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471 results on '"Xu, Manman"'

18. Comparison of the profiles of first-line PD-1/PD-L1 inhibitors for advanced NSCLC lacking driver gene mutations: a systematic review and Bayesian network meta-analysis

Author

Fu Wenfan, Xu Manman, Shi Xingyuan, Jiang Zeyong, Zhao Jian, and Dai Lu

Subjects
Therapeutics. Pharmacology, RM1-950
Abstract

Background: Numerous first-line immune checkpoint inhibitors (ICI) were developed for patients with advanced non-small cell lung cancer (NSCLC) lacking driver gene mutations. However, this group consists of a heterogeneous patient population, for whom the optimal therapeutic choice is yet to be confirmed. Objective: To identify the best first-line immunotherapy regimen for overall advanced NSCLC patients and different subgroups. Design: Systematic review and Bayesian network meta-analysis (NMA). Methods: We searched several databases to retrieve relevant literature. We performed Bayesian NMA for the overall survival (OS), progression-free survival (PFS), objective response rate (ORR), and treatment-related adverse events (tr-AEs) with a grade equal or more than 3 (grade ⩾ 3 tr-AEs). Subgroup analysis was conducted according to programed death ligand 1 (PD-L1) levels, histologic type, central nervous system (CNS) metastases and tobacco use history. Results: For the PD-L1 non-selective patients, sintilimab plus chemotherapy (sinti-chemo) provided the best OS [hazard ratio (HR) = 0.59, 95% confidence interval (CI):0.42–0.83]. Nivolumab plus bevacizumab plus chemotherapy (nivo-bev-chemo) was comparable to atezolizumab plus bevacizumab plus chemotherapy (atezo-bev-chemo) in prolonging PFS (HR = 0.99, 95% CI: 0.51–1.91). Atezo-bev-chemo remarkably elevated the ORR than chemotherapy (OR = 3.13, 95% CI: 1.51–6.59). Subgroup analysis showed pembrolizumab plus chemotherapy (pembro-chemo) ranked first in OS in subgroups of PD-L1

Published
2023
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39. ODF2L acts as a synthetic lethal partner with WEE1 inhibition in epithelial ovarian cancer models

Author

Li, Jie, Lu, Jingyi, Xu, Manman, Yang, Shiyu, Yu, Tiantian, Zheng, Cuimiao, Huang, Xi, Pan, Yuwen, Chen, Yangyang, Long, Junming, Zhang, Chunyu, Huang, Hua, Dai, Qingyuan, Li, Bo, Wang, Wei, Yao, Shuzhong, and Pan, Chaoyun

Subjects
Oncology, Experimental, Gene expression -- Research, Epithelial tumors -- Genetic aspects -- Development and progression, Protein kinases -- Health aspects -- Genetic aspects, Ovarian cancer -- Genetic aspects -- Development and progression, Cancer -- Research, Molecular targeted therapy -- Research, Health care industry
Abstract

WEE1 has emerged as an attractive target in epithelial ovarian cancer (EOC), but how EOC cells may alter their sensitivity to WEE1 inhibition remains unclear. Here, through a cell cycle machinery- related gene RNAi screen, we found that targeting outer dense fiber of sperm tails 2-like (ODF2L) was a synthetic lethal partner with WEE1 kinase inhibition in EOC cells. Knockdown of ODF2L robustly sensitized cells to treatment with the WEE1 inhibitor AZD1775 in EOC cell lines in vitro as well as in xenografts in vivo. Mechanistically, the increased sensitivity to WEE1 inhibition upon ODF2L loss was accompanied by accumulated DNA damage. ODF2L licensed the recruitment of PKMYT1, a functionally redundant kinase of WEE1, to the CDK1-cyclin B complex and thus restricted the activity of CDK1 when WEE1 was inhibited. Clinically, upregulation of ODF2L correlated with CDK1 activity, DNA damage levels, and sensitivity to WEE1 inhibition in patient-derived EOC cells. Moreover, ODF2L levels predicted the response to WEE1 inhibition in an EOC patient- derived xenograft model. Combination treatment with tumor-targeted lipid nanoparticles that packaged ODF2L siRNA and AZD1775 led to the synergistic attenuation of tumor growth in the ID8 ovarian cancer syngeneic mouse model. These data suggest that WEE1 inhibition is a promising precision therapeutic strategy for EOC cells expressing low levels of ODF2L., Introduction Epithelial ovarian cancer (EOC), the most common subtype of ovarian cancer, ranks fifth in cancer-related deaths among women (1, 2). EOC is more than a single disease, as it [...]

Published
2023
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42. Hepatocyte-Specific Fads1 Overexpression Attenuates Western Diet-Induced Metabolic Phenotypes in a Rat Model.

Author

Ghooray, Dushan T., Xu, Manman, Shi, Hongxue, McClain, Craig J., and Song, Ming

Subjects
*FATTY acid desaturase, *MONOUNSATURATED fatty acids, *FRUCTOSE, *ANIMAL disease models, *PHENOTYPES, *UNSATURATED fatty acids, *INSULIN
Abstract

Fatty acid desaturase 1 (FADS1) is a rate-limiting enzyme in long-chain polyunsaturated fatty acid (LCPUFA) synthesis. Reduced activity of FADS1 was observed in metabolic dysfunction-associated steatotic liver disease (MASLD). The aim of this study was to determine whether adeno-associated virus serotype 8 (AAV8) mediated hepatocyte-specific overexpression of Fads1 (AAV8-Fads1) attenuates western diet-induced metabolic phenotypes in a rat model. Male weanling Sprague-Dawley rats were fed with a chow diet, or low-fat high-fructose (LFHFr) or high-fat high-fructose diet (HFHFr) ad libitum for 8 weeks. Metabolic phenotypes were evaluated at the endpoint. AAV8-Fads1 injection restored hepatic FADS1 protein levels in both LFHFr and HFHFr-fed rats. While AAV8-Fads1 injection led to improved glucose tolerance and insulin signaling in LFHFr-fed rats, it significantly reduced plasma triglyceride (by ~50%) and hepatic cholesterol levels (by ~25%) in HFHFr-fed rats. Hepatic lipidomics analysis showed that FADS1 activity was rescued by AAV8-FADS1 in HFHFr-fed rats, as shown by the restored arachidonic acid (AA)/dihomo-γ-linolenic acid (DGLA) ratio, and that was associated with reduced monounsaturated fatty acid (MUFA). Our data suggest that the beneficial role of AAV8-Fads1 is likely mediated by the inhibition of fatty acid re-esterification. FADS1 is a promising therapeutic target for MASLD in a diet-dependent manner. [ABSTRACT FROM AUTHOR]

Published
2024
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