The main goals for urologists during the coronavirus disease 2019 (COVID-19) pandemic are to prevent their patients from getting COVID-19, protect themselves as health care professionals, and deliver optimal urology care [1]. While prioritisation strategies are being proposed [2,3], further measures are warranted for multifaceted action plans towards optimal perpetuation of urology care during the pandemic [4]. Urological telemedicine can lead to (1) fewer patient contacts, (2) lower infection rates among the staff, and (3) continuation of urological care by quarantined urologists [5]. However, the proportion of patients eligible for telemedicine, their wish to use telemedicine, and their demographic risk profile for acquiring a severe pandemic infection are unknown. In this context, we tested the potential of telemedicine in urology. We evaluated patients' eligibility for telemedicine according to the physician and examined the patients' perspective by evaluating their willingness for telemedicine.
Currently radical surgery represents the only chance of long-term survival for patients with renal cell carcinoma and tumor thrombus extension in the inferior vena cava. Median cancer specific survival is significantly higher with localized tumor. However, even with metastatic disease radical surgery can prolong survival, especially when immunotherapy is added. Fuhrman grade and tumor thrombus level are also prognostic factors.
adjuvant therapy who underwent RP were included. The median age was 64.7 years, the median preoperative PSA level was 7.9 ng/ mL, and the median follow-up was 5.2 years. We analysed pathological tumour stage, grading, number and location of PSMs, PSAfree survival, local recurrence-free survival, metastasis-free survival, prostate cancerspecific and, overall survival prospectively.
RESULTSThe overall rate of PSMs was 17.2%. The number was higher in higher stage ( P < 0.001) and higher grade tumours ( P = 0.041). For a PSM the PSA recurrence rate was 64.3%, the local recurrence rate was 18.6%, the development of distant metastasis was 15.7% and therefore much higher than in patients with negative margins (20.5%, 2.7%, and 1.5%). A PSM was an adverse predictor for PSA-free survival ( P < 0.001), local recurrence-free survival ( P = 0.002), and development of metastasis ( P = 0.003) on multivariate analysis. The number and location of PSMs was of no additional prognostic value.
CONCLUSIONS
BackgroundThe enhancer of zeste homolog 2 (EZH2) gene exerts oncogene-like activities and its (over)expression has been linked to several human malignancies. Here, we studied a possible association between EZH2 expression and prognosis in patients with renal cell carcinoma (RCC).MethodsEZH2 protein expression in RCC specimens was analyzed by immunohistochemistry using a tissue microarray (TMA) containing RCC tumor tissue and corresponding normal tissue samples of 520 patients. For immunohistochemical assessment of EZH2 expression, nuclear staining quantity was evaluated using a semiquantitative score. The effect of EZH2 expression on cancer specific survival (CSS) was assessed by univariate and multivariate Cox regression analyses.ResultsDuring follow-up, 147 patients (28%) had died of their disease, median follow-up of patients still alive was 6.0 years (range 0-16.1 years). EZH2 nuclear staining was present in tumor cores of 411 (79%) patients. A multivariate Cox regression analysis revealed that high nuclear EZH2 expression was an independent predictor of poor CSS (> 25-50% vs. 0%: HR 2.72, p = 0.025) in patients suffering from non-metastatic RCC. Apart from high nuclear EZH2 expression, tumor stage and Fuhrman's grading emerged as significant prognostic markers. In metastatic disease, nuclear EZH2 expression and histopathological subtype were independent predictive parameters of poor CSS (EZH2: 1-5%: HR 2.63, p = 0.043, >5-25%: HR 3.35, p = 0.013, >25%-50%: HR 4.92, p = 0.003, all compared to 0%: HR 0.36, p = 0.025, respectively).ConclusionsThis study defines EZH2 as a powerful independent unfavourable prognostic marker of CSS in patients with metastatic and non-metastatic RCC.
Purpose: Renal cell carcinoma harbors high numbers of infiltrating lymphocytes with apparent limited efficacy in tumor control.This study focused on the natural killer (NK) cells infiltrating renal cell carcinoma. Experimental Design: Tumor-infiltrating lymphocytes (TIL) were isolated from renal cell carcinoma and analyzed for NK cell frequency and phenotype (n = 34). NK cells were enriched and tested for effector function. Results: Two renal cell carcinoma subtypes were identified, one containing high (>20% of the lymphocyte population, n = 14), the other low (<20%, n = 20), NK cell numbers. NK cells of both groups were noncytolytic ex vivo but differed in CD16 and cytotoxic effector molecule expression as well as in their capacity to acquire cytotoxic activity: The majority of NK cells from tumors with high NK cell content (high NK-TIL) were CD16bright , whereas few CD16 bright NK cells were found in tumors with low NK cell frequencies (low NK-TIL). The CD16 dichotomy correlated with different capacities to develop cytotoxicity after short-term activation with interleukin-2 ex vivo : Low NK-TIL remained noncytolytic against K562 and unresponsive to signals via the activating receptor NKp46 despite expression of receptor and adaptor molecules. In contrast, high NK-TIL acquired cytotoxic function. As described for peripheral CD16 bright NK cells, NK cells from high-NK tumors showed high per cell expression of granzyme A, granzyme B, and perforin. NK cells from low NK-TIL resembled CD16 neg/dim peripheral NK cells with few cytotoxin + cells and lower expression of perforin.
Conclusion:The extent of NK cell infiltration and the expression of markers (CD16 and cytotoxins) predict the functional capacity of NK cells infiltrating renal cell carcinoma and can be used to characterize subgroups of renal cell carcinoma.Renal cell carcinoma (RCC) is a progressive tumor that accounts for 80% to 85% of malignant kidney tumors and 3% of all adult malignancies in the Western world (1, 2). About 30% of patients exhibit metastases at the time of diagnosis (2).Few therapeutic options exist for renal cell carcinoma because it does not respond to chemotherapy or irradiation. Renal cell carcinoma seems to be immunogenic and some patients respond to systemic immunotherapeutic agents, including IFN-a and/or interleukin-2 (IL-2; refs. 3, 4). However, it is unclear why only some patients show remarkable regression of metastatic lesions whereas others exhibit rapid tumor progression under identical cytokine therapies. Because systemic cytokine therapies often inflict serious adverse effects, it is desirable to spare nonresponding patients from treatment. Multiple studies have attempted to elucidate variables that distinguish responders from nonresponders, thereby showing prognostic significance for successful immunotherapies (5 -10). Conflicting results have been reported regarding the importance of peripheral lymphocyte subpopulations (6 -8) and the presence of higher numbers of T cells in renal cell carcinoma tissues seems to...
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