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Cancer > 14. Leukaemia > Flashcards

14. Leukaemia Flashcards

1
Q

In what age group is leukaemia the most common cancer, and the main cause of cancer death?

A
  • Most common cancer - 15-24 years

* Main cause of cancer death - 1-34 years

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2
Q

What is lymphoma and myeloma?

A
  • Lymphoma - tumour of lymphoid cells

* Myeloma - neoplasma of plasma cells

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3
Q

What is leukaemia?

A

Cancer of the white blood cells in the bone marrow

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4
Q

Do all leukaemia patients have circulating tumour cells?

A

No

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5
Q

What brings about leukaemia?

A
  • Series of mutations in a single lymphoid or myeloid stem cells
  • Normally at least 2 mutations
  • Lead to abnormalities in proliferation, differentiation and cell survival
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6
Q

What cell can give rise to both myeloid and lymphoid cells?

A

Pluripotent haematopoietic stem cell

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7
Q

What do lymphoid and myeloid stem cells give rise to?

A
  • Lymphoid - B and T lymphocytes

* Myeloid - granulocytic, monocytic, erythroid or megakaryocytic

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8
Q

Outline the first and second mutation in a blood stem cell?

A

• Initial mutation - growth advantage
- uncontrolled expansion, crowding out the normal polyclonal cells
• Second mutation - even more aggressive behaviour
- can be an interval of years between the 2 mutations

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9
Q

Why can’t leukaemia be defined as benign and malignant and what is used instead?

A
  • Normally, a concept for solid tumours is invasion (local spread) and metastasis
  • Neither can be regarded as abnormal behaviour for haematopoeitic and lymphoid cells, as they normally recirculate between tissues and blood
  • Described as chronic or acute instead
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10
Q

What is chronic and acute leukaemia?

A
  • Chronic - leukaemias that behave in a relatively benign manner
  • Acute - leukaemias that behave in a malignant manner
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11
Q

What are the 4 main types of leukaemia (refer to stem cells and types)?

A
  • Chronic lymphocytic leukaemia (CLL)
  • Chronic myeloid leukaemia (CML)
  • Acute lymphoblastic leukaemia (ALL)
  • Acute myeloid leukaemia (AML)
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12
Q

How can you remember if a lymphoid cell cancer is acute or chronic?

A
  • lymphoCYTIC = chronic

* lymphoBLASTIC = acute

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13
Q

What gene mutations can cause leukaemia?

A
  • Proto-oncogene mutation
  • Creation of a novel gene e.g. chimeric
  • Translocation may bring a normal gene under the influence of the promoter
  • Loss of function of TSG
  • Tendency to chromosomal breaks
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14
Q

What inherited or other constitutional abnormalities can contribute to leukaemogenesis?

A
  • Down’s syndrome - increased propensity to ALL and AML
  • Chromosomal fragility syndromes
  • Defects in DNA repair
  • Inherited defects of TSGs
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15
Q

What are environmental causes of leukaemogenic mutations?

A
  • Irradiation
  • Anti-cancer drugs (ironic)
  • Cigarette smoking
  • Chemicals e.g. benzene
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16
Q

Leukaemia can be seen as an acquired genetic disease, resulting from a somatic mutation - mutations can be beneficial or neutral, what does this mean?

A
  • Beneficial - rare, but can lead to reversion to a normal phenotype in some cells in individuals with an inherited abnormality
  • Neutral - mutation doesn’t give the cell any particular growth or survival advantage (no leukaemia)
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17
Q

Are mutations that contribute to leukaemogenesis more likely to be random or caused by an exogenous influence?

A

Random (nature of the human genome - side effect of the ability to evolve)

18
Q

What generally happens in AML?

A
  • Cells continue to proliferate
  • No longer mature - build up of immature cells (myeloblasts) in the BM with spread to the blood
  • Failure to produce various end blood cells - can result in anaemia
19
Q

What are the 2 reasons for a low platelet count in leukaemia?

A
  • Failure of production of normal functioning end cells

* Disseminated intravascular coagulation

20
Q

What protein is affected by a mutation in AML and CML?

A
  • AML - transcription factors
  • CML - signalling protein gene (encodes protein in signalling pathway between a cell surface receptor and nucleus - membrane receptor or cytoplasmic protein)
21
Q

Are cell kinetics and function more seriously affected in AML or CML?

A

AML

22
Q

Does the cell become independent of external signals in AML or CML?

A

CML

23
Q

How does the production of end cells differ in AML and CML?

A
  • AML - failure of production of end cells

* CML - increased production of end cells

24
Q

What is the difference between ALL and CLL?

A
  • ALL - increase in immature cells (lymphoblasts) - failure to develop into mature T and B cells
  • CLL - cells are mature, but abnormal
25
Q

What are the disease characteristics of leukaemia?

A
  • Leucocytosis - blood becomes viscous - blockages
  • Bone pain
  • Hepatomegaly
  • Splenomegaly
  • Lymphadenopathy (if lymphoid)
  • Thymic enlargement (if T lymphoid)
  • Skin infiltration - bumps from leukaemic deposits
26
Q

What are the metabolic effects of leukaemic cell proliferation?

A
  • Hyperuricaemia - high uric acid in the blood due to increased breakdown of DNA
  • Renal failure - uric acid deposition in kidneys (chronic can lead to gout)
  • Weight loss
  • Low grade fever
  • Sweating
27
Q

What does pallor at the nail beds of an AML patient suggest?

A

Anaemia

28
Q

Which leukaemia is an immunological deficit a feature of?

A
  • CLL
  • High incidence of shingles and herpes zoster
  • Susceptible to viral, fungal and bacterial infections
29
Q

Which leukaemia is largely a disease of children?

A

ALL (many have first mutation in utero, and second just before the development of the leukaemia)

30
Q

How can you tell if an ALL mutation has occurred in utero?

A

Sots of dried blood from umbilical cord

31
Q

How does the incidence of ALL change with age?

A
  • Decreases with age
  • Stays relatively low after 20yrs
  • Slow rise again from 50yrs (second, lower peak in old age)
32
Q

What does the epidemiology of ALL suggest the cause for it?

A
  • B-lineage ALL may result from delayed exposure to a common pathogen
  • Irradiation in utero
  • In utero exposure to certain chemicals
  • EBV
33
Q

Can ALL result from exposure to a mutagenic drug?

A

Rarely - normally causes AML

34
Q

What are the clinical features of ALL?

A
  • Bone pain
  • Hepatomegaly
  • Splenomegaly
  • Lymphadenopathy
  • Thymic enlargement (if T-lineage
  • Testicular enlargement
35
Q 
What causes the following features of ALL:
• Fatigue
• Breathlessness
• Fever
• Bruising
A
  • Anaemia - fatigue, breathlessness etc.
  • Neutropenia - fever, infections etc.
  • Thrombocytopenia - bruising, petechiae etc.
36
Q

What is purpura?

A

Subcutaenous bleeding - purple-coloured spots in the skin

37
Q

What do we look for in a x-ray when investigating ALL?

A

Thymus enlargement and pneumonia

38
Q

What is immunophenotyping used for in leukaemia?

A
  • Determining whether cells are of T or B-lineage
  • Done by recognising antigens expressed on the surface of the cells
  • Can recognise different stages of maturation
39
Q

Which type of analysis is useful for managing the individual leukaemia patient and what does it identify?

A
  • Cytogenic + molecular analysis
  • Identify oncogenes
  • Information about prognosis
40
Q

What is an example of a genetic chromosome abnormality in ALL and how could this be detected?

A
  • Chr 12 and 21 carry the ETV6 and RUNX1 gene respectively
  • Translocation => fusion ETV6-RUNX1 on Chr 12
  • 2 fluorescent probes - green for ETV6 and red for RUNX1 - fusion gene => yellow signal
  • This is called fluorescence in situ hybridisation (FISH)
41
Q

What is the treatment for ALL?

A
  • Red cell transfusion, platelets, and antibiotics
  • Systemic chemotherapy (oral or IV)
  • Intrathechal chemotherapy (lumbar puncture, injection into CSF)

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