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CAN > L11: Chronic Myeloid Leuaemia From Chromosome To Targeted Therapy > Flashcards

L11: Chronic Myeloid Leuaemia From Chromosome To Targeted Therapy Flashcards

1
Q

What is chronic myeloid leukaemia

A

Excess myeloid cells

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2
Q

What is a philadelphia

A

A reciprocal chromosome

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3
Q

What is the Philadelphia of CML

A

Chromosome 22 and 9

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4
Q

In a blood film with someone with CML what would it show

A 
Normal neutrophils 
Precursors of:
Metameylocytes 
Myelocytes 
Premyelocytes 
Blasts
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5
Q

What would a cml bone marrow aspirate show

A

Lots of cells together

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6
Q

Would would a cml bone marrow trophine show

A

Packed marrow with less fat (should have more fat)

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7
Q

Which chromosome does BCR gene lie on

A

Chromosome 22

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8
Q

What chromosome does ABL gene lie on

A

Chromosome 9

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9
Q

What happens to BCR and ABL

A

Fuse together to from a new gene called BCR-ABL on chromosome 22

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10
Q

How does BCR and ABL fuse

A

Via translocation

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11
Q

What does the expression of BCR-ABL lead to

A

Increased proliferation

Decreased apoptosis

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12
Q

What is the typical presentation of BCR-ABL

A 
Asymptomatic - can be incidental 
High viscosity of haematocrit- gives rise to heart failure, bleeding back of eye and renal failure
Anaemia- tiredness
Infection- WBC do not function properly 
Bleeding- due to decreased platelets 
Weight loss 
Splenomegaly
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13
Q

What are the 3 basic diagnosis technique we can use to diagnose CML

A
  • blood count and film
  • biochemistry
  • bone marrow diagnosis
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14
Q

What would a blood count and film show for the levels of haemotcrit

A

High levels of WBC
Low/high platelet
Low haemoglobin

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15
Q

What would the biochemistry test show

A

Abnormal liver
Impaired renal function
Raised lactate dehydrogenase

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16
Q

What other disease do we need to exclude

A

Bacterial infection

Other malignancy

17
Q

How can we look for BCR-ABL gene

A

By FISH (fluorescence in situ hybridisation)

18
Q

Describe what occurs in FISH

A

1) place a piece of dna
2) put primers of BCR and ABL
3) heat dna
4) primers will join to BCR and ABL and light up with fluorescence

19
Q

To find out how much BCR-ABL gene there is what test can be carried out

A

Real time quantitative PCR

20
Q

What is the acute treatment of CML

A 
Hydoxylurea 
Leukapheresis (taking WBC out to bring levels down)
Allopurinol (to treat gout)
Iv fluid (renal failure)
Analgesia
21
Q

What are the long term treatment of cml

A

Tyrosine kinase inhibitors

22
Q

Name a common example of tyrosine kinase inhibitor used in CML

A

Imatinib

23
Q

Where does imatinib bind to

A

ABL kinase pocket

24
Q

What does imatinib prevent

A

ATP from binding to the ABL tyrosine kinase so ABL cannot be phosphorylated and is inactive

25
Q

What does inactive BCR-ABL result in

A

Cell death

26
Q

How Do we monitor CML to see if treatment is working

A

Blood count should return to normal
Chromosome disappearance partial or complete?
BCR-ABL quanititaive PCR test - should decrease

27
Q

What is the problem with imatinib

A

Drug resistance

28
Q

If there is drug resistance what other alternatives can we use for treatment

A

Second generation tyrosine kinase inhibitors

29
Q

Name examples of 2nd generation tyrosine kinase inhibitors

A

Nicotinic
Dosatinib
Basutinib
Palatinib

30
Q

Apart from giving tyrosine kinase inhibitors what other alternative is available for treatment

A

Haemotopoietic stem cell transplant

31
Q

Describe how we carry out haemotopoietic stem cell transplant

A

1) give high doses of chemotherapy to kill the cells

2) then give haemotopoietic stem cells form someone else e.g sibling or unrelated donor with matched HLA-antigens

32
Q

What are the eligible patients for haemotopoietic stem cell therapy

A

Young age

Donor availability

CAN (25 decks)

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