Chromosome 1p loss evaluation in anaplastic oligodendrogliomas
Corresponding Author
Ahmed Idbaih
INSERM, Unité 711,
Université Pierre et Marie Curie-Paris6, Laboratoire Biologie des Interactions Neuron-Glie, Groupe hospitalier Pitié-Salpêtrière,
Assistance Publique-Hôpitaux de Paris, Groupe hospitalier Pitié-Salpêtrière, Service de neurologie Mazarin,
Ahmed Idbaih, MD, PhD, Laboratoire Biologie des Interactions Neuron-Glie and Service de neurologie Mazarin, Hôpital Pitié-Salpêtrière, 47-83, Boulevard de l'Hôpital, 75013 Paris, France. Email: [email protected]Search for more papers by this authorMathilde Kouwenhoven
Department of Neurology, Erasmus Medical Center, Rotterdam,
Search for more papers by this authorJudith Jeuken
Department of Pathology, Radboud University Nijmegen Medical Center, Nijmegen,
Search for more papers by this authorCatherine Carpentier
INSERM, Unité 711,
Université Pierre et Marie Curie-Paris6, Laboratoire Biologie des Interactions Neuron-Glie, Groupe hospitalier Pitié-Salpêtrière,
Search for more papers by this authorThierry Gorlia
European Organization for Research and Treatment of Cancer DataCenter, Brussels, Belgium
Search for more papers by this authorJohan M. Kros
Department of Pathology, Erasmus Medical Center, Rotterdam,
Search for more papers by this authorPim French
Department of Neurology, Erasmus Medical Center, Rotterdam,
Search for more papers by this authorJohannes L. Teepen
Department of Pathology, St. Elisabeth Hospital, Tilburg, the Netherlands, and
Search for more papers by this authorOlivier Delattre
INSERM, Unité 830,
Institut Curie, Section Recherche, Unité de Génétique et Biologie des Cancers, Paris, France,
Search for more papers by this authorJean-Yves Delattre
INSERM, Unité 711,
Université Pierre et Marie Curie-Paris6, Laboratoire Biologie des Interactions Neuron-Glie, Groupe hospitalier Pitié-Salpêtrière,
Assistance Publique-Hôpitaux de Paris, Groupe hospitalier Pitié-Salpêtrière, Service de neurologie Mazarin,
Search for more papers by this authorMartin Van Den Bent
Department of Neurology, Erasmus Medical Center, Rotterdam,
Search for more papers by this authorKhê Hoang-Xuan
INSERM, Unité 711,
Université Pierre et Marie Curie-Paris6, Laboratoire Biologie des Interactions Neuron-Glie, Groupe hospitalier Pitié-Salpêtrière,
Assistance Publique-Hôpitaux de Paris, Groupe hospitalier Pitié-Salpêtrière, Service de neurologie Mazarin,
Search for more papers by this authorCorresponding Author
Ahmed Idbaih
INSERM, Unité 711,
Université Pierre et Marie Curie-Paris6, Laboratoire Biologie des Interactions Neuron-Glie, Groupe hospitalier Pitié-Salpêtrière,
Assistance Publique-Hôpitaux de Paris, Groupe hospitalier Pitié-Salpêtrière, Service de neurologie Mazarin,
Ahmed Idbaih, MD, PhD, Laboratoire Biologie des Interactions Neuron-Glie and Service de neurologie Mazarin, Hôpital Pitié-Salpêtrière, 47-83, Boulevard de l'Hôpital, 75013 Paris, France. Email: [email protected]Search for more papers by this authorMathilde Kouwenhoven
Department of Neurology, Erasmus Medical Center, Rotterdam,
Search for more papers by this authorJudith Jeuken
Department of Pathology, Radboud University Nijmegen Medical Center, Nijmegen,
Search for more papers by this authorCatherine Carpentier
INSERM, Unité 711,
Université Pierre et Marie Curie-Paris6, Laboratoire Biologie des Interactions Neuron-Glie, Groupe hospitalier Pitié-Salpêtrière,
Search for more papers by this authorThierry Gorlia
European Organization for Research and Treatment of Cancer DataCenter, Brussels, Belgium
Search for more papers by this authorJohan M. Kros
Department of Pathology, Erasmus Medical Center, Rotterdam,
Search for more papers by this authorPim French
Department of Neurology, Erasmus Medical Center, Rotterdam,
Search for more papers by this authorJohannes L. Teepen
Department of Pathology, St. Elisabeth Hospital, Tilburg, the Netherlands, and
Search for more papers by this authorOlivier Delattre
INSERM, Unité 830,
Institut Curie, Section Recherche, Unité de Génétique et Biologie des Cancers, Paris, France,
Search for more papers by this authorJean-Yves Delattre
INSERM, Unité 711,
Université Pierre et Marie Curie-Paris6, Laboratoire Biologie des Interactions Neuron-Glie, Groupe hospitalier Pitié-Salpêtrière,
Assistance Publique-Hôpitaux de Paris, Groupe hospitalier Pitié-Salpêtrière, Service de neurologie Mazarin,
Search for more papers by this authorMartin Van Den Bent
Department of Neurology, Erasmus Medical Center, Rotterdam,
Search for more papers by this authorKhê Hoang-Xuan
INSERM, Unité 711,
Université Pierre et Marie Curie-Paris6, Laboratoire Biologie des Interactions Neuron-Glie, Groupe hospitalier Pitié-Salpêtrière,
Assistance Publique-Hôpitaux de Paris, Groupe hospitalier Pitié-Salpêtrière, Service de neurologie Mazarin,
Search for more papers by this authorAbstract
The chromosome (chr) 1p deletion is a favorable biomarker in oligodendroglial tumors and is even more powerful a marker when combined with chr 19q loss. As a result, the 1p deletion is taken into account more and more in clinical trials and the management of patients. However, the laboratory technique implemented for detection of this biomarker has been a topic of debate. To illustrate the usefulness of evaluating multiple loci, we here report two anaplastic oligodendrogliomas that were investigated using fluorescent in situ hybridization (FISH) and bacterial artificial chromosome (BAC)-array-based comparative genomic hybridization (aCGH). Indeed, segmental analysis using FISH, limited to chr 1p36 was unable to discriminate between complete and partial deletions of chrs 1p. However, complete and partial deletions of 1p are reported to have distinct clinical outcomes. Our results illustrate that aCGH (or other multiple loci technologies) provide complementary information to single locus technologies such as FISH because multiple loci technologies can evaluate the extent of the chr 1p deletion.
REFERENCES
- 1 Cairncross JG, Ueki K, Zlatescu MC et al. Specific genetic predictors of chemotherapeutic response and survival in patients with anaplastic oligodendrogliomas. J Natl Cancer Inst 1998; 90: 1473–1479.
- 2 Reifenberger J, Reifenberger G, Liu L, James CD, Wechsler W, Collins VP. Molecular genetic analysis of oligodendroglial tumors shows preferential allelic deletions on 19q and 1p. Am J Pathol 1994; 145: 1175–1190.
- 3 Smith JS, Perry A, Borell TJ et al. Alterations of chromosome arms 1p and 19q as predictors of survival in oligodendrogliomas, astrocytomas, and mixed oligoastrocytomas. J Clin Oncol 2000; 18: 636–645.
- 4 Ino Y, Zlatescu MC, Sasaki H et al. Long survival and therapeutic responses in patients with histologically disparate high-grade gliomas demonstrating chromosome 1p loss. J Neurosurg 2000; 92: 983–990.
- 5 Kujas M, Lejeune J, Benouaich-Amiel A et al. Chromosome 1p loss: a favorable prognostic factor in low-grade gliomas. Ann Neurol 2005; 58: 322–326.
- 6 Kouwenhoven MC, Kros JM, French PJ et al. 1p/19q loss within oligodendroglioma is predictive for response to first line temozolomide but not to salvage treatment. Eur J Cancer 2006; 42: 2499–2503.
- 7 Van Den Bent MJ, Carpentier AF, Brandes AA et al. Adjuvant procarbazine, lomustine, and vincristine improves progression-free survival but not overall survival in newly diagnosed anaplastic oligodendrogliomas and oligoastrocytomas: a randomized European Organisation for Research and Treatment of Cancer phase III trial. J Clin Oncol 2006; 24: 2715–2722.
- 8 Intergroup Radiation Therapy Oncology Group Trial 9402, Cairncross G, Berkey B, Shaw E et al. Phase III trial of chemotherapy plus radiotherapy compared with radiotherapy alone for pure and mixed anaplastic oligodendroglioma: Intergroup Radiation Therapy Oncology Group Trial 9402. J Clin Oncol 2006; 24: 2707–2714.
- 9 Idbaih A, Marie Y, Pierron G et al. Two types of chromosome 1p losses with opposite significance in gliomas. Ann Neurol 2005; 58: 483–487.
- 10 Jeuken J, Cornelissen S, Boots-Sprenger S, Gijsen S, Wesseling P. Multiplex ligation-dependent probe amplification: a diagnostic tool for simultaneous identification of different genetic markers in glial tumors. J Mol Diagn 2006; 8: 433–443.
- 11 Scheie D, Andresen PA, Cvancarova M et al. Fluorescence in situ hybridization (FISH) on touch preparations: a reliable method for detecting loss of heterozygosity at 1p and 19q in oligodendroglial tumors. Am J Surg Pathol 2006; 30: 828–837.
- 12 Belaud-Rotureau MA, Meunier N, Eimer S, Vital A, Loiseau H, Merlio JP. Automatized assessment of 1p36–19q13 status in gliomas by interphase FISH assay on touch imprints of frozen tumors. Acta Neuropathol (Berl) 2006; 111: 255–263.
- 13 Neuvial P, Hupe P, Brito I et al. Spatial normalization of array-CGH data. BMC Bioinformatics 2006; 7: 264.
- 14 Hupe P, Stransky N, Thiery JP, Radvanyi F, Barillot E. Analysis of array CGH data: from signal ratio to gain and loss of DNA regions. Bioinformatics 2004; 20: 3413–3422.
- 15 La Rosa P, Viara E, Hupe P et al. VAMP: visualization and analysis of array-CGH, transcriptome and other molecular profiles. Bioinformatics 2006; 22: 2066–2073.
- 16 Liva S, Hupe P, Neuvial P et al. CAPweb: a bioinformatics CGH array Analysis Platform. Nucleic Acids Res 2006; 34: W477–W481.
- 17 Jenkins RB, Blair H, Ballman KV et al. A t(1;19)(q10;p10) mediates the combined deletions of 1p and 19q and predicts a better prognosis of patients with oligodendroglioma. Cancer Res 2006; 66: 9852–9861.
- 18 Griffin CA, Burger P, Morsberger L et al. Identification of der(1;19)(q10;p10) in five oligodendrogliomas suggests mechanism of concurrent 1p and 19q loss. J Neuropathol Exp Neurol 2006; 65: 988–994.
- 19 Kubota T, Hirano A, Tanaka R, Takahashi H. Fine structural study of a cerebral tumor characterized by a honeycomb appearance after a 20-year post-mortem interval. Neuropathology 2006; 26: 158–160.
- 20 Rickert CH, Korshunov A, Paulus W. Chromosomal imbalances in clear cell ependymomas. Mod Pathol 2006; 19: 958–962.
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