Obesity and renal cell carcinoma: epidemiology, underlying mechanisms and management considerations

2009 ◽  
Vol 9 (7) ◽  
pp. 975-987 ◽  
Author(s):  
Zachary Klinghoffer ◽  
Brian Yang ◽  
Anil Kapoor ◽  
Jehonathan H Pinthus
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Underlying Mechanisms

scholarly journals Alpha-1 blocker use increased risk of subsequent renal cell carcinoma: A nationwide population-based study in Taiwan

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
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Proportional Hazards ◽  
Population Based ◽  
Cox Proportional Hazards ◽  
Research Database ◽  
Antihypertensive Medications ◽  
Increased Risk ◽  
Underlying Mechanisms

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.

scholarly journals HMGCR inhibition stabilizes the glycolytic enzyme PKM2 to support the growth of renal cell carcinoma

PLoS Biology ◽  
2021 ◽  
Vol 19 (4) ◽  
pp. e3001197
Author(s):  
Jiajun Huang ◽  
Xiaoyu Zhao ◽  
Xiang Li ◽  
Jiwei Peng ◽  
Weihao Yang ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Tumor Development ◽  
Serum Levels ◽  
Glycolytic Enzyme ◽  
Hsp90 Expression ◽  
Cholesterol Biosynthetic Pathway ◽  
Underlying Mechanisms ◽  
Rate Limiting

Renal cell carcinoma (RCC) is responsible for most cases of the kidney cancer. Previous research showed that low serum levels of cholesterol level positively correlate with poorer RCC-specific survival outcomes. However, the underlying mechanisms and functional significance of the role of cholesterol in the development of RCC remain obscure. 3-Hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) plays a pivotal role in RCC development as it is the key rate-limiting enzyme of the cholesterol biosynthetic pathway. In this study, we demonstrated that the inhibition of HMGCR could accelerate the development of RCC tumors by lactate accumulation and angiogenesis in animal models. We identified that the inhibition of HMGCR led to an increase in glycolysis via the regulated HSP90 expression levels, thus maintaining the levels of a glycolysis rate-limiting enzyme, pyruvate kinase M2 (PKM2). Based on these findings, we reversed the HMGCR inhibition-induced tumor growth acceleration in RCC xenograft mice by suppressing glycolysis. Furthermore, the coadministration of Shikonin, a potent PKM2 inhibitor, reverted the tumor development induced by the HMGCR signaling pathway.

scholarly journals Intratumoral Fibrosis in Facilitating Renal Cancer Aggressiveness: Underlying Mechanisms and Promising Targets

2021 ◽  
Vol 9 ◽  
Author(s):  
Chao Hu ◽  
Yufeng Zhao ◽  
Xuanchuan Wang ◽  
Tongyu Zhu
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cancer Cells ◽  
Renal Cell ◽  
Tumor Stroma ◽  
Biological Processes ◽  
Future Studies ◽  
Cancer Aggressiveness ◽  
Underlying Mechanisms ◽  
Renal Fibrogenesis

Intratumoral fibrosis is a histologic manifestation of fibrotic tumor stroma. The interaction between cancer cells and fibrotic stroma is intricate and reciprocal, involving dysregulations from multiple biological processes. Different components of tumor stroma are implicated via distinct manners. In the kidney, intratumoral fibrosis is frequently observed in renal cell carcinoma (RCC). However, the underlying mechanisms remain largely unclear. In this review, we recapitulate evidence demonstrating how fibrotic stroma interacts with cancer cells and mechanisms shared between RCC tumorigenesis and renal fibrogenesis, providing promising targets for future studies.

scholarly journals Cytoreductive Nephrectomy Promoted Abscopal Effect of Camrelizumab Combined With Radiotherapy for Metastatic Renal Cell Carcinoma: A Case Report and Review of the Literature

2021 ◽  
Vol 12 ◽  
Author(s):  
Min Wu ◽  
Jie Liu ◽  
Samuel Seery ◽  
Xue Meng ◽  
Jinbo Yue
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Metastatic Renal Cell Carcinoma ◽  
Renal Cell ◽  
Tumor Burden ◽  
Abscopal Effect ◽  
Cytoreductive Nephrectomy ◽  
Immune Resistance ◽  
Programmed Cell Death 1 ◽  
Underlying Mechanisms

There is little evidence around Camrelizumab combined with cytoreductive nephrectomy (CN) and radiotherapy (RT) as a treatment option for metastatic renal cell carcinoma (mRCC). The influence of CN on immune responses and the abscopal effect are not well understood. In this paper, we report a case of anti-programmed cell death-1 (PD-1) treated with combined RT once CN reduced the primary tumor burden (TB). This patient also encountered an increased response to targeted radiotherapy after immune resistance. We also observed a macrophage-to-lymphocyte ratio (MLR) peak, which may be correlated with subsequent pseudoprogression after thoracic radiotherapy. Consequently, even with the disease, this patient has remained stable. This peculiar instance suggests there is a need to investigate the underlying mechanisms of CN in promoting the abscopal effect during immunotherapy when combined with RT. It also suggests that there is a need for further investigation into the role of RT in overcoming immune resistance, and the value of MLR in predicting pseudoprogression. We hypothesize that a heavy tumor burden might suppress the abscopal effect, thereby ensuring that CN promotes it. However, radiotherapy may overcome immune resistance during oligoprogression.

scholarly journals Hereditary Leiomyomatosis and Renal Cell Cancer: Recent Insights Into Mechanisms and Systemic Treatment

2021 ◽  
Vol 11 ◽  
Author(s):  
Congwang Zhang ◽  
Lijun Li ◽  
Yipeng Zhang ◽  
Changchun Zeng
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Molecular Mechanisms ◽  
Cell Cancer ◽  
Fumarate Hydratase ◽  
Hereditary Cancer Syndrome ◽  
Cancer Syndrome ◽  
Underlying Mechanisms ◽  
Hereditary Leiomyomatosis

Hereditary leiomyomatosis and renal cell carcinoma (HLRCC) is a rare autosomal dominant hereditary cancer syndrome characterized by a predisposition to cutaneous leiomyomas, uterine leiomyomas, and renal cell carcinoma (RCC). It is known to be caused by germline mutations of the fumarate hydratase (FH) gene, which encodes an enzyme component of the citric acid cycle and catalyzes the conversion of fumarate to L-malate. Currently, there is no standardized treatment for HLRCC, which may be due in part to a lack of understanding of the underlying mechanisms. Here, the underlying molecular mechanisms by which the inactivation of FH causes HLRCC are discussed. Additionally, potential therapeutic pharmacological strategies are also summarized to provide new perspectives for the prevention and treatment of HLRCC.

scholarly journals Identification of immunization-related new prognostic biomarkers for papillary renal cell carcinoma by integrated bioinformatics analysis

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Ping Wu ◽  
Tingting Xiang ◽  
Jing Wang ◽  
Run Lv ◽  
Shaoxin Ma ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Molecular Mechanism ◽  
Renal Cell ◽  
Immune Cell ◽  
Papillary Renal Cell Carcinoma ◽  
Functional Enrichment ◽  
Clear Understanding ◽  
Protein Protein Interaction ◽  
Underlying Mechanisms

Abstract Background Despite papillary renal cell carcinoma (pRCC) being the second most common type of kidney cancer, the underlying molecular mechanism remains unclear. Targeted therapies in the past have not been successful because of the lack of a clear understanding of the molecular mechanism. Hence, exploring the underlying mechanisms and seeking novel biomarkers for pursuing a precise prognostic biomarker and appropriate therapies are critical. Material and methods In our research, the differentially expressed genes (DEGs) were screened from the TCGA and GEO databases, and a total of 149 upregulated and 285 downregulated genes were sorted. This was followed by construction of functional enrichment and protein–protein interaction (PPI) network, and then the top 15 DEGs were selected for further analysis. The P4HB gene was chosen as our target gene by repetitively validating multiple datasets, and higher levels of P4HB expression predicted lower overall survival (OS) in patients with pRCC. Results We found that P4HB not only connects with immune cell infiltration and co-expression with PD-1, PD-L2, and CTLA-4, but also has a strong connection with the newly discovered hot gene, TOX. Conclusion We speculate that P4HB is a novel gene involved in the progression of pRCC through immunomodulation.

1253: Different Survival in PT3A Renal Cell Carcinoma with Sinus Fat Invasion or Perinephric Fat Invasion

2007 ◽  
Vol 177 (4S) ◽  
pp. 413-413
Author(s):  
Marco Roscigno ◽  
Roberto Bertini ◽  
Cesare Cozzarini ◽  
Alessandra Pasta ◽  
Mattia Sangalli ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Perinephric Fat

1252: Relative Survival Following Treatment for Renal Cell Carcinoma (RCC)- A S.E.E.R. Analysis: Is Age Important?

2007 ◽  
Vol 177 (4S) ◽  
pp. 413-413
Author(s):  
Yu-Ning Wong ◽  
Brian L. Egleston ◽  
Ismail R. Saad ◽  
Robert G. Uzzo
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Relative Survival

920: Pediatric Renal Cell Carcinoma: An Aggressive Tumor with Biologic Features Distinct From Its Adult Counterpart

2007 ◽  
Vol 177 (4S) ◽  
pp. 305-305
Author(s):  
Richard A. Ashley ◽  
Jonathan C. Routh ◽  
Sameer A. Siddiqui ◽  
Brant A. Inman ◽  
Thomas J. Sebo ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Pediatric Renal Cell Carcinoma ◽  
Aggressive Tumor
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