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ENGR 1 > Leukemias1 > Flashcards

Leukemias1 Flashcards

1
Q

Two types of Leukemias

A

Acute myeloid leukemia (AML)
and
Acute lymphoblastic leukemia (ALL)

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2
Q

ALL demographics

A

75% of cases of ALL occur in children under 6 years old

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3
Q

Two types of ALL

A

B-lymphoblastic ALL (B-ALL)

T-ALL

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4
Q

3 types of B-ALL

A

B-ALL with:

  1. BCR-ABL1
  2. MLL
  3. ETV6-RUNX1
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5
Q

3 types of AML

A

Q

  1. Congenital
  2. Therapeutic
  3. AML, NOS (not otherwise specified)
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6
Q

5 cytogenic abnormalities for congenital AML

A

AML with:

  1. RUNX1-RUNX1T1
  2. CBFB-MYH11
  3. PML-RARA (APL)
  4. RBM15-MKL1
  5. MLL
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7
Q

2 causes of therapeutic AML

A
  1. aklylating agent + radiation

2. topoisomerase II inhibitors

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8
Q

molecular findings leading to AML-NOS

A
  1. FLT3 ITD
  2. NPM1
  3. CEPBA
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9
Q

“leukemic stem cell” theory

A

• Theory suggests that chemo only kills differentiating or differentiated cells, so you don’t kill the LSCs. As a result, the cancer can recur.

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10
Q

risk factors for acute leukemia

dont forget: majority of acute leukemias occur in the apparent absence of risk factors

A
  • Previous chemotherapy, especially DNA alkylating agents and topoisomerase-II inhibitors
  • Previous exposure of active marrow to ionizing radiation
  • Tobacco smoke
  • Benzene exposure
  • Genetic syndromes (Down Syndrome, Bloom, Fanconi, ataxia-telangiectasia)
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11
Q

signs and symptoms of acute leukemia at initial presentation. What are they due to?

A

• Signs and symptoms are because normal cells in the marrow are replaced by leukemic cells
○ anemia: fatigue, malaise, pallor, dyspnea
○ thrombocytopenia: bruising, petechiae, hemorrhage
○neutropenia: fever, infections

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12
Q

Rare signs and symptoms of acute leukemia

A
  • Thrombocytic events are due to increased blood viscosity (known as leukostasis and is seen where WBC count is very high)
  • DIC can be initiated by some leukemic cells
  • Direct infiltration of skin, gums, lymph nodes, and other tissues
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13
Q

ALL and AML generic marker of immaturity

A

CD34

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14
Q

ALL lymphoblast marker (not mature lymphocyte)

A

Tdt

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15
Q

ALL markers of B cell lineage

A

CD19,

CD22

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16
Q

ALL markers of T cell lineage

A

CD3, CD7

17
Q

B-ALL

  • patient age
  • sex
  • manner of manifestation
  • prognosis.
A

○ Age: more frequent in neonates and young children
○ Sex: Females > Males
○ Manifestation: B-cell lineage antigens, lack markers of mature B-cells
○ Prognosis: complete remission >95%; cure around 80%

18
Q

Does B-ALL express CD20?

A

No.

-express CD19, CD22

19
Q

T-ALL

  • patient age
  • sex
  • manner of manifestation
  • prognosis.
A

○ Age: more frequent in adolescents and young adults
○ Sex: Males > Females
○ Manifestation: T-lymphoblastic lymphoma, (mediastinal mass). Elevated WBC.
○ Prognosis: complete remission 60-80%; cure rates <50%

20
Q

% of ALL cases. How much B-ALL, how much T-ALL?

A

B-ALL: 75% of all ALL cases

T-ALL: 25% of all ALL cases

21
Q

Pt age group of (B-ALL) BCR-ABL1

-prognosis?

A

25% cases of adult B-ALL, 2% of childhood B-ALL
(more common in adults)
- Ph+: worst prognosis of any ALL!

22
Q

Pt age group of (B-ALL) MLL

-prognosis?

A

a. Most common in neonates and young infants
b. Poor prognosis
* MLL of both B-ALL and congenital AML MLL have poor prognosis

23
Q

Pt age group of (B-ALL) ETV6-RUNX1

-prognosis?

A

a. 25% of cases of childhood B-ALL

b. Very favorable prognosis!

24
Q

5 factors affecting prognosis in ALL

A
  1. Age
  2. White blood cell count
  3. Slow response to therapy / small amounts of residual disease after therapy
  4. Number of chromosomes
  5. B versus T lineage
25
Q

What has worst prognosis, B-ALL or T-ALL?-ALL

A

B-ALL

26
Q

What is the prognosis for ALL with regards to hyperdiploidy vs hypodiploidy?

A

very favorable prognosis for hyperdiploidy (>50 but <46 chromosomes).

27
Q

2 types of findings that would allow for a diagnosis of AML.

A
  1. Increased myeloblasts accounting for 20% or more of nucleated cells in the marrow or peripheral blood
  2. cytogenetic findings
    - CD34
    - CD117 (C-Kit) Myeloperoxidase
28
Q

clinical significance of Auer rod

A

clinical significance of Auer rod
Q
Myeloblasts are very generic looking, can be confused with lymphoblasts unless you see Auer rods!
• Not only does the presence of an Auer rod tell you that you have a myeloblast, it means you have an ABNORMAL myeloblast.

29
Q 
5 cytogenic abnormalities for congenital AML: Prognosis and Pt population 
1. RUNX1-RUNX1T1 
2. CBFB-MYH11 
3. RBM15-MKL1 
4. PML-RARA (APL) 
5. MLL
Q 
reveal answer
A
  1. RUNX1-RUNX1T1:
    - younger patients
    - good prognosis
  2. CBFB-MYH11:
    - younger patients
    - good prognosis
  3. RBM15-MKL1
    - infants with down syndrome
    - good prognosis
30
Q

5 cytogenic abnormalities for congenital AML:

  1. PML-RARA
    - % of AML
  2. MLL
    - prognosis?
A
  1. PML-RARA (APL)
    - 5-10% of all AML
    - prognosis not stated
  2. MLL
    - Pt not stated
    - Poor prognosis
31
Q

two reasons why it is important to recognize at initial diagnosis that a case of AML is the AML with t(15;17)(aka acute promyelocytic leukemia (APL)

A
  1. Don’t need chemo!
    - treat with all trans retinoic acid (ATRA)
  2. APL is associated with DIC
32
Q

2 main categories of therapy-related AML, and compare their latency and prognosis.

A
  1. t-AML secondary to alkylating agents or radiation:
    - Latency of 2-8 years from prior treatment
    - POOR prognosis
  2. t-AML secondary to topo-II inhibitors:
    - Latency period of 1-2 years from prior treatment
    - POOR prognosis
33
Q

3 molecular markers (abnormalities) currently used to predict prognosis in patients with AML with normal karyotype

A
  1. FLT3 - Internal tandem duplication
  2. Nucleophosmin-1 : NPM1 mut.
  3. CEBPA mutation
34
Q

Which of the 3 molecular markers for AML has poor prognosis (driving prognostic factor)?

A

Poor

ENGR 1 (29 decks)

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