The Role of Chemotherapy for Pure and Mixed Anaplastic Oligodendroglial Tumors Academic Article Book Review uri icon

abstract

  • Pure and mixed anaplastic oligodendrogliomas (AO/mixed-AOs) remain terminal primary brain tumors, without a defined optimal initial therapy, and without sufficiently active and tolerable therapies at recurrence/progression (R/P). Very heterogeneous international therapy recommendations remain. Historical advances have resulted in only modest improvements in outcome. AO/mixed-AOs with 1p/19q co-deletion are prognostically favorable, regardless of therapy, and must be identified as early as possible. Following resection, outcome data on initial therapy with radiation (RT) remain the most mature, although controversies regarding its true toxicities and optimal timing continue. Recently, the landmark RTOG 9402 and EORTC 26951 trials showed that the addition of Procarbazine, CCNU, Vincristine chemotherapy to RT, at anytime during initial therapy, prolongs progression-free survival, but not survival, and not without moderate toxicity. Despite a lack of definitive evidence, this strategy has commonly been extrapolated to Temozolomide. Chemo-sensitivity of AO/mixed-AOs provides the rationale for the chemotherapy-only strategies being explored. In the setting of recurrence/progression (R/P), chemotherapy, small molecule (targeted), biologic, and other strategies have been relatively disappointing, toxic, and cumbersome. Partly secondary to biases regarding the relative toxicities of tumor burden vs. treatment effect, therapy remains highly individualized. Future international research must prospectively evaluate health-related quality of life, toxicity, and molecular genetic markers.

publication date

  • 2009
  • 2009-08-01

keywords

  • Antineoplastic Agents
  • Brain Neoplasms
  • Clinical Trials as Topic
  • Combined Modality Therapy
  • Disease Progression
  • Genetic Markers
  • Humans
  • Medical Oncology
  • Oligodendroglioma
  • Treatment Outcome

Web of Science ID

  • 000270881300008

PubMed ID

  • 19381820

start page

  • 216

end page

  • 230

volume

  • 10