Aging and cancer最新文献

{"title":"Risk Prediction Models for Recurrence After Curative Treatment of Early-Stage or Locally Advanced Lung Cancer: A Systematic Review","authors":"Evangeline Samuel, S. Tissera, E. Paul, J. Zalcberg, R. G. Stirling","doi":"10.1002/aac2.70023","DOIUrl":"https://doi.org/10.1002/aac2.70023","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>Lung cancer remains the leading cause of cancer-related mortality worldwide. Despite advances in treatment, postoperative recurrence rates in early-stage and locally advanced non-small cell lung cancer (NSCLC) remain substantial. Prognostic models may support risk stratification and guide posttreatment management.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>To systematically identify and compare prognostic models predicting survival and recurrence outcomes in patients with NSCLC treated with curative intent.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This systematic review was conducted in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. MEDLINE, EMBASE, and the Cochrane Library were searched from inception to November 29, 2022, with an updated search to capture newly published studies. Eligible studies reported quantitative performance measures of prognostic models predicting recurrence-free survival (RFS), cancer-specific survival (CSS), or overall survival (OS) in patients with curatively treated NSCLC. Data extraction followed the CHARMS checklist, and risk of bias was assessed using the PROBAST tool. The review protocol was registered with PROSPERO (CRD42021226091).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Of 6369 screened records, 40 studies met inclusion criteria. Most models employed Cox proportional hazards regression and varied widely in predictor selection. Common predictors included age (<i>n</i> = 40), sex (<i>n</i> = 40), and tumor characteristics (<i>n</i> = 36). Radiomic features were incorporated in 11 models and were associated with improved discrimination. Reported model performance ranged from poor to excellent (AUROC 0.5–0.9), with most models demonstrating acceptable to good discrimination (AUROC > 0.7). The highest reported 3-year OS AUROC was 0.90 (95% CI: 0.85–0.95). However, only four models underwent external validation, and reporting of calibration and other performance metrics was inconsistent.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Prognostic models for survival and recurrence in resected NSCLC frequently demonstrate good discrimination but are limited by inadequate external validation and variable reporting. Future research should prioritize transparent model development, robust validation, and clinical usability to improve posttreatment decision-making.</p>\u0000 </section>\u0000 </","PeriodicalId":72128,"journal":{"name":"Aging and cancer","volume":"7 3","pages":"125-141"},"PeriodicalIF":0.0,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aac2.70023","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148974896","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":"Long-Term Follow-Up of Chemotherapy-Associated Biological Aging in Women With Early Breast Cancer","authors":"Hyman B. Muss,&nbsp;Alexis C. Wardell,&nbsp;Allison M. Deal,&nbsp;Kirsten A. Nyrop,&nbsp;Allison Ross,&nbsp;Yara G. Abdou,&nbsp;Jeffrey D. Aldrich,&nbsp;Lisa A. Cary,&nbsp;E. Claire Dees,&nbsp;Katherine E. Reeder-Hayes,&nbsp;Emily M. Ray,&nbsp;Natalia Mitin,&nbsp;Denis Tsygankov","doi":"10.1002/aac2.70022","DOIUrl":"https://doi.org/10.1002/aac2.70022","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p><i>p16^INK4a</i> (<i>p16</i>), a robust marker of cell senescence, rises rapidly and dramatically after adjuvant chemotherapy for breast cancer. We measured <i>p16</i> in peripheral blood T cells of 119 women with stage I–III breast cancer, 75 with previous adjuvant chemotherapy and 44 randomly selected women who had never received chemotherapy. <i>p16</i> was measured at least 3 years (mean, 6 years) following diagnosis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>This study aims to assess the expression of <i>p16</i> after long-term follow-up and define the trajectory of the <i>p16</i> increase in a subset of patients with baseline, 6-month post-chemotherapy, and long-term follow-up data.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods and Results</h3>\u0000 \u0000 <p>All patients were treated in accordance with national guidelines, and 53% of the chemotherapy-treated patients received anthracycline regimens. After a mean follow-up of 6 years from the end of treatment, chemotherapy-treated patients demonstrated <i>p16</i> levels corresponding to approximate age-equivalent increase of ∼14 years compared to 2.1 years in non-chemotherapy-treated patients. When compared to community-dwelling adults, <i>p16</i> expression increased markedly at 6 months post-chemotherapy, particularly among anthracycline-treated patients (corresponding to larger age-equivalent deviation: median 21.5 years vs. median 15.4 years). At long-term follow-up, both anthracycline and non-anthracycline-treated patients showed elevated but converging <i>p16</i> levels (age-equivalent median of 18.1 years vs. median 17.2 years), indicating an improvement in <i>p16</i> levels over time in anthracycline-treated patients. Age-equivalent values are reported as an interpretive aid derived from population-level <i>p16</i>–age relationship and are not intended to represent literal biological age or clock-based aging.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Early breast cancer patients treated with chemotherapy exhibited a marked increase in <i>p16</i> expression shortly after treatment completion that persists for years after treatment. The long-term impact of these changes remains uncertain but raises the possibility that chemotherapy-related cellular senescence could contribute to an increased risk of age-related comorbidities over time.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72128,"journal":{"name":"Aging and cancer","volume":"7 3","pages":"87-98"},"PeriodicalIF":0.0,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aac2.70022","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148974993","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 Is a Key Driver for Adult Acute Myeloid Leukemia","authors":"Rong Yin,&nbsp;Haojian Zhang","doi":"10.1002/aac2.70020","DOIUrl":"https://doi.org/10.1002/aac2.70020","url":null,"abstract":"<p>Aging is a progressive functional decline with increased susceptibility to human diseases. Among these age-related diseases, adult acute myeloid leukemia (AML) is a fatal hematologic malignancy characterized by aggressive clonal expansion and arrested differentiation of myeloid progenitors. Although it is known that aging plays a crucial role in AML pathogenesis, treating this age-related blood disease remains a huge challenge, which needs a deeper understanding of the mechanisms of aging in driving AML. This review updates recent advances on the relationship between aging and AML pathogenesis by focusing on the age-related intrinsic and extrinsic factors. The aging of the hematopoietic system exhibits an expansion of phenotypic hematopoietic stem cells (HSCs), skewed differentiation to myeloid lineage, decreased repopulation ability, and altered clonal behaviors. We first discuss the role of aging in regulating the fate and fitness of HSCs, and summarize how aging contributes to the accumulation of genomic alterations and clonal hematopoiesis. In the following, epigenetic and metabolic alterations in hematopoietic cells and AML pathogenesis with aging are emphasized, and the aging-related changes in extrinsic elements are also reviewed. Finally, we discuss the potential for aging intervention in treating hematopoietic malignancies. Overall, this review provides a comprehensive summary of the aging-associated intrinsic and extrinsic factors for AML pathogenesis. Targeting these aging-associated alterations in HSCs may provide new opportunities for AML intervention.</p>","PeriodicalId":72128,"journal":{"name":"Aging and cancer","volume":"7 3","pages":"99-108"},"PeriodicalIF":0.0,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aac2.70020","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148974915","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":"Mutant NPM1 in Acute Myeloid Leukemia Initiation and Maintenance","authors":"Yanan Jiang,&nbsp;Zhong Fan,&nbsp;Runmeng Liu,&nbsp;Xiaotian Zhang","doi":"10.1002/aac2.70021","DOIUrl":"https://doi.org/10.1002/aac2.70021","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Nucleophosmin (NPM1), a multifunctional nucleolar protein, plays critical roles in ribosome biogenesis, chromatin organization, and genome stability. In one-third of adult acute myeloid leukemia (AML) cases, mutations in <i>NPM1</i>, most frequently a 4-bp insertion in exon 12 generates an aberrant nuclear export signal in C-terminus, resulting in the cytoplasmic mislocalization of NPM1 (NPM1c). NPM1c defines a distinct molecular entity characterized by aberrant activation of <i>HOXA/B</i> clusters and <i>MEIS1</i>, which sustain an oncogenic transcriptional program.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>This review aims to summarize recent advances in the molecular mechanisms of NPM1c-driven leukemogenesis and discuss its implications for clonal evolution and targeted therapies.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods and Results</h3>\u0000 \u0000 <p>Recent findings revealed that NPM1c forms neomorphic chromatin-bound condensates with the Menin–MLL complex, XPO1, and the super-elongation complex, amplifying leukemogenic transcriptional hubs while suppressing HDAC activity. Within the framework of age-associated clonal hematopoiesis (CH), <i>NPM1c</i> acts as a late gatekeeping mutation that transforms preleukemic clones harboring early epigenetic lesions in <i>DNMT3A</i>, <i>TET2</i>, or <i>IDH1/2</i> into overt AML cells. Insights from mouse models support this hierarchical evolution and underscore the requirement for cooperating mutations, such as <i>FLT3-ITD</i>. Emerging therapies including Menin–MLL, XPO1, DOT1L, HBO1, and ENL inhibitors target NPM1c-driven <i>HOX/MEIS1</i> dysregulation, whereas early intervention at the CH stage in hematopoietic stem and progenitor cells (HSPCs) harboring <i>IDH</i> or <i>DNMT3A</i> mutations offers a promising preventive strategy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This review integrates mechanistic advances from biochemistry, genetic and epigenetic regulation, and clonal evolution to provide a unified model of NPM1c-mediated leukemogenesis and highlights future directions for precision therapy in AML.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72128,"journal":{"name":"Aging and cancer","volume":"7 3","pages":"109-124"},"PeriodicalIF":0.0,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aac2.70021","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148974895","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":"Natural Products as Geroprotective Modulators in Diabetic Nephropathy: A Mechanistic Framework Integrating Aging Hallmarks and the AMPK–SIRT1–Nrf2 Axis","authors":"Sherif Hamidu,&nbsp;Latif Adams,&nbsp;Eunice Ampem-Danso,&nbsp;Justice Kumi,&nbsp;Abigail Aning,&nbsp;Fatima Hamidu,&nbsp;Mustapha Abdul Mumin Mohammed,&nbsp;Ayuba Nii Darku Ankrah,&nbsp;Seth Kwabena Amponsah","doi":"10.1002/aac2.70017","DOIUrl":"https://doi.org/10.1002/aac2.70017","url":null,"abstract":"<p>Diabetic nephropathy (DN) is not merely a metabolic complication, it is an age-accelerated kidney disorder in which biological aging pathways amplify hyperglycemic injury. Mounting evidence implicates cellular senescence, mitochondrial dysfunction, chronic inflammation (“inflammaging”), and epigenetic drift as central drivers of DN progression. However, current therapies fail to address these aging mechanisms.</p><p>This review introduces a geroscience-based framework in which natural products are conceptualized as <i>geroprotective modulators</i> capable of reprogramming age-related molecular damage in the diabetic kidney. We integrate preclinical evidence showing that compounds such as resveratrol, quercetin, curcumin, ginsenosides, and berberine restore the AMPK–SIRT1–Nrf2 regulatory triad, thereby rejuvenating mitochondrial bioenergetics, suppressing inflammasome activation, and mitigating fibrosis.</p><p>A new mechanistic classification model is proposed, categorizing natural products by the specific hallmarks of aging they target; cellular senescence, mitochondrial decline, inflammaging, and epigenetic alterations rather than by chemical class. Finally, we advance a unifying hypothesis: simultaneous activation of the AMPK–SIRT1–Nrf2 axis represents the central mechanism through which diverse natural products confer renoprotection and longevity signaling in DN.</p><p>By linking geroscience to phytotherapy, this review provides a novel conceptual and mechanistic roadmap for developing multi-targeted interventions to slow kidney aging and improve outcomes in diabetic patients.</p>","PeriodicalId":72128,"journal":{"name":"Aging and cancer","volume":"7 2","pages":"52-66"},"PeriodicalIF":0.0,"publicationDate":"2026-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aac2.70017","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148292515","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":"Re-Awakening Public Attention to the Silent Pandemic of Cancer Among Older Adults in Low- and Middle-Income Countries","authors":"Ibrahim Bidemi Abdullateef,&nbsp;Sunkanmi Folorunsho,&nbsp;Abdulazeez Opeyemi Abdulganiyu","doi":"10.1002/aac2.70019","DOIUrl":"https://doi.org/10.1002/aac2.70019","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <p>As global populations age, cancer is increasingly becoming a leading cause of morbidity and mortality among older adults, particularly in low- and middle-income countries (LMICs). Despite accounting for the majority of new cancer cases and deaths, older individuals remain underrepresented in cancer research, clinical guidelines, and health policies, a trend contributing to what can be termed a “silent pandemic.” This perspective highlights the growing burden of cancer in aging populations in LMICs and critically examines the systemic gaps in prevention, diagnosis, treatment, survivorship care, and financial protection. Drawing on global and LMIC-specific evidence, the article explores key challenges such as underdiagnosis, limited access to age-sensitive screening, inadequate geriatric assessment, exclusion from clinical trials, and financial toxicity. It also provides evidence-informed recommendations to strengthen geriatric oncology care in resource-limited settings. These include integrating geriatric assessments into oncology practice, promoting age-inclusive research, expanding survivorship care and community support systems, and implementing financial protection policies. Addressing this neglected area is essential to achieving equitable cancer control and ensuring healthy aging in LMICs.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72128,"journal":{"name":"Aging and cancer","volume":"7 2","pages":"77-84"},"PeriodicalIF":0.0,"publicationDate":"2026-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aac2.70019","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148292452","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":"Cutaneous Melanoma Drives Metabolic Changes in the Aged Bone Marrow Immune Microenvironment","authors":"Alexis E. Carey,&nbsp;Murilo Ramos Rocha,&nbsp;Cheyenne Palm,&nbsp;Vania Wang,&nbsp;Denys Balandin,&nbsp;Ethan Black,&nbsp;Kevin Y. Zhang,&nbsp;Fan Huang,&nbsp;Daniel J. Zabransky,&nbsp;Yash Chhabra,&nbsp;Mareike Peters,&nbsp;Gabriel Ghiaur,&nbsp;Ashani Weeraratna","doi":"10.1002/aac2.70015","DOIUrl":"https://doi.org/10.1002/aac2.70015","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Melanoma is the deadliest form of skin cancer, with increasing incidence rates among the older population. The immune system experiences age-related changes that can impact tumor progression and treatment efficacy. Additionally, aging leads to systemic non-immune changes, such as enhanced adiposity and iron accumulation in the bone marrow (BM).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>This study aims to investigate how age-related alterations in the BM, alongside the presence of melanoma, influence the immune response and susceptibility to ferroptosis in aged mice.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods and Results</h3>\u0000 \u0000 <p>Utilizing an aged mouse model with melanoma, we observed significant changes in iron and lipid levels within the BM, as well as alterations in immune cell populations. Specifically, our findings indicate that tumor burden expands the myeloid compartment and contracts the lymphoid compartment in the BM niche. Aging increases neutral lipids within the BM, but tumor burden in aged mice appears to reverse this effect. We noted elevated intracellular neutral lipid levels in monocytes due to the tumor burden. Bone marrow–derived macrophages (BMDMs) from aged mice exhibited altered fatty acid synthase and fatty acid uptake protein expression. While aging leads to increased iron accumulation and lipid peroxidation in the BM, the presence of melanoma counteracts these changes. Disruptions in iron and lipid homeostasis heightened the risk of ferroptosis. Notably, imidazole ketone erastin and aging influenced intracellular ferrous iron levels and immune cell populations.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Overall, melanoma induces an age-specific metabolic response in the BM, which may sensitize immune cells to ferroptosis inducers.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72128,"journal":{"name":"Aging and cancer","volume":"7 2","pages":"35-51"},"PeriodicalIF":0.0,"publicationDate":"2026-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aac2.70015","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148292506","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":"Prognostic Impact of European LeukemiaNet Genetic Risk Stratification System in Adult Patients With Acute Myeloid Leukemia","authors":"Mobina Shrestha,&nbsp;Bishwas Mandal,&nbsp;Vishal Mandal,&nbsp;Asis Shrestha,&nbsp;Amir Babu Shrestha","doi":"10.1002/aac2.70018","DOIUrl":"https://doi.org/10.1002/aac2.70018","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The European LeukemiaNet (ELN) 2017 Genetic Risk Stratification System is widely used to categorize adult acute myeloid leukemia (AML) patients into prognostic groups. This study aimed to evaluate the prognostic value of ELN2017 in predicting survival outcomes and to assess the impact of clinical and molecular factors such as age, FLT3 and NPM1 mutations, and allogeneic hematopoietic stem cell transplantation (allo-HSCT).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A cohort of 186 adult AML patients was stratified into ELN2017 risk categories: favorable (19.6%), intermediate (54.6%), and adverse (25.76%). We analyzed overall survival (OS) and relapse-free survival (RFS), with subgroup analyses based on age, FLT3 and NPM1 mutation status, and allogeneic allo-HSCT.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Three-year OS was 68.09% (favorable), 45.36% (intermediate), and 22.87% (adverse). Five-year OS declined to 34.47%, 34.99%, and 13.72%, respectively. Corresponding 3-year RFS rates were 49.96%, 38%, and 12.98%, whereas 5-year RFS rates were 39.97%, 30.40%, and 6.49%. Patients aged ≥60 years showed poorer survival across all risk groups. Among FLT3-mutated cases, 5-year OS was 50% in the favorable group and 41.10% in the intermediate group. Allo-HSCT significantly improved 3-year OS in intermediate-risk patients from 33.80% to 63.00% and in adverse-risk patients from 10.10% to 46.15%.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>ELN2017 provides strong prognostic discrimination in adult AML despite the introduction of newer ELN guidelines. Patient age, FLT3/NPM1 mutations, and transplantation status further refine risk assessment and should guide individualized treatment strategies.</p>\u0000 </section>\u0000 </div>","PeriodicalId":72128,"journal":{"name":"Aging and cancer","volume":"7 2","pages":"67-76"},"PeriodicalIF":0.0,"publicationDate":"2026-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aac2.70018","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148292431","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":"Enhancing Oncological Care for India's Aging Population: Addressing the Complex Needs of Older Adults With Cancer","authors":"Nihanthy D. Sreenath,&nbsp;Mathigatta Shivarudraiah S,&nbsp;Rajath Govind,&nbsp;Kaushik M R","doi":"10.1002/aac2.70011","DOIUrl":"https://doi.org/10.1002/aac2.70011","url":null,"abstract":"<p>Cancer in older adults is a growing public health concern in India, with approximately 50% of all new cancer cases occurring in individuals aged 60 years and above, according to recent estimates from the Indian Council of Medical Research (ICMR). Older adults often present with a distinct set of medical, psychological, and social vulnerabilities that necessitate tailored approaches to cancer management. The increasing prevalence of solid malignancies among older adults presents substantial challenges for an already overburdened healthcare system.</p><p>However, oncology care in India lacks a geriatric-oriented approach, resulting in gaps in both accessibility and quality for older populations. This review provides a detailed exploration of the multidimensional issues of treating older adults with malignancies in India, examining current deficiencies in healthcare delivery, socio-economic constraints, and potential avenues for enhancing care quality through multidisciplinary collaboration, palliative care integration, and policy reform. The recommendations herein advocate for a model of care that emphasizes holistic support, ensuring dignity, accessibility, and quality outcomes for older adults with cancer in India.</p>","PeriodicalId":72128,"journal":{"name":"Aging and cancer","volume":"7 1","pages":"3-11"},"PeriodicalIF":0.0,"publicationDate":"2026-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aac2.70011","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147568507","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 Aging Blood: Cellular Origins, Circulating Drivers, and Therapeutic Potential","authors":"Hanqing He,&nbsp;Jianwei Wang","doi":"10.1002/aac2.70016","DOIUrl":"https://doi.org/10.1002/aac2.70016","url":null,"abstract":"<p>Aging is a complex and systemic biological process. As a crucial conduit linking all organs and tissues, the blood system not only reflects systemic aging phenotypes but may also actively drive the progression of organismal aging. In recent years, a series of heterochronic parabiosis and plasma transfusion experiments have revealed that exposure to young blood can restore the function of multiple organs in aged individuals, spurring growing interest in the concept of “blood-based antiaging.” Studies have identified a range of rejuvenating factors in young plasma—such as GDF11, TIMP2, and PF4—while aged blood is enriched in pro-aging signals, including CCL11, C1q, β2-microglobulin, and components of the senescence-associated secretory phenotype (SASP). These findings suggest that blood serves not only as a vehicle for youth-promoting cues but also as a reservoir of aging-inducing signals. Further research has shown that hematopoietic stem cells (HSCs), the root of the hematopoietic system, undergo functional decline, myeloid-biased differentiation, and clonal hematopoiesis during aging—key features that are tightly linked to immunosenescence, inflammaging, and multi-organ dysfunction. Transplantation of young HSCs has been demonstrated to extend lifespan and improve neurological, cardiac, and immune functions, highlighting their promising role in antiaging interventions. This review aims to systematically outline the development of blood-based rejuvenation research, focusing on the regulatory roles of circulating aging-related factors and the mechanistic underpinnings of HSC aging, and to explore future strategies and translational prospects of targeting the hematopoietic system in aging intervention.</p>","PeriodicalId":72128,"journal":{"name":"Aging and cancer","volume":"7 1","pages":"21-31"},"PeriodicalIF":0.0,"publicationDate":"2026-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/aac2.70016","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147569376","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}