scholarly journals Risk factors for dementia onset in older adults with metastatic renal cell carcinoma

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 701-702
Author(s):  
Samuel Miller ◽  
Lauren Wilson ◽  
Melissa Greiner ◽  
Jessica Pritchard ◽  
Tian Zhang ◽  
...  

Abstract Renal dysfunction is a driver of dementia. It is also associated with renal cell carcinoma, possibly the result of the tumor itself or from cancer treatment. This study evaluates metastatic renal cell carcinoma (mRCC) as a risk factor for developing mild cognitive impairment or dementia (MCI/D) as well as the impact of RCC-directed therapies on the development of MCI/D. We identified all patients diagnosed with mRCC in SEER-Medicare from 2007-2015. The main outcome was incident MCI/D within one year of mRCC diagnosis or cohort entry. Exclusion criteria included age <65 at mRCC diagnosis and diagnosis of MCI/D within preceding year of mRCC diagnosis. Patients with mRCC (n=2,533) were matched to non-cancer controls (n=7,027) on age, sex, race, comorbidities and year. Cox proportional hazards regression showed that having mRCC (HR 8.52, 95% MCI/D 6.49-11.18, p<0.001) and being older (HR 1.05 for 1-year age increase, 95% MCI/D 1.03-1.07, p<0.001) were predictive of developing MCI/D. A second Cox proportional hazards regression of only patients with mRCC revealed that neither those initiating treatment with oral anticancer agents (OAAs) nor those who underwent nephrectomy were more likely to develop MCI/D. Black patients had a higher risk of dementia compared to white patients (HR 1.92, 95% MCI/D 1.02-3.59, p=0.047). In conclusion, patients with mRCC were more likely to develop MCI/D than those without mRCC. The medical and surgical therapies evaluated were not associated with increased incidence of MCI/D. The increased incidence of MCI/D in older adults with mRCC may be the result of the pathology itself.

2018 ◽  
Vol 36 (6_suppl) ◽  
pp. 693-693
Author(s):  
Kyle A Blum ◽  
Renzo DiNatale ◽  
Alejandro Sanchez ◽  
Nirmal T John ◽  
Eden Axler ◽  
...  

693 Background: Sarcomatoid differentiation is associated with poor clinical outcomes and is present in approximately 4% of patients with renal cell carcinoma (sRCC). However, limited studies have evaluated the impact of sarcomatoid differentiation among patients, especially with lower stage pT1−2 disease. Methods: This study evaluated 3,850 patients with RCC who underwent partial or radical nephrectomy between 2000−2017. Patients were divided into four groups for analysis: pT1−2NxMx RCC without sarcomatoid features, pT1−2NxMx sRCC, pT3−4 RCC without sarcomatoid features and pT3−4 sRCC. Clinicopathological outcomes including sex, race, age, primary histology, lymph node involvement and margin status were compared between groups using Chi−squared and T-tests. Overall survival rates were analyzed by constructing Kaplan−Meier curves, p−values were calculated using log−rank tests and fitting Cox proportional hazards models for adjusted analyses. Results: Among 3,850 cases, 168 (4.4%) sRCC patients were identified. Of these, 33 (19.6%) were pT1−2. The mean overall follow up time was 59.9 months. When comparing CSS between groups, survival was poorer in patients with sarcomatoid features regardless of pT stage (p < 0.0001). Of note, CSS was worse in sRCC pT1−2 patients compared to non−sarcomatoid pT3−4 patients. Overall survival (OS) results were similar, with sarcomatoid tumors having worse estimates on survival analysis (p < 0.0001). Conclusions: Patients with pT1−2 sRCC demonstrated worse CSS when compared to pT1-2 and pT3−T4 RCC without sarcomatoid features, regardless of primary histology. Sarcomatoid differentiation in low−stage disease may be a marker of poor oncologic outcomes requiring more vigilant surveillance and possible inclusion in adjuvant therapy trials. Our next step, which is currently ongoing, is to pursue a multi−institutional collaborative effort and establish a larger cohort of sRCC for analysis.


2013 ◽  
Vol 31 (15_suppl) ◽  
pp. e15538-e15538
Author(s):  
Peggy L. Lin ◽  
Sumanta Kumar Pal ◽  
Eric Jonasch ◽  
James E. Signorovitch ◽  
Zhimei Liu ◽  
...  

e15538 Background: NCCN guidelines recommend imaging at 2-6 months after initiation of targeted therapy for metastatic renal cell carcinoma (mRCC). This study assessed the association between guideline-adherent imaging and overall survival in mRCC. Methods: Thirty-six community-based medical oncologists/hematologists reviewed charts for ≤ 15 mRCC patients each. Included patients were aged ≥ 18 years and initiated 2nd targeted therapy in 2010 or later. Patients alive up to month 6 were categorized into 3 groups based on time of first imaging test: early (0-60 days), guideline-adherent (61-180 days), and delayed(> 180 days). Overall survival (OS) was compared using multivariable Cox proportional hazards models adjusted for age, gender, duration of mRCC, prior treatments, comorbidities, metastatic sites, 1st targeted therapy, ECOG and MSKCC status, 2nd targeted therapy, and progression status (based on symptoms or imaging) in the first 6 months on 2nd line therapy. Reasons for imaging were also assessed. Results: Among the 192 patients included in the analysis, 25 received early imaging, 136 received guideline-adherent imaging, and 31 received delayed imaging. First imaging tests were more likely due to worsening symptoms or changes in a palpable mass, as opposed to routine monitoring, among patients with delayed vs. guideline adherent imaging (20.0% vs. 7.1%, P = 0.005). After adjusting for baseline characteristics, guideline-adherent imaging was associated with a 64% lower hazard of death compared to delayed imaging (hazard ratio (HR) = 0.36, 95% confidence interval (CI) 0.14 to 0.93, P = 0.035). Adjusted 1-year survival was 82% in the guideline-adherent compared to 67% in the delayed imaging group. The hazard of death did not differ between those with early vs. guideline-adherent imaging (HR = 1.05, 95% CI 0.35-3.12, P = 0.927). Conclusions: Among patients surviving 6 months after the initiation of 2nd targeted therapy for mRCC, timely first imaging within 2-6 months, consistent with guidelines, was associated with significantly prolonged overall survival compared to delayed imaging. Further investigation is warranted with larger samples.


2017 ◽  
Vol 10 (1) ◽  
pp. 3-10 ◽  
Author(s):  
Reza Mehrazin ◽  
Essel Dulaimi ◽  
Robert G. Uzzo ◽  
Karthik Devarjan ◽  
Jianming Pei ◽  
...  

Background: The proto-oncogene c-MYC, located on chromosome 8q, can be upregulated through gain of 8q, causing alteration in biology of renal cell carcinoma (RCC). The aim of this study was to evaluate the prevalence of c-MYC through chromosome 8q gain and to correlate findings with cancer-specific mortality (CSM), and overall survival (OS). Methods: Cytogenetic analysis by conventional or Chromosomal Genomic Microarray Analysis (CMA) was performed on 414 renal tumors. Nonclear and nonpapillary RCC were excluded. Impact of gain in chromosome 8q status on CSM, OS, and its correlation with clinicopathological variables were evaluated. CSM and OS were assessed using log-rank test and the Cox proportional hazards model. Results: A total of 297 RCC tumors with cytogenetic analysis were included. Gain of 8q was detected in 18 (6.1%) tumors (9 clear cell and 9 papillary RCC), using conventional method ( n = 11) or CMA ( n = 7). Gain of 8q was associated with higher T stage ( p < 0.001), grade ( p < 0.001), nodal involvement ( p = 0.005), and distant metastasis ( p < 0.001). No association between gain of 8q and age ( p = 0.23), sex ( p = 0.46), and Charlson comorbidity index (CCI, p = 0.59) were seen. Gain of 8q was associated with an 8.38-fold [95% confidence interval (CI), 3.83–18.34, p < 0.001] and 3.31-fold (95% CI, 1.56–7.04, p = 0.001) increase in CSM and decrease in OS, respectively, at a median follow up of 56 months. Conclusion: Chromosome 8q harbors the proto-oncogene c-MYC, which can be upregulated by gain of 8q. Our findings suggest that gain of 8q, can predict aggressive tumor phenotype and inferior survival in RCC.


2017 ◽  
Vol 197 (4S) ◽  
Author(s):  
Suguru Shirotake ◽  
Hideyuki Kondo ◽  
Yota Yasumizu ◽  
Koshiro Nishimoto ◽  
Nobuyuki Tanaka ◽  
...  

2019 ◽  
Vol 201 (Supplement 4) ◽  
Author(s):  
Florian Janisch ◽  
Constantin Fühner ◽  
Christian P. Meyer ◽  
Tobias Hillemacher ◽  
Thomas Klotzbücher ◽  
...  

PLoS ONE ◽  
2020 ◽  
Vol 15 (11) ◽  
pp. e0242429
Author(s):  
Shian-Ying Sung ◽  
Trang Thi Huynh Le ◽  
Jin- Hua Chen ◽  
Teng-Fu Hsieh ◽  
Chia-Ling Hsieh

Elevated Renal cell carcinoma (RCC) risk has been associated with the use of several antihypertensive medications but has not yet been elucidated in the populations prescribed alpha-1 blockers that are commonly used in the treatment of hypertension and lower urinary tract symptoms associated with benign prostatic hyperplasia (LUTS-BPH). The aim of the present study was to investigate the association between alpha-1 blocker use and the risk of developing RCC using a nationwide population-based database in Taiwan. Patients who were treated with alpha-1 blockers for at least 28 days were identified through the Taiwan National Health Insurance Research Database from 2000 to 2010. The unexposed participants were matched with the exposed cases according to age, sex, and index year at a ratio of 3:1. Cox proportional hazards regression, stratified by sex and comorbidities and adjusted for age, was performed to estimate hazard ratios (HRs) for the risk of subsequent RCC. Among 2,232,092 subjects, patients who received alpha-1 blocker treatment had a higher risk of RCC than the unexposed group. Taking into account hypertension and BPH, the adjusted HR was significantly higher in male alpha-1 blocker users who had no BPH and either the presence (HR: 1.63, 95% confidence interval [CI] = 1.22–2.18) or absence (HR: 2.31, 95% CI = 1.40–3.81) of hypertension than in men not receiving these drugs. Taken together, male alpha-1 blocker users who had no comorbidity of BPH exhibited an increased risk for developing RCC independent of hypertension. Further study is warranted to elucidate the underlying mechanisms of this association.


2015 ◽  
Vol 194 (4) ◽  
pp. 1112-1119 ◽  
Author(s):  
Ji-Yeon Kim ◽  
Se-Hoon Lee ◽  
Kyung Chul Moon ◽  
Cheol Kwak ◽  
Hyeon Hoe Kim ◽  
...  

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Huan Zhou ◽  
Jun Dong ◽  
Liyi Guo ◽  
Xicheng Wang ◽  
Kailin Wang ◽  
...  

AbstractB7-H6, a member of the B7 family molecules, participates in the clearance of tumor cells by binding to NKp30 on NK cells. B7-H6 expression level in esophageal squamous cell carcinoma (ESCC) and the clinical value remain unknown. The goal of this study was to determine the expression of B7-H6 in ESCC and further explore its clinical significance. We retrospectively collected the clinical data of 145 patients diagnosed with ESCC between January 2007 and December 2008. The expression of B7-H6 of the pathological tissue samples was detected by immunohistochemistry. The chi-square (χ2) test was used to analyse the relationships of B7-H6 and clinicopathological characteristics. Survival and hazard functions were estimated using the Kaplan-Meier method, and survival between groups was compared using the two-sided log-rank test. The Cox proportional hazards regression model was used to adjust for the risk factors related to overall survival (OS). 133/145 (91.72%) of the ESCC tissue samples exhibited B7-H6 expression. The expression level of B7-H6 was correlated with T stage (P = 0.036) and lymphatic metastasis status (P = 0.044). High B7-H6 expression (P = 0.003) was associated with a significantly worse OS than low B7-H6 expression. Multivariate Cox proportional hazards regression analysis demonstrated that tumour size (P = 0.021), B7-H6 expression (P = 0.025) and lymphatic metastasis status (P = 0.049) were independent prognostic factors of OS for ESCC. Collectively, our findings suggest that B7-H6 is widely expressed in ESCC samples. And B7-H6 may represent a predictor of poor prognosis for ESCC.


Sign in / Sign up

Export Citation Format

Share Document