Kidney cancer (Clifton, Va.)最新文献

Objectives: To better characterize the relay of information about prostate, kidney, and bladder cancer on Twitter in relation to the COVID-19 pandemic.

Materials and methods: Tweets containing the joint hashtags "#COVID-19" and either "#bladder cancer", "#kidney cancer", or "#prostate cancer" were identified on the Twitter platform from January 1, 2020 to July 30, 2020. The Twitter handle responsible for each tweet was categorized as an Academic, Medical Education, Patient Advocacy Groups/Non-Profits, Pharmaceutical, or Other entity based on content domain. Descriptive statistics were used to summarize data on Twitter handle characteristics stratified by disease category (bladder, kidney, and prostate). Median/interquartile range and percentages were used to summarize continuous and categorical data, respectively. Number of tweets containing the relevant joint hashtags were tracked over time in relation to the cumulative United States case count of COVID-19.

Results: The content of 730 total tweets containing the joint hashtags "COVID-19" and either "#bladder cancer" (138 tweets), "#kidney cancer" (137 tweets), or "#prostate cancer" (455 tweets) from January 1, 2020 to July 31, 2020 were analyzed. We identified 326 unique Twitter handles across all disease states (62 bladder, 47 kidney, and 217 prostate-related). Academic Twitter handles accounted for the greatest number of tweets containing the joint hashtags (31%). Temporal tracking of tweets with regard to monthly U.S. COVID cases revealed that communication surged in March of 2020 and peaked in April for both bladder and kidney cancer, whereas related prostate cancer Twitter communication peaked in May of 2020.

Conclusions: As COVID-19 case counts rose in the United States initially, so too did communication surrounding COVID-19 and genitourinary cancers on Twitter. Many of these conversations were driven by academically-associated Twitter accounts.

Background: The treatment landscape for metastatic clear cell renal cell carcinoma (mRCC) is rapidly changing. It is unknown how adoption of new types of therapies may differ by patient age.

Objective: To compare trends in first-line therapy use for older (≥70 years) and younger (< 70) patients with mRCC before and after approval of nivolumab in 2015.

Methods: Using the National Cancer Database, we assessed trends in first-line therapy use by calculating the proportion of patients receiving targeted therapy, immunotherapy, or no systemic therapy by year of diagnosis. Initial systemic treatment was compared for patients diagnosed in 2016 with patients diagnosed in 2011 as a control group prior to nivolumab approval. Multivariable regression analysis was used to evaluate the interaction between year of diagnosis and elderly status for use of first-line immunotherapy or targeted therapy.

Results: From 2006 to 2016, the proportion of patients receiving any type of systemic therapy increased from 43.7% to 56.5%. On stratified multivariable regression analysis, older patients diagnosed in 2016 were 17.3 times more likely to receive first-line immunotherapy compared to those diagnosed in 2011, while younger patients were 2.3 times more likely. There was no change in targeted therapy use over this time regardless of patient age.

Conclusions: The rate of adoption of first-line immunotherapy was particularly pronounced for elderly compared to younger patients. While first-line use of immunotherapy may have allowed elderly patients to receive systemic therapy that they otherwise would not, the efficacy of these drugs in elderly patients deserves further study.

Renal cell carcinoma has traditionally been classified based on histological features. Contemporary studies have identified genomic, transcriptomic, epigenomic, and metabolomic signatures that correspond to or even transcend histological subtypes. Much remains to be learned about improving the algorithm of pan-omics integration for precision oncology, which will not only advance our understanding of RCC pathobiology and treatment response but also result in novel therapeutic opportunities. Accordingly, this review focuses on recent RCC multi-omics literature. Encouragingly, a few reports on omics integration into routinely employed prognostic risk models have shown early promise that could lay the foundation for future development of precision kidney cancer therapies. Hence, this article serves as a primer on what we have learned and how we might better realize the clinical potential of the burgeoning pan-omics data.

Introduction: There have been a number of recent advances in the management of advanced clear cell renal cell carcinoma (ccRCC). However, the majority of these studies excluded patients with non-clear cell RCC (nccRCC), and optimal management of nccRCC remains unknown.

Materials and methods: A systematic review of the literature was performed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines to evaluate systemic treatment options in locally advanced or metastatic nccRCC between 2000-2019. Randomized controlled trials, single-arm phase II-IV trials, and prospective analyses of medication access programs were included. The primary outcome measures were progression free survival (PFS), overall survival (OS), and objective response rate (ORR).

Results: A total of 31 studies were included in the final analysis. There was the highest level of evidence to support first-line treatment of nccRCC with sunitinib. Additional single-arm trials support the use of other vascular endothelial growth factor (VEGF) inhibitors with axitinib and pazopanib, as well as mammalian target of rapamycin (mTOR) inhibition with temsirolimus or everolimus +/- bevacizumab. Immune checkpoint inhibition has an emerging role in nccRCC, but optimal sequencing of available options is not clear. Prospective data to support the use of newer immunotherapy combinations are lacking. Treatment for collecting duct carcinoma remains platinum-based chemotherapy.

Conclusions: The availability of randomized trials in nccRCC is limited, and most studies include outcomes for nccRCC as a group, making conclusions about efficacy by subtype difficult. This systematic review supports consensus guidelines recommending sunitinib or clinical trial enrollment as preferred first-line treatment options for nccRCC, but also suggests a more nuanced approach to management and new options for therapy such as immune checkpoint inhibition.

Introduction: To evaluate overall survival (OS) of T1a kidney cancers stratified by histologic subtype and curative treatment including partial nephrectomy (PN), percutaneous ablation (PA), and radical nephrectomy (RN).

Materials and methods: We queried the National Cancer Data Base (2004-2015) for patients with T1a kidney cancers who were treated surgically. OS was estimated by Kaplan-Meier curves based on histologic subtype and management. Cox proportional regression models were used to determine whether histologic subtypes and management procedure predicted OS.

Results: 46,014 T1a kidney cancers met inclusion criteria. Kaplan Meier curves demonstrated differences in OS by treatment for clear cell, papillary, chromophobe, and cystic histologic subtypes (all p < 0.001), but no differences for sarcomatoid (p = 0.110) or collecting duct (p = 0.392) were observed. Adjusted Cox regression showed worse OS for PA than PN among patients with clear cell (HR 1.58, 95%CI [1.44-1.73], papillary RCC (1.53 [1.34-1.75]), and chromophobe RCC (2.19 [1.64-2.91]). OS was worse for RN than PN for clear cell (HR 1.38 [1.28-1.50]) papillary (1.34 [1.16-1.56]) and chromophobe RCC (1.92 [1.43-2.58]). Predictive models using Cox proportional hazards incorporating histology and surgical procedure alone were limited (c-index 0.63) while adding demographics demonstrated fair predictive power for OS (c-index 0.73).

Conclusions: In patients with pathologic T1a RCC, patterns of OS differed by surgery and histologic subtype. Patients receiving PN appears to have better prognosis than both PA and RN. However, the incorporation of histologic subtype and treatment modality into a risk stratification model to predict OS had limited utility compared with variables representing competing risks.

 Papillary renal cell carcinoma (PRCC) is a subtype of renal cell carcinoma (RCC) accounting for approximately 15-20% of cases and further divided into Type 1 and Type 2. Type 1 PRCC tends to have more alterations in the MET tyrosine kinase receptor than Type 2 PRCC. Treatment for RCC patients is based on studies with minimal participation from patients with PRCC; consequently, conventional therapies tend to be less effective for RCC patients with a subtype other than ccRCC (non-ccRCC). Since MET is a known alteration in PRCC, it is potential target for directed therapy. There have been many attempts to develop MET inhibitors for use in solid tumors including PRCC. The following review will discuss the current research regarding MET-targeted therapy, MET inhibitors in clinical trials, and future directions for MET inhibitors in PRCC.

An important hallmark of cancer is 'metabolic reprogramming' or the rewiring of cellular metabolism to support rapid cell proliferation [1-5]. Metabolic reprogramming through oncometabolite-mediated transformation or activation of oncogenes in renal cell carcinoma (RCC) globally impacts energy production as well as glucose and glutamine utilization in RCC cells, which can promote dependence on glutamine supply to support cell growth and proliferation [6, 7]. Novel inhibitors of glutaminase, a key enzyme in glutamine metabolism, target glutamine addiction as a viable treatment strategy in metastatic RCC (mRCC). Here, we review glutamine metabolic pathways and how changes in cellular glutamine utilization enable the progression of RCC. This overview provides scientific rationale for targeting this pathway in patients with mRCC. We will summarize the current understanding of cellular and molecular mechanisms underlying anti-tumor efficacy of glutaminase inhibitors in RCC, provide an overview of clinical efforts targeting glutaminase in mRCC, and review approaches for identifying biomarkers for patient stratification and detecting therapeutic response early on in patients treated with this novel class of anti-cancer drug. Ultimately, results of ongoing clinical trials will demonstrate whether glutaminase inhibition can be a worthy addition to the current armamentarium of drugs used for patients with mRCC.

Background: In renal cell carcinoma (RCC), angiopoietin (Ang) 2 is elevated at the time of progression on anti-vascular endothelial growth factor (VEGF) therapy and may contribute to resistance.

Objective: We tested trebananib, an Ang 1 and 2 neutralizing peptibody in patients with RCC progressing on anti-VEGF treatment.

Methods: Patients with measurable RCC progressing despite an anti-VEGF agent within 12 weeks, any number of prior treatments, and good PS were randomized to trebananib 15 mg/kg IV weekly without (Arm A) or with (Arm B) continuation of the prior anti-VEGF agent. The primary endpoint for each arm was tumor response (RECIST 1.1). Secondary endpoints included progression free survival and adverse events.

Results: Of 41 enrolled patients, 35 were eligible and started treatment (17 Arm A, 18 Arm B) with median age 60 (46-76) and 3 prior treatments (1-8). Four died prior to documented progression and 27 progressed as their first event. Both arms were stopped after interim analysis, 2 responses (11%; 95% C.I. 1-35%) were observed in Arm B. Median PFS of 2.7 (95% C.I. 2.3-4.7) months in Arm A and 5.2 (95% C.I. 2.7-10.8) months in Arm B did not support continued study. Common adverse events including fatigue, nausea, and increased creatinine were generally grade 1-2 and numerically higher in Arm B. The most common grade 3 or higher adverse events were hypertension and dyspnea.

Conclusions: While tolerable, trebananib either without or with continued anti-VEGF therapy did not show promising activity in RCC patients who recently progressed on anti-VEGF therapy alone.

The prognosis of renal tumors depends on histologic subtype. The increased use of abdominal imaging has resulted in an increase in the number of small renal incidentaloma in recent decades. Of these incidentally discovered tumors, 20% are benign lesions warranting conservative management, but most are renal cell carcinomas that warrant a more aggressive therapeutic approach due to their malignant potential. Dedicated diagnostic renal imaging is important for characterization of renal tumors to facilitate treatment planning. This review discusses the ability to detect and differentiate renal cell carcinoma subtypes, angiomyolipoma and oncocytoma based on ultrasound imaging, computed tomography, multiparametric magnetic resonance, and nuclear imaging.