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Immunology > Lecture 8: Inflammation And Breast Cancer > Flashcards

Lecture 8: Inflammation And Breast Cancer Flashcards

1
Q

What is related with helicobacter infection?

A

Gastric cancer

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2
Q

What are mechanisms to combat infections?

A

Skin Stomach acid

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3
Q

How do viral genomes arise?

A

Instrinsic functions (ability to degrade double stranded RNA)

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4
Q

What can break down vesicles that are formed during bacterial uptake?

A

Phagosomes and lysosomes

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5
Q

What does immune system attack?

A

Foreign infectious agents

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6
Q

What are infectious agents?

A

Bacteria Fungus Virus

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7
Q

What are part of the innate immune system?

A

NK cells, macrophages, dendritic cells and the granulocytes

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8
Q

What are problems associated with innate immune system?

A

These cells cannot remember pathogens to provide long lasting immunity

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9
Q

What provides an immediate inflammatory response?

A

Macrophages and neutrophils

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10
Q

Where are immune system derived from?

A

Stem cells

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11
Q

What can stem cells differentiate into?

A

Lymphoid progenitor Myeloid progenitor

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12
Q

What gives rise to the adaptive immune cells?

A

Lymphoid progenitor

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13
Q

Where does NK cells feed into?

A

Innate immune response

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14
Q

What gives rise to neutrophils, eosinophils, basophils, mast cells and monocytes?

A

Myeloid progenitor

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15
Q

What does the humoral response generate?

A

Soluble antibodies which recognise antigens and coat targets

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16
Q

What does macrophages do?

A

Neutralisation, englulfment and destruction by phagocytes

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17
Q

What does NK cells do?

A

Cells are killed by cytotoxic T cells

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18
Q

How can T cell recognise antigens ?

A

Via the TCR

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19
Q

How does immune system protect cancer?

A

Protect us from infection Resolving inflammation Recognising and killing tumour cells

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20
Q

Who postulated the idea of immunosurveillance system?

A

Paul Erlich

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21
Q

In 1959 what did scientists speculate about the immune system?

A

Urge immune system is able to monitor body and kill tumour cells before they ever become established

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22
Q

What did they speculate about cancer cells?

A

Cancer cells behave as foreign and prove an immune response

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23
Q

What was the mouse model?

A

They would take tumour from one mouse and put it into another mouse Found that tumours was destroyed Taking tumour from one mouse genotype and putting them into a completely different genotype mouse: was recognised as non-self

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24
Q

Experiment: nude mice which lacked a thymus (lack T cells)

A

No increase in tumour development

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25
Q

What do certain chemicals induce?

A

Highly immunogenic cancers

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26
Q

What is the transgenic mouse system?

A

Knocked out IFN-g receptor and RAG2

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27
Q

What happens if there is no IFN-g receptor?

A

Unable to recruit macrophages to site of infection

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28
Q

What happens if there is no RAG2?

A

Prevent B and T cell development

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29
Q

What happens when wild type and immunocompromised mice are given 3MC carcinogen?

A

Generated tumour

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30
Q

What are wild type where tumours arose categorised as and why?

A

Weak immunogenic because they are arisen in a background of a strong immune system

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31
Q

How can immune system promote Timor formation?

A

Provide selection pressure Create micro environment

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32
Q

What is immunoediting?

A

How the immune system shapes tumour immunogenecity and selection and how cancer cells edit host anti-tumour immunity

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33
Q

What are the 3 stages of immunoediting?

A

Elimination Equilibrium Escape

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34
Q

What is elimination?

A

Cancer immune system is alerted to tumour cells by cytokines and anti-tumour immune response (both innate and adaptive)

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35
Q

What is equilibrium?

A

Selection of less immunogenic tumour cells during anti-tumour response

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36
Q

What is escape?

A

Tumour evades the immune system. Stage 2 provides a selection pressure on the cancer cells to acquire mutations that evade the immune system allowing the cancer to escape

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37
Q

What has studies from immunosurveillance immunoediting show?

A

Type of Immune profile correlate with patient survival and prognosis

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38
Q

What do Melanoma patients have high levels of?

A

CD8 T cell

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39
Q

What are high levels of T regs associated with?

A

Negative prognosis (solid tumours)

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40
Q

What is inflammation?

A

Immune response of tissues due to bodily injuries

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41
Q

What are the clinical characteristics of acute inflammation?

A

Pain Heat Swelling Redness at the site of injury

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42
Q

What is acute inflammation?

A

Localised, protective response following trauma or infection

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43
Q

How is acute inflammation resolved?

A

Replacement of damaged tissue with differentiated cells that restore function

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44
Q

What can chronic inflammation result from?

A

Viral or microbial infection Environmental antigen (e.g. pollen) Autoimmune reaction Persistent activation of inflammatory molecules

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45
Q

What is chronic inflammation mediated by?

A

Monocytes and long-lived macrophages

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46
Q

What does monocytes mature into Once they leave the bloodstream and enter tissues?

A

Macrophages

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47
Q

What do macrophages do?

A

Engulf and digest microorganisms, foreign invaders and senescent cells

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48
Q

What chemical mediators do macrophages release?

A

IL-1 TNF alpha Prostaglandin

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49
Q

What do macrophages and other leukocytes release?

A

ROS and proteases that destroy the source of inflammation

50
Q

How is chronic inflammation resolved?

A

Repair of damaged tissue by replacement with fibrous connective tissue

51
Q

Who made the link between cancer and inflammation?

A

Virchow

52
Q

What did Virchow observe?

A

The presence of leukocytes in the stroma of cancer tissue

53
Q

What did Virchow hypothesise?

A

Malignancy originated at sites of chronic inflammation

54
Q

What did Epidemiological studies show?

A

Chronic inflammation can predispose people to cancer

55
Q

What are the 4 major cancer causing infections?

A

Helicobacter pylori Human papillomavirus Hepatitis B virus Hepatitis C Virus

56
Q

What bacterium induces chronic inflammation in the stomach and initiates carcinogenesis?

A

H.Pylori

57
Q

What does H.pylori colonisation lead to?

A

Superficial gastritis

58
Q

What is gastric atrophy?

A

Loss of normal glandular cells that result in reduced acid production allowing more bacterial colonisation and triggers the inflammatory response

59
Q

What does the H.plyori infect?

A

Gastric mucosa which results in gastritis

60
Q

What does the expression of IL2-beta lead to?

A

Atrophy

61
Q

What is gastric adenocarcinoma?

A

Cancer that affects stomach

62
Q

What protein does H.pylori express?

A

Cytotoxic associated protein A (cagA)

63
Q

What happens when H.pylori infects Cell?

A

CagA is injected into the cells

64
Q

What does proteins SHP-2 and Grb2 do?

A

Activate pathways that stimulate cell growth and migration

65
Q

What does H.pylori induce?

A

Pro-inflammatory mediators CIA activation of NFkB pathway

66
Q

What can chronic inflammation be a result of?

A

Non-infectious agents and infections

67
Q

What can tobacco smoke induce?

A

Chronic inflammation

68
Q

What do asbestos act as?

A

Inflammatory stimulus in lungs

69
Q

What can Asbestos predispose to?

A

Bronchioles carcinoma

70
Q

What are extrinsic driven by?

A

Inflammation condition e.g. inflammatory bowel disease

71
Q

What are intrinsic mediated by?

A

Genetic alteration - cause inflammation and neoplasia

72
Q

What does prostaglandin COC2 recruit?

A

Inflammatory cells

73
Q

What are cancer related inflammation mediated by?

A

Cell proliferation, survival, EMT Angiogenesis tumour Cell migration, invasion, metastasis inhibition of adaptive immunity altered response to hormones and chemotherapy

74
Q

What is thyroid papillary carcinoma?

A

Chromosomal rearrangement early in development of cancer that results in overexpressjon and activation of protein tyrosine kinase RET

75
Q

What does activation of RET induce?

A

Gene expression of colony stimulating factors (promote leukocyte survival and recruitment)

76
Q

What is CSF1

A

Critical protein for macrophage and monocytes recruitment

77
Q

What happens to mice that lack CSF-1?

A

Unable to recruit and differentiate macrophages

78
Q

What does lack of macrophages reduce?

A

Angiogenesis

79
Q

How are macrophages classified?

A

M1 or M2

80
Q

What does M1 activation occur in response ?

A

Pathogens via TH1 cytokines IFN-g and LPS

81
Q

What is M2 macrophage differentiation associated with?

A

TH2 cytokines (IL-4 and IL-13)

82
Q

What resembles M2 macrophages?

A

TAM

83
Q

What plays a key role in determining macrophage phenotype?

A

Hypoxia

84
Q

What are early tumours?

A

Hypoxic and necrotic

85
Q

What does TAM contain high levels of?

A

Endothelial monocytes activating: Protein II, endothelium II and necrotic debris

86
Q

When TAM become immobilised what do they upregulate?

A

HIF 1/2 that drives VEGF and Tie-2 expression - results in potent pro angiogenic environment

87
Q

When was T-regulatory cells first identified?

A

1971

88
Q

What are T cells characterised as?

A

CD4+, CD25+ and FoxP3+

89
Q

What are T regs?

A

T cells that suppress autologous cytotoxic anti-tumour immune response

90
Q

What do T cell thought to protect?

A

Host from autoimmune disease by suppressing self-reactive cells and blocking anti-tumour responses

91
Q

What does intratumoral depletion of CD4+ T cells lead to?

A

Eradication of established rumours and long term anti-tumour memory

92
Q

How does a tumour develop?

A

when T reg cell leads to suppression of t-killer cells and suppression of adaptive response

93
Q

What is a checkpoint protein on T cells?

A

PD-1

94
Q

What does PD-1 do?

A

Act as an “off switch” that helps keep the T cells from attacking other cells in body

95
Q

What cells have large amounts of PD1L1?

A

Cancer cells which help them evade immune attack

96
Q

What targets PD-1 or PD-L1?

A

Monoclonal Antibodies

97
Q

What are some examples of PD-1 inhibitors?

A

Pembrolizumab (keytruda) Nivolumab (Odiyo)

98
Q

Where are PD-1 inhibitors used in?

A

Melanoma of skin, non small cell lung cancer, kidney cancer, bladder cancer, head and neck cancers and Hodgkin lymphoma

99
Q

What are some example of PD-L1 inhibitors?

A

Atezolizumab (Tecentrig)

100
Q

Where are PD-L1 inhibitors found?

A

Bladder cancer and non-small cell lung cancer

101
Q

What happens if both PD1 and CTLA4 is blocked?

A

Block the ability of cancer cells to switch off

102
Q

What transcription factor is key mediator of the inflammatory response?

A

NF-Kb

103
Q

What is the transcription factor NFkB activated by?

A

TNF alpha, H.pylori CagA, viral proteins, carcinogens and chemotherapeutic

104
Q

What are the roles of TF NFkB?

A

Promote expression of inflammatory cytokines Polarisation of macrophages towards TAM type phenotype

105
Q

What can NFkB activation in cancer cells lead to?

A

Chemokines that initiate and maintain tumour micro environment

106
Q

What does knocking out IKK in tumour-infiltrating leukocytes inhibit?

A

Cancer related inflammation in intestine and colitis associated cancer

107
Q

What can NFkB exist as?

A

Dimer - homo or heterodimer, p50/p50 or p65/p50

108
Q

What has p50/p50 dimer been found to be responsible for?

A

Pro tumour phenotypes of TAMS

109
Q

How can NFKB activation be deceased?

A

Inhibit activating using aspirin Block degradation of IkB Prevent the translocation of NFKB into nucleus

110
Q

What target genes are inflammation, inhibit apoptosis and Mets angiogenesis induced by ?

A

Bcl-XL, Cox-2, MMP9, VEGF, IL6, TNF-a

111
Q

What vaccine prevents Cervarix?

A

HPV16/18 infection

112
Q

What had been shown to reduce cancer risk?

A

Aspirin

113
Q

What catalyses the synthesis of prostaglandin?

A

Cox-1 (constitutive) and Cox-2 (inducible)

114
Q

What is the role of prostaglandin?

A

Produce mutagens and induce cytokine synthesis as well as drive cell proliferation

115
Q

What does immunosurveillance recognise and kill?

A

Tumour cells

116
Q

What does Immunosurveillance utilise?

A

NK cells M1 type macrophages and cytotoxic T cells

117
Q

What does immunosurveillance induce?

A

Apoptosis, phagocytosis, antigen recognition and growth suppression

118
Q

How much percentage does infection and chronic inflammation account for in cancers?

A

15-20%

119
Q

What can Immune system be?

A

Pro and anti-tumourigenic

120
Q

Define immunosurveillance

A

The mechanism by which the immune system identifies and eliminates cancer cells

121
Q

What can chronic inflammation cause?

A

Oncogene activation (extrinsic)

122
Q

What does inflammation drive?

A

Oncogene activation (intrinsic)

Immunology (20 decks)

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