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Leukaemia > Introduction To Leukaemia And Malignant Haematology > Flashcards

Introduction To Leukaemia And Malignant Haematology Flashcards

0
Q

Aetiology of haematological malignancy?

Speak a little about each.

A

Combination of genetic and environmental factors.

Genetic Eg) Downs Syndrome

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1
Q

What is a haemopoietic malaignancy?

A

A clonal disease that is derived from a single cell in the bone marrow or lymphoid tissue which has undergone genetic alteration.

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2
Q

Environmental factors involved in haematological malignancy?

A

Chemicals eg) benzene –> AML
Drugs, especially previus chemotherapy –> AML
Radiation eg) atom bomb survivors in Japan
Infections

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3
Q

Can you name some infectious agents associated with haematological milignancies?

A 
Viral:
EBV and Burkitts lymphoma
HHV8 and Kaposi's Sarcoma
Bacterial: 
H. Pylori and gastric MALT lymphoma
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4
Q

What are haematological growth factors?

A

Soluble glycoprotein hormones.

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5
Q

Site of action of haematological growth factors?

A

May act locally at a site where produced or circulate in plasma.

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6
Q

What kinds of cells produce haemopoietic growth factors?

A

Many kinds of cells Eg) T lymphocytes, endothelial cells

Mainly stromal cells of the bone marrow Eg) adipocytes, fibroblasts, endothelial cells, macrophages/monocytes

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7
Q

What are stromal cells and what do they do?

A

Connective tissue cells of any organ. They support the function of the parenchymal cells of that organ.

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8
Q

What do haemopoietic growth factors do?

A

They interact at many different levels in the bone marrow, from stem cell to mature blood cell, to regulate proliferation and differentiation of haemopoietic progenitors.

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9
Q

How do haemopoietic growth factors exert their effect?

A

Exert their effect by binding to high affinity receptors on the cell surface.

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10
Q

Which haemopoietic growth factor stimulates erythropoiesis?

Where is it produced?

A

Erythropoietin.

Mainly in kidney but also in liver(early development)

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11
Q

Which haemopoietic growth factor is involved in platelet production? Where is it produced?
What does it do?

A

Thrombopoietin.
Produced by liver and kidney.
Stimulates the production of megakaryocytes.

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12
Q

What are megakaryocytes?

A

Bone marrow cells that bud off large numbers of platelets.

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13
Q

What is a cytokine? Examples?

A

Cytokines are a broad and loose category of small proteins that are important in cell signalling.
Cytokines include chemokines, interferons, interleukins, lymphokines and tumour necrosis factor.

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14
Q

What are interleukins?

What do they do?

A

Interleukins are a group of cytokines that were first seen to be expressed by WBC’s (leukocytes).
They promote the development and differentiation of T and B lymphocytes, and haematopoietic cells. (Includes NK cell)

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15
Q

For what is stem cell factor important?

A

Plays an important role in haematopoiesis, spermatogenesis and melanogenesis.

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16
Q

What are granulocytes/polymorphonuclear leukocytes (PMN)?

A

A category of WBC’s characterised by the presence of granules in their cytoplasm.
Types: neutrophils, basophils, eosinophils and mast cells

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17
Q 
Growth factors associated with:
-RBC's
-Platelets
-Monocytes
-Neutrophils
-Eosinophils
-
A 
RBC's - erythropoietin
Platelets - thrombopoietin
Monocytes - M-CSF
Neutrophils - G-CSF
Eosinophils - IL-5
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18
Q

What aspects of cell development do haematopoietic growth factors promote?

A 
Proliferation
Differentiation
Maturation
Suppression of apoptosis
Functional activation
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19
Q

Mechanism of action of haemopoietic growth factors?

A

1) GF binds to corresponding receptor (dimerisation)
2) binding activates whatever pathway is involved
3) activation of pathway –> transcription of particular genes

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20
Q

Ist three secondary pathways that may be activated by a haemopoietic growth factor.

A

JAK/STAT pathway
MPK pathway
Phosphatidyl-inositol-3-kinase (PI3K) pathway

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21
Q

Which transcription factor is needed for cell transition from G1 to S phase?

A

E2F

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22
Q

Which gene codes for a protein that inhibits the action of E2F?
How is this gene activated?

A

Rb (retinoblastoma) gene.

Gene is activated by p53.

23
Q

What is AKT?

A

A protein kinase that suppresses apoptosis.

24
Q

Outline the cell cycle.

A

M phase - mitosis, cell physically divides
Interphase:
-Where chromosomes duplicate and cell growth occurs prior to division

25
Q

What are the 3 stages of interphase?

A

G1 - cell begins to commit to replication
S phase - DNA content doubles and chromosomes replicate
G2 - cell organelles copied and cytoplasmic volume increases

26
Q

What are the roles of checkpoints in the cell cycle?

When do they occur?

A

Checkpoints act as breaks to coordinate divisions.
These breaks allow integrity of DNA to be assessed - does DNA need to be repaired?
They occur either side of S-phase.

27
Q

Which group of enzymes is responsible for progression through the cell cycle?

A

Cyclin-dependent protein kinases (Cdk’s)

28
Q

Which two classes of molecules control the checkpoints in the cell-cycle?

A

Cyclins

Cyclin-dependent kinases (Cdk’s)

29
Q

How is p53 involved in the cell cycle?

A

Acts at the G1-S checkpoint to sense damaged DNA.
p53 prevents activation of Cyclins required for the movement through the checkpoint –> allows time for repair of a potential defect.
When the defect cannot be repaired the cell undergoes apoptosis.

30
Q

Outlone the processof apoptosis.

A

1) Activation of caspases
2) Cell shrinkage
3) Cleavage of DNA
4) Condensation of nuclear chromatin
5) Fragmentation of nucleus
6) Phagocytosis of apoptotic bodies by macrophages

31
Q

2 main stimuli for the initiation of apoptosis?

A

Cell receptors: FAS/FASL

Release of cytocrome c from the mitochondria

32
Q

An example of a cell that expresses FASL?

A

Cytotoxic T-cells

33
Q

What do BAX proteins do?

Which protein upregulates expression of BAX?

A

BAX increases permeability of mitochondrial membrane –> cytochrome C release (tends to apoptosis).
p53 up-regulates BAX

34
Q

What is Bcl-2 and what does it do?

What group of genes does it fall under?

A

Bcl-2 is an antiapoptotic protein that makes mitochondrial membrane less permeable –> less cytochrome C (tends away from apoptosis).
BCL-2 is a proto-oncogene.

35
Q

2 main genes involved in the development of cancer?

A

Oncogenes

Tumour surpressor genes

36
Q

Can a translocation on a chromosome be visible under a microscope?

A

Yes.

37
Q

Which genetic alteration is associated with Chronic Myeloid Leukaemia?

A

t(9;22)

38
Q

Which genetic alteration is associated with Acute Promyelocytic Leukaemia?

A

t(15;17)

39
Q

Which genetic alteration is associated with Burkitt lymphoma?

A

t(8;14)

40
Q

What is the role of a tumour surpressor gene and give an example.

A

It is a gene responsible for protecting the organism against malignancy and regulating the cell cycle.
p53 is the most significant tumour surpressor gene.

41
Q

List the five main genetic abnormalities underlying haematopoietic malignancies.

A 
Point mutation
Translocation
Partial chromosomal deletion
Chromosomal duplication
DNA methylation/deacetylation (epigenetic alterations)
42
Q

Two mechanisms by which a translocation may caise haematological malignancy?

A

1) via the creation of a fusion gene, where 2 separate codings for different proteins end up together to produce a combination protein.
2) dysregulation, where an enhancer region (or any region that regulates rate of transcription) of one region is placed before a DNA sequence that it is not usually next to, cuasing increased or decreased transcription.

43
Q

Characteristivs of the cells in acute leukaemia?

A

Acute implies that the proliferating cells are at an early stage of development (not very differentiated).

44
Q

Characteristics of the cells in chronic leukaemia?

A

Cells are able to mature (are differentiated).

They often lose normal function and accumulate due to failure of apoptosis mechanisms.

45
Q

Outline the progression of acute leukaemia.
Characteristic of the cells involved?
Chemotherapy?

A

Onset is rapid –> death within weeks or months.
Cells involved have a defect that stops them from maturing or dying.
Requires high dose chemotherapy.

46
Q

Outline the progression of chronic leukaemia.
Characteristic of the cells involved?
Therapy?
Types?

A

Onset is slow –> death in months to years.
Proliferating cells retain their ability to differentiate.
May not require treatment. May require oral therapy or less intensive chemotherapy as opposed to that of acute.
2 types: myeloid/lymphoid

47
Q

What does the term myeloid mean?

A

Is an adjective that relates to the granulocyte precursor cell in the bone marrow.

48
Q

What does lymphoid mean?

In relation to leukaemia?

A

Resembling or pertaining to lymph or tissue of the lymphoid tissue.
When referring to leukaemia, it is a type of leukaemia affecting circulating lymphocyte cells.

49
Q

What does WHO use in the classification of leukaemias?

A

Morphology
Identification of cell surface markers (flow cytometry)
Cytogenetics/karyotyping
Molecular genetics (FISH, PCR)

50
Q

Is bone marrow failure common to all leukaemias or only some? Why does this occur?

A

Common to all leukaemias.

Occurs due to infiltration and disruption of normal tissue function.

51
Q

What are the clinical effects of bone marrow failure?

Why do all leukaemias lead to bone marrow failure?

A

Bleeding (low platelet count)
Infections (immune deficiency - such as neutropenia)
Anaemia (decreased RBC production) –> fatigue + pallor
Occurs due to malignant cells infiltrating and disrupting normal bone marrow tissue.

52
Q

Which organs can be involved in ALL?

A

Bone pain. (Commoner in children)

Testicular pain.

53
Q

What is seen commonly in AML?

A

Gum hypertrophy.

54
Q

In which group of leukaemias is lymphodenopathy and hepatosplenomegaly seen in?

A

Mostly chronic leukaemias. Some ALL.

55
Q

What metabolic abnormalities are associated with ALL and Burkitt’s Lymphoma.

A

Tumour lysis - acute rise in uric acid, K and phosphate.
Hyperuricaemia.
Fever.

Leukaemia (4 decks)

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