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NOTES: Heme/Onc > 266/268 - Leukemias (AML and ALL) > Flashcards

266/268 - Leukemias (AML and ALL) Flashcards

1
Q

On immunophenotyping, what markers prove that a cell population is made up of immature myeloid cells?

A
  • Evidence for immaturity:
    • CD34+
    • CD117+
  • Myeloid differentiation markers:
    • CD13+
    • CD33+
    • MPO+

Also - auer rods are important! Can’t see on flow but indicates myeloid lineage –> AML

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2
Q

Which translocation is most common in each of the following presentations of B-ALL?

  • Infants:
  • Children:
  • Adults:
A
  • Infants:
    • t(v;11) - KMT2A/MLL
    • The KMT2A part of chromosome 11 is moved somewhere else; not a specific location
  • Children:
    • t(12;21) - ETV6/RUNX1
    • good prognosis
  • Adults:
    • t(9;22) BCR-ABL1 (Philadephia Chromosome)
    • Can occur spontaneously or trasnform from CML
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3
Q

What are the diagnostic criteria for AML?

A

Bone marrow biopsy

  • >20% blasts in bone marrow or blood
  • Evidence of myeloid differentiation
    • ​Auer rods
    • MPO+ (NSE+ = monoblasts)
    • Myeloid-associated markers by immunophenotyping
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4
Q

What is the lineage-defining marker of T-cells?

A

CD3

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5
Q

What translocation is associated with acute promyelocytic leukemia?

What product is created?

A

t(15;17)

Creates PML-RARA; causes cells to arrest in promyelocytic stage

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6
Q

What is the lineage-defining marker of B-cells?

A

CD19

CD20 is acquired later; can be lost in malignancy (ex: classic nodular sclerosing hodgkin lymphoma)

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7
Q

Bone pain and refusal to bear weight are common symptoms of which hematopologic malignancy?

A

ALL

Due to intramedullary expansion of leukemic blasts

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8
Q

List the key differences in presentation between B-ALL and
T-ALL (often LBL)

A
  • B-ALL
    • Abrupt onset
    • symptoms related to bone marrow failure (thrombocytopenia, neutropenia, anemia)
    • B symtoms (fever, night sweats)
    • Bone pain
  • T-ALL (LBL)
    • High white count
    • anterior mediatinal mass –> SVC syndrome
    • CNS involvement
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9
Q

What is the most important prognostic factor in AML?

A

Chromosomal abnormalities

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10
Q

What is the cell of origin in AML?

A

Common myeloid progenitor

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11
Q

Which malignancy, in which population, is associated with t(12;21)?

Is this translocation prognostic?

A

B-ALL in children 1-10 years old

Favorable prognosis

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12
Q

What is the most common cancer of children?

A

ALL

Peak incidence of B-ALL is 3 years

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13
Q

What is the most important prognostic factor in ALL?

A

Time to response to induction chemotherapy

Fast response = good prognosis

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14
Q

Genomic alterations in AML can be used:

  1. For further classification
  2. For Prognostication
  3. For Targeted therapy
  4. For the detection of minimal residual disease
  5. All of the above
A

e. All of the above

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15
Q

Which part of which chromosome is most commonly involved in B-ALL in infants <1 year old?

A

11q23.3

Results in abnormal expression KMT2A

Can be translocated to various different locations (I think)

In the learning guide, the explanation for guiding question 2 is “B-ALL with t(v;11q23.3), KMT21 (or MLL) rearrangement is the most common leukemia in infants <1 year)”

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16
Q

In AML, the presence of which genetic mutation is associated with good prognosis?

A

NPM1 mutations

(Also CEBPA, but less common)

FTL3-ITD = poor prognosis

17
Q

Are abnromal karyotypes more useful for prognosis in B-ALL or T-ALL?

A

B-ALL

  • t(v;11q23) - KMT2A/MLL = poor prognosis (infants <1)
  • t(12;21) - ETV6-RUNX1 = good prognosis (children 1-10)
  • t(9;22) - BCR-ABL = poor prognosis (adults)

Chromosome abnormalities are common in T-ALL, but not prognostic. Usually involves 14q, 7p

18
Q

What is the “classic presentation” of acute promyelocytic leukemia (APL)?

A

Young patient w/ low blood counts + bleeding/bruising –> DIC + Hemorrhage (ex: subarachnoid hemorrhage)

t(15;17) forms PML-RARA -> arrest in promyelocytic stage

19
Q

What genetic syndrome is a risk factor for ALL?

A

Down syndrome

20
Q

Which chemotherapy agents pose the greatest risk for developing AML?

A
  • Alkylating agents (cyclophosphamide, bendamustine)
    • Usually has intermediate MDS phase
  • Topoisomerase-II inhibitors (Etoposide, anthracyclines)
    • No intermediate phase; usually goes straight to AML
21
Q

What is the most curable AML?

A

Acute promyelocytic leukemia (APL)

t(15;17) creates PML-RARA; treat with all-trans retinoic acid and arsenic trioxide

22
Q

Which age group at presentation has the most favorable prognosis for ALL?

A

2-10 years old

23
Q

What is the most common cell of origin in ALL (acute lympoblastic leukemia) or LBL (lymphoblastic lymphoma)

A
  • ALL
    • 85% is from B-cells (B-ALL)
      • Very young children
  • LBL
    • 90% is from T-cells
      • Adolescents
24
Q

What are the B-cell markers of immaturity? (2)

A

CD34

TdT

Immature T cells will have CD1a and CD3

25
Q

Which malignancy, in which population, is associated with t(v;11q23)?

Is this translocation prognostic?

A

B-ALL in infants <1yo

  • often t(4;11)
  • Poor prognosis :(
  • Often predicts CNS involvement
26
Q

In AML, the presence of which genetic mutation is associated with poor prognosis?

A

FTL3-ITD

NPM1 is associated with a good prognosis

27
Q

What is the treatment for APL?

A

All-trans retinoic acid (ATRA) + Arsenic trioxide (ATO)

28
Q

Which population is most commonly affeted by T-ALL/LBL?

What are the characteristic markers? (3)

A
  • Males, adolescents
  • Presents with mediastinal mass
  • Markers: TdT, cytoplasmic CD3, CD1a
29
Q

What does CNS or testicular involvement predict for the prognosis of ALL?

A

poor prognosis :(

30
Q

B-ALL with t(9;22) is most common in which population?

Is this translocation prognostic?

A
  • Adults
  • Poor prognosis

Can be a transformation from CML or arise spontaneously

31
Q

What targeted treatments can be used in B-ALL?

A

Imatinib if t(9;22) translocation

Blinatumomab otherwise

32
Q

What two translocations are associated with AML?

A
  • t(8;21)
    • large blasts w/ long sharp Auer rods
  • inv(16)
    • Atypical eosinophilic precursors

  • Both have good prognosis, unless concurrent KIT mutation*
  • Vs. AML mutations: NPM1 –> good prognosis, FTL3 –> bad prognosis*

NOTES: Heme/Onc (36 decks)

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