Evidence of overestimating prostate cancer mortality in Estonia: a population-based study.

BACKGROUND: Prostate cancer (PC) mortality statistics in Estonia has shown inconsistencies with incidence and survival trends. The aim of this population-based study was to assess the accuracy of reporting PC as the underlying cause of death and estimate the effect of misattribution in assigning cause of death on PC mortality rates. MATERIAL AND METHODS: The Estonian Causes of Death Registry (CoDR) and Cancer Registry provided data on all men in Estonia who died in 2017 and had a mention of PC on any field of the death certificate or had a lifetime diagnosis of PC. A blinded review of medical records was conducted by an expert panel to ascertain whether the underlying cause was PC or other death. We estimated the agreement between the underlying causes of death registered at the CoDR and those ascertained by medical review and calculated corrected mortality rates. RESULTS: The study population included 655 deaths. Among 277 PC deaths registered at CoDR, 164 (59%) were verified by medical review. Among 378 other deaths registered at CoDR, 17 (5%) were ascertained as PC deaths by medical review. In total, the number of PC deaths decreased from 277 to 181 and the corrected age standardized (world) mortality rate decreased from 20 to 13 per 100 000 (1.5-fold overestimation, 95% confidence interval 1.2-1.9). CONCLUSIONS: PC mortality statistics in Estonia should be interpreted with caution and possible overestimation considered when making policy decisions. Quality assurance mechanisms should be reinforced in the whole death certification process.

Impact of Blood Vessel Quantity and Vascular Expression of CD133 and ICAM-1 on Survival of Glioblastoma Patients.

Glioblastoma (GB) is the most angiogenic tumor. Nevertheless, antiangiogenic therapy has not shown significant clinical efficacy. The aim of this study was to assess blood vessel characteristics on survival of GB patients. Surgically excised GB tissues were histologically examined for overall proportion of glomeruloid microvascular proliferation (MP) and the total number of blood vessels. Also, immunohistochemical vascular staining intensities of CD133 and ICAM-1 were determined. Vessel parameters were correlated with patients' overall survival. The survival time depended on the number of blood vessels (p = 0.03) but not on the proportion of MP. Median survival times for patients with low (

Impact of tumor infiltrating CD63 positive cells on survival in patients with glioblastoma multiforme.

BACKGROUND: Glioblastoma multiforme (GBM) is the most aggressive type of brain cancer in adults. It is suggested that tumour microenvironment might influence treatment outcome. The aim of the study was to evaluate the impact of tumor infiltrating CD63 positive (CD63+) inflammatory and immune cells on treatment response and survival of GBM patients. METHODS: Forty patients were operated and received postoperative radiotherapy (±chemotherapy for recurrent disease). In surgically excised GBM tissues, the number of CD63+ cells per microscopic field was determined and correlated with patient's survival. RESULTS: Immunohistochemical parameters were examined by two independent researchers whose results were in good accordance (R=0.8, P<0.001). Median survival time of the study group was 10.0 months (95% CI 9.0-11.0). However, the survival time clearly depended on the number of CD63+ cells in GBM tissue (log rank test, P=0.003). Median survival times for patients with low (

VEGFR-2 Expression in Glioblastoma Multiforme Depends on Inflammatory Tumor Microenvironment.

Glioblastoma multiforme (GBM) is one of the most angiogenic tumors. However, antiangiogenic therapy has not shown significant clinical efficacy. The aim of our study was to evaluate the impact of inflammatory tumor microenvironment on the expression of vascular endothelial growth factor receptor 2 (VEGFR-2). Surgically excised primary GBM tissues were histologically examined for overall extent of inflammation (score 1-3). After immunohistochemistry, the tissue expression of ICAM-1 (optical density), the number of VEGFR-2 positive (VEGFR-2+) blood vessels (per microscopic field), and the endothelial staining intensity of VEGFR-2 (score 0-3) were determined. In GBM, the extent of inflammation was 1.9 ± 0.7 (group mean ± SD). Mean optical density of inflammatory mediator ICAM-1 was 57.0 ± 27.1 (pixel values). The number of VEGFR-2+ blood vessels and endothelial VEGFR-2 staining intensity were 6.2 ± 2.4 and 1.2 ± 0.8, respectively. A positive association was found between endothelial VEGFR-2 staining intensity and the extent of inflammation (p = 0.005). Moreover, VEGFR-2 staining intensity correlated with the expression level of ICAM-1 (p = 0.026). The expression of VEGFR-2, one of the main targets of antiangiogenic therapy, depends on GBM microenvironment. Higher endothelial VEGFR-2 levels were seen in the presence of more pronounced inflammation. Target dependence on inflammatory tumor microenvironment has to be taken into consideration when treatment approaches that block VEGFR-2 signaling are designed.