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Glioblastoma Multiforme
- 3. A 48-year-old Saudi female presented to ER complaining about seizures she was lethargic and apathetic when she admitted, after a year her clinical conditioned worsened by time and she died due to infections and multiple organ failure, she had a history of several further major epileptic fits subsequent 8 months prior to her death. Case study
- 4. UnremarkableSystemic review Unremarkable Past surgical history she had a history of several epileptic fits 8 months prior to her death. Past history Non-smoker and denies any past or present use of alcohol No significant family history of neurological disorders were reported or any cancer Social, family history
- 5. Gradual mental deterioration. Loss of memory. Altered speech. Inaccurate writing. She had bilateral papilloedema. +ve brisk reflexes on the right side. Clinical examination
- 7. Secondary Metastatic Lung Kidney Breast Primary Gliomas Meningiomas Schwannoma PNET Pituitary Pineal subacute cerebral infarction tumefactive demyelination cerebral abscess primary CNS lymphoma Differential diagnosis
- 8. Hx & Physical Examination Findings Investigation
- 9. Secondary Metastatic Lung Kidney Breast Primary Gliomas Meningiomas Schwannoma PNET Pituitary Pineal subacute cerebral infarction tumefactive demyelination cerebral abscess primary CNS lymphoma Differential diagnosis
- 10. Hx & Physical Examination Findings CT Scan Brain & MRI Brain Investigation
- 11. Significant mass effect in left frontal lobe, an intra axial space occupying lesion in white matter. T2 iso intense thick enhancing wall, eccentric nodule with T2 hyper intense central non enhancing necrosis, Perilesional vasogenic odema. enhancing bubbly lesion involving corpus callosum extending in right lateral ventricle. Left lateral ventricle compressed, significant mid line shift with mid brain compression
- 12. Secondary Metastatic Lung Kidney Breast Primary Gliomas Meningiomas Schwannoma PNET Pituitary Pineal Benign Primary CNS lymphoma Subacute cerebral infarction Tumefactive demyelination Cerebral abscess Differential diagnosis
- 13. MR Spectroscopy: sharp long peak of raised choline at 3.03ppm. raised choline - creatinine ratio.
- 14. Secondary Metastatic Lung Kidney Breast Primary Gliomas Meningiomas Schwannoma PNET Pituitary Pineal Benign Primary CNS lymphoma Subacute cerebral infarction Tumefactive demyelination Cerebral abscess Differential diagnosis
- 15. -Physical Examination Findings -CT Scan Brain & MRI Brain -MR Angiography Investigation
- 16. A left carotid arteriogram showed a vascular tumour approximately 7 cm in diameter in the left frontal lobe MR Angiography
- 18. Gliomas Astrocytoma Oligodendroglioma Ependymoma -Pilocytic Astrocytoma = Grade I tumour -Diffuse Astrocytoma = Grade II tumour -Anaplastic Astrocytoma = Grade III tumour -Glioblastoma = Grade IV tumour
- 19. Physical Examination Findings CT Scan Brain & MRI Brain MR Angiography Laboratory Studies ( CBC, ESR, LFTS, Tumor Makers, etc) Immunohistochemistry Investigation
- 20. . Double staining of GFAP (red) and IDH1 R132H (brown) of oligodendroglioma infiltration zone showing specific labelling of tumor cells but not of GFAP positive reactive astrocytes GFAP: Marker of glial differentiation Ki-67/MIB1: Assessment of proliferation images showing a high Ki-67 proliferation index in approximately 25%-30% of the tumor cells Immunohistochemical
- 21. Gliomas Astrocytoma Oligodendroglioma Ependymoma -Pilocytic Astrocytoma = Grade I tumour -Diffuse Astrocytoma = Grade II tumour -Anaplastic Astrocytoma = Grade III tumour -Glioblastoma = Grade IV tumour
- 22. Physical Examination Findings CT Scan Brain & MRI Brain MR Angiography Laboratory Studies ( CBC, ESR, LFTS, Tumor Makers, etc) Immunohistochemistry Microscopic examination & Biopsy Investigation
- 24. There is a U-shaped portion of pale eosinophilic tissue related to the top edge, this represents near normal grey matter with a central sulcus containing small blood vessels. To the left of the “U” is a zone of variegated tissue. irregular areas of brightly eosinophilic tissue are interspersed with basophilic zones, this is the tumour. The more homogenous tissue on the other side of the “U” is near normal white matter. Macroscopic examination
- 25. 1-vascular proliferation 2-greatly increased cellularity
- 28. (a) atypical cells; (b) mitosis; (c) vascular proliferation; (d) necrosis with “ghost ce
- 29. Gliomas Astrocytoma Oligodendroglioma Ependymoma -Pilocytic Astrocytoma = Grade I tumour -Diffuse Astrocytoma = Grade II tumour -Anaplastic Astrocytoma = Grade III tumour -Glioblastoma = Grade IV tumour
- 30. -High grade astrocytoma (anaplastic, nuclear atypia, cellular pleomorphism, mitotic activity) with either coagulation necrosis or microvascular proliferation(formerly"endothelial proliferation")- Usually hypercellular with mitotic figures (some atypical), multinucleated tumor cells, bizarre nuclei, karyorrhectic cells. -pseudopalisading necrosis -Other less common features: epithelial structures (glandular or ribbon-like), epithelioid cells with well-delineated cytoplasmic membranes, granular cells, lipidized cells, macrophages . Micro description
- 31. Externally, there is gross swelling of the left frontal lobe with marked subfalcine herniation A large tumour is present in the left frontal lobe which extends to involve the meninges. This tumour measures 8 cm in diameter numerous foci of haemorrhage and tumour necrosis. Macroscopically, the lesion appears fairly well demarcated from the surrounding brain tissue. Autopsy
- 32. Glioblastoma Multiforme Grade IV tumor The Definitive diagnosis is …?
- 34. Background Glioblastoma Multiforme: -It is the most common malignant primary tumor of the brain. -It is very aggressive, involving glial cells. -GBM is 20% of all intracranial tumors and 52% of all tissue brain tumors. -GBM incidence is only 2–3 cases per 100,000 people in Europe and North America. -GBM differ in location within the CNS, in age and sex distribution, in growth, in invasiveness, in histological features, in progression, & in response to therapy.
- 35. There are 2 variants of GBM: -Gliosarcoma -Giant Cell Glioblastoma.
- 36. Causes The exact cause is unknown but changes or loss of chromosome 17 & inactivation of p53 has a role. -Gender: Men are more affected than women. -Viruses: like CMV or SV40 may be the cause. (There is some association of GBM with polyvinyl chloride, radiation, malaria and lead exposure) -Age: above fifty years. -Ethnicity: Asians, Caucasians
- 37. Pathogenesis GBM have necrotizing tissues which are surrounded by anaplastic cells. This along with hyperplastic vessels distinguishes GBM from astrocytomas grade III.
- 38. Types of GBM:- Classical GBM: This type has extra copies of the EGFR gene in 97% of cases. They have higher expression of EGFR gene. Proneural GBM: This type shows greater alterations in IDHI, TP53, & in PDGFRA. Mesenchymal GBM: Alterations & mutations in Neurofibromatosis type 1(NF1).
- 39. Other types of GBM:- 1-Primary GBM is sixty percent. These manifest de novo . 2-Secondary GBM is 40% develop in younger patients less than forty five years of age.
- 40. Common genetic abnormalities are: -LOH: Loss of heterozygosity on arm 10q, mutation of MDM2 are specific for GBM associated with poor survival. -Epidermal growth factor receptor gene, PTEN primary GBM. -PDGF overexpressed, p53 deletes or alteres secondary GBM Rare mutations: MAC1-E1 – A, MAGE-E1 – A and NRP/B – A
- 43. Clinical Features: Headache Vomiting Impaired memory Intellectual disability Convulsions Paralysis on one side of body Personality changes Lack of emotion Seizures Poor coordination Impaired speech Reduced ability to interpret language Motor disturbance Agraphia Paresthesia Loss of positional awareness of body Sensory changes Spatial disorientation Seizures
- 44. GBM usually reappears although disease free condition is achievable. Mostly it occurs within 3 cm of the original site but may occur in 10–20% cases at distant sites. Recurrences
- 45. Prognosis without treatment is three months survival , with treatment it is upto two years. Older patients have worse prognosis. Cerebral edema is the common cause of death. Patients who receive surgery, radiotherapy, and Temozolomide chemotherapy have long –term benefit. Prognosis
Editor's Notes
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- On clinical examination she began to show a gradual mental deterioration loss of memory altered speech +inaccurate writing. she had bilateral papilloedema +ve brisk reflexes on the right side
- :Definition These are lesions which expand in volume to displace normal neural structures & may lead to increase in intra – cranial pressure
- No hx of cancer
- MR spectroscopy has been used to help distinguish between tumor and nontumor lesions in the brain. An elevated choline peak suggests neoplasm.
- subacute cerebral infarction should not have elevated choline tumefactive demyelination often has an open ring pattern of enhancement usually younger patient cerebral abscess presence of dual rim sign
- لابوراتوري المفروض اول وحده بعد الاقزامينيشن
- GFAP: Marker of glial differentiation GFAP (Glial Fibrillary Acidic Protein) has proven to be the most specific marker for cells of astrocytic origin that distinguishes differentiated astrocytes from other glial cells during the development of the central nervous system _________________________________________ Ki-67/MIB1: Assessment of proliferation Ki67/MIB1 has been established as the reference marker for assessing cellular proliferation in tumour cells. The antibody identifies actively dividing cells at all stages of the cell cycle (late G1, S, M and G2 phases), but does not recognize cells in G0 phase
- 2-greatly increased cellularity : compared to the surrounding brain tissue. Many of these tumours show striking cellular pleomorphism, tumour giant cells and bizarre mitoses – thesefeatures are not present in this case
- in a primary glial tumour equates with a high grade lesions, 3-tumour necrosis
- a) hematoxylin-eosin stain, showing highly cellular atypia with hyperchromatic pleomorphic nuclei and mitosis, surrounded by abundant microvascular hyperplasia
- Glioblastoma = Grade IV tumour:similar to that of anaplastic astrocytoma, in addition to feature of necrosis, vascular proliferation, and pseudopalisading nuclei)
- The mounted specimen shows the brain after horizontal slicing. Externally, there is gross swelling of the left frontal lobe with marked subfalcine herniation A large tumour is present in the left frontal lobe which extends to involve the meninges. This tumour measures 8 cm in diameter numerous foci of haemorrhage and tumour necrosis. Macroscopically, the lesion appears fairly well demarcated from the surrounding brain tissue.
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- Malignant transformation from a low to anaplastic astrocytoma requires one to ten years. There is genuine evidence which indicates that primary & secondary GBMs are distinct entities. Different genetic pathways involve in GBM.
- Epidermal growth factor receptor gene, PTEN more common in primary GBM. -Platelet-derived growth factor–alpha gene PDGF overexpressed, p53 deletes or alteres it is typically In secondary GBM
- Chromosomal and genetic aberrations involved in the genesis of glioblastoma. Shown are the relationships between survival, pathobiology, and the molecular lesions that lead to the formation of primary (de novo) and secondary (progressive) glioblastomas
- Clinical features largely depend on the location of the tumor than on its pathological characteristics