Moving on in our in our brain tumor series (check out the overviewastrocytoma, and pilocytic astrocytoma posts), today we’ll talk about oligodendroglioma.

Oligodendrogliomas are a fairly uncommon type of glioma (they comprise around 10% of all gliomas). They occur most commonly in patients between the ages of 30 and 50, and they often present with a several-year history of neurologic symptoms, including seizures. Many have a specific genetic alteration that confers a relatively good prognosis, and overall survival is between 5 and 10 years.

Grossly, they are grey, gelatinous masses that occur in the cerebral hemispheres (mostly in the white matter). They are usually sharply circumscribed, and may contain cystic and/or hemorrhagic regions.

Microscopically, oligodendrogliomas are composed of – surprise – oligodendrocytes. The tumor cells often look like regular old oligodendrocytes (plain-looking cells with round nuclei, finely granular chromatin, and little clear cytoplasmic halos). Check out the tumor cells in the image of a classic oligodendroglioma above for reference. There is usually a delicate capillary network, and in most cases, there is calcification (either microsopic foci or big deposits). Some cases of oligodendroglioma have more anaplastic cells, with increased mitotic activity and areas of necrosis. These are called anaplastic oligodendrogliomas, and they generally carry a worse prognosis.

Here’s something interesting: most cases of classic (not anaplastic) oligodendroglioma contain a genetic alteration that is associated with prolonged survival! This change consists of a codeletion of both 1p and 19q. Patients with this dual deletion (but no other chromosomal abnormalities) have a long-lasting response to chemotherapy and radiation.

When patients develop additional changes, though (like loss of 9p or 10q), that tends to go along with progression to anaplastic oligodendroglioma (which has a worse prognosis). It’s curious that losing 1p and 19q is a good thing, but losing 9p and 10q is a bad thing.