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Haem/Onc > Neuro Oncology, ASPHO > Flashcards

Neuro Oncology, ASPHO Flashcards

1
Q

in terms of prevalence in peds haem/onc, where do brain tumours fall?

A

most common SOLID malig…second most common malig overall after leukemia

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2
Q

what is the most common brain tumour overall?

A
  • Astrocytomas are the most common brain tumor overall (most commonly low‐grade)
  • Medulloblastomas are the most common “malignant” brain tumor
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3
Q

msot common malig brain tumour?

A

medulloblastoma

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4
Q

CNS tumours: prevalence in boys vs girls?

A

overall more prevalent in BOYS…1.2:1

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5
Q

5 survival rate for peds CNS tumours?

A

70-75%…but misleading because some worse survival outcomes and high morbidity

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6
Q

in what ways are peds brain tumours diff from adult ones?

A

histo
bio
tx
outcomes

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7
Q

etiology of brain tumours generally unknown excepet in what TWO cases?

A

history of ionizing radiation…typically hx of CNS rads from past CNS tumour or CNS leukemia…..or Genetic brain tumour predisopsoition syndrome

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8
Q

give 8 predisposition syndromes

A

NNTLGFRR
Nada’s Tumours: Never Let Go of Really Fresh Research
NF1, NF2, Tuberous sclerosis, Li Fraumeni, Gorlin’s syndrome= nevoid basal cell carcinoma sydnrome, Familial Adenomatous Polyposis (Gardner’s Turcot’s), Rhabdoid tumour predisposition syndrome, retinoblastoma (germline)

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9
Q

Neurofibromatosis Type 1: give gene, CNS lesion, other findings

A
  • NF1
  • low grade glioma (optic pathway and brainstem)
  • Cafe au lait spots, lisch nodules, axillary freckling
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10
Q

Neurofibromatosis type 2: give gene, CNS lesion, other findings

A
  • NF2
  • BIlateral acoustic schwannomas, meningiomas, ependymomas
  • increased risk of cataracts and seizures
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11
Q

Tuberous Sclerosis: give genes, characteristic CNS lesion, other findings

A
  • TSC1 and TSC2
  • Subependymal giant cell astrocytoma= SEGA
  • increased risk fo skin adn renal growths
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12
Q

Li Fraumeni: give gene, characteristic CNS lesion, other findings

A
  • TP53
  • malig glioma, choroid plexus carcinoma
  • nuemrous cancers at younger ages (breast, sarcoma, adrenal cortical carcinoma)
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13
Q

Gorlin’s syndrome= nevoid basal cell ca syndrome…give gene, characteristic cns lesion, other findings

A
  • PTCH
  • medulloblastoma
  • basal cell ca
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14
Q

rhabdoid tumour predispositon syndrome…give gene, CNS lesion, other findings

A
  • SMARCB1 and SMARCA4
  • ATRT= atypical teratoid rhabdoid tumour
  • rhabdoid tumours in kidney, schwannomatosis, usually <1 year at dx
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15
Q

retinoblastoma (germline): give gene, charactersitic CNS lesion, other findings

A
  • trilaeral Retinoblastoma (unilateral or bilateral retinoblastoma + pineoblastoma)
  • pineoblastoma in these cases is usually dx’ed after the Rb but often before age of 5
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16
Q

majority of brain tumours in kids are in ____ region…what fraction of tumours is this? what’s included in this region?

A

infratentorial; 2/3; cerebellum, pons, medulla

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17
Q

where’s the lesion: autonomic dysfunction like temp reg, thirst, hunger affected…endocrinopathies

A

hypothalamus

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18
Q

where’s the lesion? poor/loss of vision

A

occipital lobe

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19
Q

where’s the lesion? decrased sense of touch/pain, poor spatial and visual perception, poor interpretation of language

A

parietal lobe

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20
Q

where’s teh lesion? personality changes, decreased motor speech (Broca’s), seizures

A

frontal lobe

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21
Q

where’s the lesion? ataxia, muscle movement/coordination affected, posture affected

A

cerebellum

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22
Q

where’s the lesion? weakness/motor control affected, decreased consciousness, sleep/wake cycle affected

A

thalamus

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23
Q

where’s teh lesion? weakness, cranial neuropathies (III-XII), autonomic dysfunction

A

brainstem

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24
Q

where’s the lesion? seizures, poor memory, decreased lang comprehension (wernicke’s)

A

temporal lobe

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25
Q

4 non-localizing neuro onc symptoms?

A

dev delay
behavioural changes
decline in school perf
sleepiness

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26
Q

5 symptoms/signs of increased ICP?

A 
headache
emesis
sleepiness/lethargy
papilledema
full/bulging fontanelle
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27
Q

5 endocrine sx associated with brian tumours

A 
diabetes insipidus
hypoT4
wt gain or loss
panhypopit
precocious puberty
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28
Q

low grade gliomas include WHO grade __ and ___ ___ tumours

A

1;2;glial

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29
Q

name 5 LGGs

A 
pilocytic astrocytoma
oligodendroglioma
ganglioma
pleomorphic xanthoastrocytoma
diffuse fibrillary astrocytoma
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30
Q

LGGs: what % of all brain tumours in kids?

A

40-50%

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31
Q

give a LGG associated with a cancer predispo

A

SEGA assocaited with TS!

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32
Q

how do you treat SEGA?

A

historically with surgery but now MTOR inhibitors are front line

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33
Q

what % of NF1 patients develop a CNS LGG?

A

15-20%

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34
Q

do you need to biopsy a LGG in NF1?

A

not if classic appearance

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35
Q

tx indication in NF1-associated LGG?

A

only treat if affecting vision or other neuro symptoms

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36
Q

tx NF1 associated LGG how?

A

chemo= first line…usually combo of carboplat and vcr or vinblastine alone

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37
Q

what do you need to AVOID in NF1 patients? (2)

A

radiation and alkylating chemo! high risk of secondary malig!

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38
Q

dx LGGs how?

A

biopsy or resection wtih goal of COMPLETE resection whenever possible…exception= NF1 pts with classic appearance of a LGG, typically within the optic pathway (dx can be made by imaging in this case)

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39
Q

other than dx’ing primary, any other eval needed for LGG?

A

only need additional imaging if symptoms warrant or there’s a specific histo…if there’s back pain, do spine MRI…also pilomyxoid astroctyoma has higher risk of mets, so do spine MRI in this case…do NOT routinely do LP for CSF cytology in LGG

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40
Q

what’s the most common LGG histo?

A

pilocytic astrocytoma

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41
Q

pilocytic astromcytoma appears how?

A

low-mod cellularity, GFAP+, dense fibrillary areas…characertized by ROSENTHAL fibers!!!! =astrocytic cytoplasmic inclusions that are corkscrew shaped and eosniophililc on H and E

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42
Q

aberrations of what pathway are most common in LGG?

A

MAPK

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43
Q

MAPK pathway starts with FGFR…waht are teh 4 next steps?

A

Ras, BRAF, MEK, ERK

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44
Q

what’s the most common mech of BRAF activation in LGG?

A

BRAF KIAA1549 fusion…in 60-80%!

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45
Q

other than BRAF fusion give another common BRAF mut in LGG

A

BRAFV600E…10-15% of pilocytic astrocytoma…also seen in pleomorphic xanthoastrocytoma and ganglioma

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46
Q

Tx LGG how?

A

try for gross total resection if possible! then observe.:)…if residual disese/no resectable: give chemo= carbo/vcr or vbl alone or combo of thioguanine, procarbazine, ccnu, vcr (PTCV)…should not give this last regimen in NF1 bc procarbazine= alkylating!…radiation effective but avoid in young kids

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47
Q

4 late effects of CNS rads?

A

neurocognitive changes, endocrine, ototoxicity, secondary malig

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48
Q

what types of targeted therapies are being studied in LGG?

A

MEK inhibitors, BRAF inhibitors

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49
Q

LGG: OS if GTR?

A

> 90-95%

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50
Q

COG A9952: compared what? findings?

A

carboplatin/vcr vs TPCV in LGG…better EFS in TPCV on cure model analysis but more toxic

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51
Q

diencephalic syndrome occurs where?

A

diencephalon, including thalamus and hypothal

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52
Q

signs and sx of diencphalic syndrome? often caused by?

A 
FTT and emaciation
abnormal eye movements and vision issues
vomiting
hydrocephalus
...oftne caused by LGG
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53
Q

HGG = WHO grade what?

A

3-4

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54
Q

HGG grade 3=?

A

anaplastic astrocytoma

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55
Q

HGG gr 4=?

A

glioblastoma multiforme

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56
Q

HGG more common in kids or adults?

A

adults

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57
Q

HGGs are more ___ __ __ and have much ___ ___ ___ compared to LGG

A

resistant to therapy; poorer survival outcomes

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58
Q

3 RFs for HGG?

A
  • previous radiation
  • Li Fraumeni syndorme
  • Familial Adenomatous Polyposis = APC gene abnormality
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59
Q

dx HGG how?

A

biopsy/resection and path…except for DIPG!

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60
Q

goal in HGG?

A

GTR

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61
Q

evaluation for HGG?

A
  • spinal MRI

- NO need for routine LP (CSF cytology)

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62
Q

path in HGG?

A 
"Path in Very Grave CNS Maligs"
highly Cellular
high Mitotic count
Vascular proliferation
Pseudopalisating necrosis
usually GFAP+
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63
Q

DIPG stands for?

A

diffuse intrinsic pontine glioma

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64
Q

dx DIPG how?

A

imaging alone…pons enlarged..typically doesn’t enhance at dx, but this can vary

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65
Q

classic age for DIPG?

A

5-7 yrs

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66
Q

> 80% DIPG tumours have which mutaiton?

67
Q

can you completely resect DIPG?

68
Q

sx in DIPG?

A

CN symptoms, long tract signs, ataxia…symptoms are of SHORT DURATION (1-2 mos)

69
Q

therapy in DIPG?

A

focal radiotherapy = only known beneficial tx

70
Q

mean survival in DIPG is ___ months with almost all children____ __ ___ within ___ ___ regardless of ____

A

10-12; succumbing to disease; 2 years; therapy

71
Q

what constitutes diffuse midline glioma, H3 K27 mutant?

A

H3 K27M seen in WHO grade 4 lesions of the midline, most commonly pons (DIPG), thalamus, or spinal cord

72
Q

H3K27M seen in what % of DIPG?

73
Q

what other histone mutation is less common that H3K27M?

74
Q

HGG tx?

A

maximal safe surgical resection–> then focal radiation and chemo…although chemo not specifically agreed upon

75
Q

For HGGs, what age range of patients have a more indolent course?

A

infant (most commonly <3 yrs)

76
Q

5 year OS in HGG?

A

15-20%…infants slightly better

77
Q

medulloblastoma is a highly ___ and ___ ___ ___ tumour

A

aggressive; rapidly growing embryonal

78
Q

medulloblastoma located where?

A

cerebellum

79
Q

what’s more common: LGG or medullo?

80
Q

medulloblastoma: more common in males or females?

A

males almost 2:1

81
Q

RFs for medulloblastoma?

A
  • Gorlin syndrome= nevoid basal cell carcinoma syndrome, due to PTCH gene mut
  • Familial Adenomatous polyposis (like Gardeners’ and turcot’s syndrome)
82
Q

what does medullo look like on imaging?

A

large heterogenous mass in posterior fossa, often with some contrast enhancement

83
Q

Dx medullo how?

A

need tissue! try to get GTR!

84
Q

what % of medullos have mets? how?

A

30%…through CNS

85
Q

eval for medullo?

A

spine MRI AND lumbar CSF cytology

86
Q

WHEN should you do spine MRI for medullo?

A

pre-op OR 10-14 days or more post-op to avoid post-op products confounding hte MRI interpretation

87
Q

do lumbar CSF when for medullo staging?

A

at least 10-14 days post-op to avoid post-op products confounding interpretation

88
Q

path in medullo?

A
  • highly cellular
  • lots of mitosis
  • synaptophysin positive
89
Q

4 histo patterns in medullo?

A
  • classic
  • desmoplastic
  • extremely nodular
  • anaplastic/large cell
90
Q

what are the 4 major medullo molecular subgroups?

A

WNT, SHH, group 3, group 4

91
Q

which medullo molecular subgroup has hte best prog?

A

WNT! 90-100% OS

92
Q

what is ACNS1422 studying?

A

whether we can reduce therpay in pts with subgroup Wnt medullos

93
Q

how do the medullo subgroups differ by age?

A

WNT, Group 3, and Group 4 all more common in children…while SHH more common in infants and adults

94
Q

how do the medullo subgroups differ by histo?

A
  • classic can be seen in all of them
  • LCA common in SHH, group 3, group 4 but is RARE for Wnt
  • Desmoplastic/nodular, M9EN common in SHH
95
Q

Describe genetics in WNT medullo

A

Monosomy 6, nuclear beta catenin, increased risk in turcot syndrome

96
Q

describe genetics in SHH medullo

A

PTCH1/SMO/SUFU, GLI2 amplification; increased risk in gorlin syndrome

97
Q

describe genetics in group 3 medullo

A

i17q, MYC ampication

98
Q

describe gneetics in group 4 medullo

A

CDK6 amplification, MYCN amplifcation

99
Q

describe prog within the diff medullo subgroups

A

WNT: excellent
Group 3: poor
SHH: fair unless TP53 mutant…in this case, it’s POOR
Group 4: fair

100
Q

not including molecular subgroups, what = Standard risk in medullo?

A

age >3, GTR with <1.5 cm3 residual disease, no mets, NOT anaplastic histo

101
Q

what are the non-molsecular risk subgroups in medullo

A

Standard Risk
High Risk (anything not SR except infants)
Infants (age <3)

102
Q

how do you tx SR medullo?

A

-Craniospinal radiation at lower doses 2340 cGy +/- weekly vcr and boost to the PF (5400 cGy)–> then maintenance chemo

103
Q

how do you treat HR medullo?

A

full dose CS radiation = 3600 cGy, +/- weekly vcr and boost to PF (5400 cGy) followed by maintenance chemo

104
Q

how do you treat infants with medullo?

A

-induction chemo
-then high dose chemo
with auto stem cell rescue +/- radiation

105
Q

for medullo, what does M0-M4 mean?

A 
M0= no mets
M1= CSF lumbar cytology +
M2= mets in brain on MRI
M3= mets in spine on MRI
M4= mets outside of CNS (very rare!)
106
Q

5 yrs OS in SR vs. HR. vs. infant medullo?

A

SR: 75-90%
HR: 40-60%
infant: 50-70%…but don’t forget if you’re talking about the WNT ones it’s >90% at 5 yrs!

107
Q

3rd most common brain tumour in peds?

A

ependymoma

108
Q

ependyma is a ___ tumour with ___ cell ___

A

glial; ependymal; differentation

109
Q

where does ependymoma occur?

A

usually associated with a ventricular surface but can be anywhere within the CNS….cerebellum>lateral ventrciles>spinal cord

110
Q

RF for ependymoma?

111
Q

dx ependymoma how?

A

need tissue!…aim for GTR! this is important!

112
Q

staging for ependymoma?

A

-CSF cytology + spine MRI…same timing as for medullo

113
Q

ependymoma appear how on imaging?

A

hetergenous mass in PF; often patchy with heterogenous enhancement

114
Q

classic path in ependymoma?

A

presence of perivascular pseudorosettes

115
Q

what molecular finding in ependymoma would yield a poor prognosis?

A

EPN-RELA (RELA fusion)

116
Q

tx for ependymoma

A
  • aim for GTR
  • then FOCAL radiation 5400-5900 cGy (unless mets, then not focal…if metes, do 3600 cGy with boost to focal area fo 5400-5900 cGy)
  • role of chemo= unclear
  • chemo alone only if LESS THAN 1 YEAR OF AGE!
117
Q

5 yrs OS in ependymoma?

A

60-80% but MANY PATIENTS HAVE LATE RELAPSES AFTER 5 YEARS:(…may eventually succumb to their disease due to recurrence

118
Q

CSF GCTs: give 2 tumouor markers

A

AFP, beta HCG

119
Q

2 major catergories of CNS GCTs?

A

germinoma = non-secreting, better outcome!….non-germinomatous germ cell tumour= secreting= worse otucome typically

120
Q

CNS GCTs: more common where in the world?

A

Japan and other Asian countries…only 2-3% in north america, but 10-15% in Japan

121
Q

RFs for CNS GCTs?

A

none known

122
Q

how do CNS GCTs appear on imaging?

A

heterogenous and enhancing mass in suprasellar= pituitary region or in pineal region…sometimes both

123
Q

symptoms of GCT in suprasellar= pituitary reigon?

A

Diabetes insipidus, panhypopit

124
Q

symptoms of GCT in pineal region?

A

parinaud’s syndrome, increaesd ICP

125
Q

what is Parinaud’s syndrome?

A
  • paralysis of upward gaze
  • pseudo-Argyll Robertson pupil (accommodative paresis and pupils become mildly dilated and show light-near dissociation)
  • convergence-retraction nystagmus (on fast up-faze, the eyes pull in and the globes retract)
126
Q

Many GCTs are ___ and can contain a ___ of ___ and other ___ __ ___ ___ elements

A

mixed; variety; germinoma; malig germ cell tumour

127
Q

amongt the non-germinatomous gcts, there are many histo variants, including:

A

endodermal sinus tumour, yolk sac tumour, embryonal carcinoma, teratoma

128
Q

Dx GCT how?

A
  • Always do serum and CSF tumour markers at diagnosis
  • If tumour markers in serum or CSF (AFP, beta-HCG ) are elevated enough, a dx of NGGCT can be made wtihout tissue
  • if markers not diagnostic, need biopsy
  • DO need full spine MRI and lumbar CSF
129
Q

tx germinoma how?

A
  • neoadjuvant chemo (carbo/etop x 4 cycles)
  • then radiation (dose depends on response to chemo but ranges from 3000-3600 cGy and includes whole ventricle…….OR could just do radiation alone at 4000-4500 cGy but we don’t really do this anymore!
130
Q

tx non-germinatous gct how?

A

neoadjuvant chemo then XRT (extent and dose controversial)

131
Q

in both germinoma and NGGCT, ___ __ ___ often advocated after ___ ___ if __ ___ remains prior to ____ to decipher ___ ___, whihc coudl be ___ ___, ___ ___, or ___

A

second-look surgery; neoadjuvant chemo; residual mass; radiotherapy; residual mass; scar tissue, malig tumour, teratoma…think growing teratoma syndrome= malig comonent shrinks away, but teratoma grows and need to remove iwth srugery!

132
Q

5 yr OS for germinoma?

133
Q

5 yr OS in NGGCT?

A

80-90%…subgroup though with poorer responses (less than partial responses to chemo)

134
Q

AT/RT stands for?

A

atypical teratoid rhabdoid tumour

135
Q

AT/RT is a __ ___ tumour typically seen in ___ ___ adn ___, about __ % of all pediatric CNS tumours

A

rare embryonal; young children; infants; 2

136
Q

eval for AT/RT?

A

do need spine MRI and lumbar CSF

137
Q

historically, prog for AT/RT is very ___ but what has helped change this?

A

poor; combinign chemo (auto stem cell rescue or “sarcoma-like” therapy) +/- radiation

138
Q

immunohistochem in AT/RT?

A

loss of INI-1

139
Q

Rhabdoid tumour predisopsoition syndrome is a germline mutation in ___ and ____ (___ or ___) associated with increased risk of AT/RT, other ___ tumours (commonly in ___), and _____

A

SMARCB1; SMARCA4; INI-1; hSNF5; rhabdoid; kidney; schwannomatosis

140
Q

choroid plexus tumours represent ___ % of all peds brain tumours; most commonly lcoated in the ___ ___

A

1-2%; lateral ventricles

141
Q

3 types of choroid plexus tumours?

A

choroid plexus papilloma
atypical choroid plexus papilloma
choroid plexus carcinoma

142
Q

choroid plexus tumours usually present in ___ ___/___ with signs of ___ ___ ___

A

younger children/infants ;increased intracranial pressure

143
Q

goal in choroid plexus tumours?

A

GTR! which is usually curative for choroid plexus papilloma specfiically

144
Q

outcomes for choroid plexus carcinoma are___ despite a variety of multimodal therapies with __ and ___

A

variable; chemo; radiation

145
Q

choroid plexus carcinoma OS at 5 yrs?

146
Q

RF for choroid plexus carcinoma?

A

Li Fraumeni

147
Q

craniopharyngioma is a rare __ tumour thought to be due to ____ origin

A

epithelial; maldevelopmental

148
Q

craniopharyngioma represents ___ % of all peds brain tumours

149
Q

how does crainopharyngioma present?

A

headaches, emesis, visual field cut, endocrionpathies

150
Q

most common location for craniopharyngioma?

A

suprasellar/pituitary

151
Q

imaging of craniopharyngioma looks like?

A

mixed solid and cystic mass at the suprasellar region

152
Q

path of craniopharyngioma?

A

squamous epithelium lining cystic cavities, often containing calcium and keratin

153
Q

tx for craniopharyngioma?

A

GTR!..if can’t do or diseases progresses, do focal rads

154
Q

although PFS and OS are ___ for craniopharyngioma, many pts have numerous ___ affecting __ __ __ (eg: 4?)

A

good; co-morbidiites; quality of life; endocrionpathies, behavioural issues; visual dysfunction; seziures…but actually considered “benign low grade tumour”

155
Q

after CNS radiation, inreased risk of what seocnary brain tumours most commonly?

A

HGG, meningioma

156
Q

secondary brain tumours after rads usually occur when?

A

7-10 yrs after radiation

157
Q

risk of secondary brain tumour after radiation?

158
Q

give 4 late effects of CNS radiation

A 
neurocognitive decline
ototoxicity
endocrine dysfunction(hypothyroidism, GH def, delayed puberty)
secondary malig
cerebrovascular events
159
Q

late effect of cyclophos?

A

infertility

160
Q

late effect of cisplatin?

A

ototoxicity

161
Q

late effect of etop?

A

secondary malig

162
Q

late effect of IT mtx?

A

leukoencephalopathy

163
Q

late effect of doxo?

A

cardiac dysfunction

Haem/Onc (30 decks)

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