Impact of the comprehensive geriatric assessment on treatment decision in geriatric oncology
BMC CANCER
Authors: Sourdet, Sandrine; Brechemier, Delphine; Steinmeyer, Zara; Gerard, Stephane; Balardy, Laurent
Abstract
BackgroundThe comprehensive geriatric assessment (CGA) is the gold standard in geriatric oncology to identify patients at high risk of adverse outcomes and optimize cancer and overall management. Many studies have demonstrated that CGA could modify oncologic treatment decision. However, there is little knowledge on which domains of the CGA are associated with this change. Moreover, the impact of frailty and physical performance on change in cancer treatment plan has been rarely assessed.MethodsThis is a cross-sectional study of older patients with solid or hematologic cancer referred by oncologists for a geriatric evaluation before cancer treatment. A comprehensive geriatric assessment was performed by a multidisciplinary team to provide guidance for treatment decision. We performed a multivariate analysis to identify CGA domains associated with change in cancer treatment plan.ResultsFour hundred eighteen patients, mean age 82.85.5, were included between October 2011 and January 2016, and 384 of them were referred with an initial cancer treatment plan. This initial cancer treatment plan was changed in 64 patients (16.7%). In multivariate analysis, CGA domains associated with change in cancer treatment plan were cognitive impairment according to the MMSE score (p=0.020), malnutrition according to the MNA score (p=0.023), and low physical performance according to the Short Physical Performance Battery (p=0.010).Conclusion p id=Par Cognition, malnutrition and low physical performance are significantly associated with change in cancer treatment plan in older adults with cancer. More studies are needed to evaluate their association with survival, treatment toxicity and quality of life. The role of physical performance should be specifically explored.
Protective Effects of Chlorogenic Acid on Cerebral lschemia/Reperfusion Injury Rats by Regulating Oxidative Stress-Related Nrf2 Pathway
DRUG DESIGN DEVELOPMENT AND THERAPY
Authors: Liu, Dequan; Wang, Huilin; Zhang, Yangang; Zhang, Zhan
Abstract
Introduction: Cerebral ischemia-reperfusion (CI/R) injury is caused by blood flow recovery after ischemic stroke. Chlorogenic acid (CGA, 5-O-caffeoylquinic acid) is a major polyphenol component of Coffea canephora, Coffea arabica L. and Mate (Ilex paraguariensis A. StHil.). Previous studies have shown that CGA has a significant neuroprotective effect and can improve global CI/R injury. However, the underlying molecular mechanism of CGA in CI/R injury has not been fully revealed. Materials: In this study, CI/R rat model was constructed. The rats were randomly divided into nine groups with ten in each group: Control, CGA (500 mg.kg-1), CI/R, CI/R + CGA (20 mg.kg-1), CI/R + CGA (100 mg.kg-1), CI/R + CGA (500 mg.kg-1), ML385 (30 mg.kg-1), CI/R + ML385 (30 mg.kg-1), CI/R + CGA + ML385. Cerebral infarction volume was detected by TTC staining. Brain pathological damage was detected by H&E staining. Apoptosis of cortical cells was detected by TUNEL staining. The expression of related proteins was detected by RT-qPCR and Western blotting. Results: Step-down test and Y maze test showed that CGA dose-dependently mitigated CI/R-induced brain damage and enhanced learning and spatial memory. Besides, CGA promoted the expression of BDNF and NGF in a dose-dependent manner and alleviated CI/R-induced nerve injury. Moreover, CGA increased the activity of SOD and the level of GSH, as well as decreased production of ROS and LDH and the accumulation of MDA. Notably, CGA attenuated oxidative stress-induced brain injury and apoptosis and inhibited the expression of apoptosis-related proteins (cleaved caspase 3 and caspase 9). Additionally, CGA reversed CI/R induced inactivation of Nrf2 pathway and promoted Nrf2, NQO-1 and HO-1 expression. Nrf2 pathway inhibitor ML385 destroyed this promotion. Discussion: All the data indicated that CGA had a neuroprotective effect on the CI/R rats by regulating oxidative stress-related Nrf2 pathway.