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Exercise Immunology > Cancer > Flashcards

Cancer Flashcards

1
Q

What is cancer?

A

A mass of cells that grows rapidly, refuses to die and spreads to a secondary site
A genetic disorder
Also an issue of genetic control

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2
Q

What gives cancer a survival advantage?

A

Mutations

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3
Q

Examples of germline (genetic) cancer mutations?

A

BRAC1 and BRAC2 - linked to breast cancer

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4
Q

Examples of somatic (acquired throughout life) cancer mutations?

A

p53

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5
Q

Effects of tumour suppressor genes?

A

Inhibit growth and division
Promote DNA repair
Switched on and off in healthy cells

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6
Q

How do tumour suppressor genes regulate healthy cell growth and division?

A

Fast growth in early stages
Slowed growth as you get older
Repairing damage and wounds

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7
Q

What is the catastrophic effect of mutations in tumour suppressor genes and oncogenes?

A

They give rise to inappropriate activation of cell growth and division

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8
Q

Effect of oncogenes?

A

Mitogenic signals

Promote growth and division

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9
Q

How do oncogenes regulate growth and division?

A

They tend to be always switched on

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10
Q

What percentage of cancer-related deaths are caused by secondary metastases?

A

90%

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11
Q

What is a secondary metastasis?

A

When cancer cells settle is a different part of the body from the primary tumour

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12
Q

What cells make up tumours?

A

Tumour cells
Stromal cells
Stem cells

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13
Q

What cells contribute to new tumours?

A

Cancer stem cells

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14
Q

What is the cluster of differentiation for cancer stem cells?

A

CD44++/CD24-

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15
Q

Which immune cells protect against cancer?

A

Natural killer cells
Dendritic cells
B-cells
T-cells

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16
Q

How do NK cells protect against cancer?

A

Tumours lose MHC 1 meaning it is more activating receptors will bind, this signals to the NK cells that the cell needs to be destroyed
Cytokine activity
Cytokine release

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17
Q

During the NK response what cytokine activity occurs in response to cancer?

A

Secretion of granzymes

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18
Q

During the NK response what cytokines are released in response to cancer?

A 
IFN-y
THF-a
GM-CSF
CCL1
CCL2
CCL3
CCL4
CCL5
CXCL8
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19
Q

What is the NK immune response occurs in response to cancer?

A

Non-specific anti-tumour immunity

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20
Q

How do dendritic cells protect against cancer?

A

Antigen-presenting cell engulfs the antigen (from the tumour cells) and breaks it down into antigenic fragments called peptide fragments. These then bind to MHC class 1 (Tc) and class 2 (Th and B-cell) receptors where they present the antigen to naive T and B-cells

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21
Q

How do B-cells protect against cancer?

A

They differentiate into plasma cells that secrete antibodies specific to the antigen
Memory cells

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22
Q

How do T-cells protect against cancer?

A

Th1, Th2 and Tc response

Memory cells

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23
Q

What are the 3 E’s of immunosurveillance?

A

Elimination
Equilibrium
Escape

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24
Q

What does Elimination stand for in the 3 E’s of immunosurveillance?

A

The innate and adaptive immune system destroys the weakest cancer cells
Darwinian Survival of the Fittest

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25
Q

What is the Darwinian Survival of the Fittest?

A

In the struggle for survival, the fittest win out at the expense of their rivals because they succeed in adapting themselves best to their environment

26
Q

What does Equilibrium stand for in the 3 E’s of immunosurveillance?

A

A small subpopulation survives and lies dormant

27
Q

What does Escape stand for in the 3 E’s of immunosurveillance?

A

A clonal outgrowth of surviving cancer cells

28
Q

What is the dendritic, B-cell, and T-cell immune response occurs in response to cancer?

A

Specific anti-tumour immunity

29
Q

What cells contribute to non-specific anti-tumour immunity?

A

NK cells

30
Q

What cells contribute to specific anti-tumour immunity?

A

Dendritic cells
B-cells
T-cells

31
Q

Examples of intrinsic mechanisms cancer uses to evade the immune system?

A

Loss of antigen
Hidden cell surface antigens
No expression of MHC class 1 or other co-stimulators
Engage inhibitors molecules (PD-L1)
Secrete factors that suppress anti-tumour immunity (TGF-B)

32
Q

Examples of extrinsic mechanisms cancer uses to evade the immune system?

A

Recruit stromal cells with immunomodulatory properties

  • Mesenchymal stem cells (MSC’s)
  • tumour-associated macrophages promote growth
  • T-regs suppress T-cell response to a tumour
  • myeloid-derived suppressor cells (MDSC’s)
33
Q

Examples of extrinsic mechanisms cancer uses to evade the immune system?

A

Recruit stromal cells with immunomodulatory properties

  • Mesenchymal stem cells (MSC’s)
  • tumour-associated macrophages promote growth
  • T-regs suppress T-cell response to a tumour
  • myeloid-derived suppressor cells (MDSC’s)
34
Q

Exercise reduces the risk of which cancers? (Moore et al. 2015)

A 
Oesophageal adenocarcinoma
Liver
Lung
Kidney
Gastric cardia
Endometrial
Myeloid leukemia (blood)
Myeloma (blood)
Colon
Head
Neck
Rectal
Bladder
Breast
35
Q

Exercise increases the risk of which cancer? (Moore et al. 2015)

A

Malignant melanoma (skin)

36
Q

How can exercise protect against cancer? (Brown et al. 2012)

A

Sex hormones
Metabolic hormones
Inflammation and adiposity
Immune function

37
Q

How can exercise affect sex hormones that helps protect against cancer? (Browen et al. 2012)

A

Positive dose-dependent manner with sex hormones and breast cancer risk in females (free estradiol, oestrone and testosterone)
Reduced oestrogen in breast cancer survivors
Physical activity has more favourable biochemistry compared to sedentary
Negative dose-dependent manner with sex hormone-binding globulin and breast cancer risk
Indirect - mediated by reductions in adiposity

38
Q

How can exercise affect metabolic hormones that helps protect against cancer? (Browen et al. 2012)

A

Insulin and insulin growth factor-1 (IGF-1) can increase tumour growth and inhibit apoptosis
Exercise improved insulin sensitivity
Promotes carcinogenesis in rats, which in concerning for Type 2 diabetic
Risk elevated with intravenous insulin injections
Circulating IGF-1 can change in response to nutritional changes -> high intake of protein and dairy have higher blood levels of IGF-1

39
Q

How can exercise affect inflammation and adiposity that help protect against cancer? (Browen et al. 2012)

A

Increased inflammatory cytokines (IL-6, CRP and TNF-a) are associated with a higher risk factor for cancer
Chronic inflammation promotes cancer
Exercise reduces inflammatory cytokines in obese individuals
Body composition is a mediator to the effects of exercise and inflammatory markers

40
Q

How can exercise affect immune function that helps protect against cancer? (Browen et al. 2012)

A

Immunodeficiency increases cancer risk
Exercise improves the quality of life in prostate cancer - treatment was more manageable
Moderate intensity exercise increases T-cells, NK-cells, and neutrophils mobilisation and activity

41
Q

Exercise effects on tumour growth and spread? (Pedersen et al. 2016; Hojman et al. 2018)

A

Voluntary wheel running in mice reduces cancer cell growth by 67%
No change in the existing size of the tumour in both mice and humans
Cancer cell incubated with exercise serum from fewer tumours when inoculated into mice

42
Q

Exercise effects of tumour metabolism? (Hojman et al. 2018)

A

Warburg effect and glycolysis - cancer cells exclusively convert glucose to pyruvate through the lactate pathway
Cancer cells are more susceptible to exercise-induced energy stress - increased expression of GLUT-1 transporters

43
Q

Exercise effects of tumour metabolism? (Hojman et al. 2018)

A

Warburg effect and glycolysis - cancer cells exclusively convert glucose to pyruvate through the lactate pathway
Cancer cells are more susceptible to exercise-induced energy stress - increased expression of GLUT-1 transporters

44
Q

Exercise effect on chemotherapy in patients? (Schaff et al. 2018)

A 
Increase vasculature (angiogensis) - augmented treatent efficacy
Enhanced drug tolerance - can withstand higher doses
45
Q

Exercise effects on anti-tumour immune response? (Hojman er al. 2018)

A

Patients with more NK and Tc cells typically have a better prognosis
Exercise mobilises NK and Tc cells
Increased blood flow -> increased shear stress -> increased ‘SOS’ signals via B-agrenergic signalling -> greater recruitment of immune cells

46
Q

Effects of moderate intensity exerise in cancer patients? (Kruijsen-Jaarsma et al. 2017)

A

Increased NK cell cytotoxic activity
Increased lymphocyte proliferation
Increased number of granulocytes
No changes in the number of leukocytes, lymphocytes, NK cells, T-cells, CRP, and pro- and anti-inflammatory mediators
Exercise was most beneficial for patients with a compromised immune function

47
Q

Impact of exercise on immune function in cancer patients? (Koelvyn et al. 2017)

A

Switch from M1 (pro-inflammatory) to M2 (anti-inflammatory) monocytes

48
Q

Cons of using the 2D model of the impact of exercise on cancer?

A

Cannot replicate what happens in the body

49
Q

Cons of using the mouse model of the impact of exercise on cancer?

A

Cannot replicate humans

Mice do not have fibroblasts

50
Q

Pros or using the 3D model of the impact of exercise on cancer?

A

More closely resembles tumours in vivo
Tumour cell-cell interaction in 3D
Tumour stroma cell interactions in 3D
Ease of visualisation

51
Q

Uses of modeling the tumour microenvironment in 3D?

A

Measuring growth and invasiveness

Measuring expression of markers of invasiveness

52
Q

What is EMT?

A

Epithelial-to-mesenchymal transition (EMT)

53
Q

Which cells are the most chemoresistance?

A

Cancer stem cells

54
Q

What is the effect of EMT?

A

Lose epithelial markers (E-cadherin) and gain mesenchymal markers (fibronectin and vimentin)
Lose basement membrane integrity (low laminin B-1)

55
Q

Which cells frequently undergo EMT?

A

Malignant cancer cells

56
Q

Impact of cycling on spheroid growth? (Masters Project)

A 
Protocol (1wk washout)
 - control
 - moderate intensity
 - high intensity
Results
 - high-intensity cycling exercise reduced the rate of growth of spheroids
57
Q

Impact of training on spheroid growth? (Master Project)

A 
Protocol
 - untrained swimmers
 - trained swimmers
 - elite swimmers
Results
 - there were reductions in the rate of growth of spheroids following exercise in the untrained and elite swimmers
58
Q

From the review by Idorn & Thor (2017) what do we know about the impact of exercise on immune function?

A

NK cells are required for exercise-mediated repression of tumour growth - but not B or T-cells
Adrenaline is also key for exercise-associated improved anti-tumours immune control 0 but not exclusively as you can recreate with exogenous administration
IL-6 is both pro- and anti-inflammatory and is involved in NK cell homing
The most pronounced effect seen with exercise initiated prior to inoculation of cancer cells
NK cells are important in the very early phases of tumourigenesis
Other specific immune cells are more important later on

59
Q

From the review by Idorn & Thor (2017) what are the limitations to research assessing the impact of exercise on immune function?

A

Exercise is often self-reported
Confounding factors - other lifestyle factors
Mouse models - leuwis lung cancer, B16 melanoma, DEN-induced liver cancer, spontaneous melanoma model DrM1
Microarray - pros and cons
Activation of T-cells as a by-product of NK cell cytotoxicity
The majority of patients don’t respond to immunotherapy
Lack of predictive markers to indicate responsiveness

60
Q

From the review by Idorn & Thor (2017) how might exercise work as an adjuvant to chemotherapy or immunotherapy?

A

Exercise increases vasculature -> allowing chemotherapy to get to more tumour cells
Exercise enables people to withstand higher doses and have fewer symptoms

Exercise Immunology (3 decks)

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