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HD 2 > Cancer in children > Flashcards

Cancer in children Flashcards

1
Q

How many children are affected by cancer in the UK

A

1/500

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2
Q

What % of childhood cancers are brain tumours

A

25

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3
Q

What are the effects of cancer treatment exaggerated in childhood

A

Chemotherapy gets incorporated into dividing cells, there are lots of dividing cells in childhood as they’re growing and developing

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4
Q

What is an embryological tumour

A

Malignancies originating in developing tissues and organ systems

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5
Q

What does cancer arise from

A

Accumulation of genetic aberrations in somatic cells

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6
Q

What do aberrations consist of

A

Mutations and chromosome defects

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7
Q

How do oncogenes act

A

By gain of function

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8
Q

Does one or both allele need to be activated in oncogenes

A

Just one

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9
Q

Name 4 ways in which oncogenes are activated

A

Mutation
Chromosome translocation
Gene amplification
Retroviral insertion

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10
Q

How do tumour suppresor genes acts

A

By loss of function

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11
Q

Do you need to inactivate both alleles for tumour suppressor genes to cause cancer

A

Yes

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12
Q

Describe the two hit model for tumour suppressor genes

A

Deletion/ mutation in somatic or inherited cells

Then a second hit

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13
Q

What forms can the ‘second hit’ in the 2 hit model take

A 
Loss
Loss and duplication
Chromosome deletion
Mutation 
Recombination
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14
Q

Another name for Wilm’s tumour

A

Nephroblastoma

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15
Q

How many children are affected by Wilm’s tumour

A

1/10,000

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16
Q

How does Wilm’s tumour usually present

A

Asymptomatic abdominal mass without metastasis

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17
Q

What is WAGR?

A

Wilm’s tumour
Aniridia
Genito-urinary abnormalities
Mental Retardation

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18
Q

Name a predisposition syndrome associated with Wilms tumour

A

Beckwith-Wiedeman Syndrome

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19
Q

What cells does Wilm’s tumour arise from?

A

Pluripotent embryonic renal precursors

20
Q

What 3 cell types present in embryonic kidney and are found in Wilm’s tumour>

A

Blastema
Epithelia
Stroma

21
Q

What does Wilm’s tumour resemble?

A

Nephrogenic mesenchyme

22
Q

What somatic genes are inactivated in Wilms tumour (3)

A

WT1
WTX
TP53

23
Q

What gene is activated in wilms tumour

A

CTNNB1

24
Q

What germline altercations occur in Wilm’s tumour

A

WT1 gene

1GF2/H19 locus

25
Q

What is the function of WT1

A

Key role in uteric branching

26
Q

What happens if WT1 expression doesn’t increase as it should?

A

WT1 stuck in condensate stage

Kidney remains immature embryological stage

27
Q

In what age do retinoblastomas usually occur

A

Children under 5 years

28
Q

Symptoms of retinoblastoma

A

Leukocoria (white pupil)
Eye pain
Redness
Vision problems

29
Q

In what % of cases in retinoblastoma metastatic

A

10-15%

30
Q

What is the cellular origin of retinoblastoma

A

Cone precursor cells

31
Q

What is the normal role of RB1 protein

A

Phosphorylation of RB1 releases ERF inducing transition from G1 to S in cell cycle

32
Q

What happens when there is no RB1

A

No regulation from G1 phase to S phase

33
Q

As well as RB1 loss, what other molecular changes occur in retinoblastoma

A

MYCN activation

MDM2 or MDM3 amplification leading to inactivation of p53

34
Q

What is a neuroblastoma

A

Tumour of the sympathetic nervous system usually arising in the adrenal gland or sympathetic ganglia

35
Q

What is the most common cancer in first year of life

A

Neuroblastoma

36
Q

What % of neuroblastoma are metastatic

A

50

37
Q

What is the cellular origin of neuroblastoma

A

Derived from sympatho-adrenal lineage of the neural crest during development

38
Q

Name 2 key genes involved in development of neuroblasotoma

A

MYCN

ALK

39
Q

What does it mean if child have >10 copies of MYCN gene

A

Usually a worse outcome of neuroblastoma

40
Q

Where do deletions occur in neuroblastoma

A

1p and 11q

41
Q

What targeted therapy can be used to treat neuroblastoma

A

Crizotinib against ALK mutation

42
Q

What is the most common malignancy in children

A

Acute lymphoblastic leukaemia

43
Q

What do ALL patients present with

A

Bruising or bleeding
Pallor or fatigue
Infection due to anaemia

44
Q

What organs can often by infiltrated by ALL

A

Liver
Spleen
Lymph nodes

45
Q

What cell does ALL with MLL translocation affect

A

Pro-B cells

CD 19

46
Q

What cell does ALL with high hyperdiploidy or TEL-AML1 translocation affect

A

Pre-B

CD19 and CD10

47
Q

Is pro-b or pre-b ALL favourable?

A

Pre-B

HD 2 (26 decks)

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