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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
What do certain chemicals induce?
Highly immunogenic cancers
26
What is the transgenic mouse system?
Knocked out IFN-g receptor and RAG2
27
What happens if there is no IFN-g receptor?
Unable to recruit macrophages to site of infection
28
What happens if there is no RAG2?
Prevent B and T cell development
29
What happens when wild type and immunocompromised mice are given 3MC carcinogen?
Generated tumour
30
What are wild type where tumours arose categorised as and why?
Weak immunogenic because they are arisen in a background of a strong immune system
31
How can immune system promote Timor formation?
Provide selection pressure Create micro environment
32
What is immunoediting?
How the immune system shapes tumour immunogenecity and selection and how cancer cells edit host anti-tumour immunity
33
What are the 3 stages of immunoediting?
Elimination Equilibrium Escape
34
What is elimination?
Cancer immune system is alerted to tumour cells by cytokines and anti-tumour immune response (both innate and adaptive)
35
What is equilibrium?
Selection of less immunogenic tumour cells during anti-tumour response
36
What is escape?
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
37
What has studies from immunosurveillance immunoediting show?
Type of Immune profile correlate with patient survival and prognosis
38
What do Melanoma patients have high levels of?
CD8 T cell
39
What are high levels of T regs associated with?
Negative prognosis (solid tumours)
40
What is inflammation?
Immune response of tissues due to bodily injuries
41
What are the clinical characteristics of acute inflammation?
Pain Heat Swelling Redness at the site of injury
42
What is acute inflammation?
Localised, protective response following trauma or infection
43
How is acute inflammation resolved?
Replacement of damaged tissue with differentiated cells that restore function
44
What can chronic inflammation result from?
Viral or microbial infection Environmental antigen (e.g. pollen) Autoimmune reaction Persistent activation of inflammatory molecules
45
What is chronic inflammation mediated by?
Monocytes and long-lived macrophages
46
What does monocytes mature into Once they leave the bloodstream and enter tissues?
Macrophages
47
What do macrophages do?
Engulf and digest microorganisms, foreign invaders and senescent cells
48
What chemical mediators do macrophages release?
IL-1 TNF alpha Prostaglandin
49
What do macrophages and other leukocytes release?
ROS and proteases that destroy the source of inflammation
50
How is chronic inflammation resolved?
Repair of damaged tissue by replacement with fibrous connective tissue
51
Who made the link between cancer and inflammation?
Virchow
52
What did Virchow observe?
The presence of leukocytes in the stroma of cancer tissue
53
What did Virchow hypothesise?
Malignancy originated at sites of chronic inflammation
54
What did Epidemiological studies show?
Chronic inflammation can predispose people to cancer
55
What are the 4 major cancer causing infections?
Helicobacter pylori Human papillomavirus Hepatitis B virus Hepatitis C Virus
56
What bacterium induces chronic inflammation in the stomach and initiates carcinogenesis?
H.Pylori
57
What does H.pylori colonisation lead to?
Superficial gastritis
58
What is gastric atrophy?
Loss of normal glandular cells that result in reduced acid production allowing more bacterial colonisation and triggers the inflammatory response
59
What does the H.plyori infect?
Gastric mucosa which results in gastritis
60
What does the expression of IL2-beta lead to?
Atrophy
61
What is gastric adenocarcinoma?
Cancer that affects stomach
62
What protein does H.pylori express?
Cytotoxic associated protein A (cagA)
63
What happens when H.pylori infects Cell?
CagA is injected into the cells
64
What does proteins SHP-2 and Grb2 do?
Activate pathways that stimulate cell growth and migration
65
What does H.pylori induce?
Pro-inflammatory mediators CIA activation of NFkB pathway
66
What can chronic inflammation be a result of?
Non-infectious agents and infections
67
What can tobacco smoke induce?
Chronic inflammation
68
What do asbestos act as?
Inflammatory stimulus in lungs
69
What can Asbestos predispose to?
Bronchioles carcinoma
70
What are extrinsic driven by?
Inflammation condition e.g. inflammatory bowel disease
71
What are intrinsic mediated by?
Genetic alteration - cause inflammation and neoplasia
72
What does prostaglandin COC2 recruit?
Inflammatory cells
73
What are cancer related inflammation mediated by?
Cell proliferation, survival, EMT Angiogenesis tumour Cell migration, invasion, metastasis inhibition of adaptive immunity altered response to hormones and chemotherapy
74
What is thyroid papillary carcinoma?
Chromosomal rearrangement early in development of cancer that results in overexpressjon and activation of protein tyrosine kinase RET
75
What does activation of RET induce?
Gene expression of colony stimulating factors (promote leukocyte survival and recruitment)
76
What is CSF1
Critical protein for macrophage and monocytes recruitment
77
What happens to mice that lack CSF-1?
Unable to recruit and differentiate macrophages
78
What does lack of macrophages reduce?
Angiogenesis
79
How are macrophages classified?
M1 or M2
80
What does M1 activation occur in response ?
Pathogens via TH1 cytokines IFN-g and LPS
81
What is M2 macrophage differentiation associated with?
TH2 cytokines (IL-4 and IL-13)
82
What resembles M2 macrophages?
TAM
83
What plays a key role in determining macrophage phenotype?
Hypoxia
84
What are early tumours?
Hypoxic and necrotic
85
What does TAM contain high levels of?
Endothelial monocytes activating: Protein II, endothelium II and necrotic debris
86
When TAM become immobilised what do they upregulate?
HIF 1/2 that drives VEGF and Tie-2 expression - results in potent pro angiogenic environment
87
When was T-regulatory cells first identified?
1971
88
What are T cells characterised as?
CD4+, CD25+ and FoxP3+
89
What are T regs?
T cells that suppress autologous cytotoxic anti-tumour immune response
90
What do T cell thought to protect?
Host from autoimmune disease by suppressing self-reactive cells and blocking anti-tumour responses
91
What does intratumoral depletion of CD4+ T cells lead to?
Eradication of established rumours and long term anti-tumour memory
92
How does a tumour develop?
when T reg cell leads to suppression of t-killer cells and suppression of adaptive response
93
What is a checkpoint protein on T cells?
PD-1
94
What does PD-1 do?
Act as an “off switch” that helps keep the T cells from attacking other cells in body
95
What cells have large amounts of PD1L1?
Cancer cells which help them evade immune attack
96
What targets PD-1 or PD-L1?
Monoclonal Antibodies
97
What are some examples of PD-1 inhibitors?
Pembrolizumab (keytruda) Nivolumab (Odiyo)
98
Where are PD-1 inhibitors used in?
Melanoma of skin, non small cell lung cancer, kidney cancer, bladder cancer, head and neck cancers and Hodgkin lymphoma
99
What are some example of PD-L1 inhibitors?
Atezolizumab (Tecentrig)
100
Where are PD-L1 inhibitors found?
Bladder cancer and non-small cell lung cancer
101
What happens if both PD1 and CTLA4 is blocked?
Block the ability of cancer cells to switch off
102
What transcription factor is key mediator of the inflammatory response?
NF-Kb
103
What is the transcription factor NFkB activated by?
TNF alpha, H.pylori CagA, viral proteins, carcinogens and chemotherapeutic
104
What are the roles of TF NFkB?
Promote expression of inflammatory cytokines Polarisation of macrophages towards TAM type phenotype
105
What can NFkB activation in cancer cells lead to?
Chemokines that initiate and maintain tumour micro environment
106
What does knocking out IKK in tumour-infiltrating leukocytes inhibit?
Cancer related inflammation in intestine and colitis associated cancer
107
What can NFkB exist as?
Dimer - homo or heterodimer, p50/p50 or p65/p50
108
What has p50/p50 dimer been found to be responsible for?
Pro tumour phenotypes of TAMS
109
How can NFKB activation be deceased?
Inhibit activating using aspirin Block degradation of IkB Prevent the translocation of NFKB into nucleus
110
What target genes are inflammation, inhibit apoptosis and Mets angiogenesis induced by ?
Bcl-XL, Cox-2, MMP9, VEGF, IL6, TNF-a
111
What vaccine prevents Cervarix?
HPV16/18 infection
112
What had been shown to reduce cancer risk?
Aspirin
113
What catalyses the synthesis of prostaglandin?
Cox-1 (constitutive) and Cox-2 (inducible)
114
What is the role of prostaglandin?
Produce mutagens and induce cytokine synthesis as well as drive cell proliferation
115
What does immunosurveillance recognise and kill?
Tumour cells
116
What does Immunosurveillance utilise?
NK cells M1 type macrophages and cytotoxic T cells
117
What does immunosurveillance induce?
Apoptosis, phagocytosis, antigen recognition and growth suppression
118
How much percentage does infection and chronic inflammation account for in cancers?
15-20%
119
What can Immune system be?
Pro and anti-tumourigenic
120
Define immunosurveillance
The mechanism by which the immune system identifies and eliminates cancer cells
121
What can chronic inflammation cause?
Oncogene activation (extrinsic)
122
What does inflammation drive?
Oncogene activation (intrinsic)

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