Search

Background: Assess clinical outcomes of focal radiotherapy (RT) in patients with limited brain metastasis (LBM) with whole brain RT (WBRT) avoidance. Methods: Patients diagnosed with LBM were entered into a database between January 2010 and February 2017. Patients were recommended WBRT avoidance with focal therapy and three‐monthly magnetic resonance imaging. The primary endpoint was overall survival. Secondary endpoints included progression‐free survival, initial‐site failure (ISF), distant brain relapse (DBF), leptomeningeal disease and rate of WBRT. Analysis involved Kaplan–Meier survival estimate with log‐rank tests and Cox‐regression analysis. Results: One hundred and sixty‐six patients were managed with median follow‐up of 13 months and median overall survival of 15 months (95% confidence interval (CI) 10.8–19.2). Eighty‐three patients had central nervous system (CNS) relapse with median progression‐free survival of 11 months (95% CI 6.7–15.3), of which most failures were DBF (83.1%) with 27 ISF (32.5%). Of the ISFs, 12 (43%) had surgery alone, six had chemotherapy alone and nine received RT. Surgery or chemotherapy alone compared with RT had a significantly higher incidence of ISF with a hazard ratio of 4.96 (P < 0.0001, 95% CI 2.10–11.83) and 6.54 (P = 0.001, 95% CI 2.26–18.87), respectively. WBRT was utilized in only 24 patients, with 83% patients free of WBRT at 12 months. On univariate analysis, number of metastases (P = 0.04), symptomatic extracranial disease (P = 0.04) and early CNS relapse within 6 months (P < 0.01) had worse survival. No grade 3–4 toxicity events were noted in 129 patients undergoing RT. Conclusion: Focal RT has a low rate of ISF with low toxicity in patients with LBMs. CNS progression was mainly DBF with low rates of salvage WBRT. Oligometastatic brain metastasis can be treated with focal radiotherapy safely. Radiotherapy toxicity is low with focal brain radiotherapy. Rates of neurological death and whole brain radiotherapy are acceptably low with focal therapies. [ABSTRACT FROM AUTHOR]

Background: Evaluate survival of patients diagnosed with glioblastoma multiforme (GBM) managed with adjuvant intensity modulated radiation therapy and temozolomide since the introduction of the European Organisation for Research and Treatment of Cancer and National Cancer Institute of Canada Clinical Trials Group (EORTC‐NCIC) protocol. Methods: All patients with GBM managed between May 2007 and December 2014 with EORTC‐NCIC protocol were entered into a prospective database. The primary endpoint was the median survival. Univariate predictors of survival were evaluated with respect to tumour resection, age and Eastern Cooperative Oncology Group (ECOG) performance status using log‐rank comparisons. Results: Two hundred and thirty‐three patients were managed under the protocol and analysed for outcome. The median age was 57 years; the rate of gross total resection, subtotal resection and biopsy were 47.2%, 35.2% and 17.6%, respectively. At progression, 49 patients had re‐resection, and in addition to second‐line chemotherapy, 86 patients had Bevacizumab including 26 with re‐irradiation. Median survival was 17.0 months (95% CI: 15.4–18.6). On univariate evaluation, extent of resection (P = 0.001), age, ECOG performance status and recursive partitioning analysis class III were shown to significantly improve survival (P < 0.0001). The median survival for gross total resection, age <50 years, ECOG 0–1 and recursive partitioning analysis class III were 21, 27, 20 and 47 months, respectively. Conclusion: This study confirms the significant improvement in median survival in GBM that has occurred in recent years since introduction of the EORTC‐NCIC protocol. Further improvements have occurred presumably related to subspecialized care, improved resection rates, sophisticated radiotherapy targeting and early systemic salvage therapies. However, the burden of the disease within the community remains high and the median survival improvements over time have plateaued. [ABSTRACT FROM AUTHOR]

Context Recent case reports detail the successful use of temozolomide in the management of aggressive pituitary tumours. O6-methylguanine-DNA methyltransferase (MGMT) is a DNA repair protein that counteracts the effect of temozolomide. Objective To study MGMT expression in pituitary tumours and consider whether MGMT expression is associated with response to temozolomide therapy in aggressive pituitary tumours. Patients We report two patients with aggressive pituitary tumours treated with temozolomide, one who responded to temozolomide and the other who did not. MGMT expression was assessed in a further 88 archived pituitary tumour samples. Design MGMT expression was assessed by immunohistochemistry. MGMT promoter methylation was studied by methylation-specific polymerase chain reaction (MSP), sequencing of MGMT was performed and loss of heterozygosity (LOH) analysis undertaken. Results Low MGMT expression and MGMT promoter methylation were found in the pituitary tumour of the patient who responded to temozolomide. Conversely, high MGMT expression was seen in the patient demonstrating a poor response to temozolomide. Eleven out of 88 archived tumour samples (13%) had low MGMT expression. Prolactinomas were more likely to have low MGMT expression compared with other pituitary tumour subtypes ( P < 0·001). There was no significant difference in MGMT expression between invasive and noninvasive tumours, or between recurrent and nonrecurrent tumours. A significant inverse correlation was found between MGMT expression and promoter methylation ( P = 0·012). Conclusion MGMT expression as assessed by immunohistochemistry may predict response to temozolomide therapy in patients with aggressive pituitary tumours. MGMT promoter methylation is likely to explain low MGMT expression in some, but not all, pituitary tumours. [ABSTRACT FROM AUTHOR]

Deep brain stimulation therapy is increasingly gaining acceptance in the management of levodopa-induced dyskinesia and fluctuations in idiopathic Parkinson's disease. It is generally not recommended for the other forms of parkinsonism such as progressive supranuclear palsy or multiple system atrophy where the response to levodopa is usually poor and disease progression more rapid, making any benefit short-lived. Here, we present an autopsy-confirmed case of 'minimal-change' multiple system atrophy in whom pallidal stimulation surgery was effective in abolishing severe levodopa-induced dyskinesia. © 2005 Movement Disorder Society [ABSTRACT FROM AUTHOR]

Objectives The objectives of the present study are to review the technique of endoscopic staple-assisted esophagodiverticulostomy (ESED) for the treatment of Zenker's diverticulum and to describe our e-perience and modifications with ESED and the advantages of ESED over previous treatments of Zenker's diverticulum. Study Design Retrospective review of 74 cases of ESED performed for the treatment of Zenker's diverticulum. Methods Patient's records were retrospectively reviewed and tabulated for age, se-, size of diverticulum, symptoms, duration of symptoms, operative time, length of postoperative hospital stay, oral intake, complications, and relief of symptoms. Results The senior author (r.l.s.) previously reported results in 36 cases of ESED performed in 34 patients with Zenker's diverticulum. We have performed an additional 38 cases of ESED in 37 patients between March 1997 and August 1999. The rate of success of ESED was similar between the two series. The average perioperative time, time until oral intake, and length of postoperative hospital stay decreased in the second series. Overall, there were no mortalities and few complications with ESED. Compared with other forms of treatment of Zenker's diverticulum, such as Dohlman's procedure, diverticulectomy, and diverticulopexy, ESED has a similar rate of success, decreased perioperative time, decreased convalescence, and decreased mortality and complications. Conclusions Cost-effectiveness, safety, and efficacy of ESED offer new advantages over previously used treatments for Zenker's diverticulum. These results continue to support the use of ESED as the initial treatment of choice for patients with Zenker's diverticulum. [ABSTRACT FROM AUTHOR]