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Molecular basis of disease > Introduction to Lymphoma and Myeloma > Flashcards

Introduction to Lymphoma and Myeloma Flashcards

1
Q

Lymphoma

A

group of heterogenous cancers of mature lymphocytes that develop in lymph organs (B & T cells)

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2
Q

Cause of lymphoma

A

Not clear, but many known to be due to specific gene mutations and chromosomal translocations

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3
Q

Main functions of the lymphatic system

A

· blood filtration/purification
· removal of excess fluids from tissues
· absorption and transport of lipids
· immune system activation

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4
Q

Lymph nodes

A

small lymph organs carrying out the functions of the lymphatic system
-located throughout the entire body

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5
Q

Types of lymph organs

A

Primary lymph organs

  • sites where stem cells can divide and become immunocompetent
  • thymus & bone marrow

Secondary lymph organs

  • sites where most of the immune responses occur
  • lymph nodes, spleen, appendix, Peyer’s patches, tonsil & adenoids
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6
Q

Effect of lymphoma (uncontrolled division of B & T cells)

A

Growth of certain lymph organs

  • e.g. lymph nodes (adenopathy)
  • e.g. spleen (splenomegaly)

Cancer cells spread to other tissues through lymphatic system

Might infiltrate in bone marrow (detectable in blood) and/or other organs

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7
Q

Clinical significance if lymphoma spreads to bone marrow

A

If it spreads to bone marrow, it can be deceiving and make us think it is leukaemia, when really it is a type of bone marrow infiltration of lymphoma.

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8
Q

Classification of Lymphoma

A

Traditional classification of lymphoma includes:
· Non-Hodgkin’s Lymphoma
· Hodgkin’s Lymphoma

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9
Q

Prevalence of Hodgkin’s lymphoma

A

Hodgkin’s lymphoma is not very prevalent. It is not even among the 20 most common cancers in the UK and represent <1% of new cancer cases each year. Hodgkin’s lymphoma has two different peaks of incidence:

  • At adolescence
  • Males over 50
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10
Q

Prevalence of Non-Hodgkin’s lymphoma

A

Non-Hodgkin’s lymphoma is more prevalent is tightly associated with age. It is more prevalent at older ages and is the 6th most common cancer in the UK.

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11
Q

Presentation of Lymphoma

A

Warning signs of lymphoma:

  • Fever
  • Swelling of face and neck
  • Lump in your neck, armpits or groin
  • Excessive sweating at night
  • Itchiness
  • Unexpected loss of weight
  • Loss of appetite
  • Breathlessness
  • Feeling of weakness
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12
Q

Diagnosis of Lymphoma

A

· Lymph Node Biopsy

  • analyse microscopic sample
  • then immunophenotyping done including by flow cytometry, FISH and NGS

· PET Scans

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13
Q

Interpretation of PET Lymphoma Scans

A

PET Scans show how much the lymphoma has spread and therefore give us an idea of what stage the lymphoma is.

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14
Q

Aetiology of lymphoma

A

Lymphoma is a multifactorial disorder (causes are not well known):

  • Malfunctioning of the body’s immune system
  • Exposure to certain infections (e.g. Epstein Barr Virus)

The triggers are unknown but most of lymphomas occur when a B cell develops/acquires a mutation in its DNA.

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15
Q

What is Hodgkin’s lymphoma?

How does Hodgkin’s lymphoma present?

A

clonal B-cell malignancy

non-painful enlarged lymph node(s)

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16
Q

Risk factors of Hodgkin’s Lymphoma

A

~50% of cases due to Epstein-Barr Virus (EBV)

Family history

HIV/AIDS

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17
Q

Diagnosis of Hodgkin’s lymphoma

A

Excisional lymph node biopsy

> Reed-Sternberg cell under microscope (abnormal B lymphocytes)

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18
Q

Characteristics of Reed-Sternberg cell

A
  • Bi-lobal nucleus
  • Enormous
  • Seen in a sea of normal B lymphocytes
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19
Q

Treatment of Hodgkin’s Lymphoma

A
  • Chemotherapy +/- radiation

- Stem cell transplant

20
Q

Prognosis of Hodgkin’s Lymphoma

A

5-year survival ~50-90% depending on age, stage and histology
-good results in young adults (97%)

21
Q

What is Non-Hodgkin’s Lymphoma?

A

complex group of blood cancers that include all types of lymphomas except the Hodgkin lymphomas

can be subdivided into grades:

  • high grade
  • low grade
  • high and low grade
22
Q

How does Non-Hodgkin lymphoma present?

A

enlarged lymph node(s)

  • some forms are slow and others are faster
  • general lymphoma symptoms
23
Q

Causes of Non-Hodgkin Lymphoma

A

Chromosome Translocations

24
Q

Risk factors of Non-Hodgkin Lymphoma

A

Virus Infections:

-e.g. EBV (HHv4) in Burkitt’s lymphomas in immunosuppressed patients

-e.g. Human T-cell leukaemia
virus in adult T-cell lymphoma

25
Q

How does EBV (HHV4) cause Non-Hodgkin’s lymphoma?

A

> directly transforms B-lymphocytes in culture due to viral oncogene LMP-1

> over half of all normal individuals carry latent EBV infection, but they do not develop lymphomas due to effective immune surveillance by cytotoxic T-cells

> HOWEVER, in highly immunosuppressed individuals (e.g. following organ transplant or HIV) the endogenous latent EBV may transform B-cells which are no longer eliminated by cytotoxic T-cells

> Develop high grade lymphoma

26
Q

Prognosis of Non-Hodgkin Lymphoma

A

overall 5-year survival rate ~70%

27
Q

Immunoglobulin expression in B-cells

A

· Ig genes are highly expressed in B-cells.

· Each Ig gene has a powerful tissue specific enhancer which enhances the expression of the Ig gene by activating the promoter of the rearranged V segment

*many lymphomas carry chromosome translocations involving the Ig heavy chain or light chain loci (chromosome 14).

28
Q

Follicular lymphoma (Non-Hodgkin’s)

A

t(14;18)(q32;q21)

  • this translocation brings together the BCL-2 gene (chr18) and the enhancer of the immunoglobulin (chr14)
  • enhancer will regulate the promoter of the BCL-2 gene, which is an apoptosis inhibitor
  • upregulation of this gene causes increased apoptosis inhibition, and cells will therefore survive and give rise to lymphoma
29
Q

Burkitt’s lymphoma (Non-Hodgkin’s)

A

t(8;14)(q24;32)= common translocation
>C-myc proto-oncogene (chr 8) and Ig gene (chr 14) are brought together
>enhancer of the Ig will regulate the promoter of the C-myc
>enhancer upregulates expression of C-myc, promoting cell proliferation and lymphoma

30
Q

Classifications of Non-Hodgkin’s lymphoma

A

Low Grade:
· Normal tissue architecture partially preserved-normal cell of origin recognisable
· Divide slowly
· May be present for many months before diagnosis
· Behave in an indolent fashion

High Grade:
· Loss of normal tissue architecture-normal cell of origin hard to determine
· Divide rapidly
· Present for a matter of weeks before diagnosis

· May be life-threatening

31
Q

Diagnosis of Non-Hodgkin’s lymphoma

A

Immunophenotyping

Cytogenetics- FISH (for chromosomal translocations)

Light chain restriction

PCR (to detect clonal Ig gene rearrangement)

32
Q

Treatment for Non-Hodgkin’s lymphoma

A
  • Chemotherapy
  • Radiotherapy
  • Stem cell transplant
  • Monoclonal Ab therapy- Rituximab (anti-CD20)
33
Q

Mechanism of action of Rituximab

A

Monoclonal antibody against CD20
-Rituximab binds all the CD20 molecules present on the cell surface of abnormal B-cells. As a consequence, immune system will recognise them and kill the abnormal B-cells.

34
Q

Myeloma

A

tumour of the bone marrow

antibodies produced by plasma cells are abnormal

-plasma cells synthesise a single monoclonal antibody called paraprotein (M component)

35
Q

Myeloma cells

A

abnormal plasma cells

36
Q

Presentation of myeloma

A

Initially: asymptomatic

Later: bone pain, bleeding, frequent infections and anaemia

37
Q

Cause of myeloma

A

unknown

38
Q

Risk factors of myeloma

A

Obesity
Radiation exposure
Family history
Certain chemicals

39
Q

Aspects of myeloma which give rise to clinical features

A

1) Suppression of normal bone marrow
2) Bone marrow resorption and calcium release
3) Pathological effects of paraprotein

40
Q

Bone marrow resorption and calcium release in myeloma

A

a) Myeloma cells produce cytokines (esp. IL-6) which will activate bone marrow stromal cells to release another cytokine RANKL→ osteoclast activation (lytic lesions of bone, bone pain, fractures)
b) Calcium released from bone causes hypercalcaemia (multiple symptoms including mental disturbance)

41
Q

Suppression of normal bone marrow in myeloma causes…

A

Anaemia
Recurrent infections
Bleeding tendency

42
Q

Pathological effects of paraprotein in myeloma

A

Paraprotein

  • precipitates in kidney tubules, causing renal failure
  • deposited as amyloid in many tissues
  • 2% of cases develop hyperviscosity syndrome → stroke & heart attack
43
Q

Diagnosis of myeloma

A

· Serum electrophoresis for paraprotein (𝛾 Ig)
· Urine electrophoresis for paraprotein (𝛾 Ig)
· Bone marrow biopsy for increased levels of plasma cells
· Erythrocyte sedmentation rate (ESR)- high due to stacking of the RBCs
· Flow cytometry and cytogenetic to detect cause
· Radiological investigation of skeleton for lytic lesions

44
Q

Treatment of myeloma

A

· Radiotherapy
· Chemotherapy
· Allogenic haematopoietic transplantation (ASCT) in young patients

45
Q

Prognosis of myeloma

A

Chemo + ASCT

-overall 5-year survival rate ~35%

Molecular basis of disease (31 decks)

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