Latest news with #Interleukin-6
Yahoo
25-03-2025
- Business
- Yahoo
MAIA Biotechnology Announces Poster Presentation at ESMO's European Lung Cancer Congress 2025
Poster highlights potential predictive biomarker for therapeutic response in advanced non-small cell lung cancer (NSCLC) CHICAGO, March 25, 2025--(BUSINESS WIRE)--MAIA Biotechnology, Inc., (NYSE American: MAIA) ("MAIA", the "Company"), a clinical-stage biopharmaceutical company developing targeted immunotherapies for cancer, today announced that an abstract detailing a potential predictive biomarker for THIO treatment was selected for poster presentation at the European Lung Cancer Congress 2025 (ELCC 2025) taking place, March 26-29, in Paris, France. ELCC is a program of the European Society for Medical Oncology (ESMO). "We are proud to join ELCC 2025, a premier conference focused directly on the science of thoracic oncology," said Vlad Vitoc, M.D., CEO of MAIA. "Our poster features our latest findings on cytokine Interleukin-6 (IL-6) as a potential predictive immune response biomarker for THIO sequenced with a checkpoint inhibitor. Predictive biomarkers can further illuminate THIO's unique mechanisms of action which have shown exceptional efficacy in our Phase 2 clinical trial." Presentation details: Title: Phase 2 Study of Telomere-Targeting Agent THIO Sequenced by Cemiplimab in Immune Checkpoint Inhibitor-Resistant Advanced NSCLC: Interleukin-6 as a Potential Predictive Biomarker Abstract number: 997 Date: March 28, 2025 Time: 12:00 p.m. CET Presenter: Tomasz Jankowski, M.D., Ph.D. – Lead investigator for THIO-101 Phase 2 clinical trial Poster access: MAIA's poster will be available at on March 28, 2025 The European Lung Cancer Congress is a collaborative effort of the most important multidisciplinary societies representing thoracic oncology specialists, working together to advance science, disseminate education and improve the practice of lung cancer specialists worldwide. About Ateganosine Ateganosine (THIO, 6-thio-dG or 6-thio-2'-deoxyguanosine) is a first-in-class investigational telomere-targeting agent currently in clinical development to evaluate its activity in Non-Small Cell Lung Cancer (NSCLC). Telomeres, along with the enzyme telomerase, play a fundamental role in the survival of cancer cells and their resistance to current therapies. The modified nucleotide 6-thio-2'-deoxyguanosine induces telomerase-dependent telomeric DNA modification, DNA damage responses, and selective cancer cell death. Ateganosine-damaged telomeric fragments accumulate in cytosolic micronuclei and activates both innate (cGAS/STING) and adaptive (T-cell) immune responses. The sequential treatment with ateganosine followed by PD-(L)1 inhibitors resulted in profound and persistent tumor regression in advanced, in vivo cancer models by induction of cancer type–specific immune memory. Ateganosine is presently developed as a second or later line of treatment for NSCLC for patients that have progressed beyond the standard-of-care regimen of existing checkpoint inhibitors. About MAIA Biotechnology, Inc. MAIA is a targeted therapy, immuno-oncology company focused on the development and commercialization of potential first-in-class drugs with novel mechanisms of action that are intended to meaningfully improve and extend the lives of people with cancer. Our lead program is ateganosine, a potential first-in-class cancer telomere targeting agent in clinical development for the treatment of NSCLC patients with telomerase-positive cancer cells. For more information, please visit Forward Looking Statements MAIA cautions that all statements, other than statements of historical facts contained in this press release, are forward-looking statements. Forward-looking statements are subject to known and unknown risks, uncertainties, and other factors that may cause our or our industry's actual results, levels or activity, performance or achievements to be materially different from those anticipated by such statements. The use of words such as "may," "might," "will," "should," "could," "expect," "plan," "anticipate," "believe," "estimate," "project," "intend," "future," "potential," or "continue," and other similar expressions are intended to identify forward looking statements. However, the absence of these words does not mean that statements are not forward-looking. For example, all statements we make regarding (i) the initiation, timing, cost, progress and results of our preclinical and clinical studies and our research and development programs, (ii) our ability to advance product candidates into, and successfully complete, clinical studies, (iii) the timing or likelihood of regulatory filings and approvals, (iv) our ability to develop, manufacture and commercialize our product candidates and to improve the manufacturing process, (v) the rate and degree of market acceptance of our product candidates, (vi) the size and growth potential of the markets for our product candidates and our ability to serve those markets, and (vii) our expectations regarding our ability to obtain and maintain intellectual property protection for our product candidates, are forward looking. All forward-looking statements are based on current estimates, assumptions and expectations by our management that, although we believe to be reasonable, are inherently uncertain. Any forward-looking statement expressing an expectation or belief as to future events is expressed in good faith and believed to be reasonable at the time such forward-looking statement is made. However, these statements are not guarantees of future events and are subject to risks and uncertainties and other factors beyond our control that may cause actual results to differ materially from those expressed in any forward-looking statement. Any forward-looking statement speaks only as of the date on which it was made. We undertake no obligation to publicly update or revise any forward-looking statement, whether as a result of new information, future events or otherwise, except as required by law. In this release, unless the context requires otherwise, "MAIA," "Company," "we," "our," and "us" refers to MAIA Biotechnology, Inc. and its subsidiaries. View source version on Contacts Investor Relations Contact +1 (872) 270-3518ir@ Sign in to access your portfolio
Associated Press
17-03-2025
- Health
- Associated Press
Astronauts' Health During Space Missions: Nichi BRITE and Neu REFIX Beta Glucans Could Benefit by Neutrophil-to-Lymphocyte Ratio, IL-6 Control, the Immune Biomarkers of Aging and Longevity
Neutrophil to Lymphocyte ratio (NLR) is a critical biomarker of health of astronauts during space mission, and that of aging related illnesses, inflammaging, longevity and cancer prognosis. Oral consumption of AFO-202 strain of Aureobasidium pullulans produced Nichi BRITE and N-163 strain produced Neu REFIX together in pre-clinical and clinical studies having safely and beneficially modified NLR, are considered holding potential to help maintain astronauts health during space flight and also to bridge the gap between health span and life span by ' Me-Byo' phenomenon as published in Frontiers in Immunology while Neu REFIX standalone yielding enhanced dystrophin, an additional benefit that might help prevent muscle loss during space missions. This press release features multimedia. View the full release here: Astronauts during space missions, deep-sea researchers, high-altitude climbers, and workers exposed to radiation hazards, are highly prone to hastened process of aging and inflammaging, reflected by increase in NLR, Interleukin-6, gut dysbiosis and immune dysfunction. Going by earlier pre-clinical & clinical studies where oral consumption of Nichi BRITE and Neu REFIX beta-glucans have shown to safely and beneficially modify those biomarkers including reduction of D-Dimer and Ferritin, besides Neu REFIX standalone reducing skeletal muscle fibrosis are considered holding potentials for benefitting those undertaking expeditions in hostile conditions. Upon validation, they could be included in the guidelines as an ingredient especially for space foods. These exo-polysaccharide beta glucans produced by unique strains of Aureobasidium Pullulans are food supplements and not a drug or remedy for any illness. Research outcomes are not to be construed as medical advice. Astronauts during space travel are exposed to ionizing radiation, circadian rhythm disruption and microgravity leading to stress, inflammation and immune dysfunction which reflects as an increase in NLR. There has been no safe intervention using a food supplement reported yet beneficially modifying NLR, according to the authors. They added that Nichi BRITE reporting immune enhancement and anti-cancer effects, Neu REFIX for its immune modulation and anti-fibrotic effects apart from enhanced gravisensing dystrophin in pre-clinical and clinical studies; when consumed together efficiently enhances butyrate, an indicator of health and longevity through beneficial gut microbiome modulation are worth further research in simulated microgravity and for vulnerable populations, specially immunocompromised and in auto-immune diseases. These potentials may bridge the gap between health span and lifespan. Neu REFIX has been granted ODD and RPD by US FDA for treatment of Duchenne Muscular Dystrophy (DMD). Hastening process of aging & inflammaging during space flight and muscle mass reduction similar to old age reflected by NLR and dystrophin levels, being beneficially modified by these unique exo-polysaccharide beta glucans manufactured in Japan as food supplements open a new area of research which could help space travel and also aging & longevity related health indices. Research could also be of help in the health and resilience of individuals working in harsh environmental conditions such as deep-sea researchers, high-altitude climbers, polar expeditions and workers prone to radiation hazards. *B-1,3-1,6 glucan is a listed food additive in MHLW, Japan; Not a drug or remedy to any illness. Research findings should not be construed as medical advice. Not GRAS, EFSA certified. SOURCE: GN Corporation Co Ltd Copyright Business Wire 2025. PUB: 03/17/2025 05:22 AM/DISC: 03/17/2025 05:21 AM
See - Sada Elbalad
07-03-2025
- Health
- See - Sada Elbalad
Poor Sleep Weakens Immunity
Dr. Magdy Badran Poor sleep weakens immunity and raises inflammation. Poor sleep quality may rapidly trigger immune system changes, potentially contributing to long-term inflammatory diseases like obesity, diabetes, and cardiovascular disease. Even a single night of sleep deprivation can alter immune cell profiles to resemble those seen in obesity, a condition linked to chronic inflammation. Increased Pro-Inflammatory Cytokines Poor sleep significantly alters immune function by increasing the production of pro-inflammatory cytokines, which are signaling molecules that regulate immune responses and inflammation. When sleep is inadequate—either due to short duration, fragmented sleep, or irregular sleep patterns, the immune system shifts toward a pro-inflammatory state, leading to widespread physiological consequences. Interleukin-6 (IL-6) plays a crucial role in regulating immune responses and inflammation. Sleep deprivation has been shown to increase IL-6 levels, promoting chronic low-grade inflammation, which is linked to cardiovascular disease, diabetes, and depression. C-Reactive Protein (CRP) is a biomarker of systemic inflammation, and its levels rise with sleep deprivation. High CRP levels have been linked to an increased risk of cardiovascular disease, stroke, and metabolic disorders. Interleukin-1β (IL-1β) is involved in sleep regulation but becomes excessively activated during sleep disturbances, leading to an increase in neuroinflammation, which has been associated with neurodegenerative conditions like Alzheimer's disease. While inflammation is necessary for fighting infections, chronic low-grade inflammation suppresses immune defenses, making individuals more susceptible to infections. Tumor Necrosis Factor-alpha Tumor Necrosis Factor-alpha (TNF-α) is a pro-inflammatory cytokine that plays a crucial role in immune system activation, inflammation, and cellular signaling. Poor sleep—whether due to sleep deprivation, fragmented sleep, or irregular sleep patterns—has been strongly linked to elevated TNF-α levels, contributing to a wide range of inflammatory and metabolic disorders. TNF-α follows a circadian rhythm, meaning its levels fluctuate naturally throughout the day and night. Sleep disturbances, such as insufficient sleep or shift work, disrupt this cycle, leading to persistently high TNF-α levels, which promote systemic inflammation. Sleep deprivation triggers oxidative stress and immune system overactivation, leading to excessive TNF-α release. This can result in chronic low-grade inflammation, which is associated with numerous diseases. Sleep is essential for immune regulation and recovery. During deep sleep, anti-inflammatory processes help balance immune function. However, poor sleep prevents this regulation, allowing TNF-α to remain elevated for extended periods. Reduced Anti-Inflammatory Response Sleep plays a critical role in regulating inflammation, helping the body recover, repair tissues, and maintain a balanced immune response. Sleep enhances the production of anti-inflammatory cytokines, which help counteract inflammation. Sleep deprivation reduces these protective molecules, allowing unchecked inflammation to damage tissues and organs. Chronic sleep deprivation disrupts the hypothalamic-pituitary-adrenal (HPA) axis, causing prolonged elevations in cortisol, the stress hormone. While cortisol initially suppresses inflammation, persistent high levels lead to immune system exhaustion, making the body unable to regulate inflammatory responses effectively. Melatonin, a sleep hormone, has anti-inflammatory and antioxidant properties. Sleep disruption lowers melatonin levels, increases oxidative stress and systemic inflammation. The gut microbiome plays a major role in immune regulation and inflammation control. Poor sleep disrupts gut bacteria, leading to increased gut permeability ("leaky gut"), which triggers inflammation and increases the risk of autoimmune and metabolic diseases. Impaired Immune Surveillance Immune surveillance is the body's ability to detect and eliminate harmful pathogens, abnormal cells, and potential threats, including cancerous cells. Quality sleep is essential for maintaining a strong immune defense, as it regulates the production, function, and coordination of immune cells. However, poor sleep disrupts this critical process, increasing vulnerability to infections, autoimmune diseases, and even cancer. Reduced Natural Killer (NK) cells are specialized immune cells that identify and destroy virus-infected cells and cancer cells. Sleep deprivation reduces NK cell function by up to 72%, allowing harmful cells to survive and multiply. This increases the risk of viral infections (e.g., flu, COVID-19) and cancer progression. T cells play a key role in recognizing and eliminating pathogens and infected cells. Poor sleep reduces the adhesion ability of T cells, making them less effective in targeting infections. This leads to longer recovery times from illnesses and higher susceptibility to diseases. Antibodies are produced after exposure to pathogens or vaccinations, helping the body develop long-term immunity. Sleep deprivation significantly reduces vaccine effectiveness, lowering the body's ability to produce protective antibodies. Studies show that people who sleep less than 6 hours per night have weaker immune responses to vaccines, including flu and hepatitis vaccines. Persistent inflammation disrupts immune signaling, impairing the body's ability to detect and neutralize threats efficiently. During deep sleep, the glymphatic system flushes out toxins and waste products from the brain, including beta-amyloid, which is linked to Alzheimer's disease. Poor sleep reduces glymphatic clearance, leading to toxin buildup, neuroinflammation, and increased risk of neurodegenerative diseases. Regulatory T cells Regulatory T cells (Tregs) are essential for maintaining immune balance, preventing excessive inflammation, and protecting against autoimmune diseases. These cells suppress overactive immune responses, ensuring that the immune system does not mistakenly attack the body's own tissues. Poor sleep disrupts Treg activity, leading to immune dysregulation, which increases the risk of chronic inflammation and autoimmune disorders such as rheumatoid arthritis, lupus, multiple sclerosis, and inflammatory bowel disease (IBD). Additionally, reduced Treg function can exacerbate allergic reactions and asthma by allowing excessive inflammatory responses. Restoring healthy sleep patterns is crucial for maintaining Treg function, reducing inflammation, and lowering the risk of immune-related diseases. Disrupted REM Sleep and Circadian Rhythms REM sleep plays a vital role in immune regulation, enhancing T cell function, natural killer cell activity, and antibody production, which strengthen the body's defense against infections and diseases. It helps balance pro-inflammatory and anti-inflammatory cytokines, preventing excessive inflammation. Disrupted circadian rhythms due to inadequate REM sleep weaken immune surveillance, making the body more vulnerable to infections, inflammation, and chronic diseases. The circadian clock regulates T cells, natural killer cells, and cytokine production, ensuring a timely and efficient immune response. When REM sleep is insufficient, this balance is disrupted, leading to reduced T cell activation, lower NK cell activity, and increased pro-inflammatory cytokines like TNF-α and IL-6. Over time, this immune dysfunction raises the risk of autoimmune diseases, cancer, and metabolic disorders. Inflammatory Diseases Linked to Poor Sleep Chronic inflammation from poor sleep contributes to the development of atherosclerosis, hypertension, and heart disease. Conditions such as rheumatoid arthritis, lupus, and multiple sclerosis are exacerbated by sleep deprivation, as the immune system becomes hyperactive and attacks healthy tissues. Poor sleep increases insulin resistance and promotes weight gain, contributing to type 2 diabetes and obesity-related inflammation. Sleep disruption has been linked to neurodegenerative diseases such as Alzheimer's and Parkinson's. Individuals with poor sleep are 3-4 times more likely to develop colds, flu, and respiratory infections. Sleep deprivation weakens mucosal immunity, increasing the risk of sinusitis, pneumonia, and bronchitis. The World Health Organization (WHO) classifies shift work (which disrupts sleep patterns) as a probable carcinogen due to its effects on immune suppression. Poor sleep is linked to higher risks of breast, prostate, and colorectal cancer, as immune cells fail to eliminate abnormal cells efficiently. Tips to Support Immunity Through Better Sleep Prioritize 7-9 hours of quality sleep – Deep sleep optimizes immune cell function and recovery. Avoid late-night screen exposure – reduce blue light before bed to support melatonin production, which strengthens immunity. Ensure a dark, cool sleep environment – darkness boosts melatonin, while a cooler temperature promotes deeper sleep. Eat a nutrient-rich diet – consume foods rich in zinc, vitamin C, and probiotics to enhance immune resilience. Engage in moderate exercise – regular movement boosts NK cell activity, but excessive exercise before bed can disrupt sleep. Manage stress and cortisol levels –practices like meditation and deep breathing can help.
