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Glioblastoma
- 2. 4 week history of 67 years-old caucasian headache “especially male patient, no when I wake up”, significant PMH memory loss; right- sided mild motor weakness T1-weighted axial MRI with T2-weighted axial MRI intravenous contrast
- 3. The most common primary brain tumors are the gliomas (approximately 60%) Among all gliomas, Glioblastoma is the most common and most aggressive tumor “Glioblastomas are densely cellular, pleomorphic tumors with mitotic activity and either microvascular proliferation or necrosis”
- 4. Classification Pilocytic astrocytoma (WHO I) Diffuse astrocytoma (WHO II) Anaplastic astrocytoma (WHO III) Glioblastoma (WHO IV)
- 5. Epidemiology Most common primary brain tumor (15%) 2-3 new cases per 100.000 people/y It affects >45 adults preferentially Men to female ratio 3:2 slightly more common in whites Overall median survival after optimal therapy is 12 months
- 6. Rarely, glioblastomas presents with meningeal dissemination, causing meningeal gliomatosis symptoms
- 8. Prognostic factors Tumor grade
- 9. Prognostic factors Tumor grade Age
- 10. Prognostic factors Tumor grade Age Extent of surgery
- 11. Prognostic factors Tumor grade Age Extent of surgery Karnofsky PS
- 12. Prognostic factors for survival of patients with glioblastoma: Recursive partitioning analysis. Neuro- oncology 2004; 6:231. Copyright © 2004 Duke University Press.
- 14. CT scan results provide a high degree of confidence for this type of tumor but it is not usually adopted
- 15. MRI is the most useful technique
- 16. MRI is the most useful technique low signal area
- 17. MRI is the most useful technique low signal area cystic areas
- 18. MRI is the most useful technique low signal area cystic areas internal high signal areas
- 19. MRI is the most useful technique low signal area cystic areas internal high signal areas irregular enhanced border
- 21. high signal area
- 22. high signal area hemorrhagic and flow voids
- 23. high signal area hemorrhagic and flow voids midline shift and mass effect
- 24. high signal area hemorrhagic and flow voids midline shift and mass effect diffuse edema
- 25. PET scanning is a useful adjunct in GBM cases, especially in the follow-up after resection Differential diagnosis between recurrent or residual masses and scars or radiation necrosis is difficult with MRI - TC PET scans is helpful in these cases
- 27. Treatment is consistent with 3typical procedures: SURGERY RADIATION CHEMOTHERAPY
- 28. The initial treatment for GBM is total resection with preservation of neurologic function preoperative imaging MRI - PET frameless stereotaxis with cortical stimulation and language assessments intraoperative techniques operating rooms equipped with CT - MRI scanners can guide the resection in “real time”
- 29. Biopsy Subtotal resection Gross total resection
- 30. Biopsy Subtotal resection cutout at 78% Gross total resection
- 31. Radiation dose of 6000 cGy administered in 5 days showed a median survival of 42 weeks Temozolomide has been shown to improve: median progression-free survival (+2 months) overall survival (+2 months) likelihood of being alive in 2 years (26% vs 10%)
- 32. Genetic background and new treatments
- 33. Alterations of receptor tyrosine kinases (such as EGFR) that activate PI3K signaling, leading to hyperproliferation and increased cell survival Dysregulation of the p53 pathway that lead to effects such as reduced apoptosis L o s s o f c e l l - c y c l e c o n t r o l v i a disruption of Rb signaling pathway
- 34. VEGF: bevacizumab, cediranib, XL184, enzastaurin EGFR: nimotuzumab PDGF: imatinib Vaccines Integrin inbitor: cilengitide Gene therapy Histone deactylase hinibitors: cilengitide, thalidomide Intratumoral drug Radio- administration: immunoconjugates carmustine polymer wafer, CED
- 35. VEGF: bevacizumab, cediranib, XL184, enzastaurin EGFR: nimotuzumab PDGF: imatinib Patients should Vaccines be Integrin inbitor: cilengitide Gene therapy encouraged to Histone deactylase hinibitors: cilengitide, thalidomide participate in clinical Intratumoralstudies whenever drug Radio- administration: immunoconjugates possible carmustine polymer wafer, CED
- 36. Thank you
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- primary vs secondary GBM\n
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- they often miss small tumors (including lower-graded masses)\nmultifocal form is not clearly depicted\noverlapping images: diffuse multiple sclerosis, infarct with hemorrhagic transformation,\nbrain abscess, ecc\n
- hemorrhagic foci\ninternal flow voids, neovascularity\n
- hemorrhagic foci\ninternal flow voids, neovascularity\n
- hemorrhagic foci\ninternal flow voids, neovascularity\n
- hemorrhagic foci\ninternal flow voids, neovascularity\n
- hemorrhagic foci\ninternal flow voids, neovascularity\n
- hemorrhagic foci\ninternal flow voids, neovascularity\n
- hemorrhagic foci\ninternal flow voids, neovascularity\n
- hemorrhagic foci\ninternal flow voids, neovascularity\n
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- similar diagnostic image quality in both fusions and PET alone\n
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- Malignant gliomas are characterized by poorly defined tumor margins with infiltration of neoplastic cells along white matter fibers and the perivascular spaces, which can extend well beyond the tumor margin as defined by the surgeon or by radiographic studies\n
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- progenitor cells vs adult cells\nSeveral gene mutations account for molecular and biologic background of GBM. In spite of the gene involved, all mutations lead to damaging one of these 3 key-regulatory pathways:\nPDGF, EGFR, IGF-1, IDH CDKN2A, CDKN2B, RB1, CDK4\n
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