brain cancer Archives - Amazing Health Advances

New Research Promises Advances to Brain Cancer Treatment

The AHA! Team — Tue, 03 Sep 2024 08:23:36 +0000

Zachy Hennessey via Israel21c – By starving tumors of glucose, researchers may have found an innovative way of selectively killing cancer cells while sparing healthy ones. A team of researchers at Ben-Gurion University has unveiled a novel approach to treating brain cancer by targeting the survival mechanisms of tumor cells under glucose starvation. Their findings, published May 14 in Nature Communications, suggest that accelerating the metabolic processes of tumor cells during glucose starvation could cause them to quickly exhaust their energy supplies and die. Research head Prof. Barak Rotblat, along with co-lead researcher Gabriel Leprivier of the Institute of Neuropathology at University Hospital Düsseldorf, discovered that tumors have less glucose compared to normal tissue. The top priority of cancer cells might be survival rather than growth This observation challenges the belief that cancer cells are primarily focused on rapid proliferation. Instead, the researchers propose that the top priority of cancer cells might be survival rather than growth. Triggering a burst of growth under glucose starvation could lead to the cells running out of energy. Cells regulate their growth based on energy availability, synthesizing fats and proteins when energy is plentiful and halting these processes when energy is scarce to avoid burning out. Tumors are often in a state of glucose starvation. By identifying and disabling the molecular mechanisms that enable their survival under these conditions, the researchers aim to selectively target cancer cells while sparing healthy ones. New research promises advances to brain cancer treatment “We may be able to target just the cancer cells and not regular cells at all, which would be a very promising step forward on the path to personalized medicine and therapeutics that do not affect healthy cells the way chemotherapy and radiation do,” Rotblat explained. The team focused on the mTOR (Mammalian Target of Rapamycin) pathway, which plays a key role in regulating cell growth based on energy levels. They identified a protein within this pathway, 4EBP1, as essential for cells to survive glucose starvation. 4EBP1 inhibits the enzyme ACC1 in the fatty acid synthesis pathway, a mechanism that cancer cells exploit to thrive in low-glucose environments. “Our discovery about glucose starvation and the role of antioxidants opens a therapeutic window to pursue a molecule which could treat glioma [brain cancer],” Rotblat noted. The potential application of this research could extend to other types of cancers. Rotblat’s team is now collaborating with BGN Technologies (BGU’s tech-transfer company) and the National Institute for Biotechnology in the Negev to develop a molecule that will block 4EBP1. This intervention would force glucose-starved tumor cells to continue synthesizing fats, depleting their energy reserves and leading to cell death. The research highlights a new direction in the pursuit of cancer treatments that target cancer cells specifically, offering a potential alternative to conventional treatments such as chemotherapy and radiation that affect healthy cells. To read the original article click here.

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The Cognitive Side Effects of Radiation Treatment

AHA Publisher — Fri, 01 Jul 2022 07:00:52 +0000

Benedette Cuffari, M.Sc. via News-Medical – Although radiation treatment is one of the primary methods to treat both brain tumors and brain metastases, it can be associated with several adverse effects that can be difficult to diagnose and manage. Introduction Many different types of cancer will often be treated with therapeutic ionizing irradiation. When used to treat benign and malignant conditions in the brain, cranial radiation therapy (CRT) is often used for both curative and palliative purposes. Regardless of where the radiation treatment is localized, nervous system injury can occur through several mechanisms. For example, irradiation treatment that damages blood vessels that supply the brain or endocrine organs with oxygen can cause secondary neurological effects. Similarly, CRT can directly damage normal neurological structures adjacent to the benign or malignant tissue of interest. Several factors can determine the damage caused by radiation treatment to the nervous system. These include the total radiation dose and dose per fraction delivered to the nervous system, the total volume of the nervous system that was irradiated, if any, the amount of time that has passed since the radiation was completed, and whether the patient has any comorbidities that might increase the intensity of radiation side effects, such as diabetes or hypertension. Acute and Early Delayed Damage Several different types of radiation can be used in the clinical setting, including photons, electrons, protons, and other particle-based radiation. Typically, CRT will be delivered in either X-rays or gamma rays, both photons, through external sources like teletherapy or directly into the tissue of interest through implanted or injectable radioisotopes. Primary neurologic damage that is caused by radiation can be classified according to the time between after the radiation treatment was administered and when the patient began to experience symptoms related to this damage. Acute neurologic damage after radiation, which typically arises within minutes to days after the radiation treatment, is often associated with a rise in intracranial pressure, likely due to acute vasogenic edema. These patients can experience a wide range of symptoms, including nausea, headache, vomiting, somnolence, fever, and worsening neurologic symptoms. However, acute encephalopathy due to radiation treatment will rarely cause cerebral herniation or death. Comparatively, early delayed neurologic damage after CRT, which typically takes several weeks to months for symptoms to develop, is often due to demyelination of surrounding structures. Some possible symptoms of this type of neurologic damage can include headache, lethargy, and worsening of lateralizing signs. Late Delayed Damage The third type of neurologic damage that can occur following CRT is referred to as late delayed damage, which may not cause symptoms to appear for several months or even years after the radiation treatment. Late delayed neurologic damage to the brain can include radiation necrosis (RN), stroke-like migraine attacks after radiation therapy (SMART syndrome), and cerebral atrophy. RN is estimated to occur between 5% and 25% of CRT patients; however, the true incidence of this condition has not been fully established. Several possible mechanisms have been proposed to be responsible for RN. These include disruption to the blood-brain barrier that increases brain permeability, or the CRT directly damages glial cells. Some common symptoms that patients with RN may experience include headaches, nausea, cognitive impairment, seizures, or focal deficits related to the location of their irradiated tumor. SMART syndrome is considered a rare complication of CRT that can occur between one and ten years after treatment. Some characteristic symptoms of SMART syndrome include migraine-like headaches associated with transient neurologic signs that may or may not be accompanied by seizures. Cerebral atrophy typically only arises after whole-brain irradiation, rather than more localized CRT treatments like gamma-knife. Although patients with cerebral atrophy may not report any symptoms at all, others may experience memory loss that can be severe in some cases. References Kaley, T. J., & Deangelis, L. M. (2021). Chapter 28 – Neurologic Complications of Chemotherapy and Radiation Therapy. In: Aminoff’s Neurology and General Medicine; 521-537. https://www.clinicalkey.com/#!/content/book/3-s2.0-B9780128193068000289. Tanguturi, S. K., & Alexander, B. M. (2018). Neurologic Complications of Radiation Therapy. Neurologic Clinics 36(3); 599-625. doi:10.1016/j.ncl.2018.04.012. Vellayappan, B., Tan, C. L., Yong, C., et al. (2018). Diagnosis and Management of Radiation Necrosis in Patients With Brain Metastases. Frontiers in Oncology 8(395). doi:10.3389/fonc.2018.00395. To read the original article click here.

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Do Cell Phones Affect Cognitive Function?

AHA Publisher — Mon, 21 Feb 2022 08:00:34 +0000

Michael Greger M.D. FACLM via Nutrition Facts – The World Health Organization concluded that cell phone radiation may cause brain tumors, but what about effects on cognitive function? “At present, we do not know precisely the degree to which the risk of cancer and other adverse health effects are increased by the exposure to the RF [radiofrequency] fields from cell phones, smart meters, and other wireless devices.” You may recall that I explored the brain tumor data in my video Does Cell Phone Radiation Cause Cancer?, but what other potential adverse health effects might there be? For example, how might radiofrequency fields affect brain function? That’s the topic of my video Do Mobile Phones Affect Brain Function?. “The dramatic increase in use of cellular telephones has generated concern about possible negative effects of radiofrequency signals delivered to the brain. However, whether acute cell phone exposure affects the human brain is unclear.” So, researchers decided to put it to the testusing PET scan technology. What did they find? As you can see at 0:44 in my video, elevated brain activity was found in the region of the brain closest to the antenna after 50 minutes of exposure to a cell phone call. What does that actually mean, though? Well, it’s evidence that the human brain has at least some sensitivity to the effects of cell phone radiation. The increased metabolism in brain regions closest to the antenna “suggest that brain absorption of [cell phone emissions] may enhance the excitability of brain tissue.” The potential health consequences of this are unknown, though the results suggest that “cell phone use can possibly affect brain function,” potentially affecting neurotransmitter and neurochemical brain activities. Perhaps this can explain the changes in psychological test outcomes observed after exposure to cell phone radiation. Although earlier studies failed to find an effect of short-term cell exposure on human cognitive performance, a 2017 review noted that “several studies indicate an increase in cortical excitability and/or efficiency with EMF exposure,” which may translate out into measurable cognitive effects. What’s more, this “cortical excitability”—excitability of the outer layer of the brain tied to cell phone exposure—“might also underpin disruptions in sleep” while at the same time being “associated with faster reaction time.” If you expose people to active cell phones while they play a computer game, the subjects can actually respond faster compared to sham exposure, meaning placebo exposure of the same scenario but with the cell phone turned off. This empowered the industry to claim that while it may be the case that cell phone radiation does affect brain function after all, the effects are positive! A decrease in reaction time upon exposure to microwave radiation from cell phones “helps people better respond to different threatening situations. Therefore these exposures can decrease the probability of human errors and reduce destructive accidents.” But, as you can see at 2:40 in my video, the difference in reaction time was only a few thousandths of a second. When all the studies are put together, “the effects seem to be so small that implications for human performance in everyday life can be practically ruled out.” As you can see at 2:57 in my video, there was a study that found that heavy cell phone users did better on a test of the ability to filter out irrelevant information, but this improvement in focused attention may just be because heavy cell phone users have a lot of practice carrying on conversations in crowded places, “rather than a direct effect of mobile phone use on cognition.” Overall, electromagnetic fields from cell phones “do not seem to induce cognitive or psychomotor [fine motor skill] effects.” Nonetheless, one has to worry about “the existence of sponsorship and publication biases.” Studies may have conflicts of interest, such as being funded by cellphone companies, and perhaps were designed in a way to skew the results or were quietly shelved and never published if they showed anything negative. In fact, researchers compared the source of funding and results of studies of the health effects of mobile cell phone use and “found that the studies funded exclusively by industry were indeed substantially less likely to report significant effects…that may be relevant to health.” It would look suspicious if all the industry studies showed no adverse effects, though, so some have accusedthe industry of taking obfuscation to a new level. “Although the industry-funded studies were significantly more likely to be negative”—that is, show no effects—“as expected, no two positive studies reported the same effect, and the few attempts to do so failed. Thus the apparent message of the studies dovetailed well with the [industry’s] position that there are no reproducible biological effects.” So, industry wasn’t only denying the existence of effects; it was also denying the existence of reproducible effects. It’s like this: If all of the industry-funded studies universally found no adverse effects of cell phone use, in contrast to the findings of independent research, the industry-funded research program could have been more easily dismissed. As well, industry researchers couldn’t publish adverse health effects because that would be bad for business. So, they came up with a wide hodge-podge of conflicting results. In this way, it seems they can better protect themselves. Was this all part of “a well-designed legal strategy” to fight off lawsuits? We may never know. We do know that when the World Health Organization announced that cell phones may cause brain tumors, the cellphone industry went into damage control to attack the agency, similar to when the WHO came out against second-hand tobacco smoke. “Sowing confusion and manufacturing doubt is a well-known strategy used by the tobacco and other industries.” Key Takeaways The World Health Organization (WHO) has found that radiation from cell phones may cause brain tumors. Researchers investigated the impact of radiofrequency signals from cellular devices on the brain and found, via PET scan technology, evidence of at least some sensitivity to the effects of cell phone radiation. Potential health consequences have not yet been determined, but results suggest cellphone usage may affect brain function and seems to increase “cortical excitability,” which may be linked to both sleep disruption and “faster reaction time,” though the difference may be only a few thousandths of a second. Research funded by the mobile phone industry was found to be substantially less likely to report significant health effects and “no two positive studies reported the same effect, and the few attempts to do so failed.” In this way, industry-funded studies had a broad range of conflicting results, which may have been calculated. To read the original article click here.

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Asthma May Reduce Risk of Brain Tumors — But How?

AHA Publisher — Mon, 13 Dec 2021 08:00:44 +0000

Washington University in St. Louis via Newswise – There’s not much good that can be said about asthma, a breathing disease in which the airways become narrowed and inflamed. But there’s this: People with asthma seem to be less likely to develop brain tumors than others. And now, researchers at Washington University School of Medicine in St. Louis believe they have discovered why. It comes down to the behavior of T cells, a type of immune cell. When a person — or a mouse — develops asthma, their T cells become activated. In a new mouse study, researchers discovered that asthma causes the T cells to behave in a way that induces lung inflammation but prevents the growth of brain tumors. What’s bad news for the airways may be good news for the brain. The findings, available online in Nature Communications, suggest that reprogramming T cells in brain tumor patients to act more like T cells in asthma patients could be a new approach to treating brain tumors. “Of course, we’re not going to start inducing asthma in anyone; asthma can be a lethal disease,” said senior author David H. Gutmann, MD, PhD, the Donald O. Schnuck Family Professor of Neurology. “But what if we could trick the T cells into thinking they’re asthma T cells when they enter the brain, so they no longer support brain tumor formation and growth? These findings open the door to new kinds of therapies targeting T cells and their interactions with cells in the brain.” The idea that people with inflammatory diseases, such as asthma or eczema, are less prone to developing brain tumors was first proposed more than 15 years ago, based on epidemiologic observations. But there was no obvious reason why the two very different kinds of diseases would be linked, and some scientists questioned whether the association was real. Gutmann is an expert on neurofibromatosis (NF), a set of complex genetic disorders that cause tumors to grow on nerves in the brain and throughout the body. Children with NF type 1 (NF1) can develop a kind of brain tumor known as an optic pathway glioma. These tumors grow within the optic nerves, which carries messages between the eyes and the brain. Gutmann, director of the Washington University NF Center, noted an inverse association between asthma and brain tumors among his patients more than five years ago but didn’t know what to make of it. It wasn’t until more recent studies from his lab began to reveal the crucial role that immune cells play in the development of optic pathway gliomas that he began to wonder whether immune cells could account for the association between asthma and brain tumors. Jit Chatterjee, PhD, a postdoctoral researcher and the paper’s first author, took on the challenge of investigating the association. Working with co-author Michael J. Holtzman, MD, the Selma and Herman Seldin Professor of Medicine and director of the Division of Pulmonary & Critical Care Medicine, Chatterjee studied mice genetically modified to carry a mutation in their NF1 genes and form optic pathway gliomas by 3 months of age. Chatterjee exposed groups of mice to irritants that induce asthma at age 4 weeks to 6 weeks, and treated a control group with saltwater for comparison. Then, he checked for optic pathway gliomas at 3 months and 6 months of age. The mice with asthma did not form these brain tumors. Further experiments revealed that inducing asthma in tumor-prone mice changes the behavior of their T cells. After the mice developed asthma, their T cells began secreting a protein called decorin that is well-known to asthma researchers. In the airways, decorin is a problem. It acts on the tissues that line the airways and exacerbates asthma symptoms. But in the brain, Chatterjee and Gutmann discovered, decorin is beneficial. There, the protein acts on immune cells known as microglia and blocks their activation by interfering with the NFkappaB activation pathway. Activated microglia promote the growth and development of brain tumors. Treatment with either decorin or caffeic acid phenethyl ester (CAPE), a compound that inhibits the NFkappaB activation pathway, protected mice with NF1 mutations from developing optic pathway gliomas. The findings suggest that blocking microglial activation may be a potentially useful therapeutic approach for brain tumors. “The most exciting part of this is that it shows that there is a normal communication between T cells in the body and the cells in the brain that support optic pathway glioma formation and growth,” said Gutmann, who is also a professor of genetics, of neurosurgery and of pediatrics. “The next step for us is to see whether this is also true for other kinds of brain tumors. We’re also investigating the role of eczema and early-childhood infections, because they both involve T cells. As we understand this communication between T cells and the cells that promote brain tumors better, we’ll start finding more opportunities to develop clever therapeutics to intervene in the process.” To read the original article click here.

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Targeted Drug Combination Shows Unprecedented Activity in Some Highly Aggressive Brain Tumors

AHA Publisher — Wed, 01 Dec 2021 08:00:09 +0000

Dana-Farber Cancer Institute via Newswise – A combination of two targeted cancer drugs showed unprecedented, “clinically meaningful” activity in patients with highly malignant brain tumors that carried a rare genetic mutation, according to a clinical trial report by investigators from Dana-Farber Cancer Institute. The drug combination, which blocked an overactive cell-growth signaling pathway, shrank tumors by 50% or more in one-third of 45 patients with hard-to-treat high-grade gliomas, including glioblastomas, the most aggressive brain tumor. The patients were selected for the trial because their tumors carried a genetic mutation known as v600E in the BRAF gene. This mutation is found in only two to three percent of patients with high-grade gliomas but is found in up to 60% of certain types of low-grade gliomas. The study included 13 patients with low-grade gliomas. Of those patients, nine had an objective response to treatment with the drug combination, for a response rate of 69%. “This is the first time that any targeted drug has been shown to work in glioblastoma in a clinical trial,” said Patrick Wen, MD, first author of the report in The Lancet Oncology and director of the Center for Neuro-Oncology at Dana-Farber. With all current chemotherapy treatments for glioblastomas, the response rate is no better than five per cent, he said, which contrasts with the 33 percent response rate achieved by the combination. The response rate was even higher – about 40 % – in patients younger than 40 years of age, according to Wen. The two drugs paired in the study were dabrafenib and trametinib. Both drugs target proteins in the MAPK pathway, a signaling chain of proteins that acts as a switch for cell growth and can become stuck in the “on” position, causing uncontrolled growth leading to tumors. Three patients had complete responses – their tumors no longer could be seen on imaging scan – and 12 had partial shrinkage of their tumors. The patients were not cured, but those who responded to the drugs experienced remarkably durable benefits – by one assessment, the median duration of response was 13.6 months, and by another assessment, it was 36.9 months. The findings are from an ongoing phase 2 study called ROAR (Rare Oncology Agnostic Research) that has been enrolling patients since 2014 in 27 community and academic cancer centers in 13 countries. The study is a so-called “basket” trial, which seeks to enroll patients who share a common tumor characteristic – in this case the BRAF v600E mutation – although they may have an array of different cancers. The ROAR study includes patients with thyroid and biliary tract cancers, gastrointestinal stromal tumors, hairy cell leukemia, multiple myeloma, low- and high-grade glioma brain tumors, and others. The study is designed to determine the overall response rate of dabrafenib combined with trametinib in patients with BRAF V600E-mutated cancers. The BRAF protein is a growth signaling protein kinase that plays a role in regulating the MAPK signaling pathway. BRAF V600E mutations drive cancer by activating the MAPK pathway, which is made up of many proteins, resulting in uncontrolled cell growth and the development of a tumor. The drugs used in this study, dabrafenib and trametinib, are oral drugs that block parts of the overactive MAPK signaling pathway. Dabrafenib inhibits an enzyme, B-Raf, and trametinib inhibits molecules called MEK1 and MEK2, which are part of the MAPK pathway. They have been used in combination to treat melanoma, non-small cell lung cancer, and thyroid cancer. Gliomas are cancer that originate in the glia – the supporting cells of the brain – not the brain neurons themselves. Gliomas comprise about 80 percent of all malignant brain tumors. Some are slow-growing low-grade gliomas, while others are aggressive high-grade gliomas including glioblastomas that are difficult to remove and almost always recur. No important advances in treating gliomas in recent years, the authors of the report said, but there have been isolated reports of the combination of dabrafenib and trametinib showing activity in gliomas. Their report from the ROAR study “is the first time that a combination of BRAF inhibitor (dabrafenib) and a MEK inhibitor (trametinib) have shown notable activity in these difficult-to-treat gliomas, including glioblastomas which have historically shown resistance to therapies.” Although the drugs only helped patients whose tumors carried the rare V600E mutation, Wen said the results were encouraging “because people were starting to think you will never have any targeted therapies for glioblastoma.” He added that there is emerging evidence that there may be other targets in gliomas that could be blocked by designer drugs. To read the original article click here.

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Research Breakthrough Could Mean Better Treatment for Patients with Most Deadly Form of Brain Tumor

AHA Publisher — Fri, 22 Oct 2021 07:00:36 +0000

Queen Mary University of London via Newswise – Scientists studying the most common and aggressive type of brain tumour in adults have discovered a new way of analysing diseased and healthy cells from the same patient. Crucially, the work which has been funded by the charity Brain Tumour Research could pave the way for truly personalised treatment for patients diagnosed with glioblastoma multiforme (GBM). Only 25% of patients with this type of brain tumour survive for more than one year and just 5% live for more than five years. A team at the Brain Tumour Research Centre of Excellence at Queen Mary University of London has established an entirely new experimental research pipeline which, in a trial involving ten patients, has revealed new insights into how GBM develops, identifying potential new targets for individualised treatments. It could also help predict a patient’s response to drugs currently in clinical use for other diseases which would be extremely valuable as the average survival time for this type of brain tumour is just 12 to 18 months. Their paper, Comparative epigenetic analysis of tumour initiating cells and syngeneic EPSC-derived neural stem cells (SYNGN) in glioblastoma, is published in the high impact journal Nature Communications today (Thursday 21 October). Professor Silvia Marino, who leads the team, said: “We have used this powerful technique to identify changes in the function of genes that occur in GBM that do not entail a change in the genetic code (epigenetics). This has revealed new insights for how GBM develops and identified potential new targets for individualised treatments.” By using a combination of laboratory work and sophisticated analytical computer programmes, the team at Queen Mary has identified significant molecular differences which could be exploited to develop new treatments. It is an innovative approach enabling the comparison of normal and malignant cells from the same patient helping to identify genes that play a role in growth of the tumour. The research is particularly significant as GBM is the most common malignant brain tumour in adults. Its aggressive nature means it spreads extensively into surrounding brain tissue making complete removal by surgery almost impossible. It is extremely resistant to radiotherapy and chemotherapy meaning it is very likely to recur following treatment. Hugh Adams, spokesman for Brain Tumour Research, said: “The complex nature of this particular tumour type means that the standard of care for these patients has not changed in a generation so this research brings much-needed hope for the future. One of the main challenges in developing effective treatments for GBM is that the tumour exhibits significant variation between patients and there can even be significant variation within a single patient’s tumour. These variations can arise from change to the cell’s genetic code – known as mutations – combined with changes to how specific genes are controlled. “There is strong evidence that GBM cells develop from neural stem cells but previous studies have not been able to compare tumour cells and their putative cell of origin from the same person. Prof Marino and her team have now harnessed state-of-the-art stem cell technologies and next-generation DNA sequencing methods to compare diseased and healthy cells from the same patient. Their results have shown how this approach can reveal novel molecular events that appear to go awry when GBM develops, thereby identifying targets for potentially new treatments.” The results of the team’s work have shown how this approach can reveal novel molecular targets for potentially new treatments. For example, the results reveal how some GBM tumours can control the movement of regulatory T cells, a type of immune cell and has also revealed epigenetic changes that could be used to predict the response to drugs currently in clinical use. Brain tumours kill more children and adults under the age of 40 than any other cancer yet historically just 1% of the national spend on cancer research has been allocated to this devastating disease. Brain Tumour Research funds sustainable research at dedicated centres in the UK. It also campaigns for the Government and the larger cancer charities to invest more in research into brain tumours in order to speed up new treatments for patients and, ultimately, to find a cure. The charity is calling for a national annual spend of £35 million in order to improve survival rates and patient outcomes in line with other cancers such as breast cancer and leukaemia and is also campaigning for greater repurposing of drugs. www.braintumourresearch.org To read the original article click here.

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Cure for Deadly Brain Cancer May Be on Its Way

AHA Publisher — Thu, 15 Apr 2021 07:00:16 +0000

Brian Blum via Israel21c – Glioblastoma is a particularly aggressive form of brain cancer, accounting for half of all primary brain cancers. It has a 40 percent survival rate after a year and just 5% after five years, even after surgery, radiation and chemotherapy. Researchers at Tel Aviv University have discovered a potential treatment, tested on mice and 3D lab models so far. If it works on humans, glioblastoma could become “chronic but manageable,” says Prof. Ronit Satchi-Fainaro, director of the university’s Cancer Biology Research Center and Cancer Research and Nanomedicine Laboratory. “It could even cure it completely.” What Satchi-Fainaro and her team discovered is that glioblastoma results in part from a failure in the brain’s immune system, which leads to the amplification of cancerous cell division. This immune system misstep is tied to the secretion of a protein called P-Selectin (SELP) which, when bound to the brain’s microglia immune cells, alters their function so that, rather than inhibiting the spread of cancer cells, they do the opposite. Since cells communicate with each other via proteins, the researchers investigated which proteins are secreted when the microglia encounter glioblastoma cells. They found that six proteins were overexpressed. Satchi-Fainaro next blocked each of the six proteins in turn, to see if one in particular was the main culprit in blocking the brain’s immune function. It was SELP that was disrupting the immune system and boosting the tumors. SELP normally helps cells – white blood cells in particular – travel inside the body. The problem is that “the encounter between glioblastoma cells and microglia cells causes them to express SELP in large quantities,” Satchi-Fainaro explains. That allows the cancer cells to travel and penetrate the brain tissue. The tumor “corrupts and reeducates” the microglia so that instead of defending the brain against cancer, it generates more SELP. But when SELP was inhibited, the tumor cells had a slower division rate, stopped migrating to the brain and were less invasive. The positive result (for the mice at least): the cancer’s progression in the brain was dramatically hindered. Dramatic Effects For the study, Satchi-Fainaro and her team modified hundreds of mice to give them glioblastoma. All the mice with tumors died within weeks. However, those given a chemical compound that blocks production of the SELP protein all recovered. The same effect was found on tumor cells taken from human patients and inserted into a 3D model of the human brain in a lab. ISRAEL21c profiled Satchi-Fainaro in our article on bio-convergence. where we looked at her work with 3D-printed tumors that allow cancer physicians to “try out” drugs on a perfect copy of the actual tumor. While addressing brain cancer was Satchi-Fainaro’s main goal in her glioblastoma study, another benefit has been discovered: Inhibiting SELP can ease the pain associated with sickle cell anemia. The next step is proving that inhibiting SELP is safe in humans. If so, Satchi-Fainaro hopes that approval of the treatment will be given quickly. “Glioblastoma patients need new treatments immediately,” she says. “Glioblastoma is the deadliest type of cancer in the central nervous system, accounting for most malignant brain tumors. It is aggressive, invasive, and fast-growing, making it resistant to existing treatments, with patients dying within a year of the cancer’s onset. Moreover, glioblastoma is defined as a ‘cold tumor’, which means that it does not respond to immunotherapeutic attempts to activate the immune system against it.” She adds: “Our treatment may be the needed breakthrough in the battle against the most daunting cancer of all. It is paving the way for a new therapy for a disease that hasn’t had anything new in terms of treatment over the last decade.” The study, published in the journal Nature Communications, was led by PhD student Eilam Yeini in collaboration with neurosurgeons from Tel Aviv Sourasky Medical Center, who supplied glioblastoma tissue samples removed during surgery. Neurosurgeons from Johns Hopkins University and the Lieber Institute in the United States supplied healthy brain tissue from autopsies. Satchi-Fainaro recently won the Youdim, Bruno, Humboldt and Kadar Family Awards for outstanding research in 2020. Her groundbreaking study was funded by the Israel Cancer Research Fund, the European Research Council, the Morris Kahn Foundation, the Israel Cancer Association and the Israel Science Foundation. To read the original article click here. For more articles from Israel21c click here.

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Scientist Uses Microbubbles to Explode Cancer Cells

AHA Publisher — Mon, 10 Aug 2020 07:00:58 +0000

Naama Barak via Israel21c – An international team of researchers led by an Israeli scientist has developed a noninvasive technology to kill breast cancer cells, an innovation that in the future could perhaps also be used to treat diseases such as brain cancer, Alzheimer’s and Parkinson’s. The groundbreaking technique, developed by Tel Aviv University’s Tali Ilovitsh during her post-doctorate period at Stanford University, uses low-frequency ultrasound to burst microscopic tumor-targeted bubbles. Her research was recently published in the journal Proceedings of the National Academy of Sciences. “Microbubbles are microscopic bubbles filled with gas, with a diameter as small as one-tenth of a blood vessel. At certain frequencies and pressures, soundwaves cause microbubbles to act like balloons: microbubbles expand and shrink periodically, and thus allow an increased transfer of substances from the blood vessel to the surrounding tissue,” Ilovitsh explained. “We discovered that using lower frequencies than those applied before causes microbubbles to expand drastically until they explode. We understood that this discovery can be used as a tumor-treatment platform and started injecting microbubbles into tumors directly.” Two-Pronged Approach The research team injected microbubbles into tumors in engineered mice. The microbubbles were tumor-targeted, meaning that they attached to the tumor cells’ membranes at the moment of explosion. “Around 80 percent of tumor cells were killed in the explosion, which is already positive,” Ilovitsh says. “The targeted treatment, which is safe and cheap, managed to destroy most of the tumor.” And yet, to prevent the cancer from spreading, the researchers needed to destroy every cancer cell. “That is why we injected an immunotherapeutic gene alongside the microbubbles, which acts as a Trojan horse and signals the immune system to attack the cell,” Ilovitsh said. This gene that alerts the immune system to attack normally cannot enter cancer cells. Introduced by the exploding microbubbles, it managed to enter the cells that were not killed by the explosion and signal to the body that they were cancerous. “The cancer cells were hit by the explosion, and through the holes that were created the gene we inserted into the microbubbles was transferred inside. Cancer cells that managed to heal and close themselves absorbed the gene that makes them produce a substance alerting the immune system to attack the cell,” Ilovitsh explained. “In fact, our model mice had tumors on both sides of the body. Despite the fact that we injected microbubbles only to the tumor on one side, the immune system attacked the other side as well,” she relates. Ilovitsh intends to use the technology that she developed as a noninvasive treatment for brain-damaging diseases such as Alzheimer’s, Parkinson’s and brain tumors. “The blood-brain barrier does not allow medications to pass through, but microbubbles can expand and enable a temporary opening of the barrier, thus letting the treatment reach its target without requiring an operation,” she said. To read the original article click here. For more articles from Israel21c click here.

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Seismic Imaging Technology Could Deliver Finely Detailed Images of the Human Brain

AHA Publisher — Fri, 13 Mar 2020 07:00:22 +0000

Imperial College London via EurekAlert – The Imperial College London and UCL researchers say their proof-of-concept study, published today in npj Digital Medicine, paves the way for the development of high-fidelity clinical imaging of the human brain that could be superior to existing technology. Unlike existing brain imaging methods like MRI, CT and PET scanning, the technology could be applied to imaging any patient, and could be suitable for the continuous monitoring of high-dependency patients. It could be delivered by a relatively small device, which would also potentially make it portable via ambulance and enable fast investigation in advance of arrival to hospital. The researchers are confident the technology will be safe as sound waves are already used for ultrasound scanning and this technology uses similar sound intensities. Ultrasound cannot easily penetrate through bone, whereas the new device, which is designed to be worn like a helmet, is able to overcome this barrier. The new approach is of special value in patients investigated for stroke – the second most common cause of death and most common cause of adult neurological disability – where rapid, universally applicable, high-fidelity imaging is essential. Lead author Dr Lluís Guasch, of Imperial’s Department of Earth Science and Engineering, said: “An imaging technique that has already revolutionised one field – seismic imaging – now has the potential to revolutionise another – brain imaging.” Professor Bryan Williams Director NIHR UCL Hospitals Biomedical Research Centre, which partly funded the research, said: “This is an extraordinary and novel development in brain imaging which has huge potential to provide accessible brain imaging in routine clinical practice to evaluate the brain in head trauma, stroke and a variety of brain diseases. “If this lives up to its promise it will be a major advance. It is also a fabulous illustration of how the collaboration between engineers and clinicians, using methods from another sphere of science, can bring ground-breaking innovation into medical care.” Transcending Disciplines Earth scientists use seismic data and a computational technique called full waveform inversion (FWI) to map the inside of the earth. Seismic data from earthquake detectors (seismometers) are plugged into FWI algorithms that extract 3D images of the Earth’s crust that can be used to predict earthquakes and search for reservoirs of oil and gas. Now Imperial researchers have adapted this approach to medical imaging, developing a method that uses sound waves with the ultimate aim of producing high-resolution images of the brain. They built a helmet lined with an array of acoustic transducers that each sends sound waves through the skull. The ultrasound energy that propagates through the head is recorded and fed via the helmet into a computer. FWI is then used to analyse the reverberations of the sound throughout the skull, constructing a 3D image of the interior. The researchers tested their helmet on a healthy volunteer and found that the quality of the recorded signals was sufficient for the algorithm to generate a detailed image, and they are confident the scattered energy from the brain will be interpretable. Using computer modelling, they also found they could obtain high-resolution images with sound frequencies low enough to penetrate the skull at safe intensities. They created detailed computer simulations based on the properties of different types of human brain tissue to establish that sound waves would be effective for composing high-resolution images of the brain. Dr Guasch said: “This is the first time FWI has been applied to the task of imaging inside a human skull. FWI is normally used in geophysics to map the structure of the Earth, but our collaborative, multidisciplinary team of earth scientists, bioengineers and neurologists are using it to create a safe, cheap and portable method of generating 3D ultrasound images of the human brain.” Potential Clinical Use Magnetic Resonance Imaging (MRI) is generally the best method for obtaining high-resolution images of the brain, and its use is currently essential to the investigation of many neurological disorders including stroke, brain cancer, and brain injury. Nonetheless, MRI requires large, complex, expensive, non-portable machines cooled to three degrees above absolute zero, and it cannot be used on patients for whom the presence of metallic implants or foreign bodies cannot be scrupulously ruled out. This makes emergency use in patients with potentially altered consciousness, such as those suspected of stroke, difficult or impossible. The researchers say that if it proves successful in human trials, their device will overcome these obstacles. Study co-author Professor Parashkev Nachev, of UCL, said: “This is a vivid illustration of the remarkable power of advanced computation in medicine. Combining algorithmic innovation with supercomputing could enable us to retrieve high-resolution images of the brain from safe, relatively simple, well-established physics: the transmission of soundwaves through human tissue. “The practicalities of MRI will always limit its applicability, especially in the acute setting, where timely intervention has the greatest impact. Neurology has been waiting for a new, universally applicable imaging modality for decades: full-waveform inversion could well be the answer.” Next, the researchers will build a new prototype for live imaging of normal human brains as the first step to a device that could be evaluated in clinical contexts. To read the original article click here.

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