Aging and cancer最新文献

{"title":"The Long Term Effects of a 12-Session Community Exercise Program on Health Measures in Cancer Patients","authors":"Isaac Oppong,&nbsp;Roozbeh Naemi","doi":"10.1002/aac2.70003","DOIUrl":"https://doi.org/10.1002/aac2.70003","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Purpose</h3>\u0000 \u0000 <p>To assess the long-term effects of a community cancer exercise program on quality of life, fatigue, weight, waist circumference, physical activity levels, lower extremity strength, body mass index (BMI), heart rate, and blood pressure, across non-metastatic and metastatic patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A total of 918 participants (F/M: 1.77; mean age = 61 years, SD = 13.233) diagnosed with cancer within the last five years completed a 12-session guided physical activity program. Sessions included functional, aerobic, and resistance training aligned with ACSM guidelines for cancer patients. Blood pressure, quality of life, fatigue, BMI, lower extremity strength, body weight, and physical activity levels were measured at baseline, 12 sessions, and at 6 months, and 12 months during follow-up. The Wilcoxon signed-rank test was used to assess changes over time.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Significant improvements were observed in physical activity levels, health-related quality of life, and overall quality of life, sustained at 6- and 12-month follow-ups. Waist circumference, fatigue, and blood pressure significantly decreased across all time points. Lower extremity strength improved up to 6 months but was not significant at 12 months. No significant changes were observed in body weight or BMI. Non-metastatic patients experienced significant improvements in blood pressure, waist circumference, fatigue, and functional ability, while metastatic patients maintained their baseline health measures, suggesting a stabilizing effect.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This study demonstrates that a community-based exercise program benefits non-metastatic cancer patients by improving quality of life, physical activity levels, and functional health, while helping metastatic patients maintain health outcomes. These findings highlight the importance of structured exercise programs in cancer care and support their implementation in real-world settings.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72128,"journal":{"name":"Aging and cancer","volume":"6 2","pages":"54-68"},"PeriodicalIF":0.0,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aac2.70003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144315266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aging-Driven Blood–Brain Barrier Dysfunction and Its Impact on CNS Cancer Susceptibility: A Comprehensive Narrative Review","authors":"Quang La,&nbsp;Aiman Baloch,&nbsp;David F. Lo","doi":"10.1002/aac2.70002","DOIUrl":"https://doi.org/10.1002/aac2.70002","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Aging significantly affects the structural and functional integrity of the blood–brain barrier (BBB), increasing the susceptibility of the central nervous system (CNS) to both primary and metastatic cancers. As the BBB deteriorates, it promotes tumor cell infiltration, alters drug permeability, and contributes to a proinflammatory microenvironment that supports tumor progression. These age-related changes present major obstacles in the effective treatment of CNS malignancies in elderly patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This review synthesizes current literature on the mechanisms of BBB aging and its impact on CNS cancer development and treatment. It examines key structural alterations, such as tight junction protein loss, endothelial dysfunction, and pericyte reduction, as well as functional changes including impaired immune regulation and transporter dysfunction. The review also evaluates therapeutic challenges and emerging strategies to overcome the BBB barrier in the aging brain.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Aging induces BBB dysfunction by weakening cellular junctions, disrupting the neurovascular unit, and promoting chronic neuroinflammation. These alterations facilitate tumor cell entry and survival in the brain and reduce the effectiveness of cancer therapies due to impaired drug delivery. Promising interventions, including nanoparticle-based therapies, focused ultrasound techniques, and targeted chemoimmunotherapy, are under development to enhance therapeutic outcomes in elderly patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The age-related breakdown of the BBB contributes significantly to increased cancer risk and therapeutic resistance in the CNS. Addressing BBB dysfunction through age-specific interventions and advanced drug delivery strategies is critical to improving outcomes for older adults with CNS malignancies. Further research into the molecular pathways of BBB aging will support the development of personalized and effective treatments.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72128,"journal":{"name":"Aging and cancer","volume":"6 2","pages":"46-53"},"PeriodicalIF":0.0,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aac2.70002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144315396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding and Overcoming Immunotherapy Resistance in Skin Cancer: Mechanisms and Strategies","authors":"Shreya Singh Beniwal,&nbsp;Abhimanyu Chiraparambil Radhakrishnan,&nbsp;Ayanchetty Haripraba,&nbsp;Saif Syed,&nbsp;Gajawada Pragna,&nbsp;Ayush Dwivedi,&nbsp;Akash Rawat,&nbsp;Daniela Castro Calderón,&nbsp;Martin Cevallos-Cueva","doi":"10.1002/aac2.70000","DOIUrl":"https://doi.org/10.1002/aac2.70000","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Background&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Immunotherapy that includes immune checkpoint inhibitors (ICI) is a revolutionary arm of the treatment of skin cancers like melanoma, basal cell carcinoma, and squamous cell carcinoma. Despite this leap in clinical advances, a critically challenging area in this field is emerging resistance to immunotherapy that limits its efficaciousness in a profound segment of the population. This resistance can be classified as primary resistance, in which cancers fail to respond to initial regimen, or acquired resistance that develops after there is a favorable initial response. A comprehensive understanding of the basic mechanisms and figuring out novel strategies to combat resistance are necessary to improve patient outcomes.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Methods&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;A comprehensive review of recent studies was conducted with focus on preclinical and clinical evidence related to immunotherapy resistance in skin cancer with a wide literature search on databases such as PubMed, Cochrane, and Google Scholar with keywords, including “skin cancer,” “immunotherapy,” “malignant melanoma,” “drug resistance,” “mechanisms,” and “strategies” published in the last 15 years.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Results&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;This study aims to establish a review of the molecular and cellular mechanisms that contribute to development of drug resistance in skin cancer and to gauge emerging strategies to overcome these barriers. Insights into these mechanisms were classified into tumor-intrinsic factors, like genetic and epigenetic changes, and tumor-extrinsic factors, such as changes in tumor microenvironment (TME) and systemic immunosuppression. Therapeutic strategies that included combination therapies, newer checkpoint inhibitors, and modulation of the TME were evaluated. Key mechanisms leading to drug resistance identified include tumor-intrinsic factors, including mutations in signaling pathways, tumor-extrinsic factors, including immunosuppressive cells and changes in the TME, such as hypoxia that contributed to drug resistance. Upcoming strategies to counteract resistance included combination approaches, adoptive T-cell therapy, and newer immunomodulatory agents that target resistance pathways.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Conclusions&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;There is a complex interplay of cancer and immune microenvironmental mechanisms that leads to development of immunotherapy resistance in skin tumor patients. A multi-pronged approach with focus in fields of genomics and immunology as well as bioinformatics is required, along with combinat","PeriodicalId":72128,"journal":{"name":"Aging and cancer","volume":"6 2","pages":"33-45"},"PeriodicalIF":0.0,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aac2.70000","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144315078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deciphering Aging, Genetic, and Epigenetic Heterogeneity in Cancer Evolution: Toward Personalized Precision Preventative Medicine","authors":"Lamis Naddaf,&nbsp;Sheng Li","doi":"10.1002/aac2.12078","DOIUrl":"https://doi.org/10.1002/aac2.12078","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Cancer's inherent ability to evolve presents significant challenges for its categorization and treatment. Cancer evolution is driven by genetic, epigenetic, and phenotypic diversity influenced by microenvironment changes. Aging plays a crucial role by altering the microenvironment and inducing substantial genetic and epigenetic heterogeneity within an individual's somatic cells even before cancer initiation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>This review highlights the clinical significance of epigenetic mechanisms in cancer evolution, focusing on hematopoietic and solid tumors. The review aims to explore opportunities for integrating evolutionary principles and data science into cancer research.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The review synthesizes recent advancements in omics technologies, single-cell sequencing, and genetic barcoding to elucidate epigenetic mechanisms and aging's role in cancer evolution.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Epigenetic mechanisms' high plasticity generates heritable phenotypic diversity, driving malignant evolution toward poor prognosis. Advances in single-cell sequencing and genetic barcoding enable the precise detection and tracking of biomarkers, allowing early, personalized interventions. Incorporating data science into cancer research has the potential to map, predict, and prevent cancer evolution effectively.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Understanding cancer evolution through novel technologies and data analysis offers a proactive approach to cancer prevention and treatment. By predicting key evolutionary events and leveraging personalized strategies, patient outcomes can be improved, and healthcare burdens reduced, marking a transformative shift in oncology.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72128,"journal":{"name":"Aging and cancer","volume":"6 1","pages":"19-29"},"PeriodicalIF":0.0,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aac2.12078","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143602539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inflammation Promotes Aging-Associated Oncogenesis in the Lung","authors":"Catherine Pham-Danis,&nbsp;Shi B. Chia,&nbsp;Hannah A. Scarborough,&nbsp;Etienne Danis,&nbsp;Travis Nemkov,&nbsp;Vadym Zaberezhnyy,&nbsp;Jessica L. Christenson,&nbsp;Emily K. Kleczko,&nbsp;Andre Navarro,&nbsp;Andrew Goodspeed,&nbsp;Elizabeth A. Bonney,&nbsp;Charles A. Dinarello,&nbsp;Carlo Marchetti,&nbsp;Raphael A. Nemenoff,&nbsp;Kirk C. Hansen,&nbsp;James DeGregori","doi":"10.1002/aac2.12077","DOIUrl":"https://doi.org/10.1002/aac2.12077","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Lung cancer is the leading cause of cancer death in the world. While cigarette smoking is the major preventable factor for cancers in general and lung cancer in particular, old age is also a major risk factor. Aging-related chronic, low-level inflammation, termed inflammaging, has been widely documented; however, it remains unclear how inflammaging contributes to increased lung cancer incidence.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>The aim of this study was to establish connections between aging-associated changes in the lungs and cancer risk.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We analyzed public databases of gene expression for normal and cancerous human lungs and used mouse models to understand which changes were dependent on inflammation, as well as to assess the impact on oncogenesis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Analyses of GTEx and TCGA databases comparing gene expression profiles from normal lungs, lung adenocarcinoma, and lung squamous cell carcinoma of subjects across age groups revealed upregulated pathways such as inflammatory response, TNFA signaling via NFκB, and interferon-gamma response. Similar pathways were identified comparing the gene expression profiles of young and old mouse lungs. Transgenic expression of alpha 1 antitrypsin (AAT) partially reverses increases in markers of aging-associated inflammation and immune deregulation. Using an orthotopic model of lung cancer using cells derived from EML4-ALK fusion-induced adenomas, we demonstrated an increased tumor outgrowth in lungs of old mice while NLRP3 knockout in old mice decreased tumor volumes, suggesting that inflammation contributes to increased lung cancer development in aging organisms.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>These studies reveal how expression of an anti-inflammatory mediator (AAT) can reduce some but not all aging-associated changes in mRNA and protein expression in the lungs. We further show that aging is associated with increased tumor outgrowth in the lungs, which may relate to an increased inflammatory microenvironment.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72128,"journal":{"name":"Aging and cancer","volume":"6 1","pages":"3-18"},"PeriodicalIF":0.0,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aac2.12077","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143602595","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biophysical Approach to Understand Life and Cancer","authors":"Nuri Faruk Aykan","doi":"10.1002/aac2.12075","DOIUrl":"https://doi.org/10.1002/aac2.12075","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>From the perspective of biology, the characteristics of life can be categorized as cellular organizations, homeostasis, metabolism, growth, reproduction and heredity, response to stimuli and adaptation to the environment. From the perspective of physics, living organisms are highly ordered, complex, thermodynamically open systems; they are in non-equilibrium phase. According to the second law of thermodynamics, every system in the universe is going to the disorder spontaneously. Maximum entropy signifies a thermodynamic equilibrium which means the death. Today, cancer is a major global health problem and despite the explosive development of our knowledge about the carcinogenesis the “war on cancer” has not yet been won.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>To examine life and cancer together based on current biophysical approach and to shed light on new paradigms.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials &amp; Methods</h3>\u0000 \u0000 <p>A systematic literature search for publications on a thermodynamic approach to understand life and cancer was conducted in PubMed without language restrictions. The reference lists of identified studies were also used as additional knowledge.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Living organisms exchange entropy and they gain information from the external environment. Information can be stored as memory. Life is a category of emergence like art composed from correct modules. On the contrary, cancer is the emergence of a disease formed by incorrect modules. Cancer is a chaotic disease at least for a limited period and cannot arise from healthy functional tissue units. Chaos of the lower level may be associated with the entropy increase of upper level.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Biologic chaos control is possible.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72128,"journal":{"name":"Aging and cancer","volume":"5 3","pages":"70-90"},"PeriodicalIF":0.0,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aac2.12075","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142244438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Considerations for the Use of the DNA Damage Marker γ-H2AX in Disease Modeling, Detection, Diagnosis, and Prognosis","authors":"Holly Hosking,&nbsp;Wayne Pederick,&nbsp;Paul Neilsen,&nbsp;Andrew Fenning","doi":"10.1002/aac2.12074","DOIUrl":"https://doi.org/10.1002/aac2.12074","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>DNA double-strand breaks are known to be the most lethal kind of DNA damage as they cause genomic instability. Visualization and quantification of these breaks are possible via staining of the phosphorylated histone H2A variant H2AX at serine 139 with the anti-phospho-histone H2AX (γ-H2AX) antibody.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The literature was searched with the following keywords: DNA damage, double-strand break, PBMC, DNA repair, H2AX, γ-H2AX.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Discussion</h3>\u0000 \u0000 <p>This review discusses various methods for the quantification of γ-H2AX and the use of γ-H2AX in cell culture, tissue biopsies, and peripheral blood mononuclear cells. The current research into basal DNA damage as quantified by γ-H2AX is discussed in relation to cancer.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This review suggests that γ-H2AX has the potential for use in the prediction of cancer risk when applied to healthy tissue and peripheral blood mononuclear cells.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72128,"journal":{"name":"Aging and cancer","volume":"5 3","pages":"62-69"},"PeriodicalIF":0.0,"publicationDate":"2024-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aac2.12074","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142244899","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From Hyperinsulinemia to Cancer Progression: How Diminishing Glucose Storage Capacity Fuels Insulin Resistance","authors":"Irina Kareva","doi":"10.1002/aac2.12073","DOIUrl":"https://doi.org/10.1002/aac2.12073","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Type 2 diabetes (T2D) is a complex metabolic disorder characterized by insulin resistance, hyperglycemia, and hyperinsulinemia. A significant portion of individuals with T2D are unaware of their condition until it has reached advanced stages. T2D is also associated with an increased risk and worse prognosis of cardiovascular disease, cognitive decline, and cancer. Understanding the mechanisms underlying the emergence of insulin resistance is critical for improving early detection and therapeutic interventions.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>An updated framework is proposed to describe the emergence of insulin resistance that precedes the development of T2D. The model focuses on the impact of diminishing capacity to store excess glucose, which can occur due to a multitude of factors, including age-related muscle loss. The model is used to simulate responses to oral glucose tolerance tests (OGTTs) to capture the transition from a normal to a diabetic phenotype, as defined by the Kraft criteria. Additionally, the model is used to explore how the metabolic environment influences tumor progression, drawing on experimental data regarding the impact of transient diabetic phenotypes and hyperinsulinemia on cancer therapy efficacy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The model successfully demonstrates that reduced glucose storage capacity can qualitatively reproduce the progression from normal to diabetic phenotypes observed in OGTT responses. Furthermore, it shows that tumor progression or regression is highly dependent on the host's metabolic environment, particularly hyperinsulinemia. This aligns with experimental results that connect drug-induced hyperinsulinemia to a loss of therapeutic efficacy against tumors, whereas the reversal of the diabetic phenotype could restore drug sensitivity and treatment response.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This study highlights the critical role of hyperinsulinemia, even in normoglycemic individuals, in both the progression of T2D and the modulation of cancer therapy outcomes. Addressing hyperinsulinemia emerges as a promising strategy to enhance cancer treatment efficacy and improve overall health outcomes in patients with or at risk for T2D.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72128,"journal":{"name":"Aging and cancer","volume":"5 3","pages":"51-61"},"PeriodicalIF":0.0,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aac2.12073","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142244898","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Gut Microbiome in Aging and Ovarian Cancer","authors":"Gena M. Dominique,&nbsp;Catherine Hammond,&nbsp;M. Sharon Stack","doi":"10.1002/aac2.12071","DOIUrl":"https://doi.org/10.1002/aac2.12071","url":null,"abstract":"<p>The gut microbiome changes with age and affects regions beyond the gut, including the ovarian cancer tumor microenvironment. In this review summarizing the literature on the gut microbiome in ovarian cancer and in aging, we note trends in the microbiota composition common to both phenomena and trends that are distinctly opposite. Both ovarian cancer and aging are characterized by an increase in proinflammatory bacterial species, particularly those belonging to phylum Proteobacteria and genus <i>Escherichia</i>, and a decrease in short-chain fatty acid producers, particularly those in <i>Clostridium</i> cluster XIVa (family Lachnospiraceae) and the Actinobacteria genus <i>Bifidobacterium</i>. However, although beneficial bacteria from family Porphyromonadaceae and genus <i>Akkermansia</i> tend to increase with normal, healthy aging, these bacteria tend to decrease in ovarian cancer, similar to what is observed in obesity or unhealthy aging. We also note a lack in the current literature of research demonstrating causal relationships between the gut microbiome and ovarian cancer outcomes and research on the gut microbiome in ovarian cancer in the context of aging, both of which could lead to improvements to ovarian cancer diagnosis and treatment.</p>","PeriodicalId":72128,"journal":{"name":"Aging and cancer","volume":"5 1-2","pages":"14-34"},"PeriodicalIF":0.0,"publicationDate":"2024-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aac2.12071","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141488589","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Trending toward gero-electroceuticals that target membrane potential for reprogramming aging and lifespan","authors":"Siamak Tabibzadeh,&nbsp;Olen R. Brown","doi":"10.1002/aac2.12070","DOIUrl":"10.1002/aac2.12070","url":null,"abstract":"<p>Ion gradients across cell membranes generate voltage potentials that are involved in a wide range of biological processes. According to the membrane hypothesis of aging, aging is inextricably linked to a decrease in resting membrane potential (<i>V</i>_mem). Alterations in ion channel activity and membrane fluidity caused by aging disrupt bioelectric homeostasis, increase intracellular calcium and potassium concentrations, induce abnormal mechanistic target of rapamycin (MTOR)- and AMPK-regulated metabolism and energy dissipation, and decrease proliferation and regeneration. Failure to maintain ion channel activity and membrane potential leads to cell senescence or death. There is evidence that by manipulating ion channel activities, a cryptic memory can be recalled to restore lost proliferative or regenerative abilities. Reversal or prevention of senescence, aging phenotypes, and longevity may be achieved by fine-tuning mitochondrial membrane polarization. Therefore, there is optimism that deciphering the bioelectric codes that govern cell functions will lead to the development of new gero-electroceuticals that restore cell function and prevent tissue loss during aging.</p>","PeriodicalId":72128,"journal":{"name":"Aging and cancer","volume":"5 1-2","pages":"3-13"},"PeriodicalIF":0.0,"publicationDate":"2024-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aac2.12070","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141369715","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}