scholarly journals p21-activated kinase 1 (PAK1) expression correlates with prognosis in solid tumors: A systematic review and meta-analysis

Oncotarget ◽  
2016 ◽  
Vol 7 (19) ◽  
pp. 27422-27429 ◽  
Author(s):  
Fang Fang ◽  
Jian Pan ◽  
Yi-Ping Li ◽  
Gang Li ◽  
Li-Xiao Xu ◽  
...  
Cancers ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 998 ◽  
Author(s):  
Alice Indini ◽  
Fausto Petrelli ◽  
Gianluca Tomasello ◽  
Erika Rijavec ◽  
Antonio Facciorusso ◽  
...  

We performed a systematic review and meta-analysis to evaluate the role of gastric acid suppressant use on outcomes of tyrosine kinase inhibitors (TKIs) and oral chemotherapy. We identified all research evaluating the effect of GAS (gastric acid suppressants) use on patients receiving oral chemotherapy or TKIs for solid tumors. The pooled hazard ratios (HRs) and 95% confidence interval (95%CI) for overall survival (OS) and progression-free survival (PFS) were calculated with a fixed-effects or a random effects model. The study population included n = 16 retrospective studies and 372,418 patients. The series concerned gastrointestinal tract tumors (n = 5 studies), renal cell carcinomas (RCC, n = 3 studies), non-small cell lung cancers (NSCLC, n = 5 studies), and soft tissue sarcomas or mixed histologies solid tumors in n = 3 studies. The pooled HRs for OS and PFS were 1.31 (95%CI: 1.20–1.43; p < 0.01) and 1.3 (95%CI 1.07–1.57; p < 0.01) for GAS and no GAS users, respectively. Only studies of EGFR (epidermal growth factor receptor) mutated NSCLC patients receiving TKIs and those with colorectal cancer receiving oral chemotherapy showed a significant correlation between GAS and poor survival. Our study supports the evidence of a possible negative impact of concomitant GAS therapy on survival outcomes of patients receiving oral anti-cancer drugs.


Oncotarget ◽  
2016 ◽  
Vol 8 (1) ◽  
pp. 303-314 ◽  
Author(s):  
Li-Na Zhou ◽  
Yue Tan ◽  
Ping Li ◽  
Ping Zeng ◽  
Min-Bin Chen ◽  
...  

2019 ◽  
Vol 30 ◽  
pp. v25 ◽  
Author(s):  
M.G. McNamara ◽  
T. Jacobs ◽  
M. Frizziero ◽  
R. Pihlak ◽  
A. Lamarca ◽  
...  

2018 ◽  
Vol 49 (1) ◽  
pp. 134-143 ◽  
Author(s):  
Cheng-Peng Yu ◽  
Shu-Fang Fu ◽  
Xuan Chen ◽  
Jing Ye ◽  
Yuan Ye ◽  
...  

Background/Aims: Indoleamine 2,3-dioxygenase 1 (IDO1) is a heme-containing enzyme catalyzing the initial and rate-limiting steps in the kynurenine pathway, which converts tryptophan into kynurenine. Upregulation of IDO1 decreases tryptophan levels and increases the accumulation of kynurenine and its metabolites. These metabolites can affect the proliferation of T cells. Increasing evidence has shown that IDO1 is highly expressed in various cancer types and associated with poor prognosis of cancer patients. However, the results were inconsistent. Methods: We searched the Web of Science, PubMed, Embase and Cochrane library databases to identify studies evaluating the prognostic value of IDO1 in cancer patients. Pooled hazard ratios (HRs) or odds ratios (ORs) with 95% confidence intervals (CIs) were calculated by using fixed-effects/random-effects models. Results: This systematic review and meta-analysis included 2706 patients from 24 articles. The results indicated a shorter overall survival in patients with high expression of IDO1 (hazard ratio [HR] = 2.03, 95% confidence interval [CI]: 1.56-2.63). Furthermore, disease-free survival was worse in patients with high expression of IDO1 (HR = 2.47, 95% CI: 1.46-4.20). Additionally, the pooled odds ratios (ORs) showed that increased IDO1 was significantly associated with tumor differentiation (OR = 1.81, 95% CI: 1.05-3.12), distant metastasis (OR = 1.45, 95% CI: 1.02-2.06), and poor clinical stage (OR = 1.89, 95% CI: 1.13-3.17). However, no significant correlation was observed of increased IDO1 expression with age, sex, lymph node metastasis, and tumor size. Conclusion: High expression of IDO1 is associated with poor clinical outcomes. IDO1 could serve as a biomarker of prognosis and a potential predictive factor of clinicopathology in various cancers. Further studies should be performed to verify the clinical utility of IDO1 in human solid tumors.


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