12. • M/E-
• Elongated Bipolar cells
( elongated hair like
processes)
• Rosenthal fibers with
eosinophilic protein droplets
• mural nodule may be
highly vascular; often
calcifications
• Vascular changes are
common –
glomeruloid vascular
proliferation and vascular
hyalinization
15. • Positive stains
• GFAP (strong), PTAH, PAS (protein droplets), alpha-1-antichymotrypsin (protein
droplets)
• Neoplastic astrocytes have intermediate cytoplasmic filaments. These filaments, has protein-glial
fibrillary acidic protein (GFAP), can be detected by I/H/C
• GFAP- positive
17. • Pleomorphic xanthoastrocytoma
• WHO grade II
• Occurs in temporal lobes of children and young adults
• Gross
• Usually cystic
• M/E-
• Pleomorphic cells (occasional xanthomatous change),
• Perivascular lymphocytic cuffing, scattered eosinophilic granular bodies,
reticulin rich network
• No necrosis and no mitosis.
19. • Positive stains
• GFAP and S100
• Reticulin, class III beta tubulin (73%)
• Variable expression of neuronal markers including synaptophysin
20. • D/D-
• Glioblastoma and giant cell glioblastoma
• Malignant fibrous histiocytoma
• Other cystic lesions, especially those with a cyst-mural nodule
architecture (pilocytic astrocytoma and ganglioglioma
21. Infiltrative astrocytoma
• Site-
Infiltrative astrocytomas are usually found in the cerebral
hemispheres,
• Age-
most common in patients between 30 and 60.
• Presentation-
Patients most commonly present with seizures, headaches, and
focal neurologic deficits (depending on where the tumor is).
23. • Diffuse astrocytoma
• Most common adult tumor.
• 80% of adult primary brain tumors
• Location: Usually supratentorial
• Age-4th to 6th decades
• MRI-
• Ill defined, non enhancing lesion with mass effect and variable peritumoral
edema.
24. • Gross-
Poorly defined infiltrative
tumor that distorts
the brain.
C/S-
Firm / soft & gelatinous, Cystic degeneration
25. • M/E-
• Mild to moderate glial
cellularity
• Variable nuclear
pleomorphism
• Fibrillary background
due to astrocytic process
28. • Anaplastic astrocytoma
• Grading: WHO grade III/IV
● Age and sex: mean age 45 years; male predominance
● Site: usually supratentorial, but can be anywhere in CNS;
● MRI:
• Usually heterogeneous or
patchy enhancement
29. Gross-
Anaplastic astrocytoma
predominantly
occupying the right temporal lobe.
The tumour is ill-defined and
appears as a homogeneous mass.
Note the large cyst in the periphery
of the neoplasm and shift of
midline structures
towards the left hemisphere.
30. This astrocytoma
had densely cellular
areas with back-to-
back nuclei,
moderate nuclear
pleomorphism, and
increased mitotic
activity. However,
necrosis or
endothelial
proliferation - the
two hallmarks of
Glioblastoma - were
absent.
31. • M/E-
• Increase in cellularity
• Nuclear pleomorphism
• Hyperchromasia
• May have mitosis
• No necrosis
32. • D/D-
● Anaplastic oligodendroglioma:
• hypercellular with loosely cohesive and single cells, moderate
pleomorphism, vacuolated background, mitotic activity
● Anaplastic oligoastrocytoma:
• conspicuous oligodendroglioma and astrocytoma components
• Glioblastoma
33. • Anaplastic astrocytoma Glioblastoma
• Increase in cellularity Dense cellularity
• Nuclear pleomorphism
• Hyperchromasia
• May have mitosis Mitosis
• No necrosis Necrosis & vascular proliferation
34. Gemistocytic astrocytoma
Dense eosinophilic cytoplasm & eccentrically
displaced nucleus.
Gemistocytes are frequently
found in other fibrillary
astrocytomas &
oligodendrogliomas. Some
authors require at 20% of
tumor cells to be gemistocytic
before using the designation of
gemistocytic astrocytoma.
This tumor appears to be
composed of an almost
pure population of gemistocytic cells.
36. • D/D-
• Gliosis:
• Hypertrophy of cells rather than hyperplasia, even distribution
• Subependymal giant cell tumor: intraventricular, larger nuclei,
non-infiltrative
• Ganglioglioma: neoplastic neurons
37. • Glioblastoma
• WHO grade IV
• "Multiforme" due to variegated gross appearance (firm white areas, yellow necrotic
areas, hemorrhagic areas and cystic areas) as well as diverse histological features
• Sites
• Usually supratentorial;
• Either primary (de novo, with with p53 mutation) or secondary (transformed from
grade II/III astrocytoma)
• MRI
• Contrast enhancing (ring pattern),
• large surrounded by peritumoral edema.
• (parietal lobe)
38. • Gross-
glioblastoma is a poorly defined
intra-axial mass with variegated
(multiform) appearance due to
necrosis and hemorrhage.
• A 9.0 cm tumor with foci of
hemorrhage and necrosis
involving the left temporal lobe.
40. • M/E-
• Densely cellular with nuclear
pleomorphism
• Necrosis in a serpentine pattern
• Tumour cells crowded along the
edges of necrosis - pseudopalisading
• When vascular cell proliferation
is extreme, the tuft forms a ball-like
structure, the glomeruloid body
41. • Besides necrosis with nuclear pseudopalisading, the presence of endothelial
proliferation is another histologic hallmark of glioblastomas.
44. • Gliomatosis Cerebri-
• WHO Grade- III/IV
• Neoplastic astrocyte infiltrates
• the multiple region of brain or
• in some cases the entire brain .
• H/P-
• Largely composed of elongated,
hyperchromatic glial cells
Mitosis.
No necrosis or
microvascular proliferation
46. Oligodendroglioma
• WHO grade- II/IV
• Gross
• well-circumscribed, gelatinous,
gray masses, often with cysts,
focal hemorrhage,
& calcification
47. • M/E-
• Sheets of regular cells with
spherical nuclei & perinuclear halo
(fried egg)
(perinuclear halo artifact due to fixation,
and is not present in frozen sections)
• Calcifications-90% cases,
• Arborizing thin capillaries
• (chicken
wire pattern)
48.
49. • Positive stains
OLIG2, Leu7, S100, MAP2 (strong)
• D/D-
• Clear cell ependymoma: enhancing, well-circumscribed, perivascualr
pseudorosettes, dot- or ring-like EMA+
• Clear cell meningioma: extra-axial, enhancing, PAS+, EMA+
• Metastatic clear cell carcinoma: enhancing, well-circumscribed,
EMA+, CK+; molecular testing for 1p/19q deletion may be helpful, but some
oligodendrogliomas are negative for the deletion
• Pituitary adenomas: chromogranin+, pituitary hormone+
52. Ependymoma
• Slowly growing tumor of ependymal cells arising from walls of
ventricles or spinal canal
• Grade II/!V
• MRI-
• Well circumscribed lesions
with variable enhancement
56. • D/D-
Glioma:
• no true rosettes,
• no cell-cell junctions,
• no intracytoplasmic microvilli-lined lumina
57. Anaplastic Ependymoma
• Grade- III /IV
• Rare; usually infants and children
• Cerebrum/ cerebellum of children / young adults, but all ages and locations
• M/E-
Marked hypercellularity,
nuclear atypia
high mitosis &
necrosis
58. Myxopapillary ependymoma
• Grade - I / IV
• M/E-
• Well differentiated Cuboidal to elongated tumor cells arranged around the
papillary cores with a myxopapillary appearance.
• Usually no atypia,
• no/low mitotic activity
59. MOLECULAR CHANGES IN ASTROCYTOMA-GLIOBLASTOMA
• Isocitrate dehydrogenase (IDH)
• IDH is a citric acid cycle enzyme that catalyzes that convert isocitrate to a-
ketoglutarate.
• IDH1 and IDH2 are frequently mutated in gliomas.
• IDH1 mutated in 70-80% of grade II and III astrocytomas,
oligodendrogliomas, oligoastrocytomas, & in secondary but not primary
glioblastomas.
• IDH2 mutations are more common in oligodendrogliomas
• Detection of IDH1 mutations by I/H/C is an important tool in the diagnosis of
gliomas.
60. • Tumor Protein 53 (TP53)
• It repairs DNA damage and induces apoptosis when damage
cannot be repaired. Its mutation promotes tumor formation
• TP53mutations common in diffuse astrocytoma, anaplastic
astrocytoma, and secondary glioblastoma, and help distinguish
glioma from gliosis.
• Mutations can be detected by I/H/C shows strong nuclear
staining for p53.
61. • Epidermal Growth Factor Receptor (EGFR)
Overexpression of EGFR, on 7p, occurs in 40 % of glioblastomas
(more commonly primary ones) and less frequently in lower
grade astrocytomas .