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Blood & Lymph Unit II > Malignancies > Flashcards

Malignancies Flashcards

1
Q

What is TdT a marker of?

A

Lymphoblasts, specifically

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2
Q

The Philadelphia Chromosome is seen in what percentage of cases of adult B-ALL?

A

25%

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3
Q

The Philadelphia Chromosome is seen in what percentage of cases of childhood B-ALL?

A

2%

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4
Q

What is the Philadelphia chromosome?

A

t(9;22); BCR-ABL1

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5
Q

Is the presence of the Philadelphia chromosome a marker of good or poor prognosis?

A

Poor

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6
Q

Is B-ALL with t(12;21); ETV6-RUNX1 a good or poor prognosis?

A

Very favorable prognosis

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7
Q

B-ALL with t(12;21); ETV6-RUNX1 is seen in what percentage of childhood B-ALL?

A

25%

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8
Q

What age group does T-ALL favor?

A

Adolescents and young adults

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9
Q

How does T-ALL often present?

A

A mediastinal mass

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10
Q

What is the average age of onset of AML?

A

65 years old

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11
Q

How is AML diagnosed?

A

Presence of >20% myeloblasts in marrow and/or peripheral blood

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12
Q

Which virus contributes to Hodgkin lymphoma, Burkitt lymphoma, and other non-Hodgkin lymphomas?

A

EBV

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13
Q

EBV contributes to which neoplasms?

A

Hodgkin lymphoma, Burkitt lymphoma, and other non-Hodgkin lymphomas

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14
Q

Which virus contributes to adult T cell leukemia/lymphoma?

A

HTLV-1

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15
Q

HTLV-1 contributes to which neoplasms?

A

Adult T cell leukemia/lymphoma

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16
Q

KSHV/HHV-8 contributes to which neoplasms?

A

Primary effusion lymphoma

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17
Q

Which virus contributes to primary effusion lymphoma?

A

KSHV/HHV-8

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18
Q

Which is more indolent or curable: Leukemia or Lymphoma?

A

Leukemia

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19
Q

Leukemias account for roughly what percentage of all childhood cancers?

A

37%

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20
Q

ACUTE leukemias are most often accumulation of what?

A

Blasts

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21
Q

CHRONIC leukemias are most often accumulation of what?

A

Mature cells

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22
Q

Most ALL is diagnosed in what age group?

A

< 6 years old

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23
Q

What are two categories of ALL?

A

B-ALL & T-ALL

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24
Q

What do B lymphoblasts express?

A

CD19, CD22, and/or CD79a

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25
Q

What are markers of mature B cells?

A

CD20 & surface Ig

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26
Q

B-ALL accounts for what percentage of all ALL?

A

80-85%

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27
Q

Is the 11q23;MLL cytogenetic finding of B-ALL a good or poor prognosis?

A

Poor

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28
Q

T 11q23;MLL cytogenetic finding of B-ALL is usually found in what age group?

A

Neonates & young infants

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29
Q

What gender does T-ALL favor?

A

Males

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30
Q

Which ALL is more likely to have a more elevated WBC count?

A

T-ALL

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31
Q

What is associated with a better ALL prognosis?

A

1-10 years old, B hyperdiploidy

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32
Q

What is associated with a worse ALL prognosis?

A

10yrsold, very high WBC, T hypodiploidy, slow response to Rx

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33
Q

What is about the incidence of both AML and ALL?

A

~3 cases per 100,000 per year

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34
Q

What is a general marker of immaturity on myeloblasts and lymphoblasts?

A

CD34

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35
Q

What are two markers of myeloid cells specifically?

A

CD117(C-Kit) & Myeloperoxidase

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36
Q

Where are Auer rods?

A

Only on abnormal Myeloblasts

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37
Q

What is the age group and prognosis of AML with t(8;21);RUNX1-RUNX1T1?

A

Younger patients; relatively good prognosis

38
Q

What does RUNX1 encode for?

A

Alpha subunit of core binding factor (CBF) which is necessary for hematopoiesis

39
Q

What is the age group and prognosis of AML with inv(16) or t(16/16);CBFB-MYH11?

A

Younger patients; relatively good prognosis

40
Q

What is AML with t(15/17);PML-RARA also known as?

A

Acute Promyelocytic Leukemia (APL)

41
Q

Acute Promyelocytic Leukemia (APL) is aka?

A

AML with t(15/17);PML-RARA

42
Q

What type of cell predominates in APL?

A

Abnormal promyelocytes (instead of blasts)

43
Q

What are two reasons it’s important to recognize that an AML is specifically the APL subtype?

A
  1. APL does not require traditional chemo but instead it can be treated with all-trans retinoic acid (ATRA) in combination with arsenic salts which has much less morbidity than chemotherapy
  2. APL can give rise to DIC, so it’s important to be on the lookout for this complication
44
Q

AML with t(1;22)(p13;q13);RBM15-MKL1 is most often seen in who?

A

Infants with DS

45
Q

What kind of prognosis does AML with t(1;22)(p13;q13);RBM15-MKL1 have?

A

Relatively good prognosis

46
Q

What kind of prognosis does AML with abnormalities of 11q23;MLL have?

47
Q

What is CD34 a marker of?

A

Immature lymphoblasts & myeloblasts

48
Q

Therapy-related AML (t-AML) accounts for what percentage of all cases of AML?

49
Q

What are the two different classes of t-AML?

A

Secondary to alkylating agents or radiation; Secondary to topoisomerase-II inhibitors

50
Q

What percentage of AML cases have no recurrent cytogenetic findings and normal karyotype? (AML-NOS)

51
Q

What are the three molecular markers currently used to determine prognosis of AML-NOS?

A
  1. FLT3 (poor prognosis)
  2. NPM1 (good)
  3. CEBPA Mutation (good)
52
Q

What are the two main features that characterize MDS?

A
  1. Ineffective hematopoiesis

2. Increased risk of transformation to AML

53
Q

What are the two clinical scenarios of MDS?

A
  1. Primary/Idiopathic
    a. People over 50 yrs old
    b. Insidious onset
    c. 3-5 cases per 100,000 per year
  2. Secondary/Therapy-related (t-MDS)
    a. Occurs like t-AML
    b. Usually 2-8 years after alkylating agents of radiation
    Usually contains whole or partial deletions of chromosomes 5 and/or 7
54
Q

What are some types of tests that can be used to diagnose MDS?

A

Morphologic evidence of dysplasia; presence of clonal cytogenetic abnormalities

55
Q

What are four possible causes of secondary myelodysplasia that might mimic MDS?

A

Drugs like chemi, toxicity (esp heavy metals), B12 folate etc deficiencies, viral infection

56
Q

What are the differences in diagnostic criteria and prognosis between low grade and high grade MDS?

A

• Low grade MDS: Myeloblasts account for 5% of marrow cells and >2% of peripheral blood cells. Dismal prognosis.

57
Q

What cytogenetic abnormalities can lead to MDS?

A

Monosomy 5 or 7, 5q or 7q deletions, trisomy 8

58
Q

List 2 reasons for the frequent occurrence of splenomegaly and hepatomegaly in patients with MPNs

A
  • Too many cells, get sequestered

* Extramedullary hematopoiesis

59
Q

What are three possible negative end points for MPNs?

A

development of AML, MDS, or excessive marrow fibrosis resulting in marrow failure

60
Q

What are four types of MPNs?

A
  1. Chronic Myelogenous Leukemia (CML)
  2. Polycythemia Vera (PV)
  3. Primary Myelofibrosis (PMF)
  4. Essential Thrombocythemia (ET)
61
Q

What cell type is elevated in CML?

A

Neutrophils

62
Q

What are the marrow findings of CML?

A

Small megakaryocytes with round non-lobulated nuclei; no dysplasia

63
Q

What is the common cytogenetic/molecular abnormality of CML?

A

Philadelphia chromosome

64
Q

What cell type is elevated in PV?

A

Erythrocytes (accompanied by neutrophils and platelets)

65
Q

What are the marrow findings of PV?

A

Clusters of large bizarre megakaryocytes

66
Q

What is the common cytogenetic/molecular abnormality of PV?

A

Mutation of the JAK2 gene encoding the JAK2 cell signaling protein

67
Q

What are the major complications of PV?

A

Venous & Arterial Thrombosis

68
Q

Thrombosis is what vessels make you suspect PV?

A

Mesenteric, portal, and splenic veins

69
Q

What cell type is elevated in PMF?

A

Proliferation of granulocytic & megakaryocytic lineages

70
Q

What cell type is elevated in ET?

A

Thrombocytes

71
Q

What are the marrow findings of PMF?

A

Large bizarre clustered megakaryocytes

72
Q

What are the marrow findings of ET?

A

Large bizarre clustered megakaryocytes (even larger and more bizarre than PMF)

73
Q

What is the common cytogenetic/molecular abnormality of PMF?

A

JAK2 mutation in 50% of cases

74
Q

What is the common cytogenetic/molecular abnormality of ET?

A

JAK2 mutation in 50% of cases

75
Q

What is the most common treatment for PV?

A

Serial phlebotomy (blood letting) and aspiring therapy

76
Q

What are CD10 and BCL6 markers of?

A

Germinal B-cells and derived lymphomas

77
Q

What molecular markers do Reed-Sternberg (RS) cells express?

A

CD30 and CD15

78
Q

What is the main difference between CLL and SLL?

A

In SLL, extramedullary sites predominate

79
Q

What is the median age of SLL and which gender predominates?

A

65, M:F 2:1

80
Q

What is the most common genetic abnormality of SLL?

A

deletion of 13q14

81
Q

What specific cells are associated with Follicular Lymphoma?

A

Germinal B cells

82
Q

What is the median age of Follicular Lymphoma, and what gender does it prefer?

A

60 years, M:F 1:1

83
Q

What is the common genetic abnormality of Follicular Lymphoma?

A

Positive for BCL2, which suppresses apoptosis

84
Q

What is the median age of Mantle Cell Lymphoma, and what gender does it prefer?

A

60 years, M:F 2:1

85
Q

What is the common genetic abnormality of Mantle Cell Lymphoma?

A

Positive for Cyclin D1 (BCL1)

86
Q

What are the characteristics of the cells affected by Burkitt’s Lymphoma?

A

Medium sized B cells with basophilic cytoplasm and an increased mitotic rate

87
Q

What are the two subcategories of Burkitt’s lymphoma and where in the body do they predominate?

A

Endemic BL: found in equitoria Africa, 95% EBV+, jaw & facial bones, also distal ileum, cecum, and omentum

Sporadic BL: found mostly in children/young adults, mostly ileocecal area

88
Q

What kind of cell is necessary for diagnosis of Classical Hodgkin’s Lymphoma?

A

Reed-Sternberg (RS) cells

89
Q

What are the two types of Hodgin’s Lymphomas? And what is one of them further classified into?

A

Nodular Lymphocyte-Predominant (NLPHL)

Classical Hodgkin's Lymphoma (CHLs)
     Nodular Sclerosis
     Lymphocyte-Rich
     Mixed Cellularity
     Lymphocyte-depleted
90
Q

Where does Nodular Sclerosis HL usually occur?

A

Above the diaphragm

91
Q

Where does Lymphocyte-Rich HL usually occur?

A

Below or on both sides of diaphragm

Blood & Lymph Unit II (1 decks)

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