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10 tumour microenvironment Flashcards

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1
Q

What is the tumour microenvironment (TME)?

A

he ecosystem surrounding a tumour, consisting of tumour cells, non-tumour cells, and extracellular components.

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2
Q

What are the three main components of the TME?

A

Tumour cells, non-tumour cells, and the extracellular matrix (ECM).

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3
Q

How does the TME support tumour growth?

A

It provides nutrients, survival signals, promotes immune evasion, and facilitates metastasis.

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4
Q

What are five key characteristics of tumour cells?

A

Uncontrolled proliferation, genetic instability, immune evasion, invasion/metastasis, and therapy resistance.

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5
Q

How do tumour cells evade the immune system?

A

By downregulating MHC I, secreting immunosuppressive factors, and recruiting pro-tumour immune cells.

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6
Q

What is the extracellular matrix (ECM)?

A

A network of proteins like collagen and elastin that provides structural support and stores growth factors.

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7
Q

How does the ECM contribute to tumour growth?

A

By providing a scaffold for tumour expansion, storing pro-growth signals, and influencing cell behaviour.

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8
Q

What are the major types of non-tumour cells in the TME?

A

Immune cells, stromal cells, and vascular cells.

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9
Q

Name three types of stromal cells found in the TME.

A

Cancer-associated fibroblasts (CAFs), adipocytes, and pericytes.

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10
Q

Name three types of vascular cells in the TME.

A

Endothelial cells, lymphatic cells, and pericytes.

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11
Q

What is the role of endothelial cells in the TME?

A

They support angiogenesis, create abnormal vasculature, and modulate immune responses.

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12
Q

How do endothelial cells influence metastasis?

A

By forming new blood vessels that allow tumour cells to enter circulation.

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13
Q

What are cancer-associated fibroblasts (CAFs)?

A

Fibroblasts that remodel the ECM, secrete growth factors, and promote tumour invasion.

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14
Q

How do CAFs contribute to therapy resistance?

A

By modifying the ECM, secreting protective signals, and suppressing immune responses.

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15
Q

What are the two main categories of immune cells in the TME?

A

Anti-tumour (good) and pro-tumour (bad) immune cells.

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16
Q

Name two key anti-tumour immune cells.

A

CD8+ T cells (cytotoxic T cells) and natural killer (NK) cells.

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17
Q

Name two key pro-tumour immune cells.

A

Neutrophils (PMN-MDSCs) and T regulatory cells (Tregs).

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18
Q

How do CD8+ T cells kill tumour cells?

A

By releasing perforin and granzymes or activating death receptors (FasL, TRAIL).

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19
Q

Why are CD8+ T cells important for immunotherapy?

A

They are major targets of immune checkpoint inhibitors that enhance anti-tumour immunity.

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20
Q

How do NK cells differ from CD8+ T cells?

A

NK cells kill independently of MHC I, making them effective against tumours that downregulate MHC I.

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21
Q

How do neutrophils (PMN-MDSCs) promote tumour growth?

A

By producing ROS and arginase-1, which suppress T cell activity, and by promoting angiogenesis.

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22
Q

How do T regulatory cells (Tregs) suppress immune responses?

A

Through immune checkpoints (direct suppression) and cytokine release (indirect suppression).

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23
Q

Why is the composition of the TME important?

A

It influences tumour progression, metastasis, response to therapy, and immune activity.

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24
Q

What is the difference between immune hot and cold tumours?

A

Immune hot tumours have active immune responses, while cold tumours lack immune infiltration.

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25
What is cancer immunoediting?
The process by which the immune system interacts with and shapes tumour evolution.
26
What are the three phases of cancer immunoediting?
Elimination, equilibrium, and escape.
27
What happens during the elimination phase?
The immune system detects and destroys transformed cells before a tumour forms.
28
What is another name for the elimination phase?
Immune surveillance.
29
What happens during the equilibrium phase?
The immune system controls tumour growth, but the tumour remains dormant.
30
Why can tumours persist in the equilibrium phase for years?
Because of selective immune pressure balancing tumour survival and immune response.
31
What happens during the escape phase?
Tumour cells evolve to evade immune surveillance, leading to rapid tumour progression.
32
How do tumour cells escape immune control?
By acquiring mutations, recruiting immunosuppressive cells, and modifying the TME.
33
What is the overall impact of cancer immunoediting?
It shapes the tumour microenvironment, influencing tumour survival and immune evasion.
34
How does the TME affect cancer treatment?
It impacts immune cell activity, hypoxia, ECM composition, and fibroblast function.
35
Why does hypoxia in the TME reduce treatment efficacy?
It decreases drug penetration and promotes therapy resistance.
36
How do CAFs contribute to treatment resistance?
By modifying the ECM and secreting survival signals that protect tumour cells.
37
How does the TME promote metastasis?
By enhancing tumour cell invasion, angiogenesis, and immune evasion.
38
Why do metastatic tumours have different microenvironments?
Because tumour cells adapt to new tissues and interact with local stromal components.
39
What role does angiogenesis play in the TME?
It supplies oxygen and nutrients, supporting tumour growth and metastasis.
40
How is tumour vasculature different from normal vasculature?
It is abnormal, leaky, and inefficient, contributing to hypoxia and immune evasion.
41
What are the three main components of the TME?
Tumour cells, non-tumour cells, and the ECM.
42
How does the TME contribute to immune evasion?
By recruiting immunosuppressive cells and downregulating immune signals.
43
What are the three phases of cancer immunoediting?
: Elimination, equilibrium, and escape.
44
What is the main function of CD8+ T cells?
Killing tumour cells via perforin, granzymes, and death receptors.
45
What type of immune cell is highly immunosuppressive in the TME?
T regulatory cells (Tregs).
46
How does ECM influence tumour growth?
By providing structural support and storing growth factors.
47
Why are immune hot tumours more responsive to immunotherapy?
Because they have more immune cell infiltration.
48
What is the role of pericytes in the TME?
Supporting blood vessel stability and function.
49
Why do tumours become resistant to therapy over time
Due to genetic mutations, immune evasion, and TME modifications.
50
What are the key functions of the tumour microenvironment (TME)?
The TME provides survival signals, facilitates immune evasion, supports metastasis, and influences therapy resistance.
51
How does the TME contribute to immune suppression?
By recruiting immunosuppressive cells (e.g., Tregs, MDSCs), secreting inhibitory cytokines, and modifying antigen presentation.
52
Why do tumour cells exhibit genetic instability?
Due to accumulated mutations, chromosomal abnormalities, and defective DNA repair mechanisms.
53
How do tumour cells resist therapy?
By mutating drug targets, enhancing drug efflux, altering apoptotic pathways, and modifying the TME.
54
How does the ECM store growth factors?
It binds and releases growth factors like VEGF and TGF-β, which drive tumour progression.
55
How does ECM remodelling promote tumour invasion?
CAFs degrade the ECM using enzymes like MMPs, creating pathways for tumour cells to migrate.
56
What is the role of adipocytes in the TME?
They secrete fatty acids and inflammatory cytokines that fuel tumour growth and metastasis.
57
How do pericytes affect tumour vasculature?
They stabilize blood vessels but can also promote abnormal angiogenesis in tumours.
58
How does tumour angiogenesis differ from normal angiogenesis
Tumour vessels are irregular, leaky, and poorly perfused, contributing to hypoxia.
59
What is the role of VEGF in tumour angiogenesis?
VEGF stimulates the growth of new blood vessels, promoting oxygen and nutrient supply to tumours.
60
How do CD8+ T cells recognise tumour cells?
They detect tumour antigens presented by MHC class I molecules.
61
What happens when tumour cells downregulate MHC class I?
They evade CD8+ T cells but become more vulnerable to NK cell-mediated killing.
62
How do MDSCs suppress T cell function?
By producing arginase-1, nitric oxide, and reactive oxygen species (ROS), which inhibit T cell activation.
63
How do tumour-associated macrophages (TAMs) promote tumour growth?
They secrete pro-angiogenic factors (e.g., VEGF) and immunosuppressive cytokines (e.g., IL-10, TGF-β).
64
What triggers the elimination phase of cancer immunoediting?
The immune system detects transformed cells through tumour antigens and stress signals.
65
What is the role of IFN-γ in the elimination phase?
It enhances antigen presentation, activates immune cells, and promotes tumour cell apoptosis.
66
How do tumour cells adapt in the equilibrium phase?
They acquire mutations that allow them to resist immune attacks while remaining dormant.
67
What marks the transition from equilibrium to escape?
Tumour cells accumulate enough mutations to fully evade immune recognition and suppression.
68
How does hypoxia in the TME affect chemotherapy and radiotherapy?
It reduces drug diffusion and makes tumour cells more resistant to radiation-induced DNA damage.
69
Why do cold tumours respond poorly to immunotherapy?
They lack immune cell infiltration, reducing the effectiveness of immune checkpoint inhibitors.
70
What role do CAFs play in metastasis?
They secrete ECM components and cytokines that help tumour cells invade new tissues.
71
How do tumour cells survive in circulation during metastasis?
They form clusters with platelets and immune cells, protecting them from shear stress and immune attack.
72
How do tumour cells exploit immune checkpoints to evade immunity?
They upregulate PD-L1, which binds to PD-1 on T cells, inhibiting their activity.
73
What is the function of CTLA-4 in immune suppression?
It prevents T cell activation by competing with CD28 for binding to B7 molecules on antigen-presenting cells.
74
What is a key difference between immune hot and cold tumours?
Immune hot tumours have high T cell infiltration, while cold tumours lack immune activity.
75
What is a major challenge in targeting the TME for cancer therapy?
The TME is highly adaptable and can evolve resistance to treatment.
76
Why is targeting the TME a promising strategy for cancer therapy?
Because it affects multiple aspects of tumour progression, from immune evasion to drug resistance.

cancer (11 decks)

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