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Molecular subtypes of anaplastic oligodendroglioma: implications for patient management at diagnosis.
The possibility that therapeutic decisions at the time of diagnosis might be tailored to particular genetic subtypes of anaplastic oligodendroglioma is raised, for the first time, in this group of patients in whom therapeutic management was not uniform.
Imaging Correlates of Molecular Signatures in Oligodendrogliomas
Molecular subsets of oligodendroglioma behave in biologically distinct ways. Their locations in the brain, rates of growth, and responses to therapy differ with their genotypes. Retrospectively, we
Tumor location and growth pattern correlate with genetic signature in oligodendroglial neoplasms.
It is concluded that molecular subtypes of oligodendrogliomas may arise preferentially in certain lobes of the brain and have differential patterns of growth, with tumors having allelic loss of chromosomes 1p and 19q occurring most frequently in the frontal lobes and having a tendency for widespread growth across the midline.
Long survival and therapeutic responses in patients with histologically disparate high-grade gliomas demonstrating chromosome 1p loss.
The findings raise the possibility that some high-grade gliomas with chromosome 1p loss, in addition to pure anaplastic oligodendrogliomas, may follow a more favorable clinical course.
Histopathological‐Molecular Genetic Correlations in Referral Pathologist‐Diagnosed Low‐Grade “Oligodendroglioma”
Results suggest that histological appearance correctly predicts genotype in approximately 80% of low-grade gliomas, but that tumor genotype more closely predicts chemosensitivity.
Expression of the neural cell adhesion molecule in astrocytic tumors
The aim of this study was to investigate the expression of the neural cell adhesion molecule (NCAM) in human astrocytic tumors and assess any relationship between NCAM expression and the degree of malignancy.
DMBT1 polymorphisms: relationship to malignant glioma tumorigenesis.
It is suggested that D MBT1 polymorphisms are not likely primary targets of 10q loss in malignant gliomas and do not support a major role for DMBT1 in gliomagenesis.