Meta-analysis of P53 expression and sensitivity to platinum-based chemotherapy in patients with non-small cell lung cancer

Abstract

Background: The relationship between p53 expression and chemosensitivity of non-small cell lung cancer (NSCLC) is unclear. This study aims to explore the correlation between p53 expression and sensitivity to platinum-based chemotherapy in patients with NSCLC. Methods: Pubmed, Web of Science, EMBASE, CNKI, China Wanfang databases were searched for studies on the relationship between the p53 expression and the chemosensitivity to platinum drugs in patients with NSCLC. The last search time was May 2020. Stata 15.0 software was used for statistical analysis. Results: A total of 21 studies were included, covering 1387 patients in total. The results showed that the pooled OR = 1.55 (95%CI: 1.05∼2.29, P < .05), for Asian population, the pooled OR = 1.67 (95%CI: 0.95∼3.09, P > .05), for Caucasian population, the pooled OR = 1.34 (95%CI: 0.74∼2.43), there was no significant difference between Asian and Caucasian. The results of subgroup analysis of publication year showed that, the pooled OR = 2.07 (95%CI: 1.39∼3.07, P < .01), the heterogeneity among the studies decreased remarkably after 2005. The subgroup analysis of advanced patients showed that the pooled OR = 1.93 (95%CI: 1.27∼2.93), the difference was statistically significant. Conclusion: Patients with p53 negative expression is more sensitive to platinum-based chemotherapy than those with p53 positive expression in NSCLC, especially in advanced NSCLC.

Transcriptome-based stemness indices analysis reveals platinum-based chemo-theraputic response indicators in advanced-stage serous ovarian cancer

“…These key genes were mainly involved in the ‘cell cycle’ pathway ( Figure 3(b) ). Interestingly, the selected key genes were also enriched to the platinum response-associated pathways ‘cellular senescence’ [ 19 , 20 ], ‘p53 signaling pathway’ [ 21 , 22 ], and ‘platinum drug resistance’ ( Figure 3(b) ). Cell cycle arrest was also the main molecular mechanism of the platinum anticancer effect [ 23 , 24 ].…”

“…This confirmed the uncontrolled cell proliferation was a core characteristic of OC cells as well as the ovarian cancer stem cells (OVSCSs) [ 35 ]. Previous studies reported that the pathway ‘Cell cycle’ [ 23 , 24 ], ‘Cellular senescence’ [ 19 , 20 ], ‘p53 signaling pathway’ [ 21 , 22 ], and ‘Platinum drug resistance’ were closely associated with platinum response. A recent review had summarized that an insufficient dose of platinum might lead to a cytostatic response, named dormancy, rather than cytotoxic response, through inducing cell cycle arrest and cellular senescence [ 36 ].…”

Treatment outcome according to genetic tumour alterations and clinical characteristics in digestive high-grade neuroendocrine neoplasms

“…TP53 mutations or abnormal p53 protein expression is associated with platinum resistance for several cancers [18,19]. TP53 mutations are frequent in NEC (51-89%) [15,[20][21][22].…”