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Clinical Cancer Research Vol. 7, 839-845, April 2001
© 2001 American Association for Cancer Research

Molecular Oncology, Markers, Clinical Correlates

Molecular Subtypes of Anaplastic Oligodendroglioma

Implications for Patient Management at Diagnosis1

Yasushi Ino, Rebecca A. Betensky, Magdalena C. Zlatescu, Hikaru Sasaki, David R. Macdonald, Anat O. Stemmer-Rachamimov, David A. Ramsay, J. Gregory Cairncross2 and David N. Louis

Molecular Neuro-Oncology Laboratory, Department of Pathology and Neurosurgical Service, Massachusetts General Hospital and Harvard Medical School [Y. I., H. S., A. O. S-R., D. N. L.] and Department of Biostatistics, Harvard School of Public Health, Boston, Massachusetts 02114 [R. A. B.], and Departments of Clinical Neurological Sciences, Oncology, and Pathology, University of Western Ontario and London Regional Cancer Centre, London, Ontario N6A 4L6, Canada [M. C. Z., D. R. M., D. A. R., J. G. C.]

Purpose: In a prior study of anaplastic oligodendrogliomas treated with chemotherapy at diagnosis or at recurrence after radiotherapy, allelic loss of chromosome 1p correlated with better chemotherapeutic response and overall survival. However, in this group of patients in whom therapeutic management was not uniform, loss of 1p did not identify all chemosensitive tumors, nor did all patients whose tumors harbor a 1p loss have long survival.

Experimental Design: To clarify the clinical relevance of molecular genetic testing at the time of diagnosis for patients with anaplastic oligodendrogliomas, we studied a larger, more homogeneous group of 50 patients with histologically defined anaplastic oligodendrogliomas treated with a chemotherapeutic regimen as the principal initial therapy.

Results: We demonstrate that these tumors can be divided genetically into four therapeutically and prognostically relevant subgroups. Patients whose tumors have combined but isolated losses of 1p and 19q have marked and durable responses to chemotherapy associated with long survival, with or without postoperative radiation therapy. Other tumors with chromosome 1p alterations also respond to chemotherapy, but with shorter duration of response and patient survival. Tumors lacking 1p loss can also be divided into two subgroups: those with TP53 mutations, which may also respond to chemotherapy but recur quickly, and those without TP53 mutations, which are poorly responsive, aggressive tumors that are clinically and genotypically similar to glioblastomas.

Conclusions: These data raise the possibility, for the first time, that therapeutic decisions at the time of diagnosis might be tailored to particular genetic subtypes of anaplastic oligodendroglioma.




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