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Neoplasia 2 Flashcards

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1
Q

Examples of hallmarks of cancer

A

avoiding immune destruction, polymorphic microbiomes, tumour-promoting inflammation

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2
Q

What are the 3 roles of the immune system in preventing tumours?

A
  1. eliminating/suppressing viral infections to prevent virus-induced tumours
  2. prompt elimination of pathogens and resolution of inflammation to prevent an inflammatory environment conducive to tumorigenesis
  3. immune surveillance - identifying and eliminating tumour cells on basis of tumour-specific antigens
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3
Q

Why can the relationship between the immune system and cancer be considered paradoxical?

A

immune system can eliminate (immune surveillance) but also promote cancer (inflammatory environment promotes tumorigenesis)

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4
Q

Immune surveillance definition

A

the immune system identifies and eliminates cancerous/precancerous cells before they can cause harm

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5
Q

Which mechanisms eliminate cancer cells during immune surveillance?

A

DNA repair (p53), apoptosis, immune response (e.g. phagocytosis)

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6
Q

What is the term used to describe tumour cells that are identified and eliminated by immunosurveillance?

A

highly immunogenic tumour cell

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7
Q

What is meant by a poorly immunogenic tumour cell?

A

a malignant cell with acquired gene mutations allowing them to evade immunosurveillance resulting in cancer

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8
Q

What is cancer immunoediting?

A

an extrinsic tumour suppressor mechanism that engages after cellular transformation and the failure of intrinsic tumour suppressor mechanisms

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9
Q

What are the intrinsic tumour suppressor mechanisms?

A

repair, senescence (biological ageing), apoptosis

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10
Q

What are the 3 phases of cancer immunoediting?

A

elimination, equilibrium, escape

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11
Q

What is the elimination phase of cancer immunoediting also known as?

A

immune surveillance

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12
Q

What happens during the elimination phase of cancer immunoediting?

A

immune system recognises and destroys tumour cells (immune surveillance)

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13
Q

Which cells are involved in the elimination phase of cancer immunoediting?

A

NK cells, CD8+ T cells, macrophages

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14
Q

When would the elimination phase progress to the equilibrium phase of cancer immunoediting?

A

if the immune system does not completely eliminate all transformed cells / poorly immunogenic cell escapes destruction

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15
Q

What happens during the equilibrium phase of cancer immunoediting?

A

there is a balance between immune control and tumour growth (cancer dormancy). tumour cells are contained but not all eliminated.

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16
Q

How may equilibrium represent the end stage of cancer immunoediting?

A

growth may be restrained for the lifetime of the host

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17
Q

What happens during the escape phase of cancer immunoediting?

A

tumour cells evade immune detection and control

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18
Q

How may the equilibrium phase of cancer immunoediting progress to the escape phase?

A

the cancer cells acquire further mutations to evade the immune cells to progress to clinically detectable malignancy

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19
Q

What mechanisms do tumour cells use to escape the immune system?

A

altered antigen presentation, express inhibitory molecules, produce immunosuppressive factors, resist immune effector mechanisms

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20
Q

How do tumour cells alter their antigen presentation to evade the immune system?

A

lose MHCI expression, defects in antigen processing (so no antigen is presented)

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21
Q

What are the inhibitory molecules expressed by tumour cells to evade the immune system?

A

PD-L1 (binds to PD-1 on T cells), CTLA-4 ligands (B7)

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22
Q

What immunosuppressive factors are produced by tumour cells?

A

TGF-beta, IL-10, prostaglandin E2

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23
Q

What is the function of the immunosuppressive factors produced by tumour cells?

A

they recruit immunosuppressive cells

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24
Q

Which immune effector mechanism do tumour cells resist?

A

apoptosis

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25
How do tumour cells resist apoptosis?
express anti-apoptotic molecules
26
Which cells express PD-L1?
tumour cells or immune cells (to inhibit T cells)
27
Which cells express PD-1?
T cells
28
What happens when PD-L1 on tumour/immune cells bind to PD-1 on T cells?
the T cell is deactivated (PD-L1 is an inhibitory molecule)
29
Which molecules on tumour/immune cells and T cells can interact?
MHC-TCR interact and PD-L1 and PD-1 interact
30
How are T cells activated by tumour/immune cells?
anti PD-L1 antibodies and anti PD-1 antibodies bind to PD-L1 on tumour/immune cells and to PD-1 on T cells respectively, blocking the receptors. Prevents the interaction between PD-L1 and PD-1 which would deactivate T cells
31
Examples of checkpoint proteins
B7-1, B7-2 (CTLA-4 ligands) on APCs, CTLA-4 on T cells (keep immune system in check)
32
Which cells express B7?
Antigen presenting cells
33
Which cells express CTLA-4?
T cells
34
How are T cells inactivated via the immune checkpoint pathway?
Via the binding of B7 (on APCs) to CTLA-4 (on T cells) as well as MHCII-TCR interaction
35
How are T cells activated via the immune checkpoint pathway?
anti-CTLA-4 antibody (immune checkpoint inhibitor) binds and blocks CTLA-4 (from B7 binding)
36
What are the 7 key stages of the cancer immunity cycle?
1. release of cancer cell antigens (cell death) 2. Cancer antigen presentation (APCs) 3. Priming and activation (T cells) in LNs 4. cytotoxic T cells travel to tumour via BVs 5. T cells infiltrate tumour 6. T cells recognise cancer cells 7. cancer cells are killed
37
What two opposing characteristics of the immune response dictate tumour fate?
effector immune response and tolerogenic immune response
38
Which type of immune response occurs during tumour initiation?
Tumoricidal effector response (to eliminate immunogenic cancer cells)
39
Which type of immune response is present during metastatic dissemination?
immune tolerance (tolerogenic)
40
Which cells are involved in the tumoricidal effector response?
NK cells, CD8+ T cells, Th1 CD4+ T cells, cytotoxic macrophages, neutrophils
41
Which cells are involved in immune tolerance?
Pro-tumoral macrophages, regulatory T cells, regulatory B cells, immature DCs, pro-metastatic neutrophils
42
Examples of tumour-infiltrating immune cells (either stimulate/inhibit cancer)
tumour-associated macrophages (TAM), regulatory T cells (Tregs), tumour-infiltrating lymphocytes (TILs)
43
What type of macrophage are tumour-associated macrophages (TAMs) often polarised to?
M2 (pro-tumour)
44
How do tumour-associated macrophages promote tumour growth?
promote angiogenesis, invasion, metastasis, and produce immunosuppressive cytokines
45
How do regulatory T cells (Tregs) promote tumour growth?
suppress effector T cell function (Tregs associated with poor prognosis)
46
Which cells are tumour-infiltrating lymphocytes (TILs)?
CD8+ cytotoxic T cells
47
Why is a high CD8+ TIL density associated with better prognosis?
CD8+ cytotoxic T cells eliminate tumour cells
48
Which cells form the basis for adoptive cell therapy?
CD8+ tumour-infiltrating lymphocytes
49
Function of M1 macrophages
release cytokines that induce proinflammatory and antitumor immune responses
50
Function of M2 macrophages
release anti-inflammatory cytokines that suppress the immune response and promote tumour progression
51
Which cells play a critical role in immunosurveillance?
Natural Killer cells
52
How do NK cells fulfil their anti-tumoral function?
secrete lytic granules, produce cytokines (both use activating receptors) and express death receptors
53
Which NK cell receptors lead to cytokine and lytic granule release?
activating receptors
54
Function of death receptors on NK cells
induce apoptosis
55
What is the tumour microenvironment?
a complex ecosystem surrounding the tumour that can be immunosuppressive or immunostimulatory
56
What is a tumour microenvironment made up of?
immune cells (lymphocytes, macrophages, DCs), stromal cells (fibroblasts, endothelium), ECM, soluble mediators (cytokines, chemokines)
57
What are some common benign oral neoplasms?
papilloma, fibroma, lipoma, pleomorphic adenoma
58
How are benign oral neoplasms usually treated?
surgical removal
59
Which virus is associated with the development of a papilloma?
HPV (human papillomavirus)
60
Description of papilloma
exophytic, cauliflower-like growth
61
Which is the most common oral benign tumour?
fibroma
62
Why is fibroma not considered to be a true neoplasms?
It is reactive hyperplasia
63
Description of a lipoma
soft, yellowish submucosal mass
64
What is the most common benign salivary gland tumour?
Pleomorphic adenoma
65
Which salivary glands are typically affected by pleomorphic adenoma?
major salivary glands
66
What are the common malignant oral neoplasms?
squamous cell carcinoma, verrucous carcinoma, mucoepidermoid carcinoma, adenoid cystic carcinoma
67
What percentage of oral malignancies are due to squamous cell carcinoma?
90%
68
Which areas of the oral cavity are more likely to develop SCC?
lateral tongue, floor of mouth
69
Which malignancy is verrucous carcinoma a variant of?
SCC
70
Description of verrucous carcinoma
exophytic, warty appearance
71
What is the most common malignant salivary gland tumour?
mucoepidermoid carcinoma
72
What is the route of metastasis for adenoid cystic carcinoma?
perineural invasion
73
What are the clinical manifestations of oral neoplasms?
erythroplakia/leukoplakia, non-healing ulcers, indurated masses/swellings, pain or paraesthesia, tooth mobility w/o periodontal disease, dysphagia/speech difficulties, lymphadenopathy, weight loss/systemic symptoms in advanced cases
74
What is a red patch called?
erythroplakia
75
What is a white patch called?
leukoplakia
76
What is the term used to describe abnormally enlarged lymph nodes?
lymphadenopathy
77
What are the risk factors for oral cancer?
tobacco, alcohol, HPV infection, chronic irritation, poor OH, genetic predisposition, nutritional deficiencies, previous history of oral cancer, age and gender factors
78
Which type of inflammation is important in oral carcinogenesis?
chronic inflammation
79
Why do HPV-positive tumours have a better prognosis than HPV-negative tumours?
HPV-positive tumours have distinct immune profiles with higher levels of immune infiltration
80
What are the diagnostic approaches to neoplasms?
clinical examination, imaging, biopsy, molecular testing
81
What are the aspects of clinically examining a neoplasm?
visual inspection, palpation, vital staining (toluidine blue)
82
What are the different forms of imaging used to diagnose neoplasms?
radiographs, CT, MRI, PET scan
83
What are the different types of biopsies used to diagnose neoplasms?
incision, excision, fine needle aspiration
84
What types of molecular testing can be used to diagnose neoplasms?
biomarkers, genetic analysis
85
What treatment modalities exist for neoplasms?
surgery, radiation therapy, chemotherapy, targeted therapy, immunotherapy
86
What is the primary treatment for most solid tumours?
surgery
87
What are the different types of surgeries used to treat neoplasms?
primary tumour resection, neck dissection, reconstructive procedures
88
Which treatment aims to establish local/regional control over a neoplasm?
Radiation therapy
89
What are the 2 types of radiation therapy?
external beam and brachytherapy
90
What is a systemic treatment for cancer?
chemotherapy
91
What are the 3 types of chemotherapy?
neoadjuvant, adjuvant, palliative
92
Which type of cancer treatment uses molecular specific agents?
targeted therapy
93
What are 2 forms of targeted therapy?
EGFR inhibitors, angiogenesis inhibitors
94
Which type of cancer treatment functions by enhancing the immune response?
immunotherapy
95
What are the major forms of immunotherapy?
immune checkpoint inhibitors, adopted cell transfer (TILs), cancer vaccines, cytokine therapy
96
What are the immune checkpoint inhibitors (activate T cells)?
anti PD-L1/PD-1, anti-CTLA-4
97
Example of a preventative cancer vaccine
HPV vaccine
98
What do therapeutic cancer vaccines contain?
personalised neoantigen vaccines
99
Example of cytokine therapy
IL-2, interferon-alpha
100
Definition of adoptive cell transfer
type of immunotherapy used for treating certain malignancies that enhances patient's own immune cells
101
What are the 3 steps of adoptive cell transfer?
1. collection of immune cells (from patient/donor) 2. ex vivo expansion/modification 3. reinfusion into patient
102
What are the different types of adoptive cell transfer?
CAR-T cell therapy, TIL therapy, TCR-modified T cells, NK cell therapy
103
What is the function of CAR-T cell therapy?
T cells are engineered to express chimeric antigen receptors
104
What is the function of TIL therapy?
expansion of tumour-infiltrating lymphocytes
105
What are TCR-modified T cells?
T cells that have engineered T cell receptors
106
What is the function of NK cell therapy?
NK cells expanded/activated
107
Which immunotherapy approach has been successful in haematological malignancies (e.g. leukaemia)?
adoptive cell transfer
108
What does CAR stand for?
Chimeric Antigen Receptor
109
What is CAR-T cell therapy?
A type of immunotherapy (type of adoptive cell transfer) that teaches T cells to recognise and destroy cancer
110
How do CAR-T cells recognise cancer cells?
T cells are engineered to express chimeric antigen receptors that target specific proteins (antigens) on the surface of cancer cells
111
Why are CAR-T cell receptors chimeric?
the receptor combines both antigen-binding and T-cell activating functions into a single receptor
112
How is the CAR-T cell activated when the antigen is bound?
the extracellular antigen recognition domain is linked to an intracellular signalling domain that activates the T cell
113
What happens when CAR-T cells come into contact with their targeted antigen?
CAR-T cell binds, is activated, proliferates and becomes cytotoxic
114
What are the 5 stages of CAR-T cell therapy?
1. Patient blood is removed to obtain T cells 2. CAR-T cells are engineered in the lab 3. Millions of CAR-T cells are grown 4. CAR-T cells are infused into patient 5. CAR-T cells bind to and kill cancer cells
115
What has been a challenging feature of applying CAR-T cell therapy to solid tumours?
identifying antigens that are highly expressed on the majority of cancer cells but largely absent on normal tissues
116
What are the causes of immunotherapy side effects?
enhanced immune activation
117
What organ systems can be affected by immunotherapy side effects?
any - skin, GI tract, endocrine glands, lung, liver, oral cavity
118
What potential immune-related adverse events can occur on the skin?
rash, pruritus (itchiness)
119
What immune-related adverse event can affect the GI tract?
colitis (inflammation of the colon)
120
What immune-related adverse event can affect the endocrine glands?
thyroiditis, hypophysitis (inflammation of the thyroid / pituitary gland)
121
What immune-related adverse event can affect the lung?
pneumonitis (inflammation of the lung)
122
What immune-related adverse event can affect the liver?
Hepatitis
123
What immune-related adverse event can affect the oral cavity?
mucositis, xerostomia

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