Aging and cancer最新文献

{"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}

{"title":"Risk factors for suicide in patients with pancreatic ductal adenocarcinoma: A population-based study","authors":"Chao Wang,&nbsp;Haoda Chen,&nbsp;Yuanchi Weng,&nbsp;Xiaxing Deng,&nbsp;Weishen Wang,&nbsp;Baiyong Shen","doi":"10.1002/aac2.12069","DOIUrl":"10.1002/aac2.12069","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Patients diagnosed with pancreatic ductal adenocarcinoma (PDAC) face a notable risk of suicide. However, comprehensive population-based studies on suicide risk in PDAC patients have been lacking. This study seeks to explore the suicide risk in PDAC patients and identify the specific risk factors associated with suicide-related mortality.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A cohort of 101,382 PDAC patients was extracted from the Surveillance, Epidemiology, and End Results database, spanning from January 1, 2000, to December 31, 2017. The study employed the standardized mortality ratio (SMR) to assess the relative risk of suicide in PDAC patients compared to the general US population. The Nelson–Aalen estimator and the Fine and Grey method were utilized to pinpoint the risk factors linked to suicide-specific mortality.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>PDAC patients exhibited a 3.51-fold higher risk of suicide compared to the general US population. This risk demonstrated an upward trend over the years. Notably, individuals aged 70–74 years faced a significantly elevated risk of suicide (SMR = 5.14, 95% CI: 3.10–8.03). Furthermore, there were distinct peaks in suicide risk at 1–4- and 25–28-month post-diagnoses (SMR = 15.04 and 2.72, respectively). Factors, such as gender, chemotherapy status, and marital status, emerged as significant independent predictors of suicide-specific mortality in PDAC patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This study highlights a heightened suicide risk among PDAC patients in comparison to the general US population. It underscores the crucial need for continuous monitoring of the psychological well-being of all PDAC patients. Additionally, considering the elevated risk, the application of antidepressant therapy could be beneficial for those identified as having a higher risk of suicide.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72128,"journal":{"name":"Aging and cancer","volume":"5 1-2","pages":"35-47"},"PeriodicalIF":0.0,"publicationDate":"2024-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aac2.12069","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140210884","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":"Promoting longevity with less cancer: The 2022 International Conference on Aging and Cancer","authors":"Yan Cui,&nbsp;Kai Wang,&nbsp;Danli Jiang,&nbsp;Yizhou Jiang,&nbsp;Dawei Shi,&nbsp;James DeGregori,&nbsp;Samuel Waxman,&nbsp;Ruibao Ren","doi":"10.1002/aac2.12068","DOIUrl":"10.1002/aac2.12068","url":null,"abstract":"<p>Aging and cancer are increasingly becoming big challenges for public health worldwide due to increased human life expectancy. Meanwhile, aging is one of the major risk factors for cancer. In December 2019, the first International Conference on Aging and Cancer was held in Haikou, Hainan province (island), China, preluding the establishment of the International Center for Aging and Cancer (ICAC) at Hainan, an institute dedicated to the research at the intersection of aging and cancer. Since then, the ICAC has hosted the annual conference each December in Hainan. The 2022 ICAC conference, with the theme of “promoting longevity with less cancer,” invited 17 internationally renowned scientists to share their new research and insights. Topics included DNA methylation in rejuvenation, development, and cellular senescence; lifespan regulation and longevity manipulation; metabolism and aging; cellular senescence and diseases; and novel therapeutics for cancer and antiaging/anticancer drug discovery. The forum highlighted the interconnectedness of aging and senescence with cancer evolution and risk. Although there is hope for preventing diseases like cancer by modulating systems that also control lifespan, attention has to be paid to the conflicting needs and competing demands in human biology.</p>","PeriodicalId":72128,"journal":{"name":"Aging and cancer","volume":"4 3-4","pages":"111-120"},"PeriodicalIF":0.0,"publicationDate":"2023-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aac2.12068","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136232958","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":"Detecting cellular senescence in vivo: Imagining imaging better","authors":"Zachary M. Rabinowitz,&nbsp;Lina Cui","doi":"10.1002/aac2.12067","DOIUrl":"10.1002/aac2.12067","url":null,"abstract":"<p>Methods to detect cellular senescence have become increasingly important, even more so in living animals and humans. This cellular state has been found to play fundamental roles in physiological processes as well as functioning detrimentally toward the advent or progression of pathological conditions. Importantly, the study of senescence involvement in these processes in vivo cannot be done without living-friendly technologies enabling senescence detection. Furthermore, senotherapies or therapies that selectively kill senescent cells have emerged as a new therapeutic strategy for aging and age-related diseases such as atherosclerosis, cancer, and neurodegenerative disorders and require tools to evaluate their use in vivo. As of now, our in vivo senescence detection toolkit includes genetically engineered reporter mouse models and small molecule imaging probes. Herein, we will focus on the detection of senescence in vivo, including a summary of its challenges, current detection methods and strategies, and a perspective on overcoming the current obstacles.</p>","PeriodicalId":72128,"journal":{"name":"Aging and cancer","volume":"4 3-4","pages":"97-110"},"PeriodicalIF":0.0,"publicationDate":"2023-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aac2.12067","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43749051","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}