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Histopathology > Neurooncology > Flashcards

Neurooncology Flashcards

1
Q

Where are the tumours of the CNS?

A
  • Brain and coverings
  • Spinal cord and coverings
  • Pituitary gland
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2
Q

What are the tumours of the peripheral nervous system?

A
  • Small nerves in any organ – usually neurofibromasof soft tissue or skin
  • Large nerves: cranial and spinal nerve schwannomas (acoustic neuroma most common)
  • Most are benign tumours
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3
Q

How do we classify CNS tumours?

A

By origin:

  • PRIMARY Tumours that originated within the CNS
  • SECONDARY Metastases:
    • 10x more frequent than primary tumours
    • in adults (30% of patients with systemic
    • cancer develop CNS mets)
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4
Q

How common are primary CNS tumours?

A
  • responsible for 2% of cancers in ADULTS and 25% of cancers in CHILDREN and most common cause of cancer death
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5
Q

How are primary CNS tumours classified?

A
  • Extra-axial (coverings):
    • Tumours of bone, cranial soft tissue, meninges, nerves and metastatic deposits
    • Intra-axial (parenchyma):
      • Derived from normal cell populations of the CNS (glia, neurons, vessels, connective tissue)
      • Derived from other cell types (metastases, lymphomas, germ cell tumours)
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6
Q

What are the interaxial and extraxial tumours?

A
  • Extra-axial: malignant
    • Meningothelial cells – meningioma
    • Schwann cells – schwannoma
    • Intra-axial: benign
      • Astrocytes – astrocytoma
      • Oligodendrocytes – oligodendroglioma
      • Ependyma – ependymoma
      • Neurons – neurocytoma
      • Embryonal cells – medulloblastoma
        • Children
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7
Q

What are the aetiology of CNS tumours?

A

LARGELY UNKNOWN

•Only known environmental factor:

Radiotherapy to head and neck: meningiomas, rarely gliomas

•Genetic predisposition <5% of primary brain tumours

  • Familiarity*
  • Familial syndromes*
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8
Q

What are the familial CNS tumour syndromes?

A
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9
Q

Describe the signs and symptoms of CNS tumours?

A
  • Signs & symptoms – often non-specific and subtly growing (can have a short history in aggressive lesions):
    • Intracranial HTN → headache, vomiting, changed mental state
    • Supratentorial → focal neurological deficits, seizures, personality change
    • Subtentorial → cerebellar ataxia, long tract signs, cranial nerve palsies
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10
Q

What neuroimaging do we use for CNS tumours?

A
  • CT scan / PET-CT (tracer compounds for hotspots)
  • MRI scan (multiple types)  MR-spectroscopy (metabolism), perfusion MRI, f-MRI
  • Purpose of imaging:
    • Assess tumour type Guide resection and biopsy
    • Assess post-surgery Assess response to treatment
    • Follow-up recurrence Progression
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11
Q

What is the management of CNS tumours?

A

(1) Surgery (maximal safe resection aims to obtain and extensive excision with minimal damage to the patient)

  • Resectability is dependent on the location, site and number of lesions
  • Craniotomy → debulking (subtotal and complete resections)
  • Open biopsies → inoperable but approachable tumours
  • Stereotactic biopsy → open biopsy not indicated

(2) Radiotherapy
* Used for… low and high-grade gliomas, metastases
(3) Chemotherapy

  • Used for… high-grade gliomas (temozolomide)
  • Biological agents (EGFR inhibitors, PD-1 inhibitors etc.)
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12
Q

How do we use histopathology and molecular pathology?

A
  • To provide a definitive and complete diagnosis
  • To guide treatment: predictive tests assays for target therapy
  • To assess treatment response
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13
Q

Describe the WHO classification of CNS tumours.

A
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14
Q

What. are the different tumour types and their origins?

  • Astrocytes
  • Oligodendrocytes
  • Ependyma
  • Neurons
  • Embryonal cells
  • Meningothelial cells
  • Schwann cells
A
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15
Q

Describe the use of grading ion CNS tumours?

A
  • Grading stratifies tumours by their outcomes (it is rarely based on their genetic profile) and is based on a tumour’s natural history and does not consider the response to treatment, it GUIDES treatment
    • Some tumours only have a few possible types and not all 4 (i.e. only 1 possible grade)
    • Grading tells us… survival
    • Grading does not tell us… therapy response, disease spread, cell of origin
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16
Q

Describe the 4 tier system of grading

A
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17
Q

What are the types of gliomas?

A
  • Diffuse
  • Circumscribed
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18
Q

What are diffuse gliomas?

A
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19
Q

What are circumscribed gliomas?

A

Much more stalble

20
Q

Where are the mutations in glial tumours?

A
21
Q

What is a pilocytic astrocytoma?

A
  • Most common child brain tumour (20% CNS tumours <14yo)
  • Common in neurofibromatosis I (NF1)
  • MRI: cerebellar; well circumscribed, cystic, enhancing
  • Histopathology:
    • Piloid (hairy) cell
    • Rosenthal fibres and granular bodies
    • Slow growing with low mitotic activity
      • BRAF mutation present in 70% of cases
22
Q
A

Rosenthal fibres - Pilocytic astrocytomas

23
Q

Describe diffuse gliomas.

A
24
Q

Describe diffuse astrocytomas.

A

(WHO grade II-IV):

  • Patients 20-40yo
  • Cerebral hemispheres (adults), cerebellum (children)
  • MRI: T1 hypointense, T2 hyperintense, non-enhancing lesion
    • Low choline: creatinine ratio at MR-spectroscopy
  • Low to moderate cellularity:
    • Mitotic activity negligible/absent
    • Vascular proliferation and necrosis absent
  • IDH1/2 mutation present in >80% of cases (positive prognostic factor)
  • Progression: an astrocytoma (grade II-III) eventually will become a glioblastoma (grade IV)
    • Over several years
25
Q
A

Diffuse astrocytomas, IDH mutant

26
Q
A

Progression: an astrocytoma (grade II-III) eventually will become a glioblastoma (grade IV)predict shorter time to progression

27
Q

Describe glioblastoma multiform.

A
  • Most patients >50yo
  • MRI: heterogenous, enhancing post-contrast
  • Cytology: high cellularity, high mitotic activity, microvascular proliferation (neoangiogenesis), necrosis
  • Histological criteria:
    • Pathological blood vessels
    • Blood vessel structural abnormalities (i.e. multi-layered vessels)
    • Cellularity on inspection
  • Genetics:
    • 90% of cases of GBM occur de novo and have wildtype IDH = MOST COMMON primary brain cancer
      • GBM, IDH wildtype
      • 10% of cases of GBM occur secondary to astrocytoma (progression) and have the IDH mutation

GBM, IDH mutant (positive prognostic factor)

28
Q
A

High cellularity

Neoangiogenesis (microvascular proliferation)

Necrosis

GLIOBLASTOMA MULTIFORME

29
Q

Describe meningiomas.

A
  • 38% of primary CNS tumours
  • Rare in patients < 40, incidence ↑ with age•
  • Originate from meningothelial cells of the arachnoid mater.

Any site of craniospinal axis, can be multiple (NF2)

••MRI: extraxial, isodense, contrast-enhancing•

80% Grade 1: benign, recurrence <25%

20% Grade 2: atypical, recurrence 25-50

1% Grade 3: malignant, recurrence 50-90%

30
Q
A

Psamomma bodies: calcification

MENINGIOMA

31
Q

What is the histology of meningiomas?

A
32
Q

Describe CNS metastases.

A
  • Most frequent CNS tumour in adults (10x more than intrinsic tumours)
    • Increasing incidence due to longer survival
    • Often multiple
  • Any tumour can potentially give CNS metastases, may be the first presentation of the disease
    • Origin can be challenging to determine
    • Most frequent tumours: lung, breast, melanoma
  • Very poor prognosis
33
Q
A

CNS metastases

  • epithelial cells
34
Q

Describe medulloblastomas.

A
  • EMBRYONAL TUMOUR: originates from neuroepithelialcells/neuronal precursors of the cerebellum or dorsal brainstem•
  • Rare (2 per 1,000,000 year), but second most common brain malignancy in children; also in young adults
  • Outcome considerably improved with radio-chemotherapy and subtype stratification
35
Q
A
  • Very undifferentiated cells
  • High grade
  • Homer wright rosettes
  • “Small blue round cell” tumour (i.e. it is a blastoma / of a primitive cell line – another = Wilm’s tumour)
  • Expression of neuronal markers (very little differentiation) – i.e. synaptophysin
  • Homer-Wright rosettes are a feature of primitive neuronal differentiation

MEDULOBLASTOMA

36
Q

What are the 4 histological subtypes of meduloblastomas? What are the 3 molecular subtypes?

A
37
Q

Describe the methylome profile.

A
  • Most tumours have characteristic patterns of DNA methylation of CpG islands•
  • The methylation signature is stable and reflects the tumour cell of origin or early transformed cells

→ Gives information on tumour type not progression/grade

•The DNA methylation status of a subset of CpG islands is assessed with DNA arrays and compared to a reference dataset (“Classifier”)

38
Q

What is the use of methylation classifiers?

A
39
Q
A

Metastatic deposit

40
Q
A

Pilocytic astrocytomas grade 1

41
Q
A

Survival

42
Q
A

IDH mutation

43
Q
A

Metastatic carcinom

44
Q
A

Pilocytic astrocytoma (WHO grade 1)

45
Q
A

Glioblastoma (WHO grade 4)

Histopathology (14 decks)

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