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302 Scientific basis of medicine > Cancer 1) Introduction > Flashcards

Cancer 1) Introduction Flashcards

1
Q

What is leukaemia?

A

Cancer of the blood

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2
Q

Why does leukaemia occur?

A

Failure of haematopoietic differentiation leading to accumulation of immature or dysfunctional leucocytes

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3
Q

What are the 4 types of leukaemia?

A

Acute myeloid leukaemia
Acute lymphocytic leukaemia
Chronic myeloid leukaemia
Chronic lymphocytic leukaemia

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4
Q

How do acute and chronic leukaemia differ?

A

Acute leukaemia has low WCC whereas chronic leukaemia has elevated WCC
Acute leukaemia occurs when differentiation arrests early in haematopoiesis leading to accumulating of immature lymphocytes in bone marrow
In chronic leukaemia the cells are more differentiated so have a dysfunctional phenotype

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5
Q

What is CLL characterised by?

A

Clonal disorder of mature CD5+/CD19+ B-cells

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6
Q

Describe CLL

A

Tumour found in bone marrow, peripheral blood and secondary lymphoid tissue
Immune dysfunction leading to recurrent infection and autoimmune complications
Bone marrow failuree

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7
Q

What is the epidemiology of CLL?

A

2-5/100,000 a year
Median age is 65-70yo
Incidence is increasing in younger patients and 20-30% are diagnosed below 55 years

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8
Q

What is the presentation of CLL?

A 
25-30% are asymptomatic
Enlarged lymph nodes
Repeat infections 
Abdominal discomfort due to enlarged spleen
Night sweats and fever
Weight loss and muscle wastage
Anaemia and or bruising
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9
Q

What are the causes of CLL?

A

Don’t know
Can arise following infectious disease or exposure to chemicals
Following autoimmune complications e.g. T1DM
Incidence if 1st degree relative is double

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10
Q

How is CLL diagnosed?

A

Traditional using Matutes scoring system
Blood films - structural membrane defect on B cells causing smudge smear cells
Rawstron flow cytometry

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11
Q

What is Matutes scoring system?

A

Flow cytometry based scoring system measure surface immunoglobulin CD5, CD23, CD79B and FMC7

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12
Q

What does Rawstron flow cytometry look at?

A

Kappa / lambda light chain
CD5+/CD19+ phenotype
CD20, CD23, CD200 and ROR1

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13
Q

How is CLL a multi-compartment disease?

A

Peripheral blood - non proliferating so relatively susceptible to standard chemotherapy
Lymph node CLL - higher level of proliferative drive
Bone marrow - more resistant to chemotherapy

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14
Q

Describe the interaction of CLL with lymph nodes

A

CLL B cells are often found in direct contact with CD3+ T-cells
CLL B cells are often proliferating due to T-cell help

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15
Q

Describe the rule of thirds for CLL

A

1/3 diagnosed with stage A CLL and won’t progress through disease
1/3 diagnosed with early CLL but will progress through disease and require treatment
1/3 diagnosed with advanced disease and require immediate treatment

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16
Q

What prognostic markers can be used for CLL?

A 
Lymphocyte doubling time
Cytogenetics
Sex
Age
Cellular markers - McL-1, CD49d, CD23, telomere length
17
Q

What are the requirements of a good prognostic tool?

A

Markers predict which patients are likely to progress
Markers predict whether patients will respond to treatment
Cheap and easy to perform
Must be reproducible
Markers should tell us something about the biology of the disease

18
Q

Why is clinical staging not enough?

A

CLL is a variable disease
Clinical stage is poorly prognostic for early stage and younger patients
New therapeutics are now available
Need more risk-benefit evaluation based on individuals risk of disease

19
Q

Describe the Stage A only cohort study

A

Lymphocyte doubling time (LDT) - proxy for proliferative drive for tumour. Patients with shorter LDT require earlier treatment
Cytogenetics
- low or intermediate risk cytogenetic aberrations e.g. deletions in chromosome 13q, trisomy 12
- high risk cytogenetic aberrations e.g. tp53 mutation
IGHV mutation status
Flow cytometry markers - CD38, CD49d, ZAP-70

20
Q

What chemotherapy is used for CLL treatment?

A 
Fludarabine 
Bendamustine
Pentostatin
Cyclophosphamide
Chlorambucil
21
Q

What is fludarabine?

A

Purine nucleoside analogue

22
Q

What is bendamustine?

A

Alkylating agent

23
Q

What are some targeted antibodies?

A

Rituximab
Ofatumumab
Obinutuzumab
Alemtuzumab

24
Q

What antibodies target CD20?

A

Rituximab
Ofatumumab
Obinutuzumab

25
Q

What are the mechanisms of action for the targeted antibodies?

A

Complement mediated lysis - antibody binds to complementary receptor leading to recruitment of complement to antibody and form of cell death
Antibody-dependent cytotoxicity - antibody binds to complementary receptors which flags to other cells to induce a response
Direct cytotoxic effect lading to trigger through binding to its receptor

26
Q

Give examples of targeted therapies

A

Ibrutinib
Idelalisib
ABT199
Lenalidomide

27
Q

Give examples of 1st line setting for fit patients with no comorbidities and without deletion of 17p or tp53 mutation

A 
FCR
BR
FR
PCR
Obinutuzumab + chlorambucil
28
Q

What is FCR?

A

Fludarabine + cyclophosphamide + rituximab

29
Q

What is BR?

A

Bendamustine + rituximab

30
Q

What is FR?

A

Fludarabine + rituximab

31
Q

What is PCR?

A

Pentostatin + cyclophosphamide + rituximab

32
Q

Give examples of 1st line setting for elderly with comorbidities and without deletion of 17p or tp53 mutation

A 
BR
Obinutuzumab + chlorambucil
Rituximab + chlorambucil
Rituximab
Cladribine
Fluradabine + rituximab
Chlorambucil
33
Q

What are the goals of novel therapies?

A

Use increasing understanding of biology & technology to improve therapy
Develop targeted treatments selective for malignant cells & less toxic to healthy cells
Recruit body’s immune system to fight disease
Improve effects of existing treatments in combination
Induce longer remission & ultimately cure with fewer side effects

34
Q

What is CAR-T therapy?

A

Chimeric antigen receptor T-cells

35
Q

What is the method of CAR-T therapy?

A

1) Patient’s own T-cells harvested from peripheral blood then transformed through genetic manipulation to express chimeric antigen receptor eg CD19
2) T-cells are then re-infused into patient (autologous)
3) T-cells then recognise patient’s own disease
4) patient is monitored

36
Q

How is the patient monitored for CAR-T therapy?

A

Disease response – CT scans, bone marrow biopsies, peripheral blood, flow cytometry
CAR-T cell persistence – immunohistochemistry of bone marrow biopsy, RT-PCR & flow cytometry of blood & bone marrow aspirate

302 Scientific basis of medicine (28 decks)

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