Assessment of clinical and nonclinical characteristics associated with health-related quality of life in patients with high-grade gliomas: a feasibility study.

Purpose: Results from several studies suggest that there is value in evaluating the association between nonclinical characteristics of patients and quality of life (QoL), but few studies have focused on brain cancer. The primary goal of this feasibility study was to explore the relationship between clinical factors and nonclinical factors and QoL in brain cancer patients.

Methods: Participants in this cross-sectional study were drawn from two hospital sites.

Natural history of multiple meningiomas.

Background: Asymptomatic solitary meningiomas are typically managed with clinical and radiographic follow-up. Multiple meningiomas represents a clinical entity distinct from solitary meningiomas and can be sporadic, radiation-induced, associated with neurofibromatosis, or exhibit other familial inheritance. The growth rate for multiple meningiomas is not known and therefore management of these complicated patients can be difficult.

Description of selected characteristics of familial glioma patients - results from the Gliogene Consortium.

Background: While certain inherited syndromes (e.g. Neurofibromatosis or Li-Fraumeni) are associated with an increased risk of glioma, most familial gliomas are non-syndromic.

A variable age of onset segregation model for linkage analysis, with correction for ascertainment, applied to glioma.

Background: We propose a 2-step model-based approach, with correction for ascertainment, to linkage analysis of a binary trait with variable age of onset and apply it to a set of multiplex pedigrees segregating for adult glioma.

Methods: First, we fit segregation models by formulating the likelihood for a person to have a bivariate phenotype, affection status and age of onset, along with other covariates, and from these we estimate population trait allele frequencies and penetrance parameters as a function of age (N = 281 multiplex glioma pedigrees). Second, the best fitting models are used as trait models in multipoint linkage analysis (N = 74 informative multiplex glioma pedigrees).

Insight in glioma susceptibility through an analysis of 6p22.3, 12p13.33-12.1, 17q22-23.2 and 18q23 SNP genotypes in familial and non-familial glioma.

The risk of glioma has consistently been shown to be increased twofold in relatives of patients with primary brain tumors (PBT). A recent genome-wide linkage study of glioma families provided evidence for a disease locus on 17q12-21.32, with the possibility of four additional risk loci at 6p22.

Genome-wide high-density SNP linkage search for glioma susceptibility loci: results from the Gliogene Consortium.

Gliomas, which generally have a poor prognosis, are the most common primary malignant brain tumors in adults. Recent genome-wide association studies have shown that inherited susceptibility plays a role in the development of glioma. Although first-degree relatives of patients exhibit a two-fold increased risk of glioma, the search for susceptibility loci in familial forms of the disease has been challenging because the disease is relatively rare, fatal, and heterogeneous, making it difficult to collect sufficient biosamples from families for statistical power.

Assessment of type of allergy and antihistamine use in the development of glioma.

Background: Allergies have been associated with decreased risk of glioma; but, associations between duration and timing of allergies, and antihistamine use and glioma risk have been less consistent. The objective was to investigate this association by analyzing types, number, years since diagnosis, and age at diagnosis of allergies, and information on antihistamine usage, including type, duration, and frequency of exposure.

Methods: Self-report data on medically diagnosed allergies and antihistamine use were obtained for 419 glioma cases and 612 hospital-based controls from Duke University and NorthShore University HealthSystem.

Survey of familial glioma and role of germline p16INK4A/p14ARF and p53 mutation.

There is increasing recognition of familial propensity to glioma as a distinct clinical entity beyond a few rare syndromes; however its genetic basis is poorly understood. The role of p16(INK4A)/p14(ARF) and p53 mutations in sporadic glioma provides a strong rationale for investigating germline mutations in these genes as a cause of familial glioma. To survey the familial glioma phenotype and examine the contribution of germline mutation in p16(INK4A)/p14(ARF) and p53 to the disease we have analyzed a series of 101 index familial cases collected through the GLIOGENE Consortium (http://braintumor.