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Final > Stromal-epithelial interactions and tumor immunology > Flashcards

Stromal-epithelial interactions and tumor immunology Flashcards

1
Q

Accordingly to the somatic mutation theory…
a) Genetic instability is a byproduct of carcinogenesis
b) Cancer is reversible
c) Cancer is a tissue/organismal disease
d) Cancer is not reversible
e) The default sate of cells is proliferation

A

d) cancer is not reversible

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2
Q

The first approved immunotherapies are base on :
a) Cancer vaccines
b) Immune checkpoint blockade
c) A chimeric antigen receptor that recognizes CD19
d) There are not any approved immunotherapies yet, they are all in clinical trials
e) CSF-1R inhibitors targeting tumor-associated macrophages

A

c) A chimeric antigen receptor that recognizes CD19

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3
Q

Which of the following statements on epithelial cells is true?
a) Can be derived from adipocytes, tissue-resident fibroblasts, and mesenchymal stem cells
b) Can eliminate cancer cells by apical extrusion
c) Can eliminate cancer cells following stimulation by antigen presenting cells
d) Give rise to carcinomas which account for 50% of all cancers
e) Can prevent dissemination by capturing invasive cancer cells

A

b) Can eliminate cancer cells by apical extrusion

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4
Q

Why is there so much variability in survival rates of cancer between different tumor types

A

Location of the tumor and screening

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5
Q

How do tumors arise? Whats the main driver for initiating tumors?

A

Mutations, they occur in the DNA and give rise to growth advantages

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6
Q

Whats the somatic Mutation theory (SMT)
(3 conclusions)

A
  1. Mutations are necessary for cancer to arise
  2. Mutation make a founder cell unable to control proliferation : resulting in tumour formation and assumes that the default state of a cell is quiscence
  3. Cancer is irreversible
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7
Q

Why do we get these mutations? What causes somatic mutations?

A

Error, normally there a good mechanism for the cells to repair those error
Sometimes those errore are important genes

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8
Q

Whats the somatic mutation theory of tumor progression?

A

cancer develops through the accumulation of genetic mutations in cells, leading to uncontrolled growth and the formation of tumoWrs.

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9
Q

True or false: Cancer is a single disease

A

False its not

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10
Q

Cancer may be considered a collection of rare diseases: What are the different features ?

A

Genetic, epigenetic, phenotypic, microenvironment, Clinical responses (treatment, side effects, survival)

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11
Q

Whats carcinoma: Account for 90% of all cancer and arise from…that covers…

A

Epithelial cell that covers internal and external body

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12
Q

Sarcoma: arise from … like ….

A

Arise from the cells of supporting tissues like bone, fat, cartilage, connective tissue, muscle

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13
Q

Lymphomas and leukemias: arise from… and …origin. The term leukemia is used in cancer in which the malignant cells … mainly in the…rather than growing as a solid tumor

A

arise from cells of blood and lymphatic origin. The term leukemia is used in cancer in which the malignant cells proliferate mainly in th blood stream rather than growing as a solid tumor

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14
Q

Brain cancers: arise from…

A

cells in brain tissue

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15
Q

What are the 3 characteristics of cancer

A
  1. loss of growth control (number of cells and differentiation.)
  2. Local invasion - may metastasize to distant site
  3. Altered tissue organization
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16
Q

True or false: The outer cells (peripheral) interact with the stromal microenvironment (other cell types and extracellular matrix)

A

true

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17
Q

True or false: Cancer cells dont interact with the microenvironment, even when you switch from normal tissue to pre-malignant tissue

A

False, they do interact with the microenvironment when they switch from normal tissue to pre-malignant

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18
Q

Complete sentence: Epithelial tissues are typically highly….
They have a high turnover to eliminate damaged cells
Often maintained by stem and progenitor populations

A

Proliferative

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19
Q

Complete sentence: … frequently develop from pre-malignant stages

A

Carcinoma

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20
Q

True or false: carcinoma may take year or decades to develop

A

true

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21
Q

Are mutations sufficient for cancer development in any cell?

A

No, if stem cells are mutated you have chance of cancer, but if you add mutated stem cells to more differentiated celle that didnt have upper limited capacity, nothing happens.

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22
Q

true or false: not all cells are equally susceptible and cells that already have a generative capacity are more susceptible to tumors

A

True

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23
Q

True or false: Some factors are coming in and sensitizing these tissues to be able to form a tumor (the microenvironment is really relevant for that)

A

True

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24
Q

Is inflammation associated with increased cancer incidence?

A

Yes, tissues subject to chronic inflammation generally exhibit high cancer incidence

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25
Q

Which cance is the leading cause of death in patients with liver cirrhosis?

A

Hepatocellular cancer (liver cancer)

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26
Q

What creates a pro-tumorigenic niche?

A

Stromal cells accumulating and becoming active

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27
Q

True or false: the systemic inflammatory state of an individual can affect the character of the microenvironment in premalignancies, thus leading to elimination or supporting progression to advanced disease

A

true

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28
Q

True or false: Predicted cancer incidence of lung, gastrointestinal, reproductive and skin cancers is higher in immunosuppressed organ transplant recipient

A

True

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29
Q

Is breast cancer incidence reduced in transplan recipients?

A

Yes

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30
Q

Is cancer reversible?

A

it could be.. but its rare

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31
Q

What are some possible mechanisms for spontaneous regression?

A

Silencing oncogenes, activating tumor suppressors, Epigenetic mechanisms, Tumor inhibition by growth factors, induction of differentiation, hormonal mediation, elimination of carcinogen, tumor necrosis or apoptosis, angiogenesis inhibition, immune mediation

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32
Q

What is the Tissue organization Fiel theory (TOFT) name the 3 corollaries:

A
  1. mutations lead to cancer by disrupting morphogens
  2. Mutations that induce proliferation are not needed for carcinogenesis
    3.Genetic instability is a by product of carcinogenesis
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33
Q

What does TOFT state:

A

that carcinogenesis takes place at the tissue level, as does morphogenesis

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34
Q

TOFT states that the default state of cells is…

A

proliferation… changes in the whole environment and tissue make this amenable

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35
Q

According top TOFT, carcinogenesis is reversible or irreversible?

A

Reversible

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36
Q

What are morphostats

A

Theyre genes that are involved in regulating the homeostasis of a tissue

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37
Q

What happens when theres disruption of the homoestasis

A

It can have an effect on growth …
Argues that mutations that induce proliferations are not needed

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38
Q

Epithelial Defense against cancer (EDAC) .. explain the concept

A

Its an intrisinc ability of normal epithelial cells to suppress or eliminate adjacent tumour cells

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39
Q

What are some features of EDAC

A

-Cell competition between more and less fit cells
-Non-cell autonomous functions
-Apical extrusion
-Apoptosis
-Senescence

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40
Q

What happens to mutated cells surrounded by normal cells

A

gets eliminated

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41
Q

In which organ can we see apical extrusion (popped-out of the tissue) of Ras-transformed cells

A

Lung, pancrea, intestine

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42
Q

What happens to active non-cell autonomous elimination of cells by apical extrusion (cell competition)

A

contest among cells where weaker or damaged ones get pushed out by healthier ones, keeping tissues healthy and balanced..

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43
Q

Whats basal extrusion
damaged cells get .. from the …, keeping the tissue strong by getting rid of unhealthy cells.

A

damaged cells get pushed out from the bottom of the tissue layer, keeping the tissue strong by getting rid of unhealthy cells.

44
Q

What happens to cells when theyre in the lumen

A

They die. They cant survive if theyre not in contact with neighboring cells or the basement membrane, so they go into the lumen and die

45
Q

What happens to cells when they go basally

A

After basal extrusion, the cells leaving the epithelial layer would encounter the ECM, which can influence their fate. The interaction between these extruded cells and the ECM may trigger signaling pathways that could contribute to their clearance, degradation, or potentially affect surrounding cells and tissues.

46
Q

How is cell competition regulated?

A

by the microenvironment

47
Q

They did experiment on systemic signalling that can modify the tumor microenvironment.. what was the experiment

A

they showed that obese mice didnt have the ability to extrude the cells apically, leading to retention of these cells within the epithelium

48
Q

Obese tissue (fat) VS lean tissue (no fat)

A

Obese tissue : aligned collagen, increased stiffness, hypoxic, Pro-iniflammatory state
Lean tissue : Less aligned ECM, Lower stiffness, Normoxic

49
Q

True or false: cell competition results in senescence of damaged cells

A

True

50
Q

True or false: competition is controlled by P53

A

True

51
Q

Is cell competition the same as the classical p53-mediated DNA damage response?

A

No, theyre distinct concepts

52
Q

The competition mediated by a non-cell autonomous induction growth arrest and senescence-related gene expresion in outcompeted cells with higher P53 activity… what does that mean?

A

Less competitive cells show increased activity in genes related to stopping growth and entering a non-dividing state (senescence).
These changes are connected to higher activity levels of the P53 protein, which regulates cell growth and responds to cellular stress.

53
Q

What is the DCI stage in breast cancer?

A

DCIS stands for Ductal Carcinoma In Situ, which is a non-invasive or pre-invasive form of breast cancer. It’s often referred to as stage 0 breast cancer

54
Q

myoepithelial cells dynamically prevent dissemination… by…
What kind of phenotype is it?

A

pulling tumor cells back in
Its an invasive suppressant phenotype

55
Q

What are the different cell types in the microenvironment? (name 5)

A
  • malignant cancer cells
  • immune cells
  • fibroblasts
  • adipocytes
  • vasculature
56
Q

What does a tumor microenvironment implie?

A

that tumours are heterogeneous ecosyste of cells that can have pro- and anti-tumorigeni properties…. implies that cancer is a tissue-level disease

57
Q

Can the normal (stromal phenotype) microenvironment predict the patients outcomes

A

Yes

58
Q

Whats the communication between tumor epithelium and stroma? (co-evolution process)
We have differences in … and differences in …between these departments but we get cooperation between them

A

We have differences in oxygen accessibility and differences in metabolism between these departments but we get cooperation between them

59
Q

As the tumor evolves… the microenvironment …

A

evolves and develops

60
Q

True or false: tumors are diverse in the nature of the composition proportion, and activation state of the stroma

A

True

61
Q

True or false: Bidirectional communication between tumour and stroma is key because theres a co-development of these two systems

A

True

62
Q

True or false: Different activation states at different times of tumor progression. Many stromal cells are initially repressive, and become educated by the tumor to be supportive for tumor growth and progression

A

True

63
Q

What are cancer associated fibroblasts (CAFs)

A

Theyre the most abundant cell type within the microenvironment

64
Q

What are the features of cancer associated fibroblasts

A

Resisting cell death, evading growth suppressors, inducing angiogenesis, activating invasion and metastasis, tumor-promoting inflammation

65
Q

CAFs can have different origins… what are they?

A

epithelial, fibrocytes, mesenchymal stem cells, endothelial cells, adipocytes, etc..

66
Q

What is the consequence of CAFs within the microenvironment?

A

Invasion and metastasis

67
Q

Name a fibroblast marker ,,,

A

FSP1

68
Q

true or false: Fibroblasts directly associate with and lead cancer cells during invasion

A

True , they can remodel the extracellular matric

69
Q

Whats the dynamic adhesions between fibroblasts and cancer cells?

A

Their adhesion molecules interact, and the interaction is so strong it allows the fibroblast to drag the cells

70
Q

True or fasle: Tumor microenvironment is uniforme

A

False, its not uniform

71
Q

What is the main product/role of CAFs?

A

Secretion of collagen, which is an extracellular matrix protein, and tumors tend to be stiffer than normal tissue, thats why we feel lumps and masses

72
Q

True or false: the stiffness of the tumor can impact its stiffness

A

true

73
Q

As the tumor progresses, it increases the… to modulate growth properties

A

stiffness

74
Q

True or false: non-cellular components of the stroma also influence epithelial cancer cell behaviors

A

True

75
Q

Whats hypoxia? whats the link to tumor?

A

Shortage of oxygen reaching the tissues and cells and induces activation of different transcriptional programs.
Hypoxia affects :
tumor vascularization, sensitivity to therapeutics, EMT, metastasis

76
Q

Whats the dual role of macrophages in cancer

A

Tumor Promotion(M2): Some macrophages aid tumor growth by promoting inflammation, supporting blood vessel formation (angiogenesis), and suppressing the immune response against the tumor.
Tumor Suppression (M1): Conversely, other macrophages can work to attack and destroy tumor cells, activating the immune response to eliminate cancerous cells.

77
Q

M1 is ….M2 is…

A

M1 is anti-tumor and kills tumor cells, M2 is pro-tumor and tissue remodelling, angiogenesis and tumor progression

78
Q

What are TAMS, and whats their role?

A

Tumor associated macrophages that promote metastasis in ovarian cancer

79
Q

CCL2 is one of the primary cytokines that recruits… and macrophages secrete…that is a pro-proliferative factor for many epithelial cell type

A
  • machrophages
  • Wnt1
80
Q

the macrophages that recruit, can… the extracellular matrix and create tracks that epithelial tumor cells will follow

A

remodel

81
Q

Whats the combination effect between macrophages and epithelial cells?

A

collaboration between macrophages and epithelial cells can either promote tumor growth or aid in immune responses against infections and tissue damage, depending on the circumstances.

82
Q

Immune surveillance in tumors is a mechanism in which the immune system can… and modulate ..

A

recognize tumor cells and modulate growth problems

83
Q

Tumors tend to have an extracellular matrix thats organized parallel to the edge of the tumor. it allows the cells to….

A

migrate through, along the ECM path and macrophages can come and remodel the ECM path

84
Q

True or false, antigen present tumor cells to T cells, and would induce apoptosis or cytoxic effect between tumor cells, eliminating them

A

true

85
Q

Whats the escape phase? theres a balance…

A

between the immune system and the tumor system, so no advancement of the tumor but its not regressing

86
Q

What are the 3 stages of immunoediting (3 E’s)

A
  1. Elimination - tumor cells are cleared by immune system
  2. Equilibrium - driven by stron selective pressure from adaptive ar of the immune system, including T cells
  3. Escape - establishing a global immunosuppressive state
87
Q

T cells can be modulated by several factors (3)…

A
  1. T cell exhaustion
  2. Immune checkpoint
  3. Many cells have suppressive function
88
Q

Whats T cell exhaustion
A state in which T cells become … to antigens and are … at providing T cell help or eliminating appropriate target

A

A state in which T cells become less responsive to antigens and are ineffective at providing T cell help or eliminating appropriate target

89
Q

What immune checkpoint

A

Receptor-ligand interaction that suppresses the activity of T cells

90
Q

Whats the difference between cold and hot tumors
In “cold” tumors, there aren’t many … fighting the cancer, so treatments like … don’t work as well.

In “hot” tumors, there are more … fighting, so …can be more effective.

A

In “cold” tumors, there aren’t many immune cells fighting the cancer, so treatments like immunotherapy don’t work as well.

In “hot” tumors, there are more immune cells fighting, so immunotherapy can be more effective.

91
Q

Why would we want to target microenvironment instead of the cells? or in addition to the epithelial cells?

A

enhance immune responses, overcome treatment resistance, and hinder cancer spread by disrupting the supportive environment that helps cancer cells thrive

92
Q

Immunotherapy :
Improved or induces….

A

immunological surveillance recognition and destruction of cancer cells
modify or stimulate a patients immune system

93
Q

What are the different approached of immunotherapy

A

Adoptive cell transfer (ACT - uses patients own immune cells to fight cancer)
Checkpoint inhibitors
Monoclonal antibodies
Cancer vaccine
Cytokines

94
Q

Whats adoptive cell transfer
T cells are … to recognize specific markers, known as …, found on the surface of cancer cells. These … are often presented by … molecule. The engineered T cells are designed to better recognize these antigens when presented by MHC on the surface of cancer cells. This recognition allows the T cells to target and attack the cancer cells more effectively, enhancing the immune response against the cancer

A

T cells are engineered to recognize specific markers, known ast antigen, found on the surface of cancer cells. These antigens are often presented by MHC molecule. The engineered T cells are designed to better recognize these antigens when presented by MHC on the surface of cancer cells. This recognition allows the T cells to target and attack the cancer cells more effectively, enhancing the immune response against the cancer

95
Q

What the 2 immune checkpoint blockade inhibitors

A

CTLA-4 and PD1

96
Q

What does CTLA4 do? and anti-CTLA-4?

A

Inhibits T-cell activity by outcompeting costimulatory CD28 for CD80/86
Anti-CTLA-4, helps the immune system recognize and attack cancer cells

97
Q

What PD1 and anti-CPDL or anti-PDL1

A

PD1 (programme cell death 1) is a protein that regulate the immune reponse…
Anti-PD1 or anti-PDL1 block the PD1, helping the immune system attack cancer cells

98
Q

How do monoclonal antibodies work in cancer

A

markers differentially expressed between normal stem cells and leukemic stem cells

99
Q

One way to increase association between tumor cell and T cell

A

to use bispecific antibodies

100
Q

true or false: pancreatic cancer stem cells expresses low levels of EpCAM on the surface

A

False, HIGH levels

101
Q

MT110 is a bispecific antibody that recognized CD3 and EpCam and acts as…

A

a bridge to bring the T cell in direct contact with the tumor epithelial cell.

102
Q

Cancer cell vaccines are made by

A

taking tumor cell lysates with a variety of molecules, to stimulate the immune system against the cancer cells.

103
Q

Therapeutic potential of re-educating the stroma… works by

A

instead of eliminating the macrophages, we reprogram into an anti-tumorigenic.. resulting in a decrease in the tumor promoting functions

104
Q

What are some challenges for immunotherapy

A

immunotherapy is not effective on immune cold tumors like prostate, but theres new approaches to turn the cold into hot tumors

105
Q

What happens when you add cytotoxic drugs

A

Increase of apoptosis, so machrophages in the microenvironment are activated, and are going to consume the dead cells.

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