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HEMA 2: LEC > INTRODUCTION TO HEMATOLOGIC NEOPLASM > Flashcards

INTRODUCTION TO HEMATOLOGIC NEOPLASM Flashcards

1
Q

from abnormal growth of cells of the hematopoietic system

first human cancers in which a consistent genetic defect was identified

leukemias, lymphomas, and myelodysplastic syndromes

A

Hematologic neoplasms

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2
Q
  • described a consistent shortened chromosome in seven patients with CML.
  • “Philadelphia chromosome”
A

1960 Nowell and Hungerford

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3
Q

Chromosome in CML.

A
  • “Philadelphia chromosome”
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4
Q
  • reported the t(9;22) translocation in CML
A

1973 Rowley

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6
Q
  • proliferate in lymph nodes and other lymphoid organs and tissues
A

Lymphomas

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7
Q
  • reported the t(8;14) translocation in Burkitt lymphoma
A

1982 Taub and colleagues

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8
Q
A
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9
Q
  • solid tumors of lymphoid cells

originate in the lymphatic system

A

Lymphomas

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10
Q
  • lymphoid and myeloid lineages
  • acute (precursor cell) and chronic (mature cell)
A

Leukemias

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11
Q

Categories of leukemia

A

Acute
Chronic

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12
Q
  • accumulation of precursor hematopoietic cells of a specific lineage (bone marrow and peripheral blood) - “maturation arrest”
A

Acute

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13
Q

• sudden, rapid, and fatal in weeks or months if left untreated.
- WBC count is variable

A

Acute

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14
Q
  • proliferation and accumulation of mature and maturing cells of a specific lineage
A

Chronic

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15
Q
  • insidious and slower, with a longer survival compared with acute leukemia.
  • WBC count is usually elevated
A

Chronic

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16
Q

• Hematopoietic cells in BM > replaced by leukemia cells > affects normal BM function

A

Untreated leukemias

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17
Q

Untreated leukemias

  • Bleeding ‹_____
    • Fever ‹______
    ‹ Fatigue <______
A

thrombocytopenia

neutropenia-induced infection

decreased hemoglobin concentration

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18
Q

Predominant cell type

A
C

A

Precursor cell or blast

Mature

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19
Q

Onset

A
C

A

Sudden

Insidious

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20
Q

Symptoms at presentation
A
C

A

Fever (as a result of neutropenia-induced infection)
Mucocutaneous blending (as a result of thrombocytopenia)
Fatigue (as a result of anemia)

Variable, nonspecific;
some asymptomatic

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21
Q

White blood cell count

A
C

A

Variable

Increased

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22
Q

Progression without treatment
A
C

A

Rapid; wetks to months

Slower, months to years

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23
Q

Acite lymohoid leukemia

ALL - common in…

A

young children

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24
Q

• Chronic lynphoid leukemia-CLL and myelodysplastic syndrome - common in…

A

older adults

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25
Q

/ induce genetic changes › malignant phenotype.

A

Environmental toxins

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26
Q

Exposure

(2) > lead to hematologic neoplasms

(1) > induce DNA damage in hematopoletic cells

A

Radiation ( atomic explosions) and Organic solvents

Alkylating agents (chemotherapy)

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27
Q
  • ability to insert into host cell genomes
  • genetic and epigenetic changes
A

Viruses

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28
Q
  • produce oncoproteins that
  • interfere with normal cell processes
A

Viruses

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29
Q
  • invades CD41 lymphocytes > adult T cell leukemia/lymphoma
A

HTLV-1

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30
Q

HTLV-1
- invades_____ > adult T cell leukemia/lymphoma

A

CD41 lymphocytes

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31
Q
  • invades mainly B lymphocytes > Burkitt and other non-Hodgkin lymphomas and in a subset of classic Hodgkin lymphoma.
A

Epstein-Barr virus

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32
Q
A
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33
Q

Epstein-Barr virus
- invades mainly_____ > Burkitt and other non-Hodgkin lymphomas and in a subset of classic Hodgkin lymphoma.

A

B lymphocytes

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34
Q
  • immunosuppression > risk of non-Hodgkin lymphoma
A

HIV-1

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35
Q
A
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36
Q
  • mutations in ATM
A

‹ Ataxia telangiectasia

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37
Q
  • mutation in TP53
A

~ Li-Fraumeni syndrome

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38
Q
  • mutation in genes for telomere maintenance
A

‹ Dyskeratosis congenita

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39
Q
  • mutation in one of the FA genes needed for DNA repair
A

Fanconi anemia

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40
Q

“molecular policeman” is a nuclear transcription factor that promotes cell cycle arrest and apoptosis

A

TP53

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41
Q
  • devised in the 1970s and 1980s
  • based largely on morphologic characteristics
  • routine histologic stain > distinguish lymphoid neoplasms from myeloid neoplasms
A

FAB Classification

42
Q

Published in 2001 and updated in 2008 and 2016 (______)
> clinical features, morphology, immunophenotyping, cytogenetics, and molecular genetics

A

Society for Hematopathology and the European Association for Haematopathology

43
Q

Cellular Processes perturbed in Hematologic Neoplasm

A

• chromosomal rearrangement (such as translocation or inversion),
• gain or loss of chromosomes (aneuploidy)
• total or partial gene deletion
• point mutation
• Insertion
• gene duplication/amplification

44
Q

• “initiation and maintenance of leukemia”
• hematopoietic cell - accumulates multiple, independent mutations or “multihits”
• affect cellular pathways > malignant clone

A

LEUKEMOGENESIS

45
Q

LEUKEMOGENESIS ЕХСЕРТ
_______
> one genetic mutation, the
> t(9;22) with fusion of the BCR-ABL1 genes

46
Q

Examples of Cell Proteins Altered in Hematologic Neoplasms

A

Cell cycle regulatory proteins
Nuclear transcription factors
Checkpoint control proteins
Pro- and anti-apoptotic proteins
DNA repair proteins
Signal transduction proteins
Growth factor receptors

47
Q

Results of Disruption

A

• Uncontrolled proliferation

• Loss of DNA repair capability and cell cycle control

• Block in differentiation

• Continued cell survival and inhibition of apoptosis

49
Q
  • mutation that codes for signal transduction proteins or growth factor receptors
  • activation without stimulus and without ability to suppress
A

Uncontrolled proliferation

50
Q
  • inactivating mutation or deletion of genes coding for DNA repair proteins
  • cell cycle proteins that regulate the cell cycle
  • checkpoint control proteins that arrest the cell cycle when DNA is damaged
A

• Loss of DNA repair capability and cell cycle control

51
Q
  • mutation in genes coding for nuclear transcription factors or aberrant changes in their epigenetic regulation
  • maturation arrest or dysplastic changes.
A

• Block in differentiation

52
Q
  • mutation or deletion of genes coding for propoptotic and other related proteins
  • persistence of leukemic stem cells
A

• Continued cell survival and inhibition of apoptosis

53
Q

-______ is essential to contain and control the massive cell expansion that occurs in the hematopoietic system during times of stress, infection, or hemorrhage

54
Q

Examples of Epigenetic
Mechanisms That Control Gene Expression

A

DNA methylation

Histone acetylation

microRNAs
(miRNAs)

55
Q

Hypermethylation of CpG islands in gene promoters and other noncoding DNA regions by DNA methyltransferases prevents gene transcription and expression.

A

DNA methylation

56
Q

Histone acetyltransferases keep DNA chromatin in an open configuration so transcription can accur.

Histone deacetylases (HDACs) keep DNA chromatin in a closed configuration so genes are unavailable for transcription, replication, and repair.

A

Histone acetylation

57
Q

miRNAs (small 22 nucleotide RNA segments) inhibit gene expression by specifically binding to targeted mINA transcripts, blocking their translation to protein, and causing their destablization and degradation.

A

microRNAs (miRNAs)

58
Q
  • originally were identified in tumor-forming retroviruses
  • derived from normal human cellular homologues called protooncogenes
59
Q

Oncogenes
- originally were identified in tumor-forming retroviruses
- derived from normal human cellular homologues called______

A

protooncogenes

60
Q

Protooncogenes are important in:

A

signaling pathways
cell proliferation
cell differentiation
Apoptosis

61
Q

Protooncogenes
- Mutations converts it to_____ with leukemogenic potential
- Dominant disorders

62
Q

Mutations that Activate Protooncogenes
_________
- alterations involve a structural change to the protooncogene and production of an abnormal protein product.

translocation t(9;22) forming the BCR-ABL1 fusion gene in CML and in some cases of acute lymphoblastic leukemia.

A

Qualitative

63
Q

Mutations that Activate Protooncogenes

  • overexpression of a normal protooncogene

B-lymphoid neoplasms - translocation next to the promoter of the Ig heavy chain (IGH) on chromosome 14.

A

Quantitative

64
Q

code for proteins that protect cells from malignant transformation.

slow down cell division or promote apoptosis.

A

Tumor Suppressor Genes

65
Q
  • promote malignant transformation when they are inactivated or deleted
A

tumor suppressor genes

67
Q

Tummor suppressor gene

> ____ in Li-Fraumeni syndrome

68
Q
  • involved in hematologic neoplasms.
  • Genetic instability and increased mutation rates > malignant transformation.
A

DNA Repair Genes

69
Q

> _______ gene, FA, which is important for maintaining genomic stability in hematopoietic tissues

A

Fanconi anemia

70
Q

General Categories of Therapy for Hematologic Neoplasms

A

Chemotherapy
Radiation Therapy
Supportive Therapy
Targeted Therapy
Hematopoietic stem cell transplantation

71
Q

Cell cycle effects: phase specific or phase nonspecific agents

Biochemical mode of action: alkylating agents, plant alkaloids, antimetabo-lites, antitumor antibiotics, glucocorticoids

A

Chemotherapy

72
Q

Supportive therapy
Eg

A

Growth factors and cytokines

73
Q

Targeted therapy
(3)

A

Targeted molecular therapy
Immunotherapy
Cellular therapy

74
Q

Hematopoietic stem cell transplantation
(3)

A

Syngeneic
Allogeneic
Autologous

75
Q

3 phases: induction, consolidation, and maintenance

A

Chemotherapy

77
Q
  • oral or parenteral treatment - possess antitumor properties
A

Chemotherapy

78
Q

Chemotherapy

3 phases:

A

induction, consolidation, and maintenance

79
Q

> decrease the tumor burden and achieve remission

A

Chemotherapy

80
Q

Chemotherapy

> Types of Remission
______: normocellular bone marrow, recovery of blood cell counts, and no microscopic evidence of leukemia cells
/______: absence of the cytogenetic defect determined by karyotyping methods
/______: absence of leukemia cell nucleic acid sequences

A

Hematologic

Cytogenetic

Molecular

81
Q

Affected during radiotherapy

A

hematopoietic system gastrointestinal tract v skin

82
Q
  • producing unstable ions that damage DNA
  • cause instant or delayed death of cells
A

Radiation Therapy

83
Q

Supportive therapy

  • rapidly expand the number of mature neutrophils
A

• G-CSF and GM-CSF

84
Q

Supportive therapy

  • rapidly expand the number of mature neutrophils
A

• G-CSF and GM-CSF

85
Q

Supportive therapy

  • RBC formation and recombinant forms are administered to cancer patients with anemia
A

• ЕРО

86
Q
  • act specifically on malignant cells and leave normal cells untouched.
  • the dream is to move away from nonspecific therapies
A

Targeted Therapy

87
Q

is now the first-line treatment for chronic-phase CML

  • long-term remissions of 10 years and longer
88
Q
  • high efficacy in patients with high-risk hematologic neoplasms.
A

Cellular therapy

89
Q
  • also used in hematologic neoplasms to reverse epigenetic silencing of gene
A

Epigenetic therapies

90
Q

Hematopoietic Stem Cell Transplantation

A

Bone marrow
Peripheral blood
Umbilical cord blood

91
Q
  • posterior iliac crests
  • general or regional anesthesia
A

• Bone marrow

92
Q
  • less invasive in that they are
  • harvested by pheresis after mobilization out of bone marrow by cytokines and chemokines
A

• Peripheral blood

94
Q
  • umbilical vein after the infant is delivered
  • cord is clamped and cut
A

Umbilical cord blood (UCB)

95
Q
  • patient’s own marrow or peripheral blood stem cells
A

• Autologous

96
Q
  • HLA-identical sibling or
  • HLA-matched unrelated donor
A

• Allogeneic

97
Q
  • identical twin

HEMA 2: LEC (8 decks)

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