Cancers are being frequently diagnosed in the elderly. Immunosenescence which refers to the gradual deterioration of the immune system brought on by natural age advancement, has been the key cross center in the increasing frequency and severity of cancer, aging and immunity. Monoclonal antibodies targeting immune checkpoint molecules CTLA-4, PD-1 or PD-L1 are the promising anticancer therapeutics in multiple cancer subtypes generating remarkable and long-lasting clinical responses. These immune checkpoint blockers (ICBs)have already obtained approval for the treatment of patients with metastatic melanoma, advanced/refractory non-small cell lung cancer and renal cell cancer. ICBs can not only enhance immune responses against cancer cells but can also lead to inflammatory side effects called immune-related adverse events (irAEs). As none or only a small number of older patients were enrolled in most ICBs studies, it remains difficult to confirm the impacts of ICBs on the elderly. We could expect that clinical specificity of older patients (co-medications, comorbidities and reduced functional reserve) and immunosenescence may affect the efficacy of ICBs and tolerance in this population. However, the results from meta-analysis on the efficacy of ICBs are very encouraging and suggesting that the older patients will benefit from the ICBs revolution in oncology without increased toxicity.

To elucidate the key molecules, functions, and pathways that bridge mild cognitive impairment (MCI) and Alzheimer's disease (AD), we investigated open gene expression data sets. Differential gene expression profiles were analyzed and combined with potential MCI- and AD-related gene expression profiles in public databases. Then, weighted gene co-expression network analysis was performed to identify the gene co-expression modules. One module was significantly negatively associated with MCI samples, in which gene ontology function and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis showed that these genes were related to cytosolic ribosome, ribosomal structure, oxidative phosphorylation, AD, and metabolic pathway. The other two modules correlated significantly with AD samples, in which functional and pathway enrichment analysis revealed strong relationships of these genes with cytoplasmic ribosome, protein binding, AD, cancer, and apoptosis. In addition, we regarded the core genes in the module network closely related to MCI and AD as bridge genes and submitted them to protein interaction network analysis to screen for major pathogenic genes according to the connectivity information. Among them, small nuclear ribonucleoprotein D2 polypeptide (SNRPD2), ribosomal protein S3a (RPS3A), S100 calcium binding protein A8 (S100A8), small nuclear ribonucleoprotein polypeptide G (SNRPG), U6 snRNA-associated Sm-like protein LSm3 (LSM3), ribosomal protein S27a (RPS27A), and ATP synthase F1 subunit gamma (ATP5C1) were not only major pathogenic genes of MCI, but also bridge genes. In addition, SNRPD2, RPS3A, S100A8, SNRPG, LSM3, thioredoxin (TXN), proteasome 20S subunit alpha 4 (PSMA4), annexin A1 (ANXA1), DnaJ heat shock protein family member A1 (DNAJA1), and prefoldin subunit 5 (PFDN5) were not only major pathogenic genes of AD, but also bridge genes. Next, we screened for differentially expressed microRNAs (miRNAs) to predict the miRNAs and transcription factors related the MCI and AD modules, respectively. The significance score of miRNAs in each module was calculated using a hypergeometric test to obtain the miRNApivot-Module interaction pair. Thirty-four bridge regulators were analyzed, among which hsa-miR-519d-3p was recognized as the bridge regulator between MCI and AD. Our study contributed to a better understanding of the pathogenic mechanisms of MCI and AD, and might lead to the development of a new strategy for clinical diagnosis and treatment.

This review discusses the effects and mechanisms of a ketogenic diet on neurodegenerative diseases on the basis of available evidence. A ketogenic diet refers to a high-fat, mediumprotein, and low-carbohydrate diet that leads to a metabolic shift to ketosis. This review systematically summarizes the scientific literature supporting this effective treatment approach for neurodegenerative diseases, including effects on mitochondrial function, oxidative stress, neuronal apoptosis, neuroinflammation, and the microbiota–gut-brain axis. It also highlights the clinical evidence for the effects of the ketogenic diet in the treatment of Alzheimer's disease, Parkinson's disease, and motor neuron disease. Finally, it discusses the common adverse effects of ketogenic therapy. Although the complete mechanism of the ketogenic diet in the treatment of neurodegenerative diseases remains to be elucidated, its clinical efficacy has attracted many new followers. The ketogenic diet is a good candidate for adjuvant therapy, but its specific applicability depends on the type and the degree of the disease.

Sitagliptin is an emerging oral hypoglycemic agent that inhibits the development of a wide variety of tumors. Current researches indicate that the abnormal activation of Yes‐associated protein (YAP) promotes the proliferation and poor prognosis of multiple tumors. However, the ability of sitagliptin to regulate YAP and its effects on gastric cancer (GC) cells remain unclear. Here, we first showed that sitagliptin inhibited the proliferation of GC cells, and this inhibition was regulated by Hippo pathway. Sitagliptin phosphorylated YAP in a large tumor suppressor homolog‐dependent manner, thereby inhibiting YAP nuclear translocation, and promoted YAP cytoplasm retention. This inhibition can be blocked by adenosine 5′‐monophosphate‐activated protein kinase (AMPK). Moreover, sitagliptin could reduce the expression of tumor‐testis antigen Melanoma‐associated antigen‐A3 through YAP. In conclusion, sitagliptin may have a potential inhibitory effect on GC by AMPK/YAP/melanoma‐associated antigen‐A3 pathway.

The majority of patients with common malignancies are older adults. Intrinsic complex biological changes of aging along with inflammation, immunosenescence, age-associated chronic diseases, and extrinsic environmental and psychosocial factors have significant impact on not only development and behavior of individual malignancies, but also physiologic reserve and vulnerability of older patients who suffer from them. As a result, clinical practice of geriatric oncology demands integration of careful geriatric assessment and management. This article provides an overview of basic biology of aging and its relationship with cancer. After a brief introduction about the definition and mechanisms of aging, as well as age-related biological and physiological changes, the discussion mainly focuses on recent development and insights into the relationship of frailty, inflammation, and immunity with cancer, highlighting how the new knowledge can help further improve assessment and treatment of older patients with malignancies and promote cancer research.

Purpose: Age at diagnosis has been identified as a major determinant of thyroid cancer-specific survival. But the cut-off value for age was controversial. The interaction among gender, age and histologic subtypes needed to be answered.