Although their neurocognitive performance is one of the major concerns of patients with high-grade gliomas (HGG) and although neurocognitive deficits have been described to be associated with negative outcome, neurocognitive rehabilitation is usually not integrated into the routine care of patients with malignant gliomas. In this pilot trial, a weekly group training session for attention, verbal, and memory skills was offered to patients with HGG with pre and post-training evaluation. Eleven patients, six with glioblastoma multiforme and five with WHO grade III gliomas, median age 50 years, with a Karnofsky performance score of 80-100 participated in ten group training sessions of 90 min. For evaluation at baseline and after the training by a neuropsychologist not involved in care or training of the patients, Trail Making Tests A and B (TMTA and TMTB), Hopkins Verbal Learning Test (HVLT), and the Controlled Oral Word Association Test (COWA) were used. Comparison of mean group differences between baseline and at post-training evaluation after 12 weeks revealed improvement across all neurocognitive variables. The patients showed a great diversity in their performances, with worsening, improvement, and stabilization. However, a significant group difference was detected only for the HVLT (score 19.6 +/- 8.9 at baseline, 23.6 +/- 8.8 after 12 weeks, P = 0.04). This pilot study shows that neurocognitive training in patients with HGG is feasible as group training with weekly sessions and might be able to induce improvements in attention and memory skills.

Purpose: Epithelial ovarian cancer is the most common cause of mortality from gynecologic malignancies. Due to advanced stage at diagnosis, most patients need systemic treatment in addition to surgery. Tumor necrosis factor (TNF)^related apoptosis-inducing ligand (TRAIL) is a member of the TNF family with a promising toxicity profile and synergistic activity with chemotherapeutic agents. Experimental Design: We used an arrayed panel of epithelial ovarian cancer tissue to assess the protein expression of TRAIL and the clinically most relevant members of its pathway death receptors 4 and 5 (DR4 and DR5) and the long form of FLICE inhibitory protein (FLIP L ). Results: We could show that a majority (66.2%) of the tumor tissues displayed either reduced DR4/DR5 expression (20.6%), increased FLIP L expression (39.7%), or both (5.9%) as determined by immunohistochemistry. Furthermore, higher TRAIL expression in the surrounding connective tissue but not in the tumor cells is significantly (P < 0.05) linked with favorable overall survival in advanced-stage patients. Conclusions: Mechanisms to escape the immune surveillance mediated byTRAIL are developed by ovarian cancer cells in a high percentage. TRAIL expression in the ovarian cancer microenvironment has an effect on overall survival. These findings enhance our understanding of ovarian cancer pathology and might be helpful in guidingTRAIL-based therapy in future.Despite great clinical and research efforts, the etiology of ovarian cancer remains poorly understood. A majority (90%) of these tumors stem from ovarian surface epithelium, which is similar to the mesothelial lining of other abdominal organs. Beyond family history, the most important risk factors for ovarian cancer include early menarche, late menopause, nulliparity, and in contrast, the use of anovulatory drugs that reduces the risk. The epidemiologic observation that all factors that limit the number of ovulations over lifetime are protective against ovarian cancer resulted in the so-called incessant ovulation theory decades ago (1).Over the past several years, the molecular mechanisms behind the genetic predisposition for ovarian cancer have been elucidated. Germ line mutations in BRCA1 and BRCA2, the genes responsible for hereditary breast and ovarian cancer and in hMLH1 and hMSH2, responsible for hereditary nonpolyposis colon cancer, are also the basis for a majority of cases of familial ovarian cancer. Originally identified by positional cloning, all these genes were later shown to be involved in the maintenance of genome integrity, implying that DNA repair mechanisms are under considerable challenge in ovarian tissue. Induction of apoptosis plays a pivotal role in cellular homeostasis, and in this scenario, the impairment of any of its components may result in accumulation of genetic defects, preceding cancer development (2).Apoptosis is induced either by binding of ligands to specific death receptors on cell surface or by unspecific cellular stress, which promotes cytochrome c release from mi...

Hypermethylation of TSG can be detected in serum of prostate cancer patients. Some hypermethylated TSG can be detected in serum of healthy controls. GSTP1 was not detectable in controls and correlated significantly with Gleason score and stage of disease. Therefore, this gene may be a promising new tool in prostate cancer diagnosis.

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Our data reveal valuable palliation with preservation of KPS and an option for steroid withdrawal in patients treated with BEV, supporting the role of this therapy in late-stage disease.