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Haem/Onc > ALL, ASPHO > Flashcards

ALL, ASPHO Flashcards

1
Q

Name 2 ALL abnormalities that can arise in utero

A
  • KMT2A=ALL

- Hyperdiploid ALL

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2
Q

What percent of baby with ETV/RUNX1 detectable on cord blood will develop ALL?

A

1%

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3
Q

For kids under 15, what % of leukemias are ALL? AML?

A

ALL=80%

AML=15%

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4
Q

For kids 15-19, what % of leukemias are ALL? AML?

A 
ALL= 56%
AML= 31%
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5
Q

what’s the peak age for ALL dx? AML?

A

ALL= 2-4; AML= no peak incidence

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6
Q

Childhood leuk represents what % of all new childhood cancer cases?

A

26.1%

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7
Q

Give 3 factors that have led to improved ALL survival

A
  • CNS ppx started in 1970s
  • Intensified therapies for identified risk groups with higher rates of relapse
  • Improved supportive care
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8
Q

Give 6 ALL predispo syndromes

A 
DNA CBNNRKL
DNA NotBadLuck
Down Syndrome
NF1
Ataxia Telangiectasia (T-ALL)
Noonan Syndrome
Bloom Syndrome
Li Fraumeni Syndrome

Also:
Constitutinal Robertsonia Translocation, Nijmegen Breakage syndrome, Constitutional Mismatch repair deficiencies, Klinefelter sydnrome

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9
Q

Risk increase for leukemia if T21?

A

20x

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10
Q

Higher risk of leukemia in T21 pertains to what age?

A

First 3 decades of life

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11
Q

Although the relative risk of AML is ___ than ____, ____ is more common than ___ except in the ___ yr of life

A
  • higher
  • ALL
  • DS-ALL
  • DS-AML
  • first
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12
Q

what percent of children with B-precursor ALL have DS?

A

3%

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13
Q

Which common sentinel genetic alterations in ALL are less common if DS-ALL?

A

KMT2A translocations
ETV-RUNX1
BCR/ABL rearrangement
Trisomy 4+10

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14
Q

which sentinel genetic alteration in ALL is more common if DS-ALL?

A

CRLF2 overexpression+ accompanying JAK and IL7R mutations

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15
Q

which genetic mutation has better outcome in DS-ALL than non DS ALL?

A

CRLFr

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16
Q

in general who does better non-DS or DS ALL?

A

non-DS…unless you discount common genetic mutations, then they are the same

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17
Q

there’s more mortality due to what in DS-ALL?

A

toxic related death

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18
Q

give 5 germline mutations predisposing towards ALL

A 
PAX5 G183S mutations
TP53 (hypodiploid)
ETV6 (hyper)
FANCA (hypo)
MLL3 (hypo)
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19
Q

what percent of childhood leukemia is associated with deleterious germline mutations?

A

~5%

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20
Q

Discuss concordance rates for ALL in identical twins by age…why? usually due to what genetic alteration in infants?

A

<12 mos: close to 100%
after 12 mos: 10-15%….concordance in infant twins due to early chrom translocations and transplacental trasnfer or leuk/preleuk cells to other twin…KMT2A

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21
Q

Give symptoms/signs of ALL

A
  • Bone pain/refusal to walk
  • Decreased energy, pallor, loss of appetite
  • Adenoapthy/HSM
  • mediastinal mass, SOB, unable to lie flat
  • headache, neck pain, sz, CN Palsy if CNS invovled
  • painless enlarged testes
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22
Q

TLS associated with what type of ALL

A

t-cell

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23
Q

risks of hyperleuk more in ALL or AML?

A

AML

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24
Q

What can genotype of ALL help determine? (3)

A

prognosis, tx stratification, and soemtimes use of targeted therapies (eg TKI for Ph+ ALL)

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25
Q

WHat defines NCI risk group?

A

age and WBC (doesn’t apply to T_ALL)…wbc and age at dx NOT prognostic in T-ALL!

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26
Q

what’s the strongest prognostic factor

A

response to therapy

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27
Q

About what % are SR and what % are high risk in B-ALL?

A

about 2/3 SR and about 1/3 HR

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28
Q

What indicates SR in B-ALL?

A

age 1.00-9.99 years; WBC<50,000/microliter

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29
Q

EFS in SR B-ALL?

A

90%

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30
Q

WHat indicates HR in B-ALL?

A

age>10 years OR WBC>50,000/microliter

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31
Q

5-yr EFS in HR B-ALL in non-infants?

A

75-80%

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32
Q

what % of B-ALL patients are infants? outcomes are ___

A

1%; poor

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33
Q

Describe principle re: giving diff treatment to HR groups:

A

Improviing outcomes by giving more intense tx to HR groups that LR groups would otherwise not need

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34
Q

what is the relevance of t(1;19) in B-ALL?

A

used to be associated with poor outcome, but now irrelevant if give more intense therapy

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35
Q

How does BFM redefine initial risk?

A

Gives 7 days prophase of steroids with one IT mtx to determine initial risk, then refines based on MRD and some genetics

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36
Q

what percent of ALL cases are B precursor?

A

80-85%

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37
Q

What marker distinguishes lymphoid from myeloid?

A

CD45 positive in lymphoid

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38
Q

other than CD45 + for lymphoid, what else do you see in B-precurosr ALL? (3) +3

A

CD19+, CD22+, CD79a+…MOST are also CD10+= cALLA+; TdT+, HLA-DR+

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39
Q

About half of KMT2A-R ALL lack what expression?

A

CD10

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40
Q

early B lineage ALLs are negative in what?

A

cytoplasmic immunoglobulin=cIg

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41
Q

Pre-B ALL is cIg ____ and sIg ____

A

pos, neg

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42
Q

co-expression of what myeloid antigens is common in B-precurosr ALL?

A

CD13,CD33…this does NOT make if acute leukemia of ambiguous linegage or mixed phenotype acute leuk!

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43
Q

what % of ALL are T?

A

15%

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44
Q

T-cell ALL associated with ___ WBC and ___ ___ and increased risk of ____

A

high; mediastinal masses; TLS

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45
Q

What markers does T-ALL express? (3) and often what? 4

A

CD3= cCD3+, sCD3+, TdT+

…also: CD2, 4, 7, 8

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46
Q

In T-Cell ALL what expression is variable?

A

CD10

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47
Q

most T-Cell ALL are HLA-DR ___

A

neg

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48
Q

Early Thymic precursor T-cell ALL= ETP has what markers?

A

CD3+, CD7+, weak CD5….also CD177+, CD34+, HLA-DR+, CD13+, CD33+, CD11b+…Cd1a neg, CD8 neg

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49
Q

T-cell ALL ____ to clear MRD by end of induciton

A

slower….end of consoliation MRD more important than EOI mRD

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50
Q

MPAL= mixed phenotype acute leuk= both myeloid and lymphoid features…reqiuires what?

A

expression of MPO= myeloperoxidase and B or T cell features

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51
Q

T-cell MPAL tends to overalp with what?

A

ETP ALL

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52
Q

B-cell MPAL has a hihg incidence of ___ driven leuk

A

ZNf384

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53
Q

high occurence of what in MPAL?

A

BCR/ABL1

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54
Q

Bilineal leukemia= ___population of __ and __ blasts…___ prog

A

distinct, myeloid, lymhoid…poor

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55
Q

should initial therpay with ___ for MPAL

A

ALL

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56
Q

What are the criteria for myeloid lineage assignment in MPAL?

A

MPO+ or monocytic differentiation= at least 2 of the following: nonspecific esterase, CD11c, Cd14, CD64, lysozyme

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57
Q

what are the criteria for T-lineage in MPAL?

A

Strong cytoplasmic CD3 or surface CD3

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58
Q

what are the criteria for B lineage assignment in MPAL?

A

strong CD19 with at least one of : CD79a, cytoplasmic CD22, CD10…OR weak CD19 with at least 2 of CD79a, cytoplasmic CD22, or CD10

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59
Q

study for using ALL therapy in MPAL?

A

retrospective study Orgel et al 2020…better OS

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60
Q

what are the 4 cytogenetic aneuplodies?

A

hyperdiploidy, low hypodiploidy, haploidy, ,masked hypodiploidy

61
Q

hyperdiploidy: 1-associated iwth what gains/losses? 2- incidence? outcome? age relevance?

A

gain of 4 and 10= double trisomy; ~25%= most common, excellent, less common in pts >15

62
Q

low hypodiploidy: asscoaited with waht spceific gains/losses?

A

modal number 32-39 chromsomes, <3%, poor with modern chemo, no benefit to transplant

63
Q

haploidy asscociatd with what specific gains/losses? incidence? outcome? comment?

A

<32 chroms, <3%, poor iwth modern chemo, no benefit to transplant

64
Q

masked hypodiploidy…what does this mean? incidence? outcome? benefit of hsct?

A

can masquerade as hyperdiploidy..e.xperienced cytogeneticist can ID using SNP assays…<3%..poor with modern chemo…no benfit to HSCT

65
Q

give 5 molecular sentinel translocations in B-ALL

A

ET6-RUNX1, TCF3-PBX1, KMT2A rearranged, BCR-ABL1, Myc fused to IgH, IgI or Igk

66
Q

ETV6-RUNX1: give translocation, incidence, outocme, comments

A

t(12;21)(p13, q2) (cryptic); 28%= most common, excellent, less common in pts>15yrs

67
Q

TCF3=PBX1: give translocation, incidence, outcome, comments

A

t(1;19)(q23;p13); 5% but 25% in pre B ALL, nuetral, poor outocme in older studies iwth higher incidence of CNS disease and CNS relapse

68
Q

KMT2A rearranged: give translocation, incidence, outocme, comments

A

t9v;11) (v;q23); t(11;v)(q23;v)…3%, poor but less signficant than in past, 75% of infants <1 yr have KMT2a-R

69
Q

BCR-ABL1: give transloc, incidence, outcome, comments

A

t(9;22) (q32;q11); 4%, poor with chemo alone, rate increases iwth age/treat with TKI+ chemo

70
Q

Myc fused to IgH, IgI or Igk: give translocation, icndience, outcome, comments

A

t(8;14)(q24;q32); t2(2;8)(p11;q24); t(8;22)(q24;q11)….rare…treat like burkitt NHL…burkitt leukemia

71
Q

NCI SR in B-lineage ALL: more than half have what cytogen?

A

Triple trisomy, ETV-RUNX1

72
Q

NCI HR in B-lineage ALL: more than half have what cytogen

A

neutral…but more of BCR-ABL and other less favourable cytogen

73
Q

what is Ph-like ALL?

A

defined by activated kinase gene expression similar to that of BCR-ABL1 rearranged Ph+ ALL…often associated with deletions of IKZF1

74
Q

Ph-like ALL comprimses what % of HR B-ALL in kids/adolescents?

A

15-20%

75
Q

pts with Ph-like ALL often present with WBC of what? what about EOI MRD? fare how with reg chemo?

A

WBC> 50,000/uL, high rate of MRD at EOI, relapse with reg chemo

76
Q

in ph-like all, what can help iwth EFS and OS?

A

TKIs

77
Q

in ph-like all, have >— different fusions involving 19 genes fo what types?

A

> 70; kinase, cytokine, cytokine receptor genes

78
Q

in ph-like all, sequence mutation or structural alterations seen in what 5 genes?

A

SCIRF

SH2B3, CRLF2, IL7R, RAS, FLT3

79
Q

Dasatinib, imatinib work best for what kinase mutations in Ph-like ALL?

A

ABL1, ABL2, CSF1R, PDGFRB

80
Q

Ruxolitinib works best for which kinase muations in ph-like all?

A

CRLF2, JAK2, EPOR

81
Q

about 50% of pts with ph-like all will have what rearranged?

A

CRL2…also often have JAK2 or JAK1 pt mutations

82
Q

15-20% of ph-like all pts have what rearrangmeents?

A

jak2, epor

83
Q

10-15% of ph-like have what alterations?

A

aBL class= ABL1, ABL2, PDGFRB, CSF1R

84
Q

ph-like all: lower 3 yr EFS shown in what sutdy?

A

COG AALL0232

85
Q

COGAALL0232 showed what with regards to CRLF2-rearragment?

A

do equally poorly whether or not prseent

86
Q

3 yr EFS in Ph-like ALL? source of study?

A

65%; AALL0232

87
Q

if MRD+ with pH-All, have ___ ___ outcomes

A

even worse

88
Q

in infant all, what’s the relevance of having KTM2A-R?

A

EFS is only 37-49% if present vs 69-95% otherwise

89
Q

how does infant ALL tend to present?

A

high WBC, extramedullary sites like chloromas, CNS disease, skull based disease– should image if suspicious!

90
Q

infant ALL is neg in __

A

CD10

91
Q

2 ways to risk classify infant ALL?

A

age, KMT2A-R status

92
Q

in infant ALL< KMT2A-R tends to always be present in infants < how many days old?

A

<100 days

93
Q

3 path features of infant all?

A

high expression. ofFLT3, global hypermethylation, abnormal histone modficiation

94
Q

in infant all, intensive multi agent therapy requires max ___ ___

A

supportive care…eg foley placement during chemo

95
Q

is EOI MRD prognostic in T-cell ALL?

A

no

96
Q

is age prognostic in t-cell all? WBC?

A

no, no

97
Q

what is most prognostic in t-all?

A

EOC MRD

98
Q

T-ALL presents with higher rates of what 3 things?

A

mediastinal mass, coagulopathy, TLS

99
Q

in T-ALL, which genetic lesions associated iwth prog?

A

none

100
Q

study that looked at nelarabine in t-all?

A

AALL0434

101
Q

AALL0434 showed __- outcomes in T-ALL, and ___ didn’t really matter

A

excellent, ETP= early thymic precursor

102
Q

what’s associated with higher risk of TLS?

A

higher WBC

103
Q

what’s the gen approach to SR ALL in terms of chemo?

A
  • 4 week 3-drug (Dex) induction
  • 4 week oral consolidation with intensive weekly IT
  • 8 week IM with escalating IV Mtx without rescue
  • 8-week DI phase with standard re-consolidation
  • IM 2 with escalating IV MTX (sometimes)
  • Maint with q4 week steroids/vcr pulses…as of 2020, q12 week pulses
104
Q

what’s the gen appraoch to HR ALL (and T-ALL)?

A
  • 4-week 4-drug induction (Pred 28 or Dex 14)
  • 8 week intensive IV consolidation with intensive weekly IT
  • 8 week IM wiht HD Mtx or capizzi IV Mtx + ASNase (T-ALL)
  • 8 week DI phase with intesnive re-consoidation
  • IM 2 Capizzi MTX (soemtimes)
  • Main with q4week steroids/VCR pulses…as of 2020, q12week pulses
105
Q

why do older HR kids get pred instead of dex?

A

to lower the osteonecrosis risk

106
Q

in DI for SR, you have modified BFM…in DI for HR you have modified augmented BFM, what’s the diff?

A

modified: Asp only on Day 4…modified augmented BFM: also includes additional Vcr, Asp on D43 and Vcr on D50

107
Q

in HR ALL, capizzi mtx includes Asp on what days?

A

2, 22

108
Q

how does BFM detrmine early tx response?

A

peripheral blast count after 7 days of steroids + dose of IT Mtx…wiht good repsosne being <1000 blasts/uL in peripehral blood

109
Q

how did CCG measure early tx response?

A

check day 8 for HR and day 15 for SR: BM resposne…M1<5% blasts, M2 5-25% blasts, M3 >25% blasts

110
Q

how does COG determine early tx response?

A

day 8 pripheral blood MRD adn d29 BM MRD

111
Q

what is the best predictor of outcome in terms of early tx response?

A

BM MRD at D29

112
Q

MRD should reach sensitivity of what?

A

at least 1 in 10k

113
Q

most common way to measure MRD?

A

flow

114
Q

name 3 MRD technologies

A

flow cytometry, PCR amplfication of Ig or TCR, PCR of translocation-derivied fusion transcripts

115
Q

what’s more sensitive? PCR or flow for MRD?

A

PCR

116
Q

how do you define CNS disease in leuk?

A

CNS1= 0-5 WBCS/chamber, 0 blasts, no clinical signs of CNS leuk….CNS2: <5 WBCs/chamber, presence of lbasts or negative by Steinherz-Bleyer alogorithm if traumatic tap…CNS 3: >5 WBCs/chamger, presence of blasts, signs of clinical leuk, positive by Steinherz-Bleyer if traumatic tap

117
Q

what is the radiation tx dose for CNS3?

A

1800cGy, includes posterior halves of globes of the eyes…spinal rad rarely used anymore

118
Q

often treat CNS2 how?

A

extra IT during induction

119
Q

give 4 AEs of IT chemo

A

arachnoiditis, seizures, transient stroke-like sx, rare subacute encephatlopathy, meylopathy, weakness/paraplegia linked to IT MTx

120
Q

AE of CNS irrad?

A

somnolence syndromes 5-7 weeks later

121
Q

Admin of __ ___ ___ ___ after cXRT is associated with ___ ____

A

high dose iV mtx; CNS toxicity…give hd mtx BEFORE rad!

122
Q

5 late complicatins of CNS directed therapy?

A
  • changes on neuroimaging studies, like cortical atrophy
  • impaired intellectual function adn school performance…linked to dose and age at time of rad (younger worse)
  • secondary brain tumours…meningioma highly curable (10-20 yrs later), others not
  • neuroendo changes like impaired GH responses, much lower risk if <2400 Gy
  • increased risk of obesity
123
Q

name 3 new ALL therapies

A

inotuzumab, blinatumomab, CAR t-cells

124
Q

inotuzumab: give mech of action, population studied, outcome

A

CD22-directed humanized monoclonal ab conjugated to calicheamicin…studies in adults with CD22+ with relapsed/refractory B-ALL, 80.7% complete remission /complete remission induction

125
Q

blina: give mech of action, population studied, outcome

A

blinatumomab: bispecific t cell receptor engage= BiTE taht redirects CD3+ T cells to CD19+ blasts; studies in adults with r/r ph+ b-ALL and kids with r/r B-ALL…CR in 39%

126
Q

car t cells: give mech of action, population studied, outcome

A

t cell transduced ex-vivo with chimeric anti CD19 receptor; kids with cd19+ r/r b-all, 83% CR/CRi

127
Q

immunotherapies share what 2 AEs?

A

cytokine release syndrome (associated iwth higher disease burden)…also neuro side effects

128
Q

inotuzumab associated with what AE?

A

-sinusoidal obstruction syndrome…higher risk in post-inotuzumab HSCT setting…high rates in kids

129
Q

management of CRS?

A

fluids, pressors, tociluzumab= anti-IL6

130
Q

features of CRS?

A

fever, myalgias, n/v, hypotension, resp insuff, renal insuff, coagulopathy

131
Q

neurotox after CAR-T: another name?

A

CAR-T cell realted encephalopahty syndrome= CRES

132
Q

similar neurotox to CRES also seen with?

A

blina

133
Q

sign/sx of neurotox from CAR-T?

A

h/a, dysgraphia, tremor, delirum, anxiety, sz, coma, cerebral edema, death

134
Q

manage neurotox from CAR-T how?

A

supportive care, steroids

135
Q

4 prog factors relating to relapse?

A

site of relapse (BM worse than extramedullary), time to relapse (ealrier worse), age at initial dx (very poor outcome for teens who realpse), immunophenoytpic and genetic featuers (BM relapse of T-ALL has very poor outcome)

136
Q

early relapse=?

A

<18 mos; do poorly

137
Q

late realpse?

A

> 36 mos

138
Q

For CNS, give a strong perdictor of outcome

A

time to realpse…must get effective systemic therapy!! at high risk of subsequent BM relapse!

139
Q

what % of boys have isolated teseticular relapse?

A

2%

140
Q

tx testicular realpse how?

A

intensive systemic tx + 2400 cGy bilateral testicular irradiation–> otherwise high risk of contralateral testicular realpse…leads to steriliyt, so need hormone repalcement…in europe undergo orchiectomy

141
Q

how does outcome for unrelated SCT fare vs. matched sib for ALL?

A

equal

142
Q

SCT is indicated for ALL with 1st marrow relapse at what time frame?

A

<3 yrs

143
Q

there’s an increasing role for transplant for what?

A

late marrow relapse with high MRD at ned of first course of reinduction therapy

144
Q

some believe that SCT indicated for what site of release and when?

A

early CNS relapse (<18 mos)

145
Q

other than first ALL BM relapse <3 yrs, when else is SCT indicated?

A
  • 2nd relapse

- T-ALL BM relapse

146
Q

describe relative half lives for different co-stumulatory domains in car t-cells

A

4-1BB lasts longer than CD28

147
Q

for CTL-019 CARs (novartis; including 4-1BB), what was CR rate for r/r ALL? 6 month EFS? OS? durable remissions seen how far out?

A

90%; 78%; 78%…24 mos

148
Q

list 7 long term risks for survivors of ALL

A

osteonerosis, cardiac tox, obestiy, neurocog impariment, GH def, insulin resistance, muscule weakness, peripheral neuropathy, liver tox

Haem/Onc (30 decks)

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