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4 CAN > 11 CML: from chromosomes to targeted therapy > Flashcards

11 CML: from chromosomes to targeted therapy Flashcards

1
Q

What was the first targeted medication against a cancer?

A

Imatinib

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2
Q

What 4 main types of chronic myeloproliferative diseases are there?

A

primary polycythaemia
Primary thrombocythaemia
Idiopathic myelofibrosis
chronic myeloid leukaemia

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3
Q

What is primary polycythaemia?

A

too many red cells

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4
Q

What is primary thrombocythaemia?

A

too many platelets

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5
Q

What is idiopathic myelofibrosis?

A

too much marrow fibrosis

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6
Q

What is chronic myeloid leukaemia?

A

too many neutrophils

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7
Q

Which organs get big if you’ve got too many white cells?

A

liver and spleen

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8
Q

What would CML have previously been treated with?

A

hydroxycarbamide

transplantation

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9
Q

How can you spot CML on a blood film?

A

more white cexlls
multi-lobulated cells (neuttrophils)
more precursors
blasts (undifferentiated cells which turn into myeloid cells)

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10
Q

What would you see in a bone marrow aspirate of someone with CML?

A

even more precursors than usual

perhaps more immature ones too

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11
Q

What would be observed in bone marrow trephine histology of someone with CML?

A

only some fat lobules, with lots of precursors

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12
Q

What chromosome is associated with CML?

A

Philadelphia chromosome
t(9;22) translocation
BCR:ABL keeps being made

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13
Q

What is ABL?

A

tyrosine kinase

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14
Q

How might you see BCR:ABL?

A

FISH

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15
Q

How might CML present?

A 
incidental blood count finding
bleeding problems (posterior eye)
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16
Q

What is a normal white cell count?

A

4-8

17
Q

Name 2 odd symptoms people with CML might get

A

priapism

gout

18
Q

What is priapism?

A

very painful erection

19
Q

Why might those with CML get gout?

A

uric acid build up - DNA breakdown

20
Q

What tests might you do to diagnose CML?

A

blood count and film

Biochemistry

21
Q

What might blood count and film of someone with CML show?

A

elevated white cell count

low platelets and haemoglobin

22
Q

What might biochemistry of someone with CML show?

A

abnormal liver function
impaired renal function (raised urate)
raised lactate dehydrogenase (LDH)

23
Q

What molecular tests would you do to diagnose CML?

A

FISH (interphase or metaphase)

QPCR

24
Q

Once you treat the patient, you want ot know how much of the gene is still around. How would you test this?

A

Real time quantitative PCR

25
Q

What is the principe of real time quantitative PCR?

A

each time the gene is copied, the reporter flourophore is released, giving a signal

the intensity of the signal rises exponentially

compare with known gene (ABL) to know how much BCR/ABL you have

26
Q

Name 5 acute treatment options for CML

A 
hydroxyurea
Leukapheresis
Allopurinol
IV fluids
Analgesia
27
Q

Name 3 types of chronic treatment for CML

A

Tyrosine kinase inhibitors
Intereron
Allogenic transplantation

28
Q

Name 5 Tyrosine kinase inhibitors

A 
Imatinib
Dasatinib
Nilotinib
Bosutinib
Ponatinib
29
Q

What does leukofouresis do?

A

takes out blood, spins off white cells

puts everything else back

30
Q

What does allopurinol treat?

A

gout

31
Q

What does IV do here?

A

stops renal failure

32
Q

Why give analgesics to someone with CML?

A

their spleen will be quite painful

33
Q

How does imatinib work?

A

fits into the ATP binding pocket of BCR/ABL protein

34
Q

How well do patients have to comply to have an adquate response?

A

take drug >90% of time to get adequate response

35
Q

What is the most frequently reported mechanism of resistance to imatinib?

A

BCR/ABL mutations

36
Q

What is the most effective next generation BCR:ABL inhibitor?

A

Ponatinib

even effective against T315l mutations

37
Q

What do you do if the patient just isn’t respondig to normal treatment?

Why is this so difficult?

A

Haematopoietic SC transplant (post significant chemo and radiotherapy)

patients prone to bleeding, although once they’ve recovered 6 month to a year down the line you’re alright tbh

38
Q

Why are only 30% of patients eligible for HSCT?

A

age
morbidity
donor availability

4 CAN (21 decks)

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