methylation of the MGMT promoter, there was a smaller and statistically insignificant difference in survival between the treatment groups (12.7 versus 11.8 months). Thus determination of MGMT promoter methylation status may allow the selection of patients most likely to benefit from alkylating/methylating chemotherapeutic strategies.

Uncovering the genetic and molecular basis of cancer has strengthened our understanding of cancer formation and progression. Similarly, our approach to the treatment of this disease has changed from a common therapeutic approach for a certain type of cancer to one that is tailored to the genetic profile of each tumor. The integration of the genetic profile of the tumors has been a priority in the Department of Neuropathology at the MNI/MNH. It started 6 years ago with LOH 1p and 19q in Oligodendrogliomas, and progressively as new clinical studies are published and new markers become relevant to therapy, we developed these new molecular tests in our laboratory. At this date, LOH 1p and 19q, amplification of EGFR gene and methylation status of MGMT gene are the markers the most often requested by the Oncology team. Further advances in our understanding will undoubtedly improve treatment options and patient selection.

References

(1) Vogelstein B, and Kinzler KW. Cancer Genes and the Pathways They Control. Nature Medicine. 10,2004.
(2) Louis DN et al. Focus on Central Nervous System Neoplasia. Cancer Cell. 1;2002.
(3) Esteller M, et al. Inactivation of the DNA-Repair Gene MGMT and the Clinical Response of Gliomas to Alkylating Agents. The
      New England Journal of
      Medicine. 343;19,2000.
(4) Hegi ME, et al. MGMT Gene Silencing and Benefit from Temozolomide in Glioblastoma. The New England Journal of
      Medicine. 352;10,2005.
(5) Timeline is from http://www.pbs.org/wnet/dna/timeline
(6) Figures forLOH1p/19q, methylation status and EGFR amplification provided by Marie-Christine Guiot,
     Neuropathology