Surgery may be followed up by chemotherapy, radiation, or a mix of both, but recent studies suggest that radiation does not improve overall survival (even when age, clinical data, histological grading, and type of surgery are considered). Prognosis
Oligodendrogliomas, like all other infiltrating gliomas, have a very high (almost uniform) rate of recurrence and gradually increase in grade over time. Recurrent tumors are generally treated with more aggressive chemotherapy and radiation therapy. Recently, stereotactic surgery has proven successful in treating small tumors that have been diagnosed early. Long-term survival is reported in a minority of patients. With aggressive treatment and close monitoring, it is possible to outlive the typical life expectancies for low grade oligodendroglioma. Westergaards study (1997) showed that patients younger than 20 years had a median survival of 17.5 years. For patients that are over 30, the survival rate is lower but as treatment options grow, the survival rate is higher. However, a patient with bad general health is more likely to pass sooner than those that have good general health. Another study shows a 34% survival rate after 20 years. However, as discussed above, such figures can be misleading since they do not factor in the types of treatment nor the genetic signature of the tumors. Additionally, such historic data loses significance due to the relatively long survival of patients (compared to other types of brain tumors) and the introduction of newer treatment options over time.
Uniparental disomy (UPD) occurs when a person receives two copies of a chromosome, or of part of a chromosome, from one parent and no copy from the other parent. UPD can be the result of heterodisomy, in which a pair of non-identical chromosomes are inherited from one parent (an earlier stage meiosis I error) or isodisomy, in which a single chromosome from one parent is duplicated (a later stage meiosis II error). Uniparental disomy may have clinical relevance for several reasons. For example, either isodisomy or heterodisomy can disrupt parent-specific genomic imprinting, resulting in imprinting disorders. Additionally, isodisomy leads to large blocks of homozygosity, which may lead to the uncovering of recessive genes, a similar phenomenon seen in inbred children of consanguineous partners.UPD has been found to occur in about 1 in 2,000 births. Pathophysiology
UPD can occur as a random event during the formation of egg cells or sperm cells or may happen in early fetal development. It can also occur during trisomic rescue. When the child receives two (different) homologous chromosomes (inherited from both grandparents) from one parent, this is called heterodisomic UPD. Heterodisomy (heterozygous) indicates a meiosis I error if the gene loci in question didnt cross over. When the child receives two (identical) replica copies of a single homologue of a chromosome, this is called an isodisomic UPD. Isodisomy (homozygous) indicates either a meiosis II (if the gene loci in question didnt cross over) or postzygotic chromosomal duplication.