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"Chen, Yong"
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Association between Dysphagia and Frailty in Older Adults: A Systematic Review and Meta-Analysis
Background: Increasing bodies of epidemiological evidence indicate potential associations between dysphagia and the risk of frailty in older adults. We hypothesized that older adults with symptoms of dysphagia might have a higher prevalence of frailty or prefrailty than those without dysphagia. Methods: We systematically searched the PubMed, Embase, and Cochrane Library databases for relevant studies published through 20 April 2022. Cross-sectional and longitudinal studies that examined the associations between dysphagia and the existence of frailty or prefrailty in community-dwelling, facility-dwelling, or hospitalized adults aged 50 years or older were synthesized. The Newcastle–Ottawa Scale was used to evaluate study quality. Results: The meta-analysis comprised 12 cohorts, including 5,503,543 non-frailty participants and 735,303 cases of frailty or prefrailty. Random-effect meta-analysis demonstrated a significant association between dysphagia and the risk of frailty and prefrailty (OR, 3.24; 95% CI, 2.51–4.20). In addition, we observed consistent results across the subgroups and heterogeneity assessments. Conclusions: We propose including dysphagia assessment as a critical factor in the cumulative deficit model for identifying frailty in older adults. Understanding dysphagia and the potential role of nutritional supplements in older adults may lead to improved strategies for preventing, delaying, or mitigating frailty.
Journal Article
Immunogenicity of somatic mutations in human gastrointestinal cancers
It is unknown whether the human immune system frequently mounts a T cell response against mutations expressed by common epithelial cancers. Using a next-generation sequencing approach combined with high-throughput immunologic screening, we demonstrated that tumor-infiltrating lymphocytes (TILs) from 9 out of 10 patients with metastatic gastrointestinal cancers contained CD4⁺ and/or CD8⁺ T cells that recognized one to three neo-epitopes derived from somatic mutations expressed by the patient's own tumor. There were no immunogenic epitopes shared between these patients. However, we identified in one patient a human leukocyte antigen–C*08:02–restricted T cell receptor from CD8⁺ TILs that targeted the KRASG12D hotspot driver mutation found in many human cancers. Thus, a high frequency of patients with common gastrointestinal cancers harbor immunogenic mutations that can potentially be exploited for the development of highly personalized immunotherapies.
Journal Article
Immune recognition of somatic mutations leading to complete durable regression in metastatic breast cancer
Immunotherapy using either checkpoint blockade or the adoptive transfer of antitumor lymphocytes has shown effectiveness in treating cancers with high levels of somatic mutations—such as melanoma, smoking-induced lung cancers and bladder cancer—with little effect in other common epithelial cancers that have lower mutation rates, such as those arising in the gastrointestinal tract, breast and ovary
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. Adoptive transfer of autologous lymphocytes that specifically target proteins encoded by somatically mutated genes has mediated substantial objective clinical regressions in patients with metastatic bile duct, colon and cervical cancers
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. We present a patient with chemorefractory hormone receptor (HR)-positive metastatic breast cancer who was treated with tumor-infiltrating lymphocytes (TILs) reactive against mutant versions of four proteins—SLC3A2, KIAA0368, CADPS2 and CTSB. Adoptive transfer of these mutant-protein-specific TILs in conjunction with interleukin (IL)-2 and checkpoint blockade mediated the complete durable regression of metastatic breast cancer, which is now ongoing for >22 months, and it represents a new immunotherapy approach for the treatment of these patients.
Adoptive T cell therapy induced complete and durable remission in a patient with refractory metastatic breast cancer, providing proof of principle for this approach in breast cancer therapy.
Journal Article
Polycrystalline graphene and other two-dimensional materials
This Review discusses the recent experimental and theoretical findings on polycrystalline graphene and related materials.
Graphene, a single atomic layer of graphitic carbon, has attracted intense attention because of its extraordinary properties that make it a suitable material for a wide range of technological applications. Large-area graphene films, which are necessary for industrial applications, are typically polycrystalline — that is, composed of single-crystalline grains of varying orientation joined by grain boundaries. Here, we present a review of the large body of research reported in the past few years on polycrystalline graphene. We discuss its growth and formation, the microscopic structure of grain boundaries and their relations to other types of topological defect such as dislocations. The Review further covers electronic transport, optical and mechanical properties pertaining to the characterizations of grain boundaries, and applications of polycrystalline graphene. We also discuss research, still in its infancy, performed on other two-dimensional materials such as transition metal dichalcogenides, and offer perspectives for future directions of research.
Journal Article
PARP inhibitor resistance: the underlying mechanisms and clinical implications
Due to the DNA repair defect, BRCA1/2 deficient tumor cells are more sensitive to PARP inhibitors (PARPi) through the mechanism of synthetic lethality. At present, several PAPRi targeting poly (ADP-ribose) polymerase (PARP) have been approved for ovarian cancer and breast cancer indications. However, PARPi resistance is ubiquitous in clinic. More than 40% BRCA1/2-deficient patients fail to respond to PARPi. In addition, lots of patients acquire PARPi resistance with prolonged oral administration of PARPi. Homologous recombination repair deficient (HRD), as an essential prerequisite of synthetic lethality, plays a vital role in killing tumor cells. Therefore, Homologous recombination repair restoration (HRR) becomes the predominant reason of PARPi resistance. Recently, it was reported that DNA replication fork protection also contributed to PARPi resistance in BRCA1/2-deficient cells and patients. Moreover, various factors, such as reversion mutations, epigenetic modification, restoration of ADP-ribosylation (PARylation) and pharmacological alteration lead to PARPi resistance as well. In this review, we reviewed the underlying mechanisms of PARP inhibitor resistance in detail and summarized the potential strategies to overcome PARPi resistance and increase PARPi sensitivity.
Journal Article