessing a patient’s psychological well-being.

    The researchers, who over two years spent 10 to 12 days observing each of the practices (based in Colorado, Illinois, Maine, New York, Pennsylvania and Washington) and interviewing clinicians and administrators, identified several barriers to integrating survivorship care into primary medicine.

    No distinct clinical category for clinicians to identify cancer survivors exists. “There is no diagnosis code for ‘cancer survivor’ that can be entered into the medical record, which is important if you want physicians to pay attention,” Crabtree said.
    Electronic medical records (EHR) used in primary care practices have limited capability to record information on patients’ cancer history and clinicians are not provided with actionable recommendations for follow up care.
    Medical records sometimes are lost as patients change clinicians over the years, leaving patients to report their cancer histories to their primary care doctors.

    In addition to these issues, primary care physicians are concerned about their knowledge gaps in cancer care and the need to monitor changing information in oncology. “There is nothing in the residency curriculum about cancer survivorship,” Crabtree said. “There is also nothing in Continuing Medical Education courses. It’s just not there.”

    Only by correcting these deficiencies, can comprehensive cancer survivorship services move to the forefront of primary care, the study states.

    “Seventy-five percent of survivors are seen in primary care,” the authors write, “demonstrating a reliance on primary care to address their needs; however, those needs are currently not being met.”

    Other contributors to the paper include Ellen B Rubinstein, Ph.D., formerly RWJMS and now with Department of Family Medicine, University of Michigan, Ann Arbor; Shawna V. Hudson, Ph.D., Jenna Howard O’Malley, Ph.D., Heather Sophia Lee, Ph.D., Alicja Bator, MPH (Department of Family and Community Health, RWJMS); William L. Miller, M.D., Lehigh Valley Health network, Allentown, Pennsylvania: and Jennifer Tsui, Ph.D., Rutgers Cancer Institute of New Jersey.

    See the full article here .

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    Rutgers, The State University of New Jersey, is a leading national research university and the state’s preeminent, comprehensive public institution of higher education. Rutgers is dedicated to teaching that meets the highest standards of excellence; to conducting research that breaks new ground; and to providing services, solutions, and clinical care that help individuals and the local, national, and global communities where they live.

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  • richardmitnick 1:13 pm on October 8, 2017 Permalink | Reply
    Tags: A tale of failure, , BMJ, Cancer, , , No clear evidence that most new cancer drugs extend or improve life   

    From MedicalXpress: “No clear evidence that most new cancer drugs extend or improve life” Don’t read this. 

    Medicalxpress bloc

    MedicalXpress

    [This is so sad, it is why I stay away from most cancer research on this blog.]

    October 4, 2017

    1
    Credit: CC0 Public Domain

    Even where drugs did show survival gains over existing treatments, these were often marginal, the results [BMJ] show.

    Many of the drugs were approved on the basis of indirect (‘surrogate’) measures that do not always reliably predict whether a patient will live longer or feel better, raising serious questions about the current standards of drug regulation.

    The researchers, based at King’s College London and the London School of Economics say: “When expensive drugs that lack clinically meaningful benefits are approved and paid for within publicly funded healthcare systems, individual patients can be harmed, important societal resources wasted, and the delivery of equitable and affordable care undermined.”

    The research team analysed reports on cancer approvals by the European Medicines Agency (EMA) from 2009 to 2013.

    Of 68 cancer indications approved during this period, 57% (39) came onto the market on the basis of a surrogate endpoint and without evidence that they extended survival or improved the quality of patients’ lives.

    After a median of 5 years on the market, only an additional 8 drug indications had shown survival or quality of life gains.

    Thus, out of 68 cancer indications approved by the EMA, and with a median 5 years follow-up, only 35 (51%) had shown a survival or quality of life gain over existing treatments or placebo. For the remaining 33 (49%), uncertainty remains over whether the drugs extend survival or improve quality of life.

    The researchers outline some study limitations which could have affected their results, but say their findings raise the possibility that regulatory evidence standards “are failing to incentivise drug development that best meets the needs of patients, clinicians, and healthcare systems.”

    Taken together, these facts paint a sobering picture, says Vinay Prasad, Assistant Professor at Oregon Health & Science University in a linked editorial.

    He calls for “rigorous testing against the best standard of care in randomized trials powered to rule in or rule out a clinically meaningful difference in patient centered outcomes in a representative population” and says “the use of uncontrolled study designs or surrogate endpoints should be the exception not the rule.”

    He adds: “The expense and toxicity of cancer drugs means we have an obligation to expose patients to treatment only when they can reasonably expect an improvement in survival or quality of life.” These findings suggest “we may be falling far short of this important benchmark.”

    This study comes at a time when European governments are starting to seriously challenge the high cost of drugs, says Dr Deborah Cohen, Associate Editor at The BMJ, in an accompanying feature.

    She points to examples of methodological problems with trials that EMA has either failed to identify or overlooked, including trial design, conduct, analysis and reporting.

    “The fact that so many of the new drugs on the market lack good evidence that they improve patient outcomes puts governments in a difficult position when it comes to deciding which treatments to fund,” she writes. “But regulatory sanctioning of a comparator that lacks robust evidence of efficacy, means the cycle of weak evidence and uncertainty continues.”

    In a patient commentary, Emma Robertson says: “It’s clear to me and thousands of other patients like me that our current research and development model has failed.”

    Emma is leader of Just Treatment, a patient led campaign with no ties to the pharmaceutical industry, which is calling for a new system that rewards and promotes innovation, so that more effective and accessible cancer medicines are brought within reach.

    Editorial: Do cancer drugs improve survival or quality of life? http://www.bmj.com/content/359/bmj.j4528

    Patient commentary: the current model has failed, http://www.bmj.com/content/359/bmj.j4568

    Feature: Cancer drugs: high price, uncertain value, http://www.bmj.com/content/359/bmj.j4543

    See the full article here .

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    Medical Xpress is a web-based medical and health news service that is part of the renowned Science X network. Medical Xpress features the most comprehensive coverage in medical research and health news in the fields of neuroscience, cardiology, cancer, HIV/AIDS, psychology, psychiatry, dentistry, genetics, diseases and conditions, medications and more.

     
  • richardmitnick 2:39 pm on September 26, 2017 Permalink | Reply
    Tags: , , Cancer, , Smash Childhood Cancer,   

    From WCG: “The Road Ahead for Help Fight Childhood Cancer” 

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    World Community Grid (WCG)

    26 Sep 2017
    Dr. Akira Nakagawara, MD, PhD
    CEO of the Saga Medical Center KOSEIKAN and President Emeritus, Chiba Cancer Center

    Summary
    The Help Fight Childhood Cancer researchers discuss how they’re moving forward with data analysis and continuing their search for pharmaceutical partners.

    1
    No image caption or credit.

    Background

    The Help Fight Childhood Cancer (HFCC) project was created to look for better treatments for neuroblastoma, which is refractory among childhood cancers (meaning that it is resistant to treatment). The project’s goal was to target certain cell proteins regulating cancer cell growth—such as TrkB tyrosine kinase receptor, ALK tyrosine kinase receptor, N – CYM protein and others—with the help of World Community Grid’s enormous computing power, which is donated by an international community of volunteers.

    Our research team conducted in-silico (computer simulation-based) drug discovery screening using World Community Grid to search through a library of three million small molecular compounds. We discovered a small molecule compound which competitively binds to the TrkB protein pocket to which BDNF (a specific growth factor) binds. The discovered molecule can thus prevent BDNF from binding to the TrkB protein and diminish cancer cell growth. This could lead to a new and improved treatment for neuroblastoma.

    Subsequently, the anti-tumor effect of the compound was examined using cultured cancer cells, or human neuroblastoma transplanted into mice, and this laboratory research confirmed that this small molecular compound and possibly some others could be candidates for anticancer drugs targeting TrkB. We announced this breakthrough and published our findings in the peer-reviewed, English language journal, Cancer Medicine, in 2014.

    Current Research

    Currently, we are conducting research to develop even more potent inhibitors by synthesizing small molecular compounds similar in structure to the compounds found using the screening. The road to developing commercial, approved new drugs is a tough task. We must find a pharmaceutical company that will conduct joint research and development and create a patentable compound so that this expensive effort is profitable. If any of you have contacts with a pharmaceutical company that may be interested in pursuing this venture, please introduce us.

    Additionally, using World Community Grid to screen drug candidates, we found other small molecular compounds showing the ability to inhibit the ligand BDNF. These results were presented it in another English language journal (Neurochem International, 2016). These compounds also look promising as a remedy for depression and dementia, and similarly, we are seeking a pharmaceutical company to cooperate in research and development of these.

    The N-CYM is a new protein we discovered which is implicated in neuroblastoma. A published paper about this can be found here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3879166/. Before we can screen for drug candidates, we must determine this protein’s three-dimensional structure. Therefore, we are currently working on the difficult task of crystallizing the N-CYM protein so that we can perform X-ray analysis to determine the protein’s three-dimensional structure. Once the three-dimensional structure of the protein is determined, we will screen to find inhibiting compounds in the Smash Childhood Cancer project, which is building on the work from this project.

    4
    Smash Childhood Cancer

    Regarding the development of ALK inhibitors (see article https://www.ncbi.nlm.nih.gov/pubmed/15972965), candidate compounds as inhibitors were found in the in-silico screening, and analysis on cultured cancer cells was completed. Because of the lack of research personnel, unfortunately preclinical tests have not yet progressed.

    We thank all volunteers who supported this project, and look forward to keeping you updated on the progress of this project as well as the Smash Childhood Cancer project.

    See the full article here.

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    World Community Grid (WCG) brings people together from across the globe to create the largest non-profit computing grid benefiting humanity. It does this by pooling surplus computer processing power. We believe that innovation combined with visionary scientific research and large-scale volunteerism can help make the planet smarter. Our success depends on like-minded individuals – like you.”
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  • richardmitnick 7:48 am on September 19, 2017 Permalink | Reply
    Tags: , Cancer, cGAS, How oxygen-deprived tumors survive body’s immune response, Hypoxia, MicroRNA helps cancer evade immune system,   

    From Salk: “MicroRNA helps cancer evade immune system” 

    Salk Institute bloc

    Salk Institute for Biological Studies

    September 18, 2017

    Salk researchers discover how oxygen-deprived tumors survive body’s immune response.

    The immune system automatically destroys dysfunctional cells such as cancer cells, but cancerous tumors often survive nonetheless. A new study by Salk scientists shows one method by which fast-growing tumors evade anti-tumor immunity.

    The Salk team uncovered two gene-regulating molecules that alter cell signaling within tumor cells to survive and subvert the body’s normal immune response, according to a September 18, 2017, paper in Nature Cell Biology. The discovery could one day point to a new target for cancer treatment in various types of cancer.

    1
    Visible regions of hypoxia in tumor samples correlate with cell signaling linked to suppressing the immune system. Credit: Salk Institute

    “The immunological pressure occurring during tumor progression might be harmful for the tumor to prosper,” says Salk Professor Juan Carlos Izpisua Belmonte, senior author of the work and holder of the Roger Guillemin Chair. “However, the cancer cells find a way to evade such a condition by restraining the anti-tumor immune response.”

    Cancerous tumors often grow so fast that they use up their available blood supply, creating a low-oxygen environment called hypoxia. Cells normally start to self-destruct under hypoxia, but in some tumors, the microenvironment surrounding hypoxic tumor tissue has been found to help shield the tumor.

    “Our findings actually indicate how cancer cells respond to a changing microenvironment and suppress anti-tumor immunity through intrinsic signaling,” says Izpisua Belmonte. The answer was through microRNAs.

    MicroRNAs—small, noncoding RNA molecules that regulate genes by silencing RNA—have increasingly been implicated in tumor survival and progression. To better understand the connection between microRNAs and tumor survival, the researchers screened different tumor types for altered levels of microRNAs. They identified two microRNAs—miR25 and miR93—whose levels increased in hypoxic tumors.

    The team then measured levels of those two microRNAs in the tumors of 148 cancer patients and found that tumors with high levels of miR25 and miR93 led to a worse prognosis in patients compared to tumors with lower levels. The reverse was true for another molecule called cGAS: the lower the level of cGAS in a tumor, the worse the prognosis for the patient.

    Previous research has shown that cGAS acts as an alarm for the immune system by detecting mitochondrial DNA floating around the cell—a sign of tissue damage—and activating the body’s immune response.

    “Given these results, we wondered if these two microRNA molecules, miR25 and miR93, could be lowering cGAS levels to create a protective immunity shield for the tumor,” says Min-Zu (Michael) Wu, first author of the paper and formerly a research associate in Salk’s Gene Expression Laboratory, now at Amgen.

    That is exactly what the team confirmed with further experiments. Using mouse models and tissue samples, the researchers found that a low-oxygen (hypoxia) state triggered miR25 and miR93 to set off a chain of cell signaling that ultimately lowered cGAS levels. If the researchers inhibited miR25 and miR93 in tumor cells, then cGAS levels remained high in low-oxygen (hypoxic) tumors.

    Researchers could slow tumor growth in mice if they inhibited miR25 and miR93. Yet, in immune-deficient mice, the effect of inhibiting miR25 and miR93 was diminished, further indicating that miR25 and miR93 help promote tumor growth by influencing the immune system.

    Identifying miR25 and miR93 may help researchers pinpoint a good target to try to boost cGAS levels and block tumor evasion of the immune response. However, the team says directly targeting microRNA in treatment can be tricky. Targeting the intermediate players in the signaling between the two microRNAs and cGAS may be easier.

    “To follow up this study, we’re now investigating the different immune cells that can contribute to cancer anti-tumor immunity,” adds Wu.

    Other authors on the paper include Carolyn O’Connor, Wen-Wei Tsai, and Lorena Martin of Salk; Wei-Chung Cheng, Su-Feng Chen and Kou-Juey Wu of the China Medical University, Taichung, Taiwan; Shin Nieh, Chia-Lin Liu, and Yaoh-Shiang Lin of the National Defense Medical Center, Taipei, Taiwan; and Cheng-Jang Wu and Li-Fan Lu of the University of California, San Diego.

    Funding was provided by the Razavi Newman Integrative Genomics and Bioinformatics Core Facility, the National Institutes of Health and National Cancer Institute, the Chapman Foundation and the Helmsley Charitable Trust, the G. Harold and Leila Y. Mathers Charitable Foundation, The Leona M. and Harry B. Helmsley Charitable Trust, The Moxie Foundation and UCAM.

    See the full article here .

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    Every cure has a starting point. Like Dr. Jonas Salk when he conquered polio, Salk scientists are dedicated to innovative biological research. Exploring the molecular basis of diseases makes curing them more likely. In an outstanding and unique environment we gather the foremost scientific minds in the world and give them the freedom to work collaboratively and think creatively. For over 50 years this wide-ranging scientific inquiry has yielded life-changing discoveries impacting human health. We are home to Nobel Laureates and members of the National Academy of Sciences who train and mentor the next generation of international scientists. We lead biological research. We prize discovery. Salk is where cures begin.

     
  • richardmitnick 10:42 am on July 31, 2017 Permalink | Reply
    Tags: , Cancer, , , , It wouldn’t have been obvious that PTPN2 is a good drug target for the immunotherapy of cancer, , PD-1 checkpoint inhibitors have transformed the treatment of many cancers   

    From HMS: “Attack Mode “ 

    Harvard University

    Harvard University

    Harvard Medical School

    Harvard Medical School

    7.31.17
    KAT MCALPINE

    1
    Genetic screening for cancer immunotherapy targets. Cancer cells (colored shapes), each with a different CRISPR-Cas9-mediated gene knocked out. T cells (red) destroy the cancer cells that have had essential immune evasion genes knocked out. Image: Haining Lab, Dana-Farber/Boston Children’s.

    A novel screening method developed by a team at Harvard Medical School and Dana-Farber/Boston Children’s Cancer and Blood Disorders Center—using CRISPR-Cas9 genome editing technology to test the function of thousands of tumor genes in mice—has revealed new drug targets that could potentially enhance the effectiveness of PD-1 checkpoint inhibitors, a promising new class of cancer immunotherapy.

    In findings published online today by Nature http://www.nature.com/nature/journal/v547/n7664/full/nature23270.html the Dana-Farber/Boston Children’s team, led by pediatric oncologist W. Nick Haining, reports that deletion of the PTPN2 gene in tumor cells made them more susceptible to PD-1 checkpoint inhibitors. PD-1 blockade is a drug that “releases the brakes” on immune cells, enabling them to locate and destroy cancer cells.

    “PD-1 checkpoint inhibitors have transformed the treatment of many cancers,” said Haining, HMS associate professor of pediatrics at Dana-Farber/Boston Children’s, associate member of the Broad Institute of MIT and Harvard, and senior author on the new paper. “Yet despite the clinical success of this new class of cancer immunotherapy, the majority of patients don’t reap a clinical benefit from PD-1 blockade.”

    That, Haining said, has triggered a rush of additional trials to investigate whether other drugs, when used in combination with PD-1 inhibitors, can increase the number of patients whose cancer responds to the treatment.

    “The challenge so far has been finding the most effective immunotherapy targets and prioritizing those that work best when combined with PD-1 inhibitors,” Haining said. “So, we set out to develop a better system for identifying new drug targets that might aid the body’s own immune system in its attack against cancer.

    “Our work suggests that there’s a wide array of biological pathways that could be targeted to make immunotherapy more successful,” Haining continued. “Many of these are surprising pathways that we couldn’t have predicted. For instance, without this screening approach, it wouldn’t have been obvious that PTPN2 is a good drug target for the immunotherapy of cancer.”

    Sifting through thousands of potential targets

    To cast a wide net, the paper’s first author Robert Manguso, a graduate student in Haining’s lab, designed a genetic screening system to identify genes used by cancer cells to evade immune attack. He used CRISPR-Cas9, a genome editing technology that works like a pair of molecular scissors to cleave DNA at precise locations in the genetic code, to systematically knock out 2,368 genes expressed by melanoma skin cancer cells. Manguso was then able to identify which genes, when deleted, made the cancer cells more susceptible to PD-1 blockade.

    Manguso started by engineering the melanoma skin cancer cells so that they all contained Cas9, the cutting enzyme that is part of the CRISPR editing system. Then, using a virus as a delivery vehicle, he programmed each cell with a different single-guide-RNA (sgRNA) sequence of genetic code. In combination with the Cas9 enzyme, the sgRNA codes—about 20 amino acids in length—enabled 2,368 different genes to be eliminated.

    By injecting the tumor cells into mice and treating them with PD-1 checkpoint inhibitors, Manguso was then able to tally up which modified tumor cells survived. Those that perished had been sensitized to PD-1 blockade as a result of their missing gene.

    Using this approach, Manguso and Haining first confirmed the role of two genes already known to be immune evaders—PD-L1 and CD47, drug inhibitors that are already in clinical trials. They then discovered a variety of new immune evaders that, if inhibited therapeutically, could enhance PD-1 cancer immunotherapy. One such newly found gene of particular interest is PTPN2.

    “PTPN2 usually puts the brakes on the immune signaling pathways that would otherwise smother cancer cells,” Haining said. “Deleting PTPN2 ramps up those immune signaling pathways, making tumor cells grow slower and die more easily under immune attack.”

    Gaining more ground

    With the new screening approach in hand, Haining’s team is quickly scaling up their efforts to search for additional novel drug targets that could boost immunotherapy.

    Haining says the team is expanding their approach to move from screening thousands of genes at a time to eventually being able to screen the whole genome and to move beyond melanoma to colon, lung, renal carcinoma and more. He’s assembled a large team of scientists spanning Dana-Farber/Boston Children’s and the Broad to tackle the technical challenges that accompany screening efforts on such a large scale.

    In the meantime, while more new potential drug targets are likely around the corner, Haining’s team is taking action based on their findings about PTPN2.

    “We’re thinking hard about what a PTPN2 inhibitor would look like,” said Haining. “It’s easy to imagine making a small molecule drug that turns off PTPN2.”

    This work was supported by the Broad Institute of Harvard and MIT (BroadIgnite and Broadnext10 awards) and the National Institute of General Medical Sciences (T32GM007753).

    See the full article here .

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    Established in 1782, Harvard Medical School began with a handful of students and a faculty of three. The first classes were held in Harvard Hall in Cambridge, long before the school’s iconic quadrangle was built in Boston. With each passing decade, the school’s faculty and trainees amassed knowledge and influence, shaping medicine in the United States and beyond. Some community members—and their accomplishments—have assumed the status of legend. We invite you to access the following resources to explore Harvard Medical School’s rich history.

    Harvard University campus

    Harvard is the oldest institution of higher education in the United States, established in 1636 by vote of the Great and General Court of the Massachusetts Bay Colony. It was named after the College’s first benefactor, the young minister John Harvard of Charlestown, who upon his death in 1638 left his library and half his estate to the institution. A statue of John Harvard stands today in front of University Hall in Harvard Yard, and is perhaps the University’s best known landmark.

    Harvard University has 12 degree-granting Schools in addition to the Radcliffe Institute for Advanced Study. The University has grown from nine students with a single master to an enrollment of more than 20,000 degree candidates including undergraduate, graduate, and professional students. There are more than 360,000 living alumni in the U.S. and over 190 other countries.

     
  • richardmitnick 4:45 pm on July 27, 2017 Permalink | Reply
    Tags: , , Cancer, , Putting cancers’ vulnerabilities on the map   

    From Broad: “Here there be dependencies: Putting cancers’ vulnerabilities on the map” 

    Broad Institute

    Broad Institute

    07.27.17
    Tom Ulrich

    1
    No image caption or credit.

    Cancer cells thrive despite harboring mutations that should kill them. By mapping the dependencies cancer cells rely on for survival, researchers hope to reveal new treatment opportunities.

    Cancer cells can harbor a whole gamut of genetic errors, from small mutations to wholesale swaps of DNA between chromosomes — sometimes thousands of molecular flaws that should leave them dead. But when an error impacts a critical gene, a cancerous cell will compensate by adjusting other genes’ activity — increasing expression of another member of the same pathway, for instance.

    From a researcher’s perspective, these adaptations — which allow the tumor to persist — represent dependencies: vulnerabilities that provide deeper insight into cancer biology and might serve as targets for designing new therapies, or for repurposing existing ones.

    “Much of what has been and continues to be done to characterize cancer has been based on genetics and sequencing. That’s given us the parts list,” said William Hahn, an institute member in the Broad Cancer Program and an oncologist at Dana-Farber Cancer Institute. “Mapping dependencies ascribes function to the parts and shows you how to reverse engineer the processes that underlie cancer.”

    That reasoning underlies the Cancer Dependency Map, a joint effort bringing together researchers from the Cancer Program’s Project Achilles, the Broad’s Genetic Perturbation Platform (GPP), and other teams across the institute. The team has spent nearly 15 years conducting genome-wide RNA interference (RNAi) screens on a growing number of cancer cell lines, probing thousands of genes individually for possible vulnerabilities.

    In a study conducted as part of the Slim Initiative in Genomic Medicine for the Americas and reported in Cell, the Dependency Map team describes a major set of findings: 769 strong dependencies unique to cancer cells uncovered through RNA interference (RNAi) screens of 501 cell lines representing a range of tumors. The list reveals intriguing themes in cancer cells’ survival strategies, and may also open new avenues for cancer drug development.

    Fruition long coming

    The data in the Cell paper represents an effort that reaches back to the earliest days of the Broad.

    “In the early 2000s we worked out how to do pooled RNAi screens in mammalian systems well,” which gave researchers the tools to run genome-wide screens on many cell lines at once, said GPP director and institute scientist David Root, who, with Hahn, is one of the study’s co-senior authors. “That led us to doing genome wide screens on a dozen cancer cell lines,” work that he and his colleagues published in 2008.

    RNAi effectively silences genes using small pieces of RNA called small interfering RNAs (siRNAs). These RNA tidbits bind to and call for the destruction of messenger RNAs (mRNAs) transcribed from individual genes, perturbing their expression. To run a genome-wide RNAi screen, researchers expose cells to pools of siRNAs, track the cells’ behavior, and and work back to see which genes were silenced.

    “The simplest thing one can do with perturbed cells is allow them to keep growing over time and see which ones thrive,” Root explained. “If cells with a certain gene silenced disappear, for example, it means that gene is essential for proliferation.”

    Even those first dozen cell lines held revelations. For instance, tumor cells depended heavily on genes active in their original tissues (e.g., blood cancer cells needed blood-lineage genes, lung cells needed different genes). Other relationships were specific to individual cell lines, like one between cells from a chronic myelogenous leukemia (CML) line and ABL, a known CML driver gene.

    But the team knew even then that they were not close to seeing the whole picture. “A dozen cell lines was far too few to really probe the breadth of dependencies,” Root said.

    Cancer cells can harbor a whole gamut of genetic errors, from small mutations to wholesale swaps of DNA between chromosomes — sometimes thousands of molecular flaws that should leave them dead. But when an error impacts a critical gene, a cancerous cell will compensate by adjusting other genes’ activity — increasing expression of another member of the same pathway, for instance.

    From a researcher’s perspective, these adaptations — which allow the tumor to persist — represent dependencies: vulnerabilities that provide deeper insight into cancer biology and might serve as targets for designing new therapies, or for repurposing existing ones.

    “Much of what has been and continues to be done to characterize cancer has been based on genetics and sequencing. That’s given us the parts list,” said William Hahn, an institute member in the Broad Cancer Program and an oncologist at Dana-Farber Cancer Institute. “Mapping dependencies ascribes function to the parts and shows you how to reverse engineer the processes that underlie cancer.”

    That reasoning underlies the Cancer Dependency Map, a joint effort bringing together researchers from the Cancer Program’s Project Achilles, the Broad’s Genetic Perturbation Platform (GPP), and other teams across the institute. The team has spent nearly 15 years conducting genome-wide RNA interference (RNAi) screens on a growing number of cancer cell lines, probing thousands of genes individually for possible vulnerabilities.

    In a study conducted as part of the Slim Initiative in Genomic Medicine for the Americas and reported in Cell, the Dependency Map team describes a major set of findings: 769 strong dependencies unique to cancer cells uncovered through RNA interference (RNAi) screens of 501 cell lines representing a range of tumors. The list reveals intriguing themes in cancer cells’ survival strategies, and may also open new avenues for cancer drug development.

    But the team knew even then that they were not close to seeing the whole picture. “A dozen cell lines was far too few to really probe the breadth of dependencies,” Root said.

    Watching tumors express themselves

    Over the following years, Root, Hahn, and their collaborators — including the Broad Cancer Program’s Paquita Vazquez, Aviad Tsherniak, Cancer Program associate director Jesse Boehm, and Broad chief scientific officer and Cancer Program director Todd Golub — continued to systematically screen additional cell lines until they had comprehensive RNAi data (available via a dedicated online portal) from 501 lines curated by the Broad-Novartis Cancer Cell Line Encyclopedia (CCLE), representing multiple cancer types.

    “Few places have tried to collect this kind of of data at this scale,” Hahn said. “But we felt that it was important to go after this many cell lines because it would give us a more comprehensive view.”

    The total dataset revealed some striking patterns in the genes and pathways cancer cells come to depend on. Many dependencies were cancer-specific, in that silencing them each affected only a subset of the cell lines. However, more than 90 percent of the cell lines had a strong dependency on at least one of a set of 76 genes, suggesting that many cancers rely on a relatively few genes and pathways.

    Using a set of molecular features (e.g., mutations, gene copy numbers, expression patterns) from each cell line, the team also generated biomarker-based models that helped explain the biology behind 426 of the 769 dependencies. Most of those biomarkers fell into four broad categories:

    mutation(s) of a gene

    loss of a copy or reduced expression of a gene

    increased expression of a gene

    reliance on a gene functionally or structurally related to another, lost gene (a.k.a., a paralog dependence)

    Surprisingly, more than 80 percent of the dependencies with biomarkers linked to changes (up or down) in a gene’s expression. Mutations (often used as the grounds for pursuing a gene as a drug target) accounted for merely 16 percent.

    Encouragingly, 20 percent of the dependencies the team discovered linked back to genes previously identified as potential drug targets.

    “We can’t say we’ve found everything, but we can say that the genes we’re seeing fall into a relatively small number of bins, some of which are familiar, some less so,” Hahn said. “That initial taxonomy is a great starting point for building a full map.”

    “Our results provide a starting point for therapeutic projects to decide where to focus their efforts,” said Vazquez, a study co-first author and a Cancer Dependency Map project leader. She added that while there was still much to do to validate the list, “it’s becoming increasingly easier to triangulate data and generate hypotheses as more genome-scale systematic datasets, like those from the CCLE, Genotype-Tissue Expression, and The Cancer Genome Atlas projects, become available.

    “Bringing of all the data together,” she continued, “will help us generate a truly comprehensive cancer dependency map.”

    See the full article here .

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    Broad Institute Campus

    The Eli and Edythe L. Broad Institute of Harvard and MIT is founded on two core beliefs:

    This generation has a historic opportunity and responsibility to transform medicine by using systematic approaches in the biological sciences to dramatically accelerate the understanding and treatment of disease.
    To fulfill this mission, we need new kinds of research institutions, with a deeply collaborative spirit across disciplines and organizations, and having the capacity to tackle ambitious challenges.

    The Broad Institute is essentially an “experiment” in a new way of doing science, empowering this generation of researchers to:

    Act nimbly. Encouraging creativity often means moving quickly, and taking risks on new approaches and structures that often defy conventional wisdom.
    Work boldly. Meeting the biomedical challenges of this generation requires the capacity to mount projects at any scale — from a single individual to teams of hundreds of scientists.
    Share openly. Seizing scientific opportunities requires creating methods, tools and massive data sets — and making them available to the entire scientific community to rapidly accelerate biomedical advancement.
    Reach globally. Biomedicine should address the medical challenges of the entire world, not just advanced economies, and include scientists in developing countries as equal partners whose knowledge and experience are critical to driving progress.

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  • richardmitnick 8:09 am on July 12, 2017 Permalink | Reply
    Tags: , Cancer, Chemotherapy before breast cancer surgery might fuel metastasis, , STAT,   

    From STAT via U Washington: “Chemotherapy before breast cancer surgery might fuel metastasis” 

    U Washington

    University of Washington

    1

    STAT

    July 10, 2017
    Sharon Begley

    2
    A breast cancer tumor imaged with a technique that highlights aspects of its microenvironment. National Cancer Institute/Univ. of Chicago Comprehensive Cancer Center. National Cancer Institute/Univ. of Chicago Comprehensive Cancer Center.

    When breast cancer patients get chemotherapy before surgery to remove their tumor, it can make remaining malignant cells spread to distant sites, resulting in incurable metastatic cancer, scientists reported last week.

    The main goal of pre-operative (neoadjuvant) chemotherapy for breast cancer is to shrink tumors so women can have a lumpectomy rather than a more invasive mastectomy. It was therefore initially used only on large tumors after being introduced about 25 years ago. But as fewer and fewer women were diagnosed with large breast tumors, pre-op chemo began to be used in patients with smaller cancers, too, in the hope that it would extend survival.

    But pre-op chemo can, instead, promote metastasis, scientists concluded from experiments in lab mice and human tissue, published in Science Translational Medicine.

    When breast cancer patients get chemotherapy before surgery to remove their tumor, it can make remaining malignant cells spread to distant sites, resulting in incurable metastatic cancer, scientists reported last week.

    The main goal of pre-operative (neoadjuvant) chemotherapy for breast cancer is to shrink tumors so women can have a lumpectomy rather than a more invasive mastectomy. It was therefore initially used only on large tumors after being introduced about 25 years ago. But as fewer and fewer women were diagnosed with large breast tumors, pre-op chemo began to be used in patients with smaller cancers, too, in the hope that it would extend survival.

    But pre-op chemo can, instead, promote metastasis, scientists concluded from experiments in lab mice and human tissue, published in Science Translational Medicine.

    The reason is that standard pre-op chemotherapies for breast cancer — paclitaxel, doxorubicin, and cyclophosphamide — affect the body’s on-ramps to the highways of metastasis, said biologist John Condeelis of Albert Einstein College of Medicine, senior author of the new study.

    Called “tumor microenvironments of metastasis,” these on-ramps are sites on blood vessels that special immune cells flock to. If the immune cells hook up with a tumor cell, they usher it into a blood vessel like a Lyft picking up a passenger. Since blood vessels are the highways to distant organs, the result is metastasis, or the spread of cancer to far-flung sites.

    Depending on characteristics such as how many tumor cells, blood vessel cells, and immune cells are touching each other, the tumor microenvironment can nearly triple the chance that a common type of breast cancer (estrogen-receptor positive/HER2 negative) that has reached the lymph nodes will also metastasize, Condeelis and colleagues showed in a 2014 study [NCBI] of 3,760 patients. The discovery of how the tumor microenvironment can fuel metastasis by whisking cancer cells into blood vessels so impressed Dr. Francis Collins, director of the National Institutes of Health, that he featured it in his blog.

    The new study took the next logical step: Can the tumor microenvironment be altered so that it promotes or thwarts metastasis?

    To find out, Einstein’s George Karagiannis spent nearly three years experimenting with lab mice whose genetic mutations make them spontaneously develop breast cancer, as well as mice given human breast tumors. In both cases, paclitaxel changed the tumor microenvironments in three ways, all more conducive to metastasis: The microenvironment had more of the immune cells that carry cancer cells into blood vessels, it developed blood vessels that were more permeable to cancer cells, and the tumor cells became more mobile, practically bounding into those molecular Lyfts.

    As a result, the mice had twice as many cancer cells zipping through their bloodstream and in their lungs compared with mice not treated with paclitaxel. Two other neoadjuvants, doxorubicin and cyclophosphamide, also promoted metastasis by altering the tumor microenvironment. “This showed that the tumor microenvironment is the doorway to metastasis,” Condeelis said.

    The scientists also analyzed tissue from 20 breast cancer patients who had undergone pre-op chemo (12 weeks of paclitaxel and four of doxorubicin and cyclophosphamide). Compared to before the chemo, the tumor microenvironment after treatment was more conducive to metastasis in most patients. In five, it got more than five times worse. No patient’s microenvironment got less friendly to metastasis.

    Pre-op chemo “may have unwanted long-term consequences in some breast cancer patients,” the Einstein researchers wrote.

    That finding is “fascinating, powerful, and very important,” said Julio Aguirre-Ghiso, of Mount Sinai School of Medicine, an expert in metastasis who was not involved in the study. “It raises awareness that we might have to be smarter about how we use chemotherapy.”

    Dr. Julie Gralow, a medical oncologist at the University of Washington, said that if pre-op chemo promoted metastasis, that should have shown up in studies that compared it to post-op chemo, but for the most part it hasn’t. However, that could be because only tumor cells containing certain proteins that make them especially mobile are affected in this way. “This is an interesting study, to say the least,” Gralow said. “I am willing to keep my mind open to the possibility that there are some breast cancer patients in whom things get worse” with pre-op chemo.

    One reason to question the findings, however, is that if pre-op chemo promotes metastasis in some patients, that might be expected to have shown up in studies of the therapy. Overall, in fact, those studies show [JCO] that “neoadjuvant chemotherapy does not seem to improve overall survival,” as the authors of an editorial in the Journal of Clinical Oncology wrote.

    That’s not as bad as decreasing survival, of course. But Einstein’s Dr. Maja Oktay, a co-author of the new research, cautioned that the typical length of the studies — six or so years — is too short to assess the risk of metastasis, “which can take more than 20 years” to appear, she said. Such patients might never be flagged as having metastatic cancer, let alone having it linked to pre-op chemo decades earlier, said Aguirre-Ghiso.

    On a brighter note, not all breast cancer patients have the kind of tumor microenvironment in which pre-op chemo can promote metastasis. Whether they do or not can be determined by a simple lab test, but one that is not routinely done, Condeelis said.

    Serendipitously, an experimental compound called rebastinib, being developed by Deciphera Pharmaceuticals, seems to be able to block the on-ramp to the metastasis highway. In a study currently recruiting patient volunteers [Clinical Trials.gov], the Einstein scientists (who have no financial relationship with Deciphera) are studying whether rebastinib can improve outcomes in metastatic breast cancer.

    See the full article here .

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    u-washington-campus
    The University of Washington is one of the world’s preeminent public universities. Our impact on individuals, on our region, and on the world is profound — whether we are launching young people into a boundless future or confronting the grand challenges of our time through undaunted research and scholarship. Ranked number 10 in the world in Shanghai Jiao Tong University rankings and educating more than 54,000 students annually, our students and faculty work together to turn ideas into impact and in the process transform lives and our world. For more about our impact on the world, every day.
    So what defines us —the students, faculty and community members at the University of Washington? Above all, it’s our belief in possibility and our unshakable optimism. It’s a connection to others, both near and far. It’s a hunger that pushes us to tackle challenges and pursue progress. It’s the conviction that together we can create a world of good. Join us on the journey.

     
  • richardmitnick 10:13 am on July 10, 2017 Permalink | Reply
    Tags: , Cancer, , , Personalized cancer vaccines, Personalized Cancer Vaccines Vanquish Melanoma in Small Study,   

    From SA: “Personalized Cancer Vaccines Vanquish Melanoma in Small Study” 

    Scientific American

    Scientific American

    July 6, 2017
    Sharon Begley

    The therapy trains the immune system to attack tumors.

    1
    Metastatic melanoma cells. Credit: NIH Wikimedia

    A small pilot study raises hopes that personalized cancer vaccines might prove safer and more effective than immune-based therapies already in use or further along in development. In a paper published online in Nature on Wednesday, scientists reported that all six melanoma patients who received an experimental, custom-made vaccine seemed to benefit: their tumors did not return after treatment.

    Researchers not involved in the study praised its results, but with caveats. The scientists “did a beautiful job,” said MD Anderson Cancer Center’s Greg Lizee, an expert in tumor immunology, who called the results “very encouraging.” But because the study did not include a comparison group of patients who received standard treatment and not the vaccine, he cautioned, “it’s not completely proved yet that the lack of [cancer] recurrence was due to the vaccine.”

    See the full article here .

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    Scientific American, the oldest continuously published magazine in the U.S., has been bringing its readers unique insights about developments in science and technology for more than 160 years.

     
  • richardmitnick 7:07 am on July 10, 2017 Permalink | Reply
    Tags: , Cancer, , Explainer: what is cancer radiotherapy and why do we need proton beam therapy?, , Proton Beam Therapy, Radiation cancer therapy,   

    From COSMOS via U Sidney: “Explainer: what is cancer radiotherapy and why do we need proton beam therapy?” 

    U Sidney bloc

    University of Sidney

    COSMOS

    10 July 2017
    Paul Keall

    Proton beam therapy is radiation therapy that uses heavier particles instead of the X-rays used in conventional radiotherapy.

    2
    1
    Both above from New Jersey’s ProCure Proton Therapy Center

    In the 2017 federal budget, the government dedicated up to A$68 million to help set up Australia’s first proton beam therapy facility in South Australia. The government says this will help Australian researchers develop the next generation of cancer treatments, including for complex children’s cancers.

    Proton beam therapy is radiation therapy that uses heavier particles (protons) instead of the X-rays used in conventional radiotherapy. These particles can more accurately target tumours closer to vital organs, which can be especially beneficial to patients suffering from brain cancer and children whose organs are still developing and are more vulnerable to damage.

    So, the facility will also be an alternative to conventional radiotherapy for treating certain cancer. But what is traditional radiotherapy, and how will access to proton beam therapy improve how we manage cancer?

    What is radiotherapy?

    Radiotherapy, together with surgery, chemotherapy and palliative care, are the cornerstones of cancer treatment. Radiotherapy is recommended for half of cancer patients.

    It is mostly used when the cancer is localised to one or more areas. Depending on the cancer site and stage, radiotherapy can be used alone or in combination with surgery and chemotherapy. It can be used before or after other treatments to make them more effective by, for example, shrinking the tumour before chemotherapy or treating cancer that remains after surgery.

    Most radiotherapy treats cancer by directing beams of high energy X-rays at the tumour (although other radiation beams, such as gamma rays, electron beams or proton/heavy particle beams can also be used).

    The X-rays interact with tumour cells, damaging their DNA and restricting their ability to reproduce. But because X-rays don’t differentiate between cancerous and healthy cells, normal tissues can be damaged. Damaged healthy tissue can lead to minor symptoms such as fatigue, or, in rare cases, more serious outcomes such as hospitalisation and death.

    Getting the right amount of radiation is a fine balance between therapy and harm. A common way to improve the benefit-to-cure ratio is to fire multiple beams at the tumour from different directions. If they overlap, they can maximise the damage to the tumour while minimising damage to healthy tissue.

    How it works

    3
    A drawing of the X-ray machine used by Wilhelm Röntgen to produce images of the hand. Golan Levin/Flickr, CC BY-SA

    Wilhelm Röntgen discovered X-rays in 1895 and within a year, the link between exposure to too much radiation and skin burns led scientists and doctors to pursue radiation in cancer treatment.

    There are three key stages in the radiotherapy process. The patient is first imaged – using such machines as computer tomography (CT) or magnetic resonance imaging (MRI). This estimates the extent of the tumour and helps to understand where it is with respect to healthy tissues and other critical structures.

    In the second stage, the doctor and treatment team will use these images and the patient’s case history to plan where the radiation beams should be placed – to maximise the damage to the tumour while minimising it to healthy tissues. Complex computer simulations model the interactions of the radiation beams with the patient to give a best estimate of what will happen during treatment.

    4
    A single radiotherapy treatment takes 15 to 30 minutes. IAEA Imagebank/Flickr, CC BY

    During the third, treatment-delivery stage, the patient lies still while the treatment beam rotates, delivering radiation from multiple angles.

    Each treatment generally takes 15 to 30 minutes. Depending on the cancer and stage, there are between one and 40 individual treatments, typically one treatment a day. The patient cannot feel the radiation being delivered.

    Benefits and side effects

    Radiotherapy’s targeting technology has made a significant difference to many cancers, in particular early-stage lung and prostate cancers. It is now possible to have effective, low toxicity treatments for these with one to five radiotherapy sessions.

    For early-stage lung cancer studies estimate with radiotherapy, survival three years after diagnosis is at 95%. For prostate cancer, one study estimates survival at the five year mark is about 93%.

    Side effects for radiotherapy vary markedly between treatment sites, cancer stages and individual patients. They are typically moderate but can be severe. A general side effect of radiotherapy is fatigue.

    5
    Radiotherapy is often used to treat brain tumours. Eric Lewis/Flickr, CC BY

    Other side effects include diarrhoea, appetite loss, dry mouth and difficulty swallowing for head and neck cancer radiotherapy, as well as incontinence and reduction in sexual function for pelvic radiotherapy.

    Long-term effects of radiotherapy are a concern, particularly for children. For instance, radiation to treat childhood brain tumours can have long-lasting cognitive effects that can affect relationships and academic achievement.

    Again doctors will need to weigh up the risks and benefits of treatment for individual patients. Proton beam therapy is arguably most beneficial in these cases.

    Other radiotherapy challenges

    There are several challenges to current radiotherapy. It is often difficult to differentiate the tumour from healthy tissue, and even experts do not always agree on where exactly the tumour is.

    Radiotherapy can’t easily adapt to the complex changes in patients’ anatomy when a patient moves – for instance, when they breathe, swallow, their heart beats or as they digest food. As a result, radiation beams can be off-target, missing the tumour and striking healthy tissue.

    Also, we currently treat all parts of the tumour equally, despite knowing some of the tumour’s regions are more aggressive, resistant to radiation and likely to spread to other parts of the body.

    The tumour itself also changes in response to the treatment, further confounding the problem. An ideal radiotherapy solution would image and adapt the treatment continuously based on these changes.

    Improvements in technology, including in imaging systems that can better find the tumour, can help overcome these challenges.


    Proton therapy requires large accelerators to give protons enough energy to penetrate deep into patients. No video credit.

    Proton beam therapy and other innovations

    Proton beam therapy will help maximise benefits for many patients, including those with cancers near the spinal cord and pelvis. It requires large accelerators to give protons enough energy to penetrate deep into patients. The energetic protons are transported into the treatment room using complex steering magnets and directed to the tumour inside the patient.

    Protons slow down and lose energy inside the patient, with most of the energy loss planned to occur in the tumour. This reduces energy loss in healthy tissues and reduces side effects.

    The problems of changing patient anatomy and physiology in other forms of radiotherapy are also challenges for proton beam therapy.

    The ConversationAustralia has a number of research teams tackling such challenges, including developing new radiation treatment devices, breathing aids for cancer patients, radiation measurement devices, shorter and more convenient treatment schedules and the optimal combination of radiotherapy with other treatments, such as chemotherapy and immunotherapy.

    See the full article here .

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    U Sidney campus

    Our founding principle as Australia’s first university was that we would be a modern and progressive institution. It’s an ideal we still hold dear today.

    When Charles William Wentworth proposed the idea of Australia’s first university in 1850, he imagined “the opportunity for the child of every class to become great and useful in the destinies of this country”.

    We’ve stayed true to that original value and purpose by promoting inclusion and diversity for the past 160 years.

    It’s the reason that, as early as 1881, we admitted women on an equal footing to male students. Oxford University didn’t follow suit until 30 years later, and Jesus College at Cambridge University did not begin admitting female students until 1974.

    It’s also why, from the very start, talented students of all backgrounds were given the chance to access further education through bursaries and scholarships.

    Today we offer hundreds of scholarships to support and encourage talented students, and a range of grants and bursaries to those who need a financial helping hand.

     
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