Analgesic use and the risk of renal cell carcinoma (RCC): Results from a large up-to-date meta-analysis.

2012 ◽  
Vol 30 (5_suppl) ◽  
pp. 395-395
Author(s):  
Eunyoung Cho ◽  
Youjin Je ◽  
Toni K. Choueiri

395 Background: Analgesics have been linked to an increased risk of developing renal cell carcinoma (RCC), but the evidence is mixed. Using a meta-analysis design of all available studies, we investigated the association between analgesic use and RCC risk. Methods: We searched the MEDLINE database to identify eligible case-control or cohort studies published in English from 1966 to July 1, 2011 for 3 categories of analgesics: acetaminophen, aspirin or other non-steroidal anti-inflammatory drugs (NSAIDs). Study-specific effect estimates were pooled to compute an overall relative risk (RR) and its 95% confidence interval (CI), using a random effects model, for each category of the analgesics. Analyses were conducted according to regular/any use and high dose or long-duration of use, separately. Results: We identified 18 studies (12 for acetaminophen, 12 for aspirin, and 5 for other NSAIDs) that were performed in 6 countries. Regular/any use of acetaminophen and other NSAIDs were each associated with an increased risk of RCC: pooled RR, 1.33 (95% CI 1.18-1.49) for acetaminophen and 1.26 (95% CI, 1.09-1.44) for other NSAIDs, respectively. For use of aspirin, we found no significant increased risk (pooled RR, 1.14 [95% CI, 0.98-1.33]). Similar risk trends were seen with high dose of analgesics intake. No significant difference in associations was found by study design (case-control vs. cohort), type of controls in case-control study (population based vs. hospital based), outcome (RCC vs. kidney cancer), and gender (male vs. female). There was no indication of publication bias for the 3 analgesics. Conclusions: In this meta-analysis of analgesics use and RCC risk, we found that use of acetaminophen and non-aspirin NSAIDs was associated with a significant increased risk of developing RCC.

2020 ◽  
Vol 35 (1) ◽  
pp. 57-64
Author(s):  
Jiajie Fang ◽  
Xuanli Xu ◽  
Qiqi Mao ◽  
Yufan Ying ◽  
Xu Zhang ◽  
...  

Background: Changes in circulating adiponectin have been related to the risks of various cancers. However, the association between circulating adiponectin and the risk of renal cell carcinoma has not been fully determined. A meta-analysis was performed to evaluate the relationship between circulating adiponectin and renal cell carcinoma risk. Methods: Observational studies that evaluated the association between circulating adiponectin and renal cell carcinoma risk were identified via a systematic search of PubMed and Embase databases. The difference between circulating adiponectin in renal cell carcinoma cases and healthy controls, and the multivariable adjusted association between circulating adiponectin and renal cell carcinoma risk were evaluated. A random effects model was used if significant heterogeneity existed; otherwise a fixed effects model was applied. Results: Eight case-control studies with 2624 renal cell carcinoma cases and 2904 healthy controls were included. Pooled results showed that circulating adiponectin was significantly lower in renal cell carcinoma cases than in healthy controls (mean difference = −1.08 ug/mL; 95% confidence interval (CI) −1.62, −0.54; P < 0.001). Higher circulating adiponectin was independently associated with a significantly lowered risk of renal cell carcinoma (adjusted odds ratio for 1 SD increment of adiponectin = 0.78; 95% CI: 0.63, 0.96; P = 0.02). Subgroup analyses according to characteristics including study design, ethnics of participants, blood samples, numbers of participants, mean ages of participants, and study quality showed consistent results. Conclusions: Lower circulating adiponectin is associated with increased risk of renal cell carcinoma. The potential pathophysiological mechanisms underlying the role of circulating adiponectin in the pathogenesis of renal cell carcinoma deserve further investigation.


2015 ◽  
Vol 25 (4) ◽  
pp. 339-344 ◽  
Author(s):  
Yonggang Shang ◽  
Shanhong Yi ◽  
Dong Cui ◽  
Guangwei Han ◽  
Chengcheng Liu

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. e20611-e20611
Author(s):  
Bilal Iqbal ◽  
Shenhong Wu

e20611 Background: Fatigue is one of the major side effects associated with targeted therapeutic agents in the treatment of renal cell carcinoma (RCC), and has negatively affected the optimal use of these drugs. Currently the risk of fatigue has not been well defined. We performed a systematic review and meta-analysis of published randomized controlled clinical trials (RCT) to determine the risk of fatigue in RCC patients treated with targeted therapy. Methods: Databases including PUBMED, Web of Science, and abstracts presented at the American Society of Clinical Oncology meetings up to October, 2012 were searched to identify relevant studies. Eligible studies included prospective RCTs in which a targeted therapy was compared to a control of non-targeted therapy (placebo or interferon) with data available. Incidences and relative risk (RR) were calculated using a random- or fixed-effects model depending on the heterogeneity of the included studies. Results: A total of 5,192 RCC patients (targeted therapy: 3023, control: 2092) from 11 RCTs were selected for analysis. The overall incidences of all-grade and high-grade (ie, grade 3 or above) fatigue were 45.4% (95% CI: 33.0-58.5%) and 7.6% (95% CI: 4.1-13.5%) respectively. The incidences varied significantly among different agents (P<0.001). In comparison with overall controls, the targeted therapy did not significantly increase the risk of all-grade (RR=1.07, 95% CI: 1.0-1.35, p=0.055) or high-grade fatigue (RR= 1.01, 95% CI: 0.68-1.50, P=0.95). However, the targeted therapy significantly increased the risk of all-grade fatigue (RR 1.60, 95% CI: 1.40-2.32; P<0.001), but not high-grade fatigue (RR 1.74, 95% CI: 0.91-3.32; P=0.095) when compared to placebo. There was no significant difference between the targeted therapy and interferon in the risk of all-grade (RR 1.02, 95% CI: 0.90-1.14; P=0.90) or high-grade fatigue (RR 0.86, 95% CI: 0.55-1.36; P=0.53). Conclusions: The targeted therapy may significantly increase the risk of fatigue in a magnitude comparable to interferon.


2009 ◽  
Vol 18 (3) ◽  
pp. 801-807 ◽  
Author(s):  
Jessica Clague ◽  
Jie Lin ◽  
Adrian Cassidy ◽  
Surena Matin ◽  
Nizar M. Tannir ◽  
...  

2008 ◽  
Vol 101 (8) ◽  
pp. 1228-1238 ◽  
Author(s):  
Kaye E. Brock ◽  
Gloria Gridley ◽  
Brian C.-H. Chiu ◽  
Abby G. Ershow ◽  
Charles F. Lynch ◽  
...  

An increased risk of renal cell carcinoma (RCC) has been linked with obesity. However, there is limited information about the contribution of dietary fat and fat-related food groups to RCC risk. A population-based case–control study of 406 cases and 2434 controls aged 40–85 years was conducted in Iowa (1986–89). For 323 cases and 1820 controls from the present study, information on dietary intake from foods high in fat nutrients and other lifestyle factors was obtained using a mailed questionnaire. Cancer risks were estimated by OR and 95 % CI, adjusting for age, sex, smoking, obesity, hypertension, physical activity, alcohol and vegetable intake and tea and coffee consumption. In all nutrient analyses, energy density estimates were used. Dietary nutrient intake of animal fat, saturated fat, oleic acid and cholesterol was associated with an elevated risk of RCC (OR = 1·9, 95 % CI 1·3, 2·9, Ptrend < 0·001; OR = 2·6, 95 % CI 1·6, 4·0, Ptrend < 0·001; OR = 1·9, 95 % CI 1·2, 2·9, Ptrend = 0·01; OR = 1·9, 95 % CI 1·3, 2·8, Ptrend = 0·006, respectively, for the top quartile compared with the bottom quartile of intake). Increased risks were also associated with high-fat spreads, red and cured meats and dairy products (OR = 2·0, 95 % CI 1·4, 3·0, Ptrend = 0·001; OR = 1·7, 95 % CI 1·0, 2·2, Ptrend = 0·01; OR = 1·8, 95 % CI 1·2, 2·7, Ptrend = 0·02; OR = 1·6, 95 % CI 1·1, 2·3, Ptrend = 0·02, respectively). In both the food groups and nutrients, there was a significant dose–response with increased intake. Our data also indicated that the association of RCC with high-fat spreads may be stronger among individuals with hypertension. These findings deserve further investigation in prospective studies.


2021 ◽  
Vol 12 ◽  
Author(s):  
Fengjun Sun ◽  
Zhuo Chen ◽  
Pu Yao ◽  
Bangbi Weng ◽  
Zhirui Liu ◽  
...  

Background: ABCG2 and ABCB1 are genes related to the pharmacokinetics of sunitinib and have been associated with its toxicity and efficacy. However, the results have been controversial. This study aimed to evaluate the associations of ABCG2 and ABCB1 polymorphisms with sunitinib-induced toxicity and efficacy in renal cell carcinoma (RCC) by meta-analysis.Methods:PubMed, EMBASE, Cochrane Library, and Web of Science were systematically searched for studies investigating the associations of the ABCG2 rs2231142 polymorphism with sunitinib-induced toxicity and the associations of the ABCB1 rs1128503 and ABCB1 rs2032582 polymorphisms with sunitinib-induced toxicity and clinical outcomes. The associations were evaluated by effect size (ES) with 95% confidence intervals (CIs).Results: Eight and five studies were included in the toxicity and efficacy analysis, respectively, including a total of 1081 RCC patients. The ABCG2 rs2231142 A allele was associated with an increased risk of sunitinib-induced thrombocytopenia and hand-foot syndrome (HFS) in Asians (ES = 1.65, 95% CI = 1.15–2.36, p = 0.006; ES = 1.52, 95% CI = 1.02–2.27, p = 0.041). However, the ABCG2 rs2231142 polymorphism was not associated with sunitinib-induced hypertension or neutropenia (ES = 1.09, 95% CI = 0.69–1.73, p = 0.701; ES = 0.87, 95% CI = 0.57–1.31, p = 0.501). Compared with the C allele, the ABCB1 rs1128503 T allele was associated with a decreased risk of sunitinib-induced hypertension but worse progression-free survival (PFS) (ES = 0.44, 95% CI = 0.26–0.77, p = 0.004; ES = 1.36, 95% CI = 1.07–1.73, p = 0.011). There was no significant association between the T allele or C allele of ABCB1 rs1128503 and overall survival (OS) (ES = 0.82, 95% CI = 0.61–1.10, p = 0.184). The ABCB1 rs2032582 T allele was associated with worse PFS than the other alleles (ES = 1.46, 95% CI = 1.14–1.87, p = 0.003), while there was no significant association between the T allele or other alleles and sunitinib-induced hypertension, HFS, or OS (ES = 0.77, 95% CI = 0.46–1.29, p = 0.326; ES = 1.02, 95% CI = 0.65–1.62, p = 0.919; ES = 1.32, 95% CI = 0.85–2.05, p = 0.215).Conclusion: The results indicate that the ABCG2 rs2231142 polymorphism may serve as a predictor of sunitinib-induced thrombocytopenia and HFS in Asians, while the ABCB1 rs1128503 polymorphism may serve as a predictor of sunitinib-induced hypertension, and both the ABCB1 rs1128503 and rs2032582 polymorphisms may serve as predictors of PFS in RCC. These results suggest a possible application of individualized use of sunitinib according to the genetic background of patients.


2013 ◽  
Vol 31 (6_suppl) ◽  
pp. 452-452
Author(s):  
Jolly Patel ◽  
Mayer N. Fishman ◽  
Dawn Goetz

452 Background: Administration of high-dose interleukin-2 (IL-2) in metastatic renal cell carcinoma (MRCC) has higher response and survival rates when compared to low dose or subcutaneous administration. In patients who achieve a response, it may be at the expense of more toxicity risk, from more doses. The association of the major response rate with the number of high dose boluses or cumulative dose received is of interest. The primary objective of this study is to evaluate a direct correlation with response and cumulative dose or the total number of doses received. Methods: A retrospective chart review was conducted of all patients at H. Lee Moffitt Cancer Center diagnosed with metastatic renal cell carcinoma who received high dose bolus IL-2 from September 30th, 1999 to September 30th, 2010. The cumulative dose and the number of doses of IL-2 received was recorded and associated with categorical complete response [CR], partial response [PR], stable disease [SD] or progressive disease [PD] response, by treating physician assessment. Sites of metastasis were also documented. The incidence of adverse effects such as renal failure, transaminitis, cardiac arrhythmias, thrombocytopenia as well as rates of infection and ICU transfers were tabulated. Results: 31 out of 55 patients analyzed were assessed at least with stable disease in response to IL-2. Six achieved a CR, 11 achieved a PR, 14 had stable disease and 24 patients had PD as best responses. Among those with CR or PR to IL-2, they received approximately 30 doses of IL-2 (p=0.027 vs. those not in that category). Converesely, those who received a higher cumulative dose were also more likely to respond (p=0.0077). With respect to adverse events, 58% of patients experienced acute renal insufficiency, 63% transaminitis, 40% arrhythmias, and 45% thrombocytopenia. 55% required dopamine use at any point and 11% required use of additional pressors; 15% required an ICU transfer at some point, and approximately 4% developed a documented infection. Conclusions: Cumulative dose or number of high dose bolus doses received is associated with a statistically significant difference in response rate, within the limitations of this retrospective analysis.


2021 ◽  
Author(s):  
YuPeng Liu ◽  
Lin Ma ◽  
YuXue Zhang ◽  
ZhiGang Wu ◽  
Xiaodong Liu

Abstract Purpose: Renal cell carcinoma (RCC) is becoming more common as a urinary system malignancy. There is a growing body of evidence supporting an important role of DNA methylation alteration involved in the initiation of RCC, but the current findings are inconsistent and controversial. Thus, we performed this systematic review and meta-analysis to comprehensively assess the associations between methylation status of tumour suppressor genes and the incidence risk of RCC. Methods: This study has been registered on PROSPERO (CRD42019130782) and was reported according to the PRISMA guidelines. We systematically searched the PubMed, EMBASE and CNKI databases for relevant studies. The effect estimates were summarized using random-effect models. Results: A total of 21 case-control studies containing 1,912 participants were included. Overall, abnormal hypermethylation of RASSF1A was associated with a significantly increased risk of RCC (OR, 6.612, 95% CI: 1.926-22.697, P = 0.003), especially in the American populations (OR, 18.429, 95% CI: 3.072-110.536, P = 0.001). An increased RCC risk was also associated with hypermethylation of SFRP1 and GSTP1 (OR, 3.995, 95% CI: 1.607-9.934, P = 0.003; OR, 4.508, 95% CI: 1.004-20.239, P = 0.049; respectively); however, the results for SFRP1 and GSTP1 were non-conclusive due to the limited number of studies included and the inconsistency across sensitivity analyses. There was no obvious association for the other genes. Conclusion: This study demonstrated a statistically and robustly positive association of aberrant hypermethylation of RASSF1A with an increased risk of developing RCC, indicating a potentially useful biomarker to predict the RCC incidence risk.


2016 ◽  
Vol 34 (2_suppl) ◽  
pp. 511-511 ◽  
Author(s):  
Joseph Clark ◽  
Michael A. Morse ◽  
Michael K.K. Wong ◽  
David F. McDermott ◽  
Howard Kaufman ◽  
...  

511 Background: HD IL-2 is FDA approved for advanced renal cell carcinoma (mRCC), however, the data supporting its use is 23 years old. In 2011, a HD IL-2 patient database was established called PROCLAIMSM, and comprises the largest active prospective collection of data from mRCC and metastatic melanoma (MM) patients receiving HD IL-2 treatment and provides longitudinal real-time insights into the clinical impact of sequencing drug treatments. These data report on the outcomes and interactions with prior targeted therapies in mRCC patients in the current era. Methods: Inclusion criteria require patients to receive at least one dose of HD IL-2. Patients who received HD IL-2 and had already undergone a post-treatment scan were not eligible. Survival analysis was performed by the method of Kaplan and Meier using datasets as of July 27, 2015. Results: The overall response rate (ORR) and median overall survival (mOS) are described in Table 1. The mOS was not reached (NR) for 364 patients. The 1, 2 and 3 year survival rates were 79%, 63%, and 51%, respectively. For patients with stable disease (SD), the mOS was not reached and the 1, 2 and 3 year survival rates were 96%, 80%, and 60% respectively. There was a significant difference in mOS between SD and progressive disease (PD) patients, NR vs 15.5 months, P<.0001. The mOS was not reached for patients regardless of whether or not they received targeted therapy (TT) prior to HD IL-2. There were 4 reported treatment-related deaths in 364 patients (1.1%), none of these patients had prior TT. Conclusions: PROCLAIM data demonstrate that SD, previously grouped with the non-responders, is associated with extended survival rates. HD IL-2 is an active 2ndline treatment option for patients who have failed TT. These data support that HD IL-2 has a favorable safety profile and remains an effective therapy for eligible patients with mRCC. Clinical trial information: NCT01415167. [Table: see text]


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