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Molecular Pathology > Non-Hodgkin’s Lymphoma > Flashcards

Non-Hodgkin’s Lymphoma Flashcards

1
Q

What is non-Hodgkin’s lymphoma?

A

A (very!) heterogenous group of lymphomas which have several things in common:

  • They are derived from lymphocytes.
  • Are not Hodgkin’s lymphoma!
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2
Q

What % of lymphomas are non-Hodgkin’s

A

85%

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3
Q

What is Burkitt’s lymphoma?

A

B-cell germinal centre lymphoma.

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4
Q

What are the 3 variants?

A

Endemic
Sporadic
Immunodeficient

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5
Q

Do they have something in common?

A

Endemic and ID variants often associated with EBV.

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6
Q

What viral infection is associated with endemic varient?

A

endemic variant is geographically associated with malaria endemic regions.

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7
Q

How is Malaria is believed to increase patient susceptibility to EBV?

A

Sporozoites downregulate TNF-a, IL-6 and MCP-1
Sporozoites upregulate IL-10
Blood stage parasite can induce expression of sFGL2.

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8
Q

c-myc is associated with strongly with Burkitt’s.

What is the common cytogenetic abnormality?

A

Common cytogenetic abnormality is t(8;14)(q24;q32)
Found in 85% of cases.
Places c-Myc under the regulatory control of IGH enhancer/promoter.

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9
Q

What about the other 15%?

A

T(2;8)(p12;q24)

T(8;22)(q24;q11)

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10
Q

The overall Morphological appearance of Burkitt’s in histology

A

“Starry skied” appearance under H&E.

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11
Q

Appearance of cytoplasm

A

Scant basophilic cytoplasm characterised by numerous lipid vacuoles

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12
Q

Appearance of nuclei

A

Round nuclei with stippled chromatin and multiple small nucleoli.

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13
Q

What other IHC stains give positive result?

A

Ki67.

Bcl-2 and Bcl-6

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14
Q

What is the Treatment for BL?

A

Similar to other lymphoma, treatment is via combination therapy.

Treatment for most NHL are very similar.

R-EPOCH has been shown to have 100% remission induction.

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15
Q

How many cycles of treatment?

A

21 day cycle.

6-8 cycles.

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16
Q

Which of the following lymphoma would rituximab work against?

A Lymphoma negatively stained with anti-CD20
B Lymphoma positively stained with anti-CD20

A

B

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17
Q

Follicular Lymphoma

A

An extremely heterogenous (and poorly understood) disease.

At least 8 sub-types

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18
Q

FL accounts for what % of non-hodgkins?

A

Accounts for ~20% of NHL cases.

~2600 cases per annum in UK.

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19
Q

Where is in situ FL found?

A

Lymph nodes (hence in situ!)

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20
Q

What is in situ FL?

A

Presents as a monoclonal expansion of malignant (?) B-cells in germinal centres.

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21
Q

Is In situ FL significant?

A

Studies suggest that ISFL can be seen as a pre-cancerous condition.
Patients have a 3% chance of transforming into FL.

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22
Q

Smoking is believed to significantly increase the risk of ISFL. By what %?

A

45% more likely to develop ISFL than non-smokers.

Interestingly this finding may not apply to other FL.

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23
Q

H&E Lymph node with ISFL (low mag)

A
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24
Q

Same lymph node but with anti-Bcl-2

A
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25
Q

Initial cytogenetic abnormality of FL

A

seems to be t(14;18)(q32;q21).

Found in majority (~90%) of ISFL cases.

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26
Q

Accumulation of other abnormalities will then cause a transformation of ISFL into FL proper. What are Examples of common FL mutations?

A 
Examples of common FL mutations include:
Chromosome 1p36 deletion (70% of cases).
KMT2D mutations (90% of cases).
CREBBP mutations (~70% of cases)
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27
Q

Aggressive transformations are associated with which mutations?

A

CD58
CDKN2B
CD79B

Transformation of FL into more aggressive forms is quite common (50%)

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28
Q

Are transformations common in malignancy?

A 
Transformations occur in many haematological malignancies and are associated with poor prognosis:
Richter transformation
CML -> ALL transformation
MDS -> AML
HL into NHL
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29
Q

What is the underlying cause of haematological malignancies and are associated with poor prognosis?

A

(almost) always genetic.

30
Q

Classification of FL

A

is via a variant of the Mann-Berard criteria (WHO modified).

31
Q

FL can be divided into 3 classifications. Describe Grade 1

A

small, cleaved centrocyte proliferation.

32
Q

Describe Grade II

A

mixed proliferation of small-cleaved centrocytes and large centroblast cells.

33
Q

Describe Grade III

A

proliferation of large centroblast cells

34
Q

Prognosis of FL

A

Prognosis for patients with FL can be variable.
Most patients diagnosed in later stages of the disease
Based on Follicular Lymphoma International Prognostic Index (FLIPI1/2)

35
Q

Follicular Lymphoma International Prognostic Index (FLIPI1/2)

A

The FILIPI scheme utilises a points based system to offer a prognosis:
>60 years olf.
>4 lymph node groups implicated.
Stage 3 or 4 disease (Ann Arbor classification).
Low Hb (<120g/L)
Increased LDH.

36
Q

Most common treatment of FL

A 
Many forms of FL are indolent and do not require active treatment (watchful waiting)
Masterly inactivity (my preferred, but slightly frowned upon wording!)
37
Q

Which type of FL can be treat with radiotherapy?

A

Localised FL

38
Q

Survival rate of FL?

A

~90% 10 year survival.

39
Q

Why is relapse common after radiotherapy?

A

Only eradiates particular parts of body, if a single cell else were will come back

40
Q

Which FL requires chemotherapeutic intervention?

A

Systemic FL

R-CHOP

41
Q

what is MALT lymphoma?

A

B-cell lymphoma originating in mucosa associated lymphoid tissue.

42
Q

What % of lymphoma are associated with MALT lymphoma?

A

<10% of all lymphoma

43
Q

What is MALT lymphoma associated with?

A

~100% of cases are associated with chronic inflammation.

44
Q

What causes MALT lymphoma?

A

~100% of MALT Lymphoma is caused by persistent H.pylori infection.

45
Q

How to diagnose H.pylori?

A

Breath test.

46
Q

Can biopsies diagnose H.pylori?

A

At least 5 biopsies taken and can be cultured and/or histologically examined.
95% sensitive for H.pylori

47
Q

What Serology tests can be used to diagnose H.pylori?

A

Anti-H.pylori antibodies.

Can be a bit like a broken pencil.

48
Q

How to culture of helicobacter?

A

H.pylori is a microaerophilic organism.
~5% atmospheric O2
Non-selective media is recommended, Horse blood agar.

49
Q

Histology of MALT lymphoma

Healthy tissue

A

MALT

50
Q

What is the incidence of T-cell lymphoma?

A

T-cell lymphoma are much rarer than B-cell lymphoma (<15% of NHL cases).
Incidence seems to be raising.
Celtic genome increases risk

51
Q

What is the classical finding of T-cell lymphoma?

A

Haemophagocytic syndrome.

52
Q

Aetiology of T-cell Lymphoma

A

is varied but can include:
EBV
HTLV1

53
Q

Human T-cell Leukaemia Virus-1 (HTLV1)

A

Retrovirus which is believed to contribute to cancer development in 5% of infected individuals.

54
Q

Is HTLV more common in animals or humans?

A

Such viruses are common in animals, not so much in humans!

55
Q

Mechanism of HTLV

A

Positive strand RNA genome and virus makes use of reverse transcriptase.

56
Q

How many specific serotypes of HTLV have geographical variation?

A

7

57
Q

Where is serotype A found?

A

A found globally.

58
Q

C?

A

C found in Asia (particularly Japan)

59
Q

The rest?

A

Rest found mainly in Africa

60
Q

Most common Cutaneous T-cell lymphoma?

A

mycoides fungoides

61
Q

Prognosis in MF

A

is generally positive (70% 10 year)
Sezary syndrome can complicate this.

Generally die with it rather than because of it (old patients)

62
Q

There is three stages of MF

Describe stage 1

A

Patchy MF

63
Q

Stage 2

A

Plaque

64
Q

Stage 3

A

tumour

65
Q

Histological appearance, what is the one key aspect?

A

Pautrier’s microabcesses are the lipid rich t cells washed away by prep of slide

66
Q

Sezary syndrome

A

Often considered as an evolution/transformation of MF.

Haematological manifestations are present.

67
Q

What kind of manifestations does SS present with?

A

Haematological manifestations are present.

68
Q

Kind of cells present?

A

Buttock cells (cerebriform cells)

69
Q

cytogenetic abnormalities are common, which three?

A

6q23-27
MYB
IL22RA2

70
Q

Treatment involves use of which monoclonal antibodies?

A

Mogamulizumab
Brentuximab vedotin

Prognosis is poor.

Molecular Pathology (10 decks)

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