The variables of the learning curve for RAPN can be obtained earlier than the same variables for LPN. RAPN had a shorter OR time and WITs. The shorter WITs, earlier in the series, led to consistently lower fluctuations in GFR and preservation of the renal function. The learning curves for each procedure need to be re-evaluated at longer intervals to ensure their accuracy.
Traditional understanding of smoking as a renal cell carcinoma risk factor applies to clear cell and papillary renal cell carcinoma but not the chromophobe subtype. These findings underscore distinct carcinogenic mechanisms underlying the various renal cell carcinoma subtypes.
Current guidelines for metastatic renal cell carcinoma (mRCC) do not recommend routine brain imaging as part of the surveillance protocol unless central nervous system (CNS) symptoms or abnormal laboratory values suggest brain involvement. We hypothesized that strict adherence to these guidelines will delay diagnosis and management of RCC brain metastases. Retrospective review of our IRB-approved kidney cancer database examined a consecutive series of subjects from 1995 to 2012. We identified all mRCC patients with radiographic evidence of renal cell brain metastasis (RCCBM). RCCBM patients were divided into two cohorts: CNS symptoms present at RCCBM diagnosis and those without symptoms present at diagnosis. Fifty-two patients within our database met criteria; CNS symptoms were present at RCCBM diagnosis in 73 % (36) of patients. Median size of RCCBM on presentation was smaller in the asymptomatic verses the symptomatic cohort (0.83 vs. 1.7 cm, p = 0.003). Multivariate analysis demonstrated presence of CNS symptoms and female gender as a survival advantage (p < 0.05) while poor performance status, history of tobacco abuse and coexistence of lung metastasis were poor indicators for survival (p < 0.05). Patients with pulmonary metastases and a history of tobacco abuse are more likely to harbor RCCBM and perhaps in the absence of CNS symptoms these subjects should have routine brain surveillance incorporated into the RCC follow up. Overall, the current urologic guidelines may be missing a subset of metastatic RCC patients who could potentially benefit from early radiation or neurosurgical intervention. This may result in improved overall survival.
Vascular endothelial growth factor (VEGF) promotes angiogenesis in a number of tumor model systems. We reported previously that estrogen supports the growth of CCL-51 cell-based mammary tumors in mice, which could be blocked with specific chemokines. We investigated whether promotion of tumor growth by estrogen, and suppression of tumor growth by chemokines, was associated with VEGF protein expression. Female C3H mice were treated with vehicle, estradiol, or with one of several chemokines for 72 h. The presence of VEGF in mammary tissue samples was detected and quantified by sodium dodecyl sulfate polyacrylamide gel electrophoresis and immunoblotting using antimurine VEGF antibodies. Estrogen significantly increased mammary VEGF expression. Cotreatment with tamoxifen or the chemokine interferon-inducible protein-10 (IP-10) suppressed the action estrogen on VEGF expression. CCL-51 tumor cells were placed into mammary tissue of C3H mice. Mice were treated every 72-h with either vehicle or estradiol, in the presence or absence of IP-10 for 21 days. Estrogen supported CCL-51 tumor growth, with an average of 2.3 tumors present/animal. Cotreatment of mice with estrogen and IP-10 resulted in significantly lower numbers of tumors in mammary tissue in comparison to animals treated with estrogen alone. VEGF levels in mammary tissue and tumors of IP-10 and estrogen cotreated mice were 40-50% less than those detected in mammary tissue of estrogen-treated mice. Our results suggest that estrogenic support of CCL-51 mammary tumor growth is related to increased VEGF expression, and that the inhibitory action of IP-10 may be related to suppressing VEGF levels in mammary tissue.
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