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  • #16
    Recently Published Study Shows Effective Treatment for Early-Stage Breast Cancer

    The TARGIT Collaborative Group (TCG) is pleased to announce publication of the long-term results of the Targeted Intraoperative Radiotherapy Trial (TARGIT-A Trial) comparing partial breast single fraction targeted intraoperative radiotherapy (TARGIT-IORT) to 3-6 week post-operative whole breast radiotherapy, demonstrating equivalent long-term outcomes between the two treatments. The results of the trial were published on August 19, 2020 in the British Medical Journal (

    The TARGIT-A Trial was a 2,298-patient multicenter, international, randomized controlled trial evaluating the use of TARGIT-IORT using the Intrabeam System (Carl Zeiss Meditec, Inc.) as a method of delivering IORT. TARGIT-IORT is typically administered in less than 30 minutes at the time of lumpectomy. TARGIT-IORT is the only method of delivering IORT widely available in the U.S. for which effectiveness has been proven in a randomized control trial.

    Dr. Valery Uhl, Radiation Oncologist and President of the TCG, stated: “We now have long-term proof that TARGIT-IORT is not only an effective—but in many ways superior—treatment for early-stage breast cancer. Every hospital where breast cancer surgery is performed should offer this form of radiation treatment to their breast cancer patients. Not only are long-term local control and cancer survival outcomes similar to whole breast radiotherapy, but mortality from other causes was lower in the IORT arm. TARGIT-IORT should be considered the new standard of treatment for early-stage breast cancer based on this large, multi-institutional, prospective, randomized controlled trial.”

    The TARGIT-A trial is largely responsible for the widespread adoption of IORT as a treatment option for early-stage breast cancer in the U.S. IORT is now covered by Medicare and most health plans. According to Breast Surgeon, Dr. Dennis Holmes, a TCG Founder and TARGIT-A Trial publication co-author, “in addition to being efficacious, separate publications have shown TARGIT-IORT to be associated with fewer side effects, improved quality of life, and reduced healthcare cost compared to whole breast radiotherapy.”

    Dr. Barry Rosen, Breast Surgeon and Secretary/Treasurer of TCG noted: “TARGIT-IORT is a safe, convenient, cost-effective alternative to WBRT that has virtually no side-effects and better cosmetic outcomes by virtue of its targeted therapy. I believe this establishes a new standard for patient-centered, precision oncology and should be offered to all breast cancer patients that meet eligibility requirements. Furthermore, the lower non-cancer mortality rates associated with IORT warrants further study.”:

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    • #17
      Study finds two drugs can reduce cancer spread after tumor removal

      A research group from Tel Aviv University (TAU) successfully reduced metastatic spread following tumor removal surgery in colorectal cancer patients.

      Using a short treatment around the time of the surgery, they were able to reduce stress responses and physiological inflammation, thus preventing the development of metastases in the years following the surgery.

      The study, recently published in the American Cancer Society journal Cancer, was led by Prof. Shamgar Ben-Eliyahu from the TAU School of Psychological Sciences and Sagol School of Neuroscience, and Dr. Oded Zmora from Shamir (Assaf Harofeh) Medical Center.

      The three-year study involved 34 patients. Over the course of 20 days — from five days prior to surgery until two weeks afterward — 16 of the patients received anti-anxiety and blood pressure-reducing drug Propranolol (Deralin) and anti-inflammatory analgesic Etodolac (Etopan), and 18 received a placebo treatment as a control group.

      Only two out of 16 patients receiving the drug treatment exhibited metastatic disease. In the control group, six out of 18 developed metastases, which is the usual rate for colorectal cancer patients.

      The treatment led to a reduction in the metastatic potential of the tumor and potentially the residual cancer cells.

      In addition, the drugs triggered good changes in patients’ white blood cell number and type, indicating a reduced chance of disease recurrence.

      “When the body is in a state of stress, whether physiological (from surgery) or psychological, this causes a release of high amounts of two types of hormones, prostaglandins and catecholamines,” Ben-Eliyahu explained.

      “These hormones suppress the activity of the immune cells, thus indirectly promoting the development of cancer metastases. In addition, these hormones also directly promote the acquisition of metastatic traits in cancer tissue.,” he continued.

      “Our study shows that inexpensive, accessible medication treatment could be used to reduce body stress responses and inflammation associated with surgery, which significantly reduces the risk of metastases that might be detected months or years after surgery.”

      Ben-Eliyahu now plans a large-scale clinical study to further test this treatment.: - https://acsjournals.onlinelibrary.wi...002/cncr.32950

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      • #18
        Up to 1,000 downwinders likely got cancer from first atomic test, study says

        As many as 1,000 New Mexicans living in communities near Trinity Site, where the first atomic bomb was detonated 75 years ago, might have developed cancer from the radioactive fallout, says a long-awaited Cancer Institute report released Tuesday.

        The institute's findings were based on a six-year study that involved computer modeling, researching historical data and interviewing 210 elderly "downwinders" who lived close enough to the blast to suffer internal radiation exposure by ingesting contaminated milk and food.

        The number of cancer victims could be less than 1,000 but is unlikely to be more, the study says.

        There's also no clear evidence the radiation was severe enough to cause genetic abnormalities that could be passed by birth to subsequent generations, the study says.

        The study's authors concede there's much uncertainty in the report because so many years have passed since the test, the government didn't conduct public studies of the test's potential impacts on communities — due to the Manhattan Project's secrecy — and cancer cases weren't tracked nationally until the 1960s.

        The report comes after decades of criticism from downwinder advocates, who have accused the federal government of refusing to acknowledge affected residents to avoid liability.:
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        • #19
          Cancer cells take over blood vessels to spread

          In laboratory studies, Johns Hopkins Kimmel Cancer Center and Johns Hopkins University researchers observed a key step in how cancer cells may spread from a primary tumor to a distant site within the body, a process known as metastasis.

          Trying to determine how groups of cells migrate to other parts of the body, the scientists used tissue engineering to construct a functional 3D blood vessel and grew breast cancer cells nearby. They observed the cancer cells reaching out to the blood vessel and taking over a patch of the cell wall. As a result of this attachment to the blood vessel, a cluster of tumor cells were easily released into the bloodstream to travel to distant sites. Cancer cells also were able to constrict blood vessels, cause them to leak, or pull on them.

          A description of the work was published online July 14 in the journal Cancer Research.

          "We observed that cancer cells can rapidly reshape, destroy or integrate into existing blood vessels," says senior study author Andrew Ewald, Ph.D., co-director of the Cancer Invasion and Metastasis Program at the Johns Hopkins Kimmel Cancer Center and professor of cell biology at the Johns Hopkins University School of Medicine. The work was conducted in close collaboration with the lab of Peter Searson, Ph.D., the Joseph R. and Lynn C. Reynolds Professor of Materials Science and Engineering, with joint appointments in the departments of biomedical engineering, oncology and physical medicine and rehabilitation.

          "Just as people going scuba diving versus ice climbing require different tools, cancer cells bring different equipment depending on the job they intend to perform," Ewald says. "Determining what that equipment is can help us understand how to stop cancer." In this case, Ewald and collaborators expected to see groups of eight to 10 cells leaving a tumor, migrating through a protein barrier and squeezing between blood vessel walls to travel.

          "We never saw that," he says. "What we kept seeing instead was that a piece of an existing tumor would take over a neighboring blood vessel wall, putting cancer cells in direct contact with the circulation, and that the cancer cells could do so in a matter of hours. They didn't have to invade past the blood vessels; they became the blood vessels, and could just release cancer cells there."

          The "mosaic" vessels that result -- named because they consist of some natural blood vessel cells and some cancer cells -- were observed in about 6% of blood vessels in human breast tumors and in a mouse model of breast cancer in this and other studies, Ewald says. They also have been found in deadly brain tumors called glioblastomas, melanoma skin cancers and gastric cancers, he says. Their presence is associated with increased distant metastases.

          The 3D model could be adapted to study additional aspects of the tumor microenvironment or to study alternate cancer types, Ewald says.:

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          • #20
            Pfizer's Ibrance kisses early breast cancer hopes goodbye with 2nd study failure

            After Pfizer’s Ibrance failed a crucial study in HR-positive, HR-negative postsurgery breast cancer patients, the company clung to hope that it could still show a benefit in a high-risk subset of those patients. But new data have officially snuffed out those hopes.

            The news didn’t surprise analysts, who widely expected a flop after Pfizer detailed its failed phase 3 Pallas trial at last month’s European Society for Medical Oncology virtual annual meeting. That study looked at Ibrance in the wider adjuvant group, showing the drug didn't deliver a benefit. In a subgroup breakdown Porges labeled “dismal,” Ibrance showed it didn’t help high-risk patients, either.

            But the Penelope-B stumble did bring a key question into sharper focus: Will its adjuvant showing hurt Ibrance in the metastatic setting, where it currently holds court?

            The way Porges sees it, it’s “inevitable that there is some spillover in terms of share of new starts in the metastatic setting,” given that Eli Lilly’s rival drug Verzenio is all lined up for an adjuvant green light after posting practice-changing data at ESMO. Adding the Lilly med to standard endocrine therapy after surgery slashed the risk of cancer recurrence by 25.3% among high-risk patients, results showed.

            The Penelope-B miss “further substantiates the hypothesis that Ibrance is an inferior molecule with less effective CDK inhibition than Lilly’s Verzenio,” Porges said.

            But RBC Capital Markets’ Randall Stanicky disagreed. “We don’t expect this to impact PFE's leading position in the metastatic setting, which as of today consists of ~79% of the CDK4/6 class,” he wrote of the Penelope-B data in his own Friday note to clients.

            Others, including Evercore ISI’s Umer Raffat, were less conclusive. Since the readout from Lilly’s successful adjuvant trial, monarchE, Ibrance hasn’t looked to be ceding its ground. “But we’ll track this dynamic over time,” he noted.

            Pfizer, for its part, has been vocal about the fact that it doesn’t expect to see its metastatic share slip.

            “I’ve got to say that all our interactions with thought leaders, through market research with medical oncologists that treat breast cancer, they look at early breast cancer very differently from metastatic,” Andy Schmeltz, global president and general manager of Pfizer's oncology unit, said in an interview ahead of ESMO, adding that “we do not expect any impact on Ibrance’s … positioning or performance in the metastatic setting.”

            But in the meantime, with an eye on clawing back a competitive edge, the company will be applying the learnings from its pair of trial misfires to up-and-coming CDK drugs in its pipeline.

            “We look forward to continuing to work with our research partners to understand subgroup data and how these could inform the development of our next-generation CDK inhibitors in early breast cancer,” Chris Boshoff, M.D., Ph.D., Pfizer’s chief development officer for oncology, said in a statement.:

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            • #21
              One drink a day raises risk of alcohol-linked cancers by 10pc

              For every seven drinks Australians have a week, their risk of developing an alcohol-related cancer rises by 10 per cent, according to a sobering new study.

              Australia's largest ever investigation of the impact of alcohol on cancer risk, published on Monday in the British Journal of Cancer, is particularly relevant because of increased consumption during the COVID-19 crisis.

              Before the pandemic, alcohol was attributed to 3500 new cancer cases each year in Australia. If the increase during COVID-19 is not reversed, this number will grow.

              The five-year study links consumption to seven prominent cancer types: liver, oesophagus, mouth, pharynx, larynx, bowel and breast.

              For NSW residents over 45, it found the relative risk of developing one of these cancers jumped by 41 per cent in “heavy drinkers”, defined as those who consumed over 28 drinks per week, compared with light drinkers who had one to three a week.

              There is low community awareness about the link between most of these cancers and alcohol, says Dr Peter Sarich, a post-doctoral research fellow at Cancer Council NSW, who led the study.

              There is an urgent need to raise awareness of the link between cancer and alcohol, says Dr Sarich.

              "While liver cancer comes first to mind with alcohol, surprisingly the biggest impact – in terms of population – is for breast and bowel cancer."

              He says currently alcohol causes 800 breast cancers and 1300 bowel cancers a year. It also causes 175 liver cancers.

              In the study, the relative risk of liver cancer rose by 48 per cent in medium volume drinkers (seven to 14 drinks a week) and by hefty 202 per cent in heavy drinkers.

              Over a lifetime, Dr Sarich says for every 100 people having more than 14 drinks per week, about five will develop cancer due to alcohol by age 85.

              This most commonly occurs in breast cancer for women and bowel cancer for men.

              He says the study, which analysed data from 226,000 participants from the Sax Institute’s 45 & Up Study, highlights the urgent need to raise awareness of the link between cancer and alcohol.

              The authors would like to see government campaigns to raise awareness. They also call for the implementation of policies to address pricing, availability and advertising of alcohol, that have been shown to help reduce alcohol use in the community.

              No amount of alcohol is regarded as healthy (despite the debate about cardiac benefits) and the current National Health and Medical Research Council guideline recommendation that Australians limit themselves to a maximum of 14 drinks per week, is set to be reduced to 10.:

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              • #22
                Morning Exercise May Lower Cancer Risk, Study Finds

                Exercising in the morning could reduce your risk of getting cancer more than doing your workout later in the day, according to recently published research.1

                In the study, which was published in Cancer Epidemiology in September, the researchers analyzed data from 2,795 people divided into two control groups and two cancer groups.

                The results indicated that the protective effect against breast and prostate cancer was most significant in the people who exercised in the morning (between the hours of 8 a.m. and 10 a.m.). The results held even when the researchers adjusted for other factors, such as participants' sleep routines and meal timing.

                Based on the new findings and earlier studies, the researchers pointed to a possible connection between cancer and circadian rhythm disruption.

                "Researchers have classified circadian disruption as a carcinogen, not unlike tobacco or asbestos,” Sean Marchese, MS, RN, a registered nurse and oncology writer at The Mesothelioma Center, tells Verywell. Marchese was not involved with the study.

                “Circadian regulatory functions are critical for many aspects of homeostasis, the body's method of regulation," Marchese says. "A disruptive circadian rhythm can impair cell cycles, DNA repair, and metabolism. Errors in any of these processes can lead to cancer, especially if disruptions continue to occur over a long period.”

                What Is Your Circadian Rhythm?

                Your circadian rhythm, also known as your sleep/wake cycle, is a 24-hour internal clock that is controlled by your brain. It tells you when it’s time to go to sleep and when it’s time to wake up. The rhythm is regulated by various hormones, two of the most notable being cortisol and melatonin.

                The circadian rhythm follows a similar pattern in everyone, but people are typically divided into three subgroups or chronotypes: morning, intermediate, and evening.

                Morning chronotypes wake up early and go to bed early, while evening chronotypes wake up later and go to bed later. Evening chronotypes usually have a sleep pattern that’s about two to three hours behind morning chronotypes. As you might expect, intermediate chronotypes fall somewhere in the middle.

                Sleep patterns are also associated with different hormonal fluctuations. Morning chronotypes have an earlier onset of melatonin production; their levels rise earlier in the evening and prompt their earlier bedtimes. For the intermediate and evening chronotypes, melatonin rises later and leads to later bedtimes.

                A disruptive circadian rhythm can impair cell cycles, DNA repair, and metabolism.
                — SEAN MARCHESE, MS, RN,

                The differences matter in the context of the recent study because the researchers found that the protective effects of early morning exercise were more significant in intermediate and evening chronotypes than in morning chronotypes.

                The researchers speculated that midday to afternoon exercise might delay a person's melatonin production even more if they were an intermediate or evening chronotype. Therefore, earlier exercise could lead to more melatonin, a balanced circadian rhythm, and reduced cancer risk.

                Keeping Your Circadian Rhythm Balanced

                When your circadian rhythm is thrown off, it can lead to difficulty sleeping through the night, insomnia, fatigue, and energy crashes during the day. Evidence has also connected a disrupted circadian rhythm to imbalanced blood sugar, negative changes in metabolism, weight gain, depression, dementia, and cancer.3

                One reason why exercise is connected to reduced cancer risk is that it helps keep your circadian rhythm balanced and functioning on a set schedule.

                Marchese adds that getting enough quality sleep and trying to keep a regular sleep schedule are also critical factors—ones that you might be able to improve by taking a closer look at your sleep habits.

                "Try not to be on your phone or other screen-based devices before bed or if you wake up in the middle of the night," Marchese says. "That light at night is what triggers the melatonin suppression and disruption to your circadian rhythm."

                What’s More Important: Sleep or Exercise?
                Ideally, you would get adequate amounts of both, but sometimes you have to choose one over the other.

                As far as your circadian rhythm is concerned, the answer is likely to make sure you're getting enough sleep. “Sufficient sleep is critical for circadian homeostasis,” Swathi Gujral, PhD, a postdoctoral fellow at the University of Pittsburgh's Brain Aging & Cognitive Health Lab, tells Verywell. “The deleterious effects for overall health of circadian cycle disruptions due to poor sleep likely outweigh the health benefits of exercising specifically in the morning hours.”

                Alpa Patel, PhD, the senior vice president of population science for the American Cancer Society, tells Verywell that rather than sacrificing good sleep and putting pressure on yourself to work out in the morning, getting regular exercise—whenever you can—is what's most important.

                The American Cancer Society recommends engaging in 150 to 300 minutes of moderate or 75 to 150 minutes of vigorous physical activity each week and limiting your sedentary activities as much as possible.4

                Future Research

                While Patel calls the new study intriguing, she adds that there is still more research to be done. While exercise is connected to a more balanced circadian rhythm and reduced risk of cancer, the time of day might be less important than getting regular exercise, no matter what the clock says.

                Patel also points out that the results of the study could have been influenced by other factors known as residual confounding factors and their overall effect on your health. While the researchers tried to account for some of these factors (such as participants' total calorie intake), there were others (such as participants' overall diet quality) that were missing. Therefore, additional research is needed before any definitive claims could be made.

                I would encourage individuals to focus on what we know is important in cancer prevention. Don’t smoke, maintain a healthy body weight, be physically active, eat a healthy diet rich in fruits and vegetables, and make sure you get your cancer prevention/early detection screenings.
                — ALPA PATEL, PHD

                Gujral adds that you should be aware of and sensitive to how your environmental and social exposures in your daily life could be disrupting your circadian rhythm—especially if these exposures are chronic and/or persistent, such as in the case of long-term shift work.:

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                • #23
                  Colon cancer screening should begin at age 45, not 50, US task force says

                  A key panel of experts on Tuesday recommended for the first time that people get screened for colorectal cancer starting at age 45, instead of age 50, pointing to new evidence of the cancer in younger people.

                  The recommendation from the U.S. Preventive Services Task Force comes after American Cancer Society recommended the same age change in 2018.

                  The draft recommendation is open for comment until Nov. 23.

                  The task force especially recommended the earlier screening for Black patients, given higher rates of the disease among Black people.

                  “New science about colorectal cancer in younger people has enabled us to expand our recommendation to screen all adults starting at age 45, especially Black adults who are more likely to die from this disease,” Michael Barry, a member of the task force, said in a statement. “Screening earlier will help prevent more people from dying from colorectal cancer.”

                  Actor Chadwick Boseman died of colon cancer at age 43 in August, placing a spotlight on the toll that the disease takes on younger adults and specifically African Americans.

                  Colorectal cancer is the third-leading cause of cancer death in the United States, but about a quarter of people aged 50 to 75 — the age range within the previous guidelines for screening — have not been screened, according to the panel.

                  “Unfortunately, not enough people in the U.S. receive this effective preventive service that has been proven to save lives,” Alex Krist, the chair of the task force, said in a statement. “We hope that this recommendation to screen people ages 45 to 75 for colorectal cancer will encourage more screening and reduce people's risk of dying from this disease.":

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                  • #24
                    Microbiome linked to chemo weight gain in cancer patients

                    Around a third of women who undergo chemotherapy treatment for breast cancer gain weight following the procedure.

                    Now Israeli scientists have a possible explanation: gut bacteria are partially responsible for metabolic changes that lead to those added pounds.

                    In a study recently published in BMC Medicine, researchers studied 33 women beginning chemotherapy for breast or gynecological cancer. The women were weighed once before the treatment, and again approximately five weeks after treatment began. Prior to treatment, a stool sample was used to genetically characterize the microbiome of each woman.

                    Nine of the women were found to have gained a significant amount of weight. The microbiome of these women exhibited a smaller diversity of gut bacteria and different bacterial strains compared to that of the women who did not experience weight gain.

                    When the researchers then transferred the gut microbiota of the women who gained weight to germ-free mice, they developed glucose intolerance and signs of chronic inflammatory condition were detected in their blood.

                    These findings suggest that bacteria are partially responsible for metabolic changes that lead to weight gain following chemotherapy and that the composition of intestinal bacteria may predict which women will gain weight during treatment.

                    “We have shown for the first time that the pre-treatment microbiome of patients that gained weight following chemotherapy is different than the microbiome of patients that did not gain weight, and that fecal transplantation from patients that gained weight results in glucose intolerance, adverse lipid changes and inflammatory changes in germ-free mice,” said Prof. Omry Koren from Bar-Ilan University.

                    Koren and his colleague Dr. Ayelet Shai, chief of oncology at the Galilee Medical Center, are conducting a follow-up study in a larger patient population and at the end of chemotherapy.

                    “We hope that in the future we will be able to identify those women who are at risk for weight gain through a simple examination and perhaps even suggest ways to prevent this phenomenon,” Shai said.:

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                    • #25
                      Testing drugs within a tumor may combat pancreatic cancer drug resistance, ‘time machine’ suggests

                      Many patients with pancreatic cancer have only about a 10% chance of survival within five years of their diagnosis because they tend to become resistant to chemotherapy, past studies have indicated.

                      A “time machine” that Purdue University engineers designed to observe pancreatic cancer behavior over time suggests a new drug testing approach that could help scientists better catch resistance.

                      The researchers found that testing potential drugs on multiple tumor cell subtypes – rather than on just one cell subtype – can reveal drug resistance that may occur due to how different cancer subtypes interact with each other.

                      The study was recently published in the Royal Society of Chemistry journal Lab on a Chip.

                      “The drug discovery and screening process has been using one cancer cell subtype and studying how it interacts with neighboring non-cancer cells, but this may overestimate the efficacy of the drug,” said Bumsoo Han, a Purdue professor of mechanical engineering and program leader of the Purdue Center for Cancer Research. Han has a courtesy appointment in biomedical engineering.

                      “By condensing time to look at how cancer cells interact within a pancreatic tumor, we found that one cancer cell subtype can not only be more drug-resistant than the others, but drug-sensitive cells can also become resistant through interaction between the subtypes.”

                      The “time machine” is a type of lab tool called a microfluidic device. These devices are gum strip-sized platforms, such as a chip or slide, where cancer cells can be cultured in channels smaller than a millimeter in diameter. The cells then grow in a lifelike environment on the platform, such as in a collagen tube that Han’s lab created to mimic the pancreatic duct.

                      Microfluidic devices are starting to become more mainstream in the drug development process because they allow scientists to test drugs in realistic simulations of a biological system using real tissue samples, but on a faster time scale than in animal models.

                      Han’s group found that about 25% of 2019 research publications indexed by PubMed, a biomedical literature database, had used microfluidic devices as models to study tumors from animals or patients.

                      But most microfluidic devices just show late-stage tumor growth. With Han’s device, scientists can load in cell lines from an animal model or patient before gene mutation has happened, enabling them to see all stages of tumor progression.

                      While findings made using microfluidic devices need to be validated in humans before being put into clinical practice, they can still shorten the drug development process by offering new research approaches.

                      The findings from Han’s device highlight the need for studying interactions between cancer cells.

                      “Not much research has been done on what kind of interaction happens within tumors, so those mechanisms of drug resistance have been overlooked,” Han said.

                      These findings are already informing the development of new drug compounds.

                      Zhong-Yin Zhang, the director of the Purdue Institute for Drug Discovery, is using Han’s microfluidic device to test a compound aimed at blocking an oncogenic process that Zhang’s lab has previously identified as playing a role in cancer development.

                      The device allows Zhang’s team to evaluate the compound not only for pancreatic cancer specifically, but also on multiple cancer cell subtypes.

                      “The nice thing about this device is that we don’t have to use as much of a compound to see how well it works,” said Zhang, who is also a distinguished professor of medicinal chemistry in Purdue’s Department of Medicinal Chemistry and Molecular Pharmacology and Department of Chemistry.

                      A patent has been issued for the microfluidic pancreatic tumor device via the Purdue Research Foundation Office of Technology Commercialization. This research is partially supported by grants from the National Institutes of Health, Purdue Center for Cancer Research and Walther Embedding Program in Physical Sciences in Oncology.:

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                      • #26
                        People who eat chili peppers may be less likely to die of heart disease and cancer, research shows

                        People who eat chili peppers may live longer and have lower risk of heart disease and cancer compared to their spice-averse counterparts, according to a new study.

                        Researchers from the Cleveland Clinic analyzed four large studies on chili peppers and health, including data from more than 570,000 people in the US, Italy, China, and Iran.

                        They found people who ate chili peppers were 26% less likely to die of heart disease, and 23% less likely to die of cancer, compared with people who rarely or never ate chilis.

                        "We were surprised to find that in these previously published studies, regular consumption of chili pepper was associated with an overall risk-reduction of all-cause, cardiovascular disease and cancer mortality. It highlights that dietary factors may play an important role in overall health," Dr. Bo Xu, senior author of the paper and a cardiologist at Cleveland Clinic, said in a press release.

                        These findings will be presented at the American Heart Association's Scientific Sessions 2020 this month.

                        It's not yet clear how much or what types of chili pepper you'd need to eat in order to experience benefit or how often you should eat them, since the studies included in this research looked at different amounts and types of chilis.

                        The research also did not prove that chili peppers directly cause better health outcomes, so more research is needed to understand how it might work.

                        "The exact reasons and mechanisms that might explain our findings are currently unknown. Therefore, it is impossible to conclusively say that eating more chili pepper can prolong life and reduce deaths, especially from cardiovascular factors or cancer," Xu said.

                        Previous research has found that hot peppers may help reduce inflammation, lower the risk of illnesses, relieve pain, and could even help people lose weight or stave off age-related cognitive decline.

                        All these benefits are linked to a specific chemical found naturally in hot peppers: capsaicin, a compound that's responsible for the spicy sensation associated with chilis.

                        Capsaicin may have originated as a defense mechanism for pepper plants to deter fungi and other organisms from eating the seeds of the plant.

                        The fiery sensation of eating a hot pepper occurs because capsaicin binds to the pain receptors in the body, and promotes the release of hormones in the body that can lower blood pressure, and improve metabolism and digestion.

                        But the irritation stimulated by capsaicin also prompts the body to produce dopamine and other endorphins to tackle the perceived threat.

                        That's why some people enthusiastically enjoy spicy foods, while other people steer clear of such pungent seasonings. If you're in the latter group, don't worry — you can still get the health benefits of capsaicin by eating milder sources such as cherry, Anaheim, and poblano peppers, or spices such as paprika.:

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                        • #27
                          Learning the lessons of COVID-19: Protecting cancer services and research through the pandemic

                          It’s going to be a tough winter for all of us.

                          Cases of COVID-19 are rising in every part of the UK, and more extensive measures to control the spread of the virus are being put in place.

                          Cancer patients – and those who think they might have cancer – have already faced huge challenges this year, with many worried about coming forward to their GP or going into hospital to get tests because of the risk of getting COVID-19. And, with a huge backlog of patients still waiting for screening, diagnostic tests and treatments, we fear that there will be a negative impact on cancer survival.

                          That’s why, today, Cancer Research UK along with 50 leaders from across the NHS and cancer community have written to the Prime Minister and First Ministers in Scotland and Wales, and First and Deputy First Ministers of Northern Ireland. The letter calls on them to stand by their commitments to improving cancer survival and make sure that everyone can still receive cancer diagnosis, treatment and care throughout the COVID-19 crisis.

                          Here, we set out where cancer services are today and the lessons we’ve learned from the first wave of COVID-19 – lessons that must be remembered and acted on as cases of COVID-19 rise again.

                          Where are we now?
                          It’s been almost 8 months since the first UK-wide lockdown, and we have a much clearer understanding of the impact the pandemic has had on cancer care.

                          The impact was felt right across the cancer pathway, with over 3 million people across the UK not able to go for cancer screening and thousands fewer people referred for tests for suspected cancer compared to normal.

                          Over 30,000 fewer people started their treatment than the same time last year too, and most cancer clinical trials were disrupted.

                          Because of the hard work of our amazing NHS staff, cancer services are getting back up and running and the situation is improving. The numbers of people being urgently referred for suspected cancer are almost back to the levels seen at the same time last year. It’s a positive sign that initiatives like the ‘Help Us Help You’ campaign by the NHS in England are working to encourage patients to see their GP if they’ve noticed anything unusual.

                          But challenges still exist. For some cancer types, such as lung cancer or urological cancers, referral numbers are still well below where they were last year. While trials are getting back up and running, this is happening slower than we would like. And even with increasing activity, there’s still huge numbers of people waiting for screening, diagnosis and treatment.

                          So it’s vital that cancer services and clinical trials can continue to recover and not go backwards again as COVID-19 cases rise again.

                          Protecting cancer services and research in future waves
                          There are already worrying signs that the NHS is beginning to feel the strain of the second wave. Governments across the UK have made it clear that health services will remain open, so they must ensure in coming months that there’s no further delays to essential cancer diagnosis, treatment and clinical trials.

                          Making sure the lessons learned in the summer are acted on will be vital.

                          First, we must ensure people feel confident to see their GP if they notice symptoms. And if those symptoms might be linked to cancer, that they get diagnostic tests quickly and safely. Many people heeded the advice to stay home and protect the NHS in the first wave. But the health system is there for everyone, including people who suspect they have cancer. Public campaigns like ‘Help Us to Help You’, and similar efforts in the devolved nations, must continue.

                          Second, we know that some cancer patients are at higher risk of complications if they catch COVID-19. So it’s critical that hospitals can provide cancer care in safe environments, including ‘COVID-protected’ spaces. A recent study showed that cancer patients who have surgery in ‘COVID-protected’ safe spaces have better outcomes, emphasising how important it is to get this right. This model has been set up all over the country and must be maintained.

                          Third, COVID-19 is tricky, as some people can be asymptomatic or infectious before they have symptoms. So, creating ‘COVID-protected’ spaces rely on a range of things to ensure they really are safe from COVID-19. Regularly testing all patient-facing staff often and quickly – whether they have symptoms or not – is a vital part of this, but it’s not clear that this is happening routinely across health systems yet.

                          Healthcare staff sickness – including in primary care – is rising because of burnout, having to self-isolate or catching COVID-19, exacerbating staff shortages that existed long before the pandemic. Ramping up testing is vital.

                          Fourth, even with all of this, the number of patients with COVID-19 and other diseases may outstrip capacity in the NHS to provide safe care. The use of the independent sector has been a positive development to keep care running when this happens, so it’s important the NHS can continue to tap into this resource.

                          While this may all sound challenging, there have been some positive developments in this crisis. Innovative diagnostics and treatments are being fast-tracked into the system, and new ways of working embedded that could help services in the long run.

                          Time to act
                          The impact of COVID-19 on people affected by cancer has already been devastating, and we can’t let things get worse again.

                          Cancer services need support now. Lessons learned earlier this year need to be put in place to minimise any future impacts of COVID-19. And cancer services must get the investment they need to continue to improve cancer outcomes.

                          Now is the time for governments across the UK to act.: https://scienceblog.cancerresearchuk...-the-pandemic/

                          Keep your friends close and your enemies closer


                          • #28
                            New Therapeutic Target Identified for Breast Cancer Treatment

                            Lemur tyrosine kinase 3 (LMTK3) is associated with cell proliferation and endocrine resistance in breast cancer. Now, a team of researchers from the University of Sussex has completed a five-year study that provides evidence for a potential new target for breast cancer treatment. It suggests that LMTK3 inhibitors could be effectively used for the treatment of breast cancer, and potentially other types of cancer.

                            Their five-year study, “The structure-function relationship of oncogenic LMTK3,” is published in Science Advances, involved researchers from seven institutions across three countries including the U.K.’s Diamond Light Source.

                            LMTK3 is a protein that has been shown to be an oncogenic regulator over the past few years. However, the lack of crystal structure has limited the understanding of LMTK3’s role and its interactions with other molecules.

                            “By solving the crystal structure of LMTK3, we have demonstrated that it possesses all of the hallmarks of an active protein kinase. LMTK3 plays a pivotal role in controlling cellular processes, and we have previously shown that active LMTK3 makes some cancer treatments (e.g., chemotherapy and endocrine therapies) less effective,” explained Georgios Giamas, professor of cancer cell signaling at the University of Sussex, who led the study.

                            “We are now in the process of taking this research to the next stage by developing LMTK3 specific drugs. We hope that in the next five years we will be undertaking clinical trials, which is incredibly quick for this type of process.”

                            Using a high-throughput homogeneous time-resolved fluorescence screen coupled with biochemical, cellular, and biophysical assays, the researchers identified a potent LMTK3 small-molecule inhibitor, C28.

                            “Functional and mechanistic studies reveal LMTK3 is a heat shock protein 90 (HSP90) client protein, requiring HSP90 for folding and stability, while C28 promotes proteasome-mediated degradation of LMTK3,” noted the researchers. “Pharmacologic inhibition of LMTK3 decreases proliferation of cancer cell lines in the NCI-60 panel, with a concomitant increase in apoptosis in breast cancer cells, recapitulating effects of LMTK3 gene silencing. Furthermore, LMTK3 inhibition reduces growth of xenograft and transgenic breast cancer mouse models without displaying systemic toxicity at effective doses. Our data reinforce LMTK3 as a druggable target for cancer therapy.

                            “It is often difficult to obtain large well diffracting crystals and LMTK3 was no exception. Through close collaboration between the OPPF and I24 and exploiting the microfocused X-ray beam at I24 to collect wedges of data from multiple crystals we were able to obtain diffraction data key to the study,” added Robin Owen, principal beamline scientist of MX beamline I24 at Diamond.

                            Their findings open a door of understanding in breast cancer and may lead to further therapies in other cancers.:

                            Keep your friends close and your enemies closer


                            • #29
                              Novel Cell Signaling Disruptor Shows Promise as Blood Cancer Treatment

                              Researchers from the University of Alberta have identified a new mechanism of cell signal inhibition that could prove beneficial to the treatment of blood cancers such as B-cell lymphomas.

                              The investigational compound PCLX-001, a N-myristoyltransferase (NMT) inhibitor, targets enzymes that perform myristoylation, the modification of proteins with the fatty acid myristate which enables membrane targeting and cell signaling.

                              “The enzymes that transfer myristate onto proteins are overexpressed in some cancer cells, meaning there’s more of those enzymes, so they have long been thought of as a logical target for cancer treatment,” explained co-author Luc G. Berthiaume, PhD, in a press release.

                              Researchers performed robotic cancer cell line screens of the compound against 300 different cancer cell types, encompassing all major cancer types, and discovered a notable sensitivity of hematological cancer cell lines, including B-cell lymphomas.

                              Treatment with PCLX-001 was found to impact myristoylation of lymphoma cell proteins and inhibit early B-cell receptor (BCR) signaling events, which malignant cancer cells can utilize for development. In addition, the drug was also found to promote degradation of B-cell tumor cells in both test-tube and animal experiments and left non-cancerous cells intact.

                              Phase 1 trials of PCLX-001 in patients with lymphoma, leukemia, breast, and colon cancer are set to begin at the cancer centers across Canada by the end of the year, according to the researchers.

                              “We think PCLX-001 is a compound with a large therapeutic window that can kill the cancer cells at a much lower concentration than what is needed to kill normal cells,” added Dr. Berthiaume. “Because of the highly selective nature of our drug, it’s often referred to as a precision medicine, and we anticipate minimal side-effects.”:

                              Keep your friends close and your enemies closer


                              • #30
                                Novel targeted therapy blocks metabolic pathways in cancer cells with specific genetic defects

                                Researchers at The University of Texas MD Anderson Cancer Center have developed a novel targeted therapy, called POMHEX, which blocks critical metabolic pathways in cancer cells with specific genetic defects. Preclinical studies found the small-molecule enolase inhibitor to be effective in killing brain cancer cells that were missing ENO1, one of two genes encoding the enolase enzyme.

                                The study results, published today in Nature Metabolism, provide proof of principle for a treatment strategy known as collateral lethality, in which an important protein is lost through genetic deletion as a bystander near a tumor suppressor gene, and a redundant protein is blocked therapeutically.

                                Enolase is an essential enzyme involved in glycolysis, a metabolic pathway that is elevated in many cancers to fuel their increased cell growth. Two genes, ENO1 and ENO2, encode slightly different but redundant versions of enolase, and several cancers, such as glioblastoma, are missing the ENO1 gene because of chromosomal loss. This leaves the cancer cells with only ENO2 to continue glycolysis, making them highly sensitive to enolase inhibitors, Muller explained.

                                Therapies that target both forms of enolase have previously been developed, but blocking ENO1 can have unwanted side effects in normal cells. Targeting ENO2 specifically is attractive because it allows for the selective treatment of cancer cells missing ENO1.

                                The research team therefore worked to generate an enolase inhibitor, called HEX, that preferentially targets ENO2 over ENO1. To improve the drug's ability to enter cells, the team created the prodrug POMHEX, which is biologically inactive until it is metabolized into HEX within cells.

                                In cancer cell lines lacking ENO1, treatment with POMHEX blocked glycolysis, inhibited cell growth and stimulated cell death. Conversely, treatment of cells with normal ENO1 showed minimal effects.

                                Further, in animal models of ENO1-deficient tumors, both HEX and POMHEX treatment was well- tolerated and effectively blocked tumor growth relative to controls, with some instances of complete tumor eradication. Taking the work one step further, the team demonstrated that the therapeutically effective dose could be safely given in multiple models, suggesting favorable future translation to the clinical studies.

                                "We were encouraged by the promising preclinical activity of these novel enolase inhibitors and that the safety profile extends to higher models. While there could be further refinements, I am optimistic that even HEX would show significant clinical activity against ENO1-deleted cancers," Muller said.

                                ENO1 deletions also occur in liver cancer, bile duct cancer and large-cell neuroendocrine lung cancers, all of which share poor prognosis and limited treatment options, Muller explained. Thus, once an optimal therapy candidate has been developed, there is potential to evaluate the ENO2 inhibitor in treating patients with multiple cancer types.:

                                Keep your friends close and your enemies closer


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