Object Cystic epithelial masses of the sellar and parasellar region may be difficult to differentiate on a clinical, imaging, or even histopathological basis. The authors review the developmental relationships and differentiating features of various epithelial lesions of the sellar region. Methods The authors performed a review of the literature to identify previous studies describing the etiological relationships and differentiating features of various cystic sellar lesions, including craniopharyngioma (CP), Rathke cleft cyst, xanthogranuloma, and dermoid and epidermoid cysts. Results There is significant evidence in the literature to support a common ectodermal origin of selected sellar and suprasellar cystic lesions, which may account for the overlap of features and transitional states observed in some cases. Research obtained from animal studies and reports of transitional cystic epithelial masses or lesions crossing over from typical to more aggressive pathological subtypes have collectively provided a solid foundation for this theory. Histological features that signify transitional entities beyond simple benign Rathke cleft cysts include squamous metaplasia, stratified squamous epithelium, and ciliated or mucinous goblet cells in squamous-papillary CPs. Several studies have identified key clinical, imaging, and histopathological features that can be used in the differentiation of these lesions. Conclusions The pattern of embryological formation of the hypothalamic-pituitary axis plays a major role in its propensity for developing cystic epithelial lesions. Subsequent inflammatory, metaplastic, and neoplastic processes may promote further progression along the pathological continuum, ranging from benign epithelial cysts to aggressive neoplastic cystic CPs. Selected clinical, imaging, and histopathological features can be used collectively to help differentiate these lesions and assign a formal diagnosis, thus accurately guiding further treatment.

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ObjectFollowing resection of a brain metastasis, stereotactic radiosurgery (SRS) to the cavity is an emerging alternative to postoperative whole-brain radiation therapy (WBRT). This approach attempts to achieve local control without the neurocognitive risks associated with WBRT. The authors aimed to report the outcomes of a large patient cohort treated with this strategy.MethodsA retrospective review identified 91 patients without a history of WBRT who received Gamma Knife (GK) SRS to 96 metastasis resection cavities between 2007 and 2013. Patterns of intracranial control were examined in the 86 cases with post-GK imaging. Survival, local failure, and distant failure were estimated by the Kaplan-Meier method. Prognostic factors were tested by univariate (log-rank test) and multivariate (Cox proportional hazards model) analyses.ResultsCommon primary tumors were non–small cell lung (43%), melanoma (14%), and breast (13%). The cases were predominantly recursive partitioning analysis Class I (25%) or II (70%). Median preoperative metastasis diameter was 2.8 cm, and 82% of patients underwent gross-total resection. A median dose of 16 Gy was delivered to the 50% isodose line, encompassing a median treatment volume of 9.2 cm3. Synchronous intact metastases were treated in addition to the resection bed in 43% of cases. Patients survived a median of 22.3 months from the time of GK. Local failure developed in 16 cavities, for a crude rate of 18% and 1-year actuarial local control of 81%. Preoperative metastasis diameter ≥ 3 cm and residual or recurrent tumor at the time of GK were associated with local failure (p = 0.04 and 0.008, respectively). Distant intracranial failure occurred in 55 cases (64%) at a median of 7.3 months from GK. Salvage therapies included WBRT and additional SRS in 33% and 31% of patients, respectively. Leptomeningeal carcinomatosis developed in 12 cases (14%) and was associated with breast histology and infratentorial cavities (p = 0.024 and 0.012, respectively).ConclusionsThis study bolsters the existing evidence for SRS to the resection bed. Local control rates are high, but patients with larger preoperative metastases or residual/recurrent tumor at the time of SRS are more likely to fail at the cavity. While most patients develop distant intracranial failure, an SRS approach spared or delayed WBRT in the majority of cases. The risk of leptomeningeal carcinomatosis does not appear to be elevated with this strategy.

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Background Risk stratification is a major challenge in bladder cancer (BC), and a biomarker is needed. Multiple studies report the neutrophil-to-lymphocyte ratio (NLR) as a promising candidate; however, these analyses have methodological limitations. Therefore, we performed a category B biomarker study. We tested whether NLR is prognostic for overall survival (OS) after curative treatment or predictive for the benefit from neoadjuvant chemotherapy (NAC). Methods We performed a secondary analysis of SWOG 8710—a randomized, phase III trial that assessed cystectomy ± NAC in 317 patients with muscle-invasive BC. We calculated NLR from prospectively collected complete blood counts. We identified 230 patients for the prognostic analysis and 263 for the predictive analysis. We evaluated NLR using proportional hazards models including pre-specified factors (age, gender, T-stage, lymphovascular invasion, treatment arm). Results With a median follow-up of 18.6 years, there were 172 and 205 deaths in the prognostic and predictive cohorts, respectively. On multivariable analysis, NLR was not prognostic for OS (HR 1.04, 95%CI [0.98–1.11], P=0.24). Furthermore, NLR did not predict for the OS benefit from NAC (HR 1.01, 95%CI [0.90 – 1.14], P=0.86). Factors associated with worse OS were older age (HR 1.05, 95%CI [1.04–1.07], P<0.001) and surgery without NAC (HR 1.39, 95%CI [1.03–1.88], P=0.03). Conclusion This is the first analysis of NLR in BC to use prospectively collected clinical trial data. In contrast to previous studies, it suggests NLR is neither a prognostic nor predictive biomarker for OS in muscle-invasive BC. Trial Registration clinicaltrials.gov Identifier NCT02756637 https://clinicaltrials.gov/show/NCT02756637