cancer therapy Archives - Amazing Health Advances

Cancers Can Be Detected in the Bloodstream Three Years Prior to Diagnosis

The AHA! Team — Fri, 20 Jun 2025 05:20:22 +0000

Johns Hopkins Medicine via Newswise – The study, partly funded by the National Institutes of Health, was published May 22 in Cancer Discovery. Genetic material shed by tumors can be detected in the bloodstream three years prior to cancer diagnosis, according to a study led by investigators at the Ludwig Center at Johns Hopkins, Johns Hopkins Kimmel Cancer Center, the Johns Hopkins University School of Medicine and the Johns Hopkins Bloomberg School of Public Health. The study, partly funded by the National Institutes of Health, was published May 22 in Cancer Discovery. Investigators were surprised they could detect cancer-derived mutations in the blood so much earlier, says lead study author Yuxuan Wang, M.D., Ph.D., an assistant professor of oncology at the Johns Hopkins University School of Medicine. “Three years earlier provides time for intervention. The tumors are likely to be much less advanced and more likely to be curable.” To determine how early cancers could be detected prior to clinical signs or symptoms, Wang and colleagues assessed plasma samples that were collected for the Atherosclerosis Risk in Communities (ARIC) study, a large National Institutes of Health-funded study to investigate risk factors for heart attack, stroke, heart failure and other cardiovascular diseases. They used highly accurate and sensitive sequencing techniques to analyze blood samples from 26 participants in the ARIC study who were diagnosed with cancer within six months after sample collection, and 26 from similar participants who were not diagnosed with cancer. At the time of blood sample collection, eight of these 52 participants scored positively on a multicancer early detection (MCED) laboratory test. All eight were diagnosed within four months following blood collection. For six of the eight individuals, investigators also were able to assess additional blood samples collected 3.1–3.5 years prior to diagnosis, and in four of these cases, tumor-derived mutations could also be identified in samples taken at the earlier timepoint. MCED tests “This study shows the promise of MCED tests in detecting cancers very early, and sets the benchmark sensitivities required for their success,” says Bert Vogelstein, M.D., Clayton Professor of Oncology, co-director of the Ludwig Center at Johns Hopkins and a senior author on the study. Detecting cancers years before their clinical diagnosis “Detecting cancers years before their clinical diagnosis could help provide management with a more favorable outcome,” adds Nickolas Papadopoulos, Ph.D., professor of oncology, Ludwig Center investigator and senior author of the study. “Of course, we need to determine the appropriate clinical follow-up after a positive test for such cancers.” The study was supported in part by National Institutes of Health grant #s R21NS113016, RA37CA230400, U01CA230691, P30 CA 06973, DRP 80057309, and U01 CA164975. Additional funding was provided by the Virginia and D.K. Ludwig Fund for Cancer Research, the Commonwealth Fund, the Thomas M Hohman Memorial Cancer Research Fund, The Sol Goldman Sequencing Facility at Johns Hopkins, The Conrad R. Hilton Foundation, the Benjamin Baker Endowment, Swim Across America, Burroughs Wellcome Career Award for Medical Scientists, Conquer Cancer – Fred J. Ansfield, MD, Endowed Young Investigator Award, and The V Foundation for Cancer Research. The Atherosclerosis Risk in Communities study has been funded in whole or in part with federal funds from the National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, under contract numbers 75N92022D00001, 75N92022D00002, 75N92022D00003, 75N92022D00004, and 75N92022D00005. To read the original article click here.

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An Old Drug with New Tricks: Hydroxychloroquine

The AHA! Team — Tue, 04 Feb 2025 06:24:47 +0000

Medical University of South Carolina via EurekAlert! – The anti-malarial drug hydroxychloroquine shows promise against cancer, but cancer cells often develop resistance. A new study from MUSC Hollings Cancer Center researchers discovered how, setting the stage for new combination therapies As the hunt for effective cancer therapies intensifies, some scientists are turning back to look at old drugs in a new light. The anti-malarial hydroxychloroquine is one such drug that has been “repurposed” to fight cancer. Despite its effectiveness at blocking the resupply of needed resources to cancer cells, clinical trial results have been disappointing, in part because cancer cells eventually become resistant to the drug. A Medical University of South Carolina Hollings Cancer Center team led by Joe Delaney, Ph.D., reports in Cell Cycle that resistance to hydroxychloroquine occurs not by restoring the cancer cells’ recycling ability, as had been expected. Rather, resistance develops due to changes in the division, metabolism and export pathways of cancer cells. These findings open the door for new combination treatments, as drugs targeting these newly identified resistance mechanisms can be administered along with hydroxychloroquine to improve outcomes. The promise of repurposed drugs Repurposing old drugs for new treatments is not a new concept. Aspirin was originally used as a painkiller, but after the discovery of its anti-coagulant properties, it was repurposed as a blood thinner to treat heart disease. Thalidomide, the infamous anti-nausea medication, has been recently repurposed as a treatment for certain types of cancer and even leprosy. As cancer therapy moves increasingly toward specific single-protein targets, some scientists, like Delaney, are swinging back to look at preexisting drugs to find robust, multi-target effects. “Targeting single proteins can be extremely effective to treat cancer,” said Delaney. “However, the more specific the treatment becomes, the more likely resistance is to occur.” Imagine a hotel hallway, and behind each door is a route for cancer development. Targeting single proteins is like welding one of the doors shut. It’s impossible to get through that door, but it’s just a matter of time before cancer picks the lock on another door and gets in. That’s why these old drugs are so promising, said Delaney – their breadth of targets padlocks several doors at once, making it that much harder for a cancer cell to work around them. “These older molecules usually work because they have many, many targets within the cell,” he said. “If we can figure out how to use them correctly, it’s harder for cancer cells to mutate all those different points that they are acting on.” The cancer-fighting promise and limitations of hydroxychloroquine Originally used as a treatment for malaria, hydroxychloroquine began to be explored as a cancer therapy in the mid-2000s. The drug is known to block autophagy, a process that essentially acts as a cell’s clean-up crew. Autophagy literally means “self-eating.” It enables cancer cells to gather up old or damaged cellular machinery and send it off either to be thrown out or recycled. “When we think of cancer, we think of uncontrolled dividing cells,” said Delaney. “Autophagy is one of those processes that really enables a cancer cell to do just that by resupplying it with resources needed for survival and division.” Despite the drug’s promise of killing cancer cells by blocking cellular recycling, most clinical trials using the drug have been disappointing. “What we don’t know is why so many of these clinical trials have failed,” said Delaney. “We’re trying to figure out why hydroxychloroquine works or doesn’t work in certain situations in cancer.” A surprising finding about resistance to hydroxychloroquine To answer these questions, researchers in the Delaney Lab embarked on a multi-omics exploration into hydroxychloroquine’s effect on ovarian and colorectal cancer cells. They treated cells with hydroxychloroquine and then used two different whole-genome screens to identify exactly what the cells were doing to evade hydroxychloroquine attacks. With these approaches, they were able to observe how cells activated or deactivated different cellular pathways in response to continued hydroxychloroquine exposure. “By using two completely different methods, we were able to home in on the true biological players in the system,” said Delaney. The researchers were surprised to find that cells weren’t modifying autophagy to survive –the door that was expected to be opened really wasn’t touched at all. Instead, cancer cells were surviving hydroxychloroquine by changing their metabolism, division and export pathways. “We thought the main interaction of hydroxychloroquine with cancer was this process of autophagy, but it appears instead that processes unrelated to autophagy may be the most important for cancer cells to survive this therapy,” said Delaney. Setting the stage for novel combination therapies With this discovery, the Hollings team hopes to identify drugs that could be administered along with hydroxychloroquine to prevent the cancer cells from becoming resistant to this therapy. “Our study has identified the potential mechanisms that we will need to target with a second drug to prevent resistance against hydroxychloroquine,” said Delaney. Combining hydroxychloroquine with drugs that affect cell division, metabolism or export could increase the effectiveness of the treatment. Additionally, using hydroxychloroquine to treat patients with cancers that already have defects in one of these newly identified pathways could be a very powerful intervention. Finally, patients without these defects could be directed to potentially more effective, less resistant treatments. “We certainly want to understand which patients would see the most benefit to get the best result from these trials,” Delaney said. Ultimately, these results from the Delaney Lab shed light on how repurposed drugs like hydroxychloroquine can be used to fight cancer more effectively. Specifically, they show that cancer cells resist hydroxychloroquine in unexpected ways. By using such information, scientists can create more effective combination treatments against cancer. # # # About MUSC Hollings Cancer Center MUSC Hollings Cancer Center is South Carolina’s only National Cancer Institute-designated cancer center with the largest academic-based cancer research program in the state. With more than 150 faculty cancer scientists and 20 academic departments, it has an annual research funding portfolio of more than $50 million and sponsors more than 200 clinical trials across the state. Hollings offers state-of-the-art cancer screenings, diagnostic capabilities, therapies and surgical techniques within its multidisciplinary clinics to provide the full range of cancer care. Dedicated to preventing and reducing the cancer burden statewide, the Hollings Office of Community Outreach and Engagement works with community organizations to bring cancer education and prevention information to affected populations. For more information, visit hollingscancercenter.musc.edu Journal Cell Cycle DOI 10.1080/15384101.2024.2402191 To read the original article click here.

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New Antibiotic Approach Proves Promising Against Lyme Bacterium

The AHA! Team — Fri, 31 May 2024 05:32:44 +0000

Duke Health – A technique that has demonstrated success against cancer tumors could also be lethal to bacteria and other pathogens DURHAM, N.C. – Using a technique that has shown promise in targeting cancer tumors, a Duke Health team has found a way to deploy a molecular warhead that can annihilate the bacterium that causes Lyme disease. Tested in cell cultures using the Borrelia burgdoferi bacterium, the approach holds the potential to target not only bacteria, but also fungi such as yeast and viruses. The findings appear in the journal Cell Chemical Biology. Duke Health team has found a way to deploy a molecular warhead that can annihilate the bacterium that causes Lyme disease “This transport mechanism gets internalized in the bacterium and brings in a molecule that causes what we’ve described as a berserker reaction – a programmed death response,” said lead author Timothy Haystead, Ph.D., professor in Duke’s Department of Pharmacology and Cancer Biology. “It wipes out the bacteria — sterilizes the culture with a single dose of light. And then when you look at what occurs with electron microscopy, you see the collapse of the chromosome.” Haystead and colleagues used a molecular facilitator called high-temperature protein G (HtpG), which is involved in protecting cells that are undergoing heat stress. This family of proteins has been the focus of drug development programs for possible cancer therapies. Studies of this protein as an antimicrobial have also been encouraging, but the Duke team’s work appears to be the first to tether an HtpG inhibitor to a drug that enhances sensitivity to light. The researchers found that the HtpG inhibitor, armed with the photosensitive drug, was rapidly absorbed into the cells of the Lyme bacteria. When hit with light, the bacteria’s cells went into disarray and ultimately collapsed, killing them. “Our findings point to a new, alternate antibiotic development strategy, whereby one can exploit a potentially vast number of previously unexplored druggable areas within bacteria to deliver cellular toxins,” Haystead said. In addition to Haystead, study authors include Dave L. Carlson, Mark Kowalewski, Khaldon Bodoor, Adam D. Lietzan, Philip Hughes, David Gooden, David L. Loiselle, David Alcorta, Zoey Dingman, Elizabeth A. Mueller, Irnov Irnov, Shannon Modla, Tim Chaya, Jeffrey Caplan, Monica Embers, Jennifer C. Miller, Christine Jacobs-Wagner, Matthew R. Redinbo, and Neil Spector (deceased). The study received funding support from the Steven and Alexander Cohen foundation and Bay Area Lyme Foundation. To read the original article click here.

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Researchers Find Natural Mechanism to Sensitize Cancer to Immunotherapy

AHA Publisher — Mon, 07 Mar 2022 08:00:02 +0000

Michigan Medicine – University of Michigan via Newswise – Researchers at the University of Michigan Rogel Cancer Center found that a cytokine, a category of protein that acts as messengers in the body, and a fatty acid can work together to trigger a type of cell death previously defined by studies with synthetic molecules. The study, published in Cancer Cell, looked at cell cultures and in vivo mouse experiments to see how the release of a T-cell cytokine called interferon gamma combined with arachidonic acid, a fatty acid, leads to a type of cell death called ferroptosis via targeting the enzyme ACSL4. Ferroptosis has been found to occur in tumor cells and play a role in cancer immunity. Understanding how ferroptosis occurs could open pathways to make immunotherapy treatments more effective. “Targeting ACSL4 may help in understanding and expanding possible immunotherapy options,” said Weiping Zou, M.D., Ph.D., director the Center of Excellence for Cancer Immunology and Immunotherapy and lead researcher on this study. Zou explains that this natural mechanism begins when activated T-cells release interferon gamma, a signaling protein. “It’s well known that interferon gamma is involved in anti-tumor responses,” said Zou. “But in this study, we defined a new way that it works.” This study shows that combining interferon gamma with arachidonic acid, a fatty acid found in the tumor microenvironment, activates ACSL4, alters tumor cell lipid pattern, and naturally induces tumor cell ferroptosis. “ACSL4-dependent tumor ferroptosis is a mode of action of killer T cells,” said Zou. “Targeting ACSL4 sensitizes cancer to immunotherapy.” Zou’s lab was the first to identify a role for ferroptosis in cancer immunity and therapy, highlighting the possibility of targeting this pathway to improve the effectiveness of immunotherapy in people with cancer. While immunotherapy has dramatically changed outcomes in melanoma, lung cancer and other cancer types, the treatments work for only about 30% of people with cancer. These new findings add more knowledge to how ferroptosis works in patients with cancer, which Zou hopes will prompt further investigation. “This study raises a lot of questions for us to keep exploring, particularly around the basic biology of cell ferroptosis, including the involvement of different fatty acids and dietary lipids, the different roles immune cells play in ferroptosis, and how to target ACSL4 and ferroptosis pathways,” Zou said. “For now, there are many unknowns, but we’ll continue to work in this space.” To read the original article click here.

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UC Researchers Engineer New Probiotic to Target and Break Down Cancer Cell Defenses

AHA Publisher — Tue, 23 Nov 2021 08:00:36 +0000

University of Cincinnati via News-Medical – Bacteria generally have a bad reputation, as people first think of certain strains that can cause serious illnesses like pneumonia or meningitis. However, there are many helpful bacteria, known as probiotics, that assist the body in different ways. University of Cincinnati researchers have now engineered a probiotic designed to target and break down cancer cell defenses, giving therapies an easier way inside to kill tumors. The findings were recently published in the journal Advanced Healthcare Materials. Nalinikanth Kotagiri, PhD, the senior author of this study, an assistant professor in UC’s James L. Winkle College of Pharmacy and a UC Cancer Center member, studies “solid cancers” or those defined as abnormal cellular growths in “solid” organs such as the breast or prostate, as opposed to leukemia, a cancer affecting the blood. Kotagiri explains many solid cancers have an extracellular matrix made up of collagen and hyaluronic acid. The matrix forms a barrier around the cells and makes it harder for antibodies and immune cells to reach the tumors. Shindu Thomas, the first author of this study and a graduate student in the Kotagiri lab, worked with E. coli Nissle, a bacteria that has been used as a probiotic for around 100 years and is different from E. coli strains that cause sickness. Through new technology, any protein or enzyme can be manufactured on the E. coli Nissle bacteria. In this case, the bacteria was engineered to secrete an abundance of smaller structures called outer membrane vesicles on the outer edge of cells. The vesicles carry the same materials present on the bacteria itself, so researchers designed the bacteria to carry an enzyme that breaks down cancers’ extracellular matrix. Kotagiri said bacteria tend to thrive in low-oxygen and immunodeficient environments, two characteristics found in solid cancers. Because of this, the specially designed bacteria are naturally drawn to these cancers. “We took advantage of this unique feature of E.coli Nissle to home and localize into these tumors. And then once bacteria are lodged there, they start making nanoscale vesicles which carry the enzyme much deeper into the tumor matrix.” Nalinikanth Kotagiri, PhD, senior author of the study After creating the new probiotic, researchers studied the bacteria’s effect on animal models of breast and colon cancer. The bacteria is delivered intravenously about four or five days prior to the cancer treatment, allowing the bacteria time to populate and break down the cancer’s defenses and prepare it to take to the treatment. After administering the bacteria and then subsequent doses of either immunotherapy or another pharmaceutical, drugs used in targeted therapy, Kotagiri said mice survived twice as long compared to those given the cancer therapy alone. Imaging showed the bacteria and enzyme were effective at breaking down the extracellular matrix and allowing the therapy to reach the cancer cells. The study found the bacteria affected the tumors but was not attacking healthy cells in other organs like the heart, lungs, liver and brain. Kotagiri said this shows the bacteria can be safe and will not cause infection in other parts of the body, but more research needs to be done to examine its safety in large animal models and potentially humans, particularly in immunodeficient environments. “This always comes with a word of caution as to how you can utilize this strategy without causing any sepsis or any overt infections in the body,” he said. Kotagiri said his lab began to look more closely at how bacterial probiotics can address biomedical problems around 2018, as there are about one to two times as many bacterial cells than human cells in your body at any given time. “There’s bacteria in the gut, on the skin, inside your lungs, inside your mouth, even inside tumors,” Kotagiri said. “So why not take advantage of that and find interesting ways to make them a bit more proactive?” If the engineered bacteria continues to prove itself safe and effective, Kotagiri said there are a wide variety of ways to engineer the bacteria for different uses, including potentially using the bacteria to treat disease conditions in the gut, mouth and skin. There is also potential to engineer the bacteria armed with multiple proteins and molecules to make a monotherapy platform (or therapy that uses one type of treatment) rather than just facilitating combination therapy, he said. “So the bacteria can essentially serve as a mothership that would carry the necessary therapeutic payload to unique niches in the body and from there it’s a self-sustaining entity,” Kotagiri said. “While the possibilities are endless there are also significant challenges. We have to be good stewards of making that kind of evidence possible for the community to understand what are the limits and what can be done.” To read the original article click here.

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Radio-Wave Therapy Is Safe for Liver Cancer Patients and Shows Improvement in Overall Survival

AHA Publisher — Mon, 02 Aug 2021 07:00:42 +0000

Wake Forest Baptist Medical Center via EurekAlert – Researchers at Wake Forest School of Medicine have shown that a targeted therapy using non-thermal radio waves is safe to use in the treatment of hepatocellular carcinoma (HCC), the most common type of liver cancer. The therapy also showed a benefit in overall survival. The study findings appear online in 4Open, a journal published by EDP Sciences. “HCC accounts for nearly 90% of all liver cancers, and current survival rates are between six and 20 months,” said Boris Pasche, M.D., Ph.D., chair of cancer biology and director of Wake Forest Baptist’s Comprehensive Cancer Center. “Currently, there are limited treatment options for patients with this advanced liver cancer.” For the study researchers used a device called TheraBionic P1, invented by Pasche and Alexandre Barbault of TheraBionic GmbH in Ettlingen, Germany, that works by delivering cancer-specific, amplitude-modulated radiofrequency electromagnetic fields (AM RF EMF) programmed specifically for HCC. The frequencies used are specific to the patient’s type of cancer as identified through tumor biopsies or blood work, Pasche said. Pasche and Barbault discovered radio frequencies for 15 different types of cancer, as previously reported in a study published in 2009 in the Journal of Experimental & Clinical Cancer Research. TheraBionic P1 is a hand-held device that emits radio frequencies via a spoon-shaped antenna, which is placed on the patient’s tongue during treatment and is administered three times a day for one hour to deliver low levels of radiofrequency electromagnetic fields throughout the patient’s body. In previous studies, the device, which received breakthrough designation from the FDA in 2019, was shown to block the growth of liver cancer cells in the body without damaging healthy cells. For the current study, 18 patients with advanced HCC participated and received treatment with the device. Researchers also analyzed previously published data on 41 patients from a phase II study and historical controls from earlier clinical trials. “Our findings show an improvement in overall survival of more than 30% in patients with well-preserved liver function and also in those with more severe disease,” Pasche said. Researchers also tracked side effects, and no patients stopped TheraBionic P1 treatment because of adverse reactions. “We’re encouraged by these initial findings,” Pasche said. “Our study shows a benefit in overall survival, and the treatment isn’t associated with any significant side effects.” Support for this study was provided by TheraBionic Inc. and funds from Wake Forest Baptist’s Comprehensive Cancer Center. Pasche noted that the study does have several limitations because of the small sample size and “selection bias inherent in the use of historical control data.” However, two additional clinical trials are underway and are being led by William Blackstock, M.D., chair of radiation oncology at Wake Forest Baptist’s Comprehensive Cancer Center. One is a single-center study to assess the safety and effectiveness of the TheraBionic device in combination with Regorafenib, a chemotherapy drug, as a second-line treatment. Another multicenter, double-blind, randomized study comparing TheraBionic with placebo will assess the safety and effectiveness of the device as a third-line therapy in the treatment of advanced HCC. To read the original article click here.

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Novel Therapeutic Agent Could Be Effective for Treating Cancers With Certain Gene Mutations

AHA Publisher — Fri, 30 Jul 2021 07:00:55 +0000

Mount Sinai Health System via News-Medical – Mount Sinai researchers have developed a therapeutic agent that shows high effectiveness in vitro at disrupting a biological pathway that helps cancer survive, according to a paper published in Cancer Discovery, a journal of the American Association for Cancer Research, in July. The therapy is an engineered molecule, named MS21, that causes the degradation of AKT, an enzyme that is overly active in many cancers. This study laid out evidence that pharmacological degradation of AKT is a viable treatment for cancers with mutations in certain genes. AKT is a cancer gene that encodes an enzyme that is frequently abnormally activated in cancer cells to stimulate tumor growth. Degradation of AKT reverses these processes and inhibits tumor growth. “Our study lays a solid foundation for the clinical development of an AKT degrader for the treatment of human cancers with certain gene mutations,” said Ramon Parsons, MD, PhD, Director of The Tisch Cancer Institute and Ward-Coleman Chair in Cancer Research and Chair of Oncological Sciences at the Icahn School of Medicine at Mount Sinai. “Examination of 44,000 human cancers identified that 19 percent of tumors have at least one of these mutations, suggesting that a large population of cancer patients could benefit from therapy with an AKT degrader such as MS21.” MS21 was tested in human cancer-derived cell lines, which are models used in laboratories to study the efficacy of cancer therapies. Mount Sinai is looking to develop MS21 with an industry partner to open clinical trials for patients. Translating these findings into effective cancer therapies for patients is a high priority because the mutations and the resulting cancer-driving pathways that we lay out in this study are arguably the most commonly activated pathways in human cancer, but this effort has proven to be particularly challenging. We look forward to an opportunity to develop this molecule into a therapy that is ready to be studied in clinical trials.” Jian Jin, PhD, Mount Sinai Professor in Therapeutics Discovery and Director of the Mount Sinai Center for Therapeutics Discovery at Icahn Mount Sinai To read the original article click here.

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Hydrogels Offer New Hope for Cancer Treatment

AHA Publisher — Fri, 16 Apr 2021 07:00:10 +0000

Tokyo University of Science via News-Medical – Hydrogels are often used as drug delivery systems, but to be effective carriers for anti-cancer drugs, they need to be responsive to varied stimuli in the tumor microenvironment. Now, scientists from Japan have developed novel hydrogels to effectively deliver drugs to tumor sites in response to temperature and pH changes in the tumor microenvironment. These multi-stimuli-responsive hydrogels can eliminate remnant cancer cells following tumor excision through controlled drug release, offering hope for effective cancer treatment. Cancer therapy in recent times relies on the use of several drugs derived from biological sources including different bacteria and viruses, among others. However, these bio-based drugs get easily degraded and therefore inactivated on administration into the body. Thus, effective delivery to and release of these drugs at target tumor sites are of paramount importance from the perspective of cancer therapy. Recently, scientists have discovered unique three-dimensional, water-containing polymers, called hydrogels, as effective drug delivery systems (DDSs). Drugs loaded into these hydrogels remain relatively stable owing to the network-like structure and organic tissue-like consistency of these DDSs. Besides, drug release from hydrogels can be controlled by designing them to swell and shrink in response to certain stimuli, or minute changes in conditions, like temperature or pH (which determines the acidity of an environment). For instance, when conditions are just the right level of acidic in the tumor microenvironment, these DDSs either shrink or swell and release the drug. However, there has been no method for the one-pot synthesis of hydrogels that respond to more than one such stimulus and degrade to release drugs at target tumor sites. Until now. Now, a team of scientists, led by Professor Akihiko Kikuchi from Tokyo University of Science, reports the production of unique degradable hydrogels that respond to changes under multiple conditions in “reducing” environments mimicking the microenvironment of tumors. In order to prepare degradable hydrogels that can release drugs in response to changes in the tumor microenvironment, we prepared hydrogels that respond to temperature, pH, and reducing environment, and analyzed their properties.” (Akihiko Kikuchi, Professor, Tokyo University of Science) In their study published in the Journal of Controlled Release, Prof. Kikuchi–along with his colleagues from Tokyo University of Science, Dr. Syuuhei Komatsu, Ms. Moeno Tago, and Ms. Yu Ando, and his collaborator on the study, Prof. Taka-Aki Asoh from Osaka University–details the steps of designing these novel hydrogels from the synthetic polymer poly(ethylene glycol) diglycidyl ether and the sulfur-containing organic compound cystamine. In response to low temperatures, these hydrogels swell up while they shrink at the physiological temperature. Additionally, the hydrogels respond to pH changes by virtue of possessing tertiary amino groups. It must be noted here that the pH of the tumor microenvironment fluctuates between 5.5 and 6.5 owing to glycolysis in the tumor cells. Under the reducing conditions of this environment, the hydrogels degrade because of the breakage of disulfide bonds and change into low molecular-weight water-soluble oligomers that are easily excreted from the body. To further test their drug release properties, the scientists loaded these hydrogels with specific proteins by exploiting their temperature-dependent swelling-deswelling behavior and tested the controlled release of drugs under acidic or reducing conditions. It was found that the amount of drug loaded onto these hydrogels could be controlled by changing the mesh size of the hydrogel polymer network by changing temperature, suggesting the possibility of customizing these DDSs for specific drug delivery. Besides, the hydrogel network structure and electrostatic interactions in the network ensured that the proteins were preserved intact until delivery, unaffected by the swelling and shrinking of the hydrogels with pH changes in the surrounding environment. The scientists found that the loaded protein drugs were completely released only under reducing conditions. Using these hydrogels and the tractability that they provide, doctors may soon be able to design “customized” hydrogels that are specific to patients, giving personalized medicine a big boost. In addition to that, this new DDS provides a way to kill cancer cells that are left behind after surgery. “The implantation of this material in the affected area after cancer resection may eliminate residual cancer cells, making it a more powerful therapeutic tool”. (Akihiko Kikuchi) As cancer tightens its vise grip around the world, treatment options need to be varied and upgraded for customized and effective therapy. This unique and simple design technique to produce multi-stimuli-responsive hydrogels for effective drug delivery to target tumor sites may just be one among several such promising techniques to mount an answer to the challenge cancer poses to humanity. To read the original article click here.

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New Treatment Extends Lives of People With Most Common Type of Liver Cancer

AHA Publisher — Thu, 14 May 2020 07:00:43 +0000

University of California, Los Angeles (UCLA), Health Sciences via Newswise – For the first time in over a decade, scientists have identified a first-line treatment that significantly improves survival for people with hepatocellular carcinoma, the most common type of liver cancer. Researchers found that the combination of atezolizumab, an immunotherapy drug that boosts the body’s natural defenses, and bevacizumab, an anti-angiogenesis drug that inhibits the growth of tumors’ blood vessels, improved overall survival and reduced the risk of death by 42%. It also decreased the risk of the disease worsening by 41%, and the percentage of patients whose cancer shrank or disappeared more than doubled. Results from the clinical trial were published today in the New England Journal of Medicine, and the combination is currently being reviewed for approval under the U.S. Food and Drug Administration’s Real-Time Oncology Reviewpilot program. “The therapy is a real game-changer for people diagnosed with this aggressive disease,” said the study’s principal investigator and lead author, Dr. Richard S. Finn, a professor of medicine at the David Geffen School of Medicine at UCLA and director of the signal transduction and therapeutics program at the UCLA Jonsson Comprehensive Cancer Center. “We now have a new therapy that not only improves survival for people with the disease, which is very challenging to treat, but that helps them live longer while maintaining a high quality of life.” Currently, people diagnosed with advanced liver cancer have limited treatment options, and the prognosis for survival is poor. Clinical treatment advancements have been few and far between. Until now, no new first-line therapy has been shown to improve survival since the drug sorafenib was approved in 2007. Both atezolizumab and bevacizumab are monoclonal antibodies — specialized drugs that attach themselves to specific proteins and disable them — and they have already been used alone and in combination with other therapies to treat other cancers. Atezolizumab targets a protein produced by cancer cells that shuts down the immune system’s infection-fighting T cells, preventing them from attacking the cancer. Bevacizumab interferes with a tumor’s blood supply, preventing the cancer from growing and spreading through the body. “By using these two drugs with different mechanisms of action together, we have increased the number of patients who respond to this treatment and have increased the duration of these responses as compared to the standard treatment, sorafenib,” said Finn. The trial included 501 people, aged 18 and over, from multiple centers worldwide, who had advanced metastatic or unresectable hepatocellular carcinoma. Two-thirds of participants were randomly assigned to receive the atezolizumab and bevacizumab combination, while one-third received sorafenib. Twelve months after the start of treatment, the rate of survival with the combination was 67.2%, compared with 54.6% for the group on sorafenib. “Liver cancer is one of the few cancers that is growing in incidence and death rate,” Finn said. “That’s why it’s so important that we now have something in the front-line setting – after more than a decade – that markedly improves survival in this very challenging disease.” According to the American Cancer Society, liver cancer incidence rates have more than tripled, and death rates have more than doubled, since 1980. Some 800,000 people are diagnosed with this cancer each year, and it is a leading cause of cancer deaths worldwide, accounting for more than 700,000 deaths annually. UCLA Health has a comprehensive liver cancer program with a multidisciplinary team to bring the latest treatments to people with all stages of liver cancer. Tecentriq (atezolizumab) and Avastin (bevacizumab) are registered trademarks of Genentech, a member of the Roche Group. To read the original article click here.

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