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Intro to immunology > Cancer Immunology > Flashcards

Cancer Immunology Flashcards

1
Q

What is cancer? (1)

A

Hyper proliferation of cells

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2
Q

What is metastasis? (2)

A

Cells in tumour mass acquire capabilities in order to change morphology and move throughout body

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3
Q

What are oncogenes? (3)

A

Drive abnormal cell proliferation
As a consequence of genetic alterations that either increase gene expression or lead to uncontrolled activity of the oncogene regulation or oncogene encoded proteins

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4
Q

What are tumour suppressor genes? (3)

A

Under normal conditions they act to inhibit cell proliferation and tumour development
In many tumors, these genes are lost or inactivated, if you remove these negative regulators of cell proliferation they contribute to the abnormal proliferation of tumour cells
Genes whose normal function is control and inhibit cellular replication.

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5
Q

What is the two-hit hypothesis? (3)

A

Most tumor suppressor genes require both alleles to be inactivated, either through mutations or through epigenetic silencing, to cause a phenotypic change

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6
Q

What are the hallmarks of cancer devised by Douglas Hanahan and Robert Weinberg? (1)

A

Comprises six biological capabilities acquired during the multistep progress to cancer

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7
Q

Describe the 6 hallmarks of cancer (6)

A

Self-sufficiency in growth signals
Insensitivity to antigrowth signals
Evading apoptosis
Tissue invasion and metastasis
Limitless replicative potential
Sustained angiogenesis

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8
Q

What is tumour heterogeneity? (2)

A

Tumours are more than insular masses of proliferating cancer cells
Instead, they are complex tissues composed of multiple distinct cell types that participate in heterotypic interactions with one another

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9
Q

What are cold tumours? (3)

A

Exclusion of CD8+ T cells and NK cells from the tumour
Immunosuppressive immune cells in tumour
Poor prognosis and response to immunotherapy

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10
Q

What are hot tumours? (3)

A

CD8+ T cells and NK cells are present in the tumour
Suppression of immunosuppressive cell types
Improved prognosis and killing of tumour cells with immunotherapy treatment

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11
Q

What are the immunological problems with cancers? (2)

A

Tumour are self cells

Contain self proteins, whichif recognisedby the immune system would result in autoimmune disease

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12
Q

What are the red flags the immune system recognises? (3)

A

Integrated stress response - Increased replicationresults in transcription and translation of proteins and macromolecules at a faster rate than normal. A lot of incorrect folding and general mechanisms of a normal cell being done poorly

Increased replication results in the use of a lot of nutrients. Anaerobic and aerobic processes that are normally carefully regulated are altered resulting in different amounts of waste products

Increased replication results in cellular stress - Recognition of Stressed induced ligands

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13
Q

How are tumour cells able to hide from the immune system? (2)

A

By reducing the expression of MHC class I on their surface
No MHC class I means tumour specific T cells activity is reduced because your T cells cant recognize whether you are non self or not

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14
Q

How can natural killer cells recognise tumour cells? (2)

A

Recognise:
- reduced MHC class I
- stress induced ligand on surface

This induces activation of NK cells

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15
Q

What are NK cells? (1)

A

Cells that have evolved to recognise and kill targets without self MHC class I and with stress induced ligand

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16
Q

What is the aim of the immune system in the tumour microenvironment? (1)

A

Recognition of unregulated growth

17
Q

What is the role of Damage Associated Molecular patterns (DAMPs) in the tumour microenvironment? (2)

A

Recognition of tumor - derived DAMPs usually initiates the activation of inflammatory signalling cascades to activate immune cells

Can also lead to sterile inflammation that can form a reinforcing loop of tumorigenesis.

18
Q

What is the integrated stress response? (2)

A

Evolutionarily conserved intracellular signaling network

ISR aims to return of homeostasis or induce cell death

19
Q

Describe the integrated stress response (3)

A

Activates the eukaryotic translation initiation factor eIF2
Triggers the translation of the key activating transcription factor ATF4 which is a multifunctional transcription regulatory protein that participates in a variety of cellular responses to different stresses or intercellular signaling molecules

20
Q

Role of Transforming Growth Factor-beta in the tumour microenvironment (3)

A

Pleotropic inhibitory cytokine

Signals via SMAD dependent and independent pathways to transcription factors that functionally inhibit immune cell function

21
Q

Role of Cyclo-oxygenase2 / Prostaglandin-E2
Inflammatory mediators in the tumour microenvironment (3)

A

Inflammatory mediators

Derived from Arachidonic Acid

Involved in homeostatic resolution of immune responses.

22
Q

Role of Indoleamine 2, 3-Dioxygenase in the tumour microenvironment (2)

A

Function is to degrade tryptophan

W degradation products have immuno-inhibitory effects

23
Q

Name the different immunomodulatory molecules in the gut (3)

A

Transforming growth factor beta
Retinoic acid
Interleukin 10

24
Q

Describe the role of transforming growth factor beta in the gut (4)

A

An inhibitory cytokine

Produced as an inactive pro-form and held inactive as a latent form

Integrins expressed in the gut epithelium, activate TGFbeta and induce regulatory T cell differentiation

TGFb in the intestines induce expression of CD8aa and CD103. CD8aa can down modulate TCR signaling so prevent over activity in the gut

25
Q

Describe the role of retinoic acid in the gut (3)

A

Produced by epithelial cells

Retinol the substrate for RA must be absorbed by from the diet

Retinol is stored in the liver and delivered to the intestines for local production of RA or the generation of Tregs

26
Q

Describe the role of Interleukin 10 in the gut (4)

A

An immunomodulatory cytokine

Signaling contributes to downregulation of TLR signalling MYD88, TRIF, TRAF6, CD14, and NFkB signalling inhibitors

Derived from Tregs

Deletion of IL10 in Tregs induces colitis.

27
Q

How are macrophages differentiated? (1)

A

By TGFb

28
Q

Describe the differences between M1 and M2 macrophages (9)

A

M1:
Pro-inflammatory
Anti-tumoral
Tissue-specific antigen presentation
Tissue injury

M2:
Anti-inflammatory
Pro-tumoral
Wound healing
Parasite clearance
Immunosuppression

29
Q

Role of tumour infiltrating lymphocytes in cancer (1)

A

Often a marker of good prognosis
suggesting role in controlling cancer

30
Q

Describe chimeric antigen receptor T cell therapy (5)

A

Acquire T cells from blood

Create CAR T cells

Grow many CAR T cells

Infuse CAR T cells into patients

CAR T cells attack cancer cells

31
Q

Problems with CAR T cell therapy (3)

A

Access to tumour microenvironment is restricted - immunosuppressive and nutrient-restricted tumour microenvironment

Tumour heterogeneity and antigen escape

CAR T cell trafficking and infiltration

32
Q

How can cancers occur (4)

A

Single point mutation in genes which can impact proliferation and change its function

Deletion in sections of genes

DNA damage - agent disrupts DNA at particular site important for cell proliferation

Genes spliced together

33
Q

What is Rb? (3)

A

P53 stops tumours from developing by:
1. In response to DNA damage and stress it will halt cell cycle
2. Inducing apoptosis
Mutations in these genes are common in lots of different cancers.

34
Q

What is P53? (3)

A

P53 stops tumours from developing by:
1. In response to DNA damage and stress it will halt cell cycle
2. Inducing apoptosis

35
Q

What is MYC? (5)

A

Oncogene
Tightly controls cell cycle state
Binds particular targets with high or low affinity at different places in cell cycle
Regulates the way cell moves through cell cycle
Myc work not working properly - keep driving proliferation

36
Q

What cells can be found in tumour microenvironment and what is important about them? (6)

A

Have a different functional output as they are altered by the tumour
Activating molecules
Dendritic cells
B/T/NK cells
Neutrophils
Macrophages etc

37
Q

What causes immune inhibition in the TME (2)

A

Transforming Growth Factor-beta
Cyclo-oxygenase 2 / Prostaglandin-E2
Indoleamine 2, 3-Dioxygenase

38
Q

Antibody targeting of tumour cells (1)

A

Bi-specific antibody

38
Q

How can we exploit the anti-tumour activity of the Immune system to
treat cancer? (3)

A

Inhibiting immune checkpoints with antibodies
T cell targeting of tumour cells
Antibody targeting of tumour cells

Intro to immunology (13 decks)

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