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2021-2022 Heme/Onc Review Rearr > 269/270 - Leukemias (AML and ALL) > Flashcards

269/270 - Leukemias (AML and ALL) Flashcards

1
Q

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

A
  • Immature
    • CD34+
    • CD117+
  • Myeloid
    • CD13+
    • CD33+
    • MPO

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

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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
  • Adults:
    • t(9;22) BCR-ABL1
    • 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
    • Bone marrow failure (thrombocytopenia, neutropenia, anemia)
    • B symtoms (fever, night sweats, generalized lymphadenopathy)
    • Bone pain (B for Bone Pain)
  • T-ALL (LBL)
    • High white count
    • SVC syndrome (T for Tall like Superior Vena Cava)
    • CNS involvement (T for Tall like Spinal Cord)
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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 [AML, No Problem Mate]

(Also CEBPA, but less common)

FTL3-ITD = poor prognosis [AML, Fuck This Life]

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

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 <1

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 [AML, Fuck this Life]

NPM1 is associated with a good prognosis [AML, No Problem Mate]

27
Q

What is the treatment for APL?

A

All-trans retinoic acid + Arsenic trioxide

28
Q

Which populationis most commonly affeted by T-ALL/LBL?

What are the characteristic markers? (3)

A

Males, adolescents

Presents with mediastinal mass

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 (Brings T-cells close to ALL cells)

32
Q

What two translocations are associated with AML?

A
  • t(8;21)
  • inv(16)
    • Atypical eosinophilic precursors
  • Both have good prognosis, unless concurrent KIT mutation*
  • Vs. mutations: NPM1 is diagnostic, FTL3 is prognostic (poor)*

2021-2022 Heme/Onc Review Rearr (36 decks)

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