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HLTH3100 > Immunity to Cancer / Cancer Checkpoints > Flashcards

Immunity to Cancer / Cancer Checkpoints Flashcards

1
Q

What are the characteristics of a benign vs malignant tumours

A
  • Benign: Localised, non-invasive, resemble tissue of origin, encapsulated, intact surface, exophytic growth, incapable of indefinite growth
  • Malignant: Invade, rapid growth, aneuploidy, ulcerated, endophytic growth, vascular permeation, metastasis to invade other tissues
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2
Q

What is malignant transformation

A
  • DNA alterations that caused cells to acquire properties of cancer
  • Small benign tumours, adenomas grow / disorganise acquiring malignant phenotype
  • Inactivation or loss of 3 tumour suppressor genes
  • Activation of one cellular proliferation oncogene
  • Induced by physical / chemical substances, ionising radiation and infectious agents
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3
Q

What is a proto-oncogene

A
  • Encode proteins that normally control cell proliferation

- Activate normal cell proliferation

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4
Q

What is an oncogene

A
  • Mutated proto-oncogene
  • Jammed accelerator, gain of function
  • Uncontrolled proliferation
  • Alterations through actions of transforming viruses, exposure to carcinogens or genetic predispositions
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5
Q

What are tumour suppressor genes

A
  • Genes that normally prevent cell proliferation that are mutated
  • Defective breaks, loss of function (recessive)
  • Uncontrolled proliferation
  • TP53: Encodes nuclear phosphoprotein involved in growth arrest, apoptosis and DNA repair
  • Rb Gene: Hereditary, one copy is mutated and second is somatically inactivated
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6
Q

What are apoptotic genes

A
  • Genes associated with cancer control, proliferation
  • Pro-apoptotic (tumour suppressor)
  • Anti apoptotic (oncogenes)
  • Dysregulation leads to failure of former / overactivity of latter, both encourage neoplastic transformation
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7
Q

What is a neoplasm / neoplastic cells

A
  • Abnormal mass of tissue, growth excess / is uncoordinated with that of normal tissues
  • New growths of cells in the body that express unique / inappropriately expressed Ag
  • Altered self gene, over expressed genes, TAAs / TSAs
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8
Q

What are TAAs vs TSAs

A
  • TAAs: Normal cellular proteins expressed at particular times of development, unregulated in tumour cells
  • TSAs: Unique to cancer, mutations in tumour cells that generate altered proteins and thus new Ag
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9
Q

What is tumour immunity

A
  • Tumour cells can evade immune activation and recognition
  • Up-regulation of anti-apoptotic mediators
  • Expression of mutated / absent death receptors
  • Poor co-stimulatory or down regulation of secondary signal molecules
  • Lack of T cell activation
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10
Q

What is immuno-editing

A
  • Dynamic process that consists of immuno-surveillance and tumour progression
  • Consists of elimination (immuno-surveillance), equilibrium (persistence) and escape (cancer progression)
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11
Q

What cells are involved in the anti-tumour response

A
  • NK cells (target neoplastic cells)
  • Adaptive immune cells (CD4 / CD8 / NK T cells)
  • Cytokines (IFN-y, IL-12, TNF-a)
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12
Q

What is involved in subverting the anti-tumour response

A
  • Chronic inflammation (increases stress signals, increased mutation, GF)
  • Anti-tumour antibodies (bind NK / macrophages, impair activities)
  • Active immunosuppression (soluble factors suppress Tregs / MDSCs)
    Reduced MHC expression (poor CTL targets, TAP, IFN-y mutations, insensitivity, decreased activation)
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13
Q

What is cancer immunotherapy

A
  • Treatment for cancer that involves cytokines that elicit / amplify or suppress immune response
  • Attempt to slow the growth of cancer cells
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14
Q

What substances are useful in immunotherapy

A
  • Used singly or in combinations
  • Cytokines (stimulate production of anti-tumour cells)
  • Autologous DCs (expanded and reintroduced, prime tumour specific T cells)
  • Tumour specific T cells (obtained from tumours, expanded and reintroduced)
  • Vaccines (enhance anti-tumour response, tumour Ag stimulating CTL response)
  • Monoclonal Ab (attached to therapeutic drug to deliver treatment directly to cancer)
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15
Q

What are the three factors that characterise the adaptive immune response to an antigen / tumour

A
  • Antigenicity: Ags promote anti-tumour immunity T cells, recognise TAAs, present to MHC
  • Adjuvanticity: Presence of non-self antigens is accompanied by danger signals, promote DC / T cell activation
  • Feedback: Homeostasis curbs immune response to remove effector cells and limit damage to healthy tissues
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16
Q

What are the mechanisms of immune evasion that can be used by tumour cell to subvert immune response

A
  • Loss of tumour recognition (decreased MHC / genetic loss of b2-microglobulin, prevent presentation of TAAs)
  • Corrupted PRR signalling (inhibition of PRR, suppresses activation of T cells / macrophages / DCs)
  • Feedback mechanisms (designed to protect, can be overridden, chronic inflammation, immunosuppressive effects)
17
Q

What is immune suppression

A
  • Immune unresponsiveness to tumour
  • Inhibitory cytokines, down regulation of MHC / Treg
  • Generation of antigen-loss variants
  • Loss of CTL function through clonal exhaustion
  • Inhibition of T cell activity
18
Q

What are checkpoint inhibitors / checkpoint inhibitor therapy

A
  • Antibodies that interfere with the function of proteins on the surface of T cells (abrogate CTL responsiveness)
  • By blocking these pathways, checkpoint inhibitors reactivate host T cell response
  • Anti-CTLA-4 or PD-1L can block the suppressive effect of tumours and allow reactivation of tumour specific CD8 CTLs
19
Q

What are exhausted T cells

A
  • Tumour microenvironment
  • Reduced proliferative and functional capacity
  • Reduced cytokine / cytolytic activity
  • Increased TCIR leading to PD1/PDL1 blockade (normally prevents tumour cells from attacking normal cells)
20
Q

What are CAR T cells

A
  • Chimaeric antigen receptor cells
  • Fusion proteins, derived from extracellular Ab and intracellular signalling molecule
  • Target surface structures
  • MHC independent recognition of tumour targets
  • Serial killers of tumour cells
21
Q

What are TCR T cells

A
  • Cells transduced with a rearranged TCR that can combine CD3
  • Specific tumour pMHC complex
  • Requires MHC expression, lifelong persistence
  • Serial killers of tumour cells

HLTH3100 (15 decks)

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