Alberto fara Skullbase

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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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  • Alberto fara Skullbase

    1. 1. Glioblastoma multiforme
    2. 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. 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” (UpToDate 2012)
    4. 4. Classification Pilocytic astrocytoma (WHO I) Diffuse astrocytoma (WHO II) Anaplastic astrocytoma (WHO III) Glioblastoma (WHO IV)
    5. 5. EpidemiologyMost 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 less then 12 months
    6. 6. Rarely, glioblastomas presents with meningeal dissemination, causing meningeal gliomatosis symptoms
    7. 7. Prognostic factors
    8. 8. Prognostic factors Tumor grade
    9. 9. Prognostic factors Tumor grade Age
    10. 10. Prognostic factors Tumor grade Age Extent of surgery
    11. 11. Prognostic factors Tumor grade Age Extent of surgery Karnofsky PS
    12. 12. Prognostic factors for survival of patients with glioblastoma: Recursive partitioning analysis. Neuro- oncology 2004; 6:231. Copyright © 2004 Duke University Press.
    13. 13. CT scan results provide a high degree of confidence for this type of tumor but it is not usually adopted
    14. 14. MRI is the most useful technique
    15. 15. MRI is the most useful technique low signal area
    16. 16. MRI is the most useful technique low signal area cystic areas
    17. 17. MRI is the most useful technique low signal area cystic areas internal high signal areas
    18. 18. MRI is the most useful technique low signal area cystic areas internal high signal areas irregular enhanced border
    19. 19. high signal area
    20. 20. high signal area hemorrhagic and flow voids
    21. 21. high signal area hemorrhagic and flow voidsmidline shift and mass effect
    22. 22. high signal area hemorrhagic and flow voidsmidline shift and mass effect diffuse edema
    23. 23. 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
    24. 24. Treatment is consistent with 3typical procedures: SURGERY RADIATIONCHEMOTHERAPY
    25. 25. 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”
    26. 26. Biopsy Subtotal resectionGross total resection
    27. 27. Biopsy Subtotal resection cutout at 78%Gross total resection
    28. 28. 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%)
    29. 29. Genetic backgroundand new treatments
    30. 30. 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
    31. 31. VEGF: bevacizumab, cediranib, XL184, enzastaurinEGFR: nimotuzumabPDGF: imatinib VaccinesIntegrin inbitor: cilengitide Gene therapyHistone deactylase hinibitors: cilengitide, thalidomide Intratumoral drug Radio- administration: immunoconjugates carmustine polymer wafer, CED
    32. 32. VEGF: bevacizumab, cediranib, XL184, enzastaurinEGFR: nimotuzumabPDGF: imatinib Patients should Vaccines beIntegrin inbitor: cilengitide Gene therapy encouraged toHistone deactylase hinibitors: cilengitide, thalidomide participate in clinical Intratumoralstudies whenever drug Radio- administration: immunoconjugates possible carmustine polymer wafer, CED
    33. 33. Thank you

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