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Module 2 > ATL Biology and Treatment > Flashcards

ATL Biology and Treatment Flashcards

1
Q

where are lymphomas predominantly found?

A

lymph nodes; lymphoid organs; spleen or GALT

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2
Q

What is involved in looking at the morphology of tumour cells?

A

architecture and cytology

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3
Q

How is cytogenetics carried out?

A

convential karyotype; FISH

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4
Q

How is the immunophenotype determined?

A

flow cytometry and immunohistochemistry

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5
Q

What is stage I lymphoma?

A

one group of nodes

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6
Q

What is stage II lymphoma?

A

> 1 group of nodes same side of diaphragm

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7
Q

What is stage III lymphoma?

A

nodes above and below the diaphragm

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8
Q

What is stage IV lymphoma?

A

spread beyond the lymphatic system eg bone marrow, liver

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9
Q

What does the suffix E in lymphoma staging mean?

A

started outside the lymph nodes

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10
Q

What are the known RFs for lymphoma?

A

constant antigenic stimulation; viral infection; immunosuppression

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11
Q

Chronic stimulation with H.pylori antigen increases the risk of which type of lymphoma?

A

gastric MALT

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12
Q

Chronic stimulation with antigen in coeliac disease increases the risk of what?

A

small bowel T cell lymphoma

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13
Q

Why is there a 60x increase in non-hodgkins lymphoma in HIV?

A

loss of T cell regulation of EBV infected B cells

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14
Q

Why are immune cells particularly at risk of malignant transformation?

A

have rapid and multiple cell division steps; lymphocytes cut and mutate their own DNA; normal development relys on apoptosis

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15
Q

what is a high prevalence of HTLV-1?

A

> 1% of adult population

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16
Q

Which subtype accounts for 70% of the ATLL cases in the UK?

A

lymphoma

17
Q

What is seen on blood film with ATLL?

A

flower cell morphology

18
Q

Where are the lesions foudn in smouldering ATLL?

A

skin or lungs

19
Q

What are the clinical features of ATLL?

A

generalised lymphadenopathy; hepatosplenomegaly;skin lesions; lytic bone lesions; hypercalcaemia and OI

20
Q

What is the proviral load?

A

% of PBMCs infected

21
Q

What transmission route is required for the development of ATLL?

A

mother-to-child

22
Q

What are the RFs for ATLL development?

A

Fhx; smoking; high provirla load (HLA type)

23
Q

What is considered a high proviral load?

A

> 4%

24
Q

How many asymptomatic carriers are high load?

A

25%

25
Q

How many high load carrier develop ATL?

A

20%

26
Q

What HLA class I allele is detrimental to host protection against HTLV1

A

HLA-B*5401

27
Q

What are the HTLV-1 serology tests available?

A

ELISA and western blot

28
Q

How do you distinguish between ATL and peripheral T cell lymphoma in asymptomatic carriers?

A

for ATL need to demonstrate a monoclonal provirus in tumours

29
Q

Why may HTLV1 infection have to happen in infancy in order to develop ATL?

A

before immune system has developed?

30
Q

Why is loss of tax expression the last hit before malignancy?

A

allows infected cells to escape the immune system, mutations acquired meaning Tax is no longer needed

31
Q

What is the oligoclonality index?

A

the spread of clones- how many of each clone present in an individual

32
Q

What is clonal succession?

A

if a subclone occupying an environmental niche is lost, another population will fill its place

33
Q

What is the treatment for lymphoma and bulky acute forms of ATLL in the UK?

A

chemo- CHOP-like regimen; allo HSCT

34
Q

What is the treatment for both acute and chronic leukaemic forms of ATL?

A

AZT and IFNa

35
Q

What killed patients qith chronic ATL?

A

half die of OI; half transform to agggressive subtype

36
Q

What is hte name of hte anti-CCR4 antibody?

A

mogamulizumab

37
Q

What is the effect of mogamulizumab in chronic ATL?

A

proviral load drops by 3-4 logs by end

Module 2 (38 decks)

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