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Cancer Y2 > Cancer as a Disease - Leukaemia > Flashcards

Cancer as a Disease - Leukaemia Flashcards

1
Q

X% of all cancers are leukaemias

A

5

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2
Q
  • Blood cancers are the most common cancers in XXX aged x-x
A

men and women aged 15‒24

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3
Q

main cause of cancer death in people aged 1‒34 years

A

Leukaemia

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4
Q
  • Leukaemias that behave in a relatively ‘benign’ manner are called ….
A

chronic

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5
Q
  • Leukaemias that behave in a ‘malignant’ manner are called …
A

acute

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6
Q

3 levels of leukaemia classification?

A

leukaemia can be acute or chronic
- Depending on the cell of origin, it can also be lymphoid or myeloid
lymphoblastic (acute lymphoid, reminds us that they’re lymphoblasts) and lymphocytic (chronic lymphoid of mature lymphocytes)

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7
Q

What lineage are lymphoid cells

A

B or T lineage

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8
Q

What lineage are myeloid cells

A

granulocytic, monocytic, erythroid or megakaryocytic

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9
Q

Leukaemia results from a series of mutations in …

A

a single stem cell

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10
Q

Three important leukaemogenic mutations that have been recognized?

A

 Mutation in a known proto-oncogene making an oncogene
 Creation of a novel gene, usually through translocation e.g. a chimaeric or fusion gene
 Dysregulation of a gene when translocation brings it under the influence of the promoter or enhancer of another gene

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11
Q

Inherited or other constitutional abnormalities can contribute to leukaemogenesis, e.g.: (4)

A

 Down’s syndrome – predisposes to ALL and AML
 Chromosomal fragility syndromes
 Defects in DNA repair
 Inherited defects of tumour-suppressor genes

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12
Q
  • Identifiable causes of leukaemogenic mutations include: (4)
A

 Irradiation
 Anti-cancer drugs
 Cigarette smoking
 Chemicals e.g. benzene

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13
Q

What happens in AML

A
  • In AML, cells continue to proliferate but they no longer mature so there is:
     A build-up of the most immature cells- myeloblasts or ‘blast cells’—in the bone marrow with spread into the blood
     A failure of production of normal functioning end cells such as neutrophils, monocytes, erythrocytes, platelets
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14
Q

What are the reasons that there a failure of production of normal functioning myeloid cells in AML

A

1 – because of maturation arrest, 2 – because of crowding out of normal bone marrow cells

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15
Q

What happens in CML

A
  • In CML, the responsible mutations usually affect a gene encoding a protein in the signalling pathway between a cell surface receptor and the nucleus
  • The protein encoded may be either a membrane receptor or a cytoplasmic protein
  • In CML, cell kinetics and function are not as seriously affected as in AML
  • However, the cell becomes independent of external signals, there are alterations in the interaction with stroma and there is reduced apoptosis so that cells survive longer and the leukaemic clone expands progressively
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16
Q

What proteins are affected in CML

A

Surface receptor or cytoplasmic proteins

17
Q

2 key differences between AML and CML

A

in AML there is a failure of production of end cells, in CML there is increased production of end cells

  • Acute lymphoblastic leukaemia has an increase in very immature cells— lymphoblasts—with a failure of these to develop into mature T and B cells
  • In chronic lymphoid leukaemias, the leukaemic cells are mature, although abnormal, T cells or B cells
18
Q

Clinical symptoms of myeloid leukaemia (7)

A

Accumulation of abnormal cells leading to:

  • Leucocytosis
  • Bone pain (if leukaemia is acute)
  • Hepatomegaly - this
  • Splenomegaly – and this is because they are good environments for proliferation of lymphoid and myeloid cells
  • Lymphadenopathy (if lymphoid)
  • Thymic enlargement (if T lymphoid)
  • Skin infiltration
19
Q

Metabolic effects of myeloid leukaemia

A
  • Hyperuricaemia
  • Renal failure – because the hyperuricaemia leads to uric acid being deposited in the kidneys
  • Weight loss
  • Low grade fever
  • Sweating
20
Q

Crowding out of normal cells in myeloid leukaemia leads to

A
  • Anaemia
  • Neutropenia
  • Thrombocytopenia
21
Q

Acute lymphoblastic leukaemia largely affects …

A

children

22
Q
  • Epidemiology suggests that B-lineage ALL may result from ….. (2)
A

delayed exposure to a common pathogen or, conversely, that early exposure to pathogens protects

23
Q

Evidence for the pathogen exposure idea of ALL causation:

A
  • Evidence relates to family size, new towns (higher rates), socio-economic class (higher classes higher rates), early social interactions (early protected), variations between countries
24
Q

Epidemiology suggests that some leukaemias in infants and young children result from:

A

 Irradiation in utero
 In utero exposure to certain chemicals
 Epstein–Barr virus infection (?)
 Exposure to a mutagenic drug (rarely)

25
Q

ACUTE LYMPHOBLASTIC LEUKAEMIA- CLINICAL FEATURES from accumulation of abnormal cells: (6)

A

 Resulting from accumulation of abnormal cells

  • Bone pain
  • Hepatomegaly
  • Splenomegaly
  • Lymphadenopathy
  • Thymic enlargement
  • Testicular enlargement
26
Q

ACUTE LYMPHOBLASTIC LEUKAEMIA- CLINICAL FEATURES Resulting from crowding out of normal cells: (3)

A
  • Fatigue, lethargy, pallor, breathlessness (caused by anaemia)
  • Fever and other features of infection (caused by neutropenia)
  • Bruising, petechiae, bleeding (caused by thrombocytopenia)
27
Q

ACUTE LYMPHOBLASTIC LEUKAEMIA- HAEMATOLOGICAL FEATURES: (5)

A
  • Leucocytosis with lymphoblasts in the blood
  • Anaemia (normocytic, normochromic)
  • Neutropenia
  • Thrombocytopenia
  • Replacement of normal bone marrow cells by lymphoblasts
28
Q

ALL investigations? (6)

A
  • Full clinical history
  • Blood count and film
  • Check of liver and renal function and uric acid
  • Bone marrow aspirate
  • Cytogenetic/molecular analysis
  • Chest X-ray
29
Q

What is cytogenetic analysis and what can it be used for?

A

Looking at chromosomes basically
- Cytogenetic/molecular genetic analysis is useful for managing the individual patient because it gives us information about prognosis

30
Q

ACUTE LYMPHOBLASTIC LEUKAEMIA- LEUKAEMOGENIC MECHANISMS:

A
  1. Formation of a fusion gene
  2. Dysregulation of a proto-oncogene by juxtaposition of it to the promoter of another gene, e.g. a T-cell receptor gene
  3. Point mutation in a proto-oncogene
31
Q

What technique is used to spot fusion genes

A

FISH - fluorescence in situ hybridization

32
Q

ALL treatment 3 levels?

A
  • Supportive care
  • Systemic chemotherapy
  • Intrathecal chemotherapy

Cancer Y2 (15 decks)

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