Special Issue "Renal Cell Carcinoma"

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: 30 November 2019

Special Issue Editor

Guest Editor
Prof. José I. López

Department of Pathology, Cruces University Hospital, Biocruces-Bizkaia Institute, University of the Basque Country (UPV/EHU), Barakaldo, Bizkaia, 48903 Spain
Website | E-Mail
Interests: translational uropathology; renal cancer; prostate cancer; urinary tract cancer

Special Issue Information

Dear Colleagues,

Renal cancer is a complex disease and a leading cause of mortality in Western countries. This tumor is regularly included in the top-ten list of the most frequent neoplasms, with around 77,000 new cases (44,120 in males and 29,700 in females) expected only in the USA in 2019. The growing aging and obesity rates detected in developed societies are factors that predict a continuous increase in the incidence of this tumor in the next decade. Further, renal cancer is a health problem of major concern considering its well-known chemo- and radio-resistance. In fact, although tyrosine kinase inhibitors and immune check-point blockade therapies are giving promising results, at present the only methods that have a direct impact on patients’ survival are early detection and surgery.

The spectrum of renal cell carcinoma subtypes is wide. Up to 70–80% of renal tumors are clear cell renal cell carcinomas, a clinically aggressive tumor subtype linked to VHL gene inactivation. Next in frequency, the papillary renal cell carcinoma category encompasses an intricate puzzle of classic and newly described entities with poorly defined limits, some of them pending definite clarification. Likewise, the chromophobe–oncocytoma duality, the so-called hybrid tumors and oncocytic neoplasms, not otherwise specified, remain to be well profiled. Finally, a growing list of very uncommon renal tumors linked to specific molecular signatures (SDH-deficient carcinomas, translocation renal cell carcinomas, etc.) fulfill the current portrait of renal cell neoplasia.

This Special Issue of Cancers intends to take a translational snapshot of the current knowledge in renal cancer, from the simplest clinical approach to the most sophisticated molecular methodology. More than ever, a multidisciplinary perspective is mandatory to solve contemporary dilemmas in this field.

Prof. José I. López
Guest Editor

Manuscript Submission Information

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Published Papers (3 papers)

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Research

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Open AccessArticle Rising Serum Uric Acid Level Is Negatively Associated with Survival in Renal Cell Carcinoma
Cancers 2019, 11(4), 536; https://doi.org/10.3390/cancers11040536
Received: 28 February 2019 / Revised: 11 April 2019 / Accepted: 11 April 2019 / Published: 15 April 2019
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Abstract
Aim and Background: To investigate the association of serum uric acid (SUA) levels along with statin use in Renal Cell Carcinoma (RCC), as statins may be associated with improved outcomes in RCC and SUA elevation is associated with increased risk of chronic kidney [...] Read more.
Aim and Background: To investigate the association of serum uric acid (SUA) levels along with statin use in Renal Cell Carcinoma (RCC), as statins may be associated with improved outcomes in RCC and SUA elevation is associated with increased risk of chronic kidney disease (CKD). Methods: Retrospective study of patients undergoing surgery for RCC with preoperative/postoperative SUA levels between 8/2005–8/2018. Analysis was carried out between patients with increased postoperative SUA vs. patients with decreased/stable postoperative SUA. Kaplan-Meier analysis (KMA) calculated overall survival (OS) and recurrence free survival (RFS). Multivariable analysis (MVA) was performed to identify factors associated with increased SUA levels and all-cause mortality. The prognostic significance of variables for OS and RFS was analyzed by cox regression analysis. Results: Decreased/stable SUA levels were noted in 675 (74.6%) and increased SUA levels were noted in 230 (25.4%). A higher proportion of patients with decreased/stable SUA levels took statins (27.9% vs. 18.3%, p = 0.0039). KMA demonstrated improved 5- and 10-year OS (89% vs. 47% and 65% vs. 9%, p < 0.001) and RFS (94% vs. 45% and 93% vs. 34%, p < 0.001), favoring patients with decreased/stable SUA levels. MVA revealed that statin use (Odds ratio (OR) 0.106, p < 0.001), dyslipidemia (OR 2.661, p = 0.004), stage III and IV disease compared to stage I (OR 1.887, p = 0.015 and 10.779, p < 0.001, respectively), and postoperative de novo CKD stage III (OR 5.952, p < 0.001) were predictors for increased postoperative SUA levels. MVA for all-cause mortality showed that increasing BMI (OR 1.085, p = 0.002), increasing ASA score (OR 1.578, p = 0.014), increased SUA levels (OR 4.698, p < 0.001), stage IV disease compared to stage I (OR 7.702, p < 0.001), radical nephrectomy (RN) compared to partial nephrectomy (PN) (OR 1.620, p = 0.019), and de novo CKD stage III (OR 7.068, p < 0.001) were significant factors. Cox proportional hazard analysis for OS revealed that increasing age (HR 1.017, p = 0.004), increasing BMI (Hazard Ratio (HR) 1.099, p < 0.001), increasing SUA (HR 4.708, p < 0.001), stage III and IV compared to stage I (HR 1.537, p = 0.013 and 3.299, p < 0.001), RN vs. PN (HR 1.497, p = 0.029), and de novo CKD stage III (HR 1.684, p < 0.001) were significant factors. Cox proportional hazard analysis for RFS demonstrated that increasing ASA score (HR 1.239, p < 0.001, increasing SUA (HR 9.782, p < 0.001), and stage II, III, and IV disease compared to stage I (HR 2.497, p < 0.001 and 3.195, p < 0.001 and 6.911, p < 0.001) were significant factors. Conclusions: Increasing SUA was associated with poorer outcomes. Decreased SUA levels were associated with statin intake and lower stage disease as well as lack of progression to CKD and anemia. Further investigation is requisite. Full article
(This article belongs to the Special Issue Renal Cell Carcinoma)
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Open AccessArticle Ghrelin Upregulates Oncogenic Aurora A to Promote Renal Cell Carcinoma Invasion
Cancers 2019, 11(3), 303; https://doi.org/10.3390/cancers11030303
Received: 21 January 2019 / Revised: 27 February 2019 / Accepted: 28 February 2019 / Published: 4 March 2019
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Abstract
Ghrelin is a peptide hormone, originally identified from the stomach, that functions as an endogenous ligand of the growth hormone secretagogue receptor (GHSR) and promotes growth hormone (GH) release and food intake. Increasing reports point out ghrelin’s role in cancer progression. We previously [...] Read more.
Ghrelin is a peptide hormone, originally identified from the stomach, that functions as an endogenous ligand of the growth hormone secretagogue receptor (GHSR) and promotes growth hormone (GH) release and food intake. Increasing reports point out ghrelin’s role in cancer progression. We previously characterized ghrelin’s prognostic significance in the clear cell subtype of renal cell carcinoma (ccRCC), and its pro-metastatic ability via Snail-dependent cell migration. However, ghrelin’s activity in promoting cell invasion remains obscure. In this study, an Ingenuity Pathway Analysis (IPA)-based investigation of differentially expressed genes in Cancer Cell Line Encyclopedia (CCLE) dataset indicated the potential association of Aurora A with ghrelin in ccRCC metastasis. In addition, a significant correlation between ghrelin and Aurora A expression level in 15 ccRCC cell line was confirmed by variant probes. ccRCC patients with high ghrelin and Aurora A status were clinically associated with poor outcome. We further observed that ghrelin upregulated Aurora A at the protein and RNA levels and that ghrelin-induced ccRCC in vitro invasion and in vivo metastasis occurred in an Aurora A-dependent manner. Furthermore, MMP1, 2, 9 and 10 expressions are associated with poor outcome. In particular, MMP10 is significantly upregulated and required for the ghrelin-Aurora A axis to promote ccRCC invasion. The results of this study indicated a novel signaling mechanism in ccRCC metastasis. Full article
(This article belongs to the Special Issue Renal Cell Carcinoma)
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Open AccessCommentary Renal Cell Carcinoma with Sarcomatoid Features: Finally New Therapeutic Hope?
Cancers 2019, 11(3), 422; https://doi.org/10.3390/cancers11030422
Received: 7 March 2019 / Revised: 21 March 2019 / Accepted: 22 March 2019 / Published: 25 March 2019
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Abstract
Renal cell carcinoma (RCC) with sarcomatoid differentiation belongs to the most aggressive clinicopathologic phenotypes of RCC. It is characterized by a high propensity for primary metastasis and limited therapeutic options due to its relative resistance to established systemic targeted therapy. Most trials report [...] Read more.
Renal cell carcinoma (RCC) with sarcomatoid differentiation belongs to the most aggressive clinicopathologic phenotypes of RCC. It is characterized by a high propensity for primary metastasis and limited therapeutic options due to its relative resistance to established systemic targeted therapy. Most trials report on a poor median overall survival of 5 to 12 months. Sarcomatoid RCC can show the typical features of epithelial-mesenchymal transition (EMT) and may contain epithelial and mesenchymal features on both the morphological and immunhistochemical level. On the molecular level, next-generation sequencing confirmed differences in driver mutations between sarcomatoid RCC and non-sarcomatoid RCC. In contrast, mutational profiles within the epithelial and sarcomatoid components of sarcomatoid RCC were shown to be identical, with TP53 being the most frequently altered gene. These data suggest that both epithelial and sarcomatoid components of RCC originate from the same progenitor cell, segregating primarily according to the underlying histologic epithelial subtype of RCC (clear cell, papillary or chromophobe). Current studies have shown that sarcomatoid RCC express programmed death 1 (PD-1) and its ligand (PD-L1) at a much higher level than non-sarcomatoid RCC, suggesting that blockade of the PD-1/PD-L1 axis may be an attractive new therapeutic strategy. Preliminary results of clinical trials evaluating checkpoint inhibitors in patients with sarcomatoid RCC showed encouraging survival data and objective response and complete response rates of up to 62% and 18%, respectively. These findings may establish a new standard of care in the management of patients with sarcomatoid RCC. Full article
(This article belongs to the Special Issue Renal Cell Carcinoma)
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