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SL32113 - Molecular Biology > Angiogenesis > Flashcards

Angiogenesis Flashcards

(66 cards)

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1
Q
A
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2
Q

What is a localised disease state?

A

A disease state where the tumour can be diagnosed in its primary location.

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3
Q

What is systemic disease?

A

A disease state where the tumour has spread beyond its primary location, making treatment harder.

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4
Q

What is angiogenesis?

A

The growth of new blood vessels sprouting from pre-existing vessels.

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5
Q

What is the role of blood vessels?

A

They bring oxygen and nutrients to cells while carrying away CO2 and cellular waste.

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6
Q

What is vasculogenesis?

A

The formation of vascular cells during embryogenesis, a tightly controlled process.

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7
Q

How does angiogenesis function in adults?

A

Limited angiogenesis occurs in adults compared to the programmed process during embryogenesis.

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8
Q

What happens after wounding in terms of angiogenesis?

A

There is a rapid outgrowth of sprouting vessels, tightly controlled even in wound healing.

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9
Q

In what conditions can angiogenesis be observed?

A

Angiogenesis can be observed in both physiological and pathological conditions.

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10
Q

What is tumour neoangiogenesis?

A

A process that is not programmed and depends on local signals, resulting in weak and leaky blood vessels.

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11
Q

How do tumours manipulate angiogenesis?

A

Tumours cause the outgrowth of new blood vessels to feed themselves by manipulating the angiogenesis system.

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12
Q

What is a challenge in chemotherapy delivery?

A

The blood vessels are very leaky, causing chemotherapeutic agents to leak into surrounding tissue.

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13
Q

What happens to a tumor as it grows?

A

It requires a blood supply because the cells in the center become hypoxic.

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14
Q

What is hypoxia in the context of tumors?

A

Hypoxia switches on a variety of genes and changes phenotypes, which is common in driving cell renewal.

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15
Q

What is the consequence of not delivering drugs to the tumor core?

A

We end up killing the outside of the tumor while the core remains unaffected.

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16
Q

What is found within the core of a tumor?

A

The core contains initiating stem cells that can drive tumor growth.

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17
Q

What happens after shrinking a tumor?

A

The tumor may start to grow again when it develops more blood vessels.

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18
Q

What causes the expression of VEGF?

A

Not enough oxygen (hypoxia)

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19
Q

What does VEGF stimulate?

A

It stimulates receptors causing the outgrowth of new vessels towards the tumour.

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20
Q

How do new vessels behave in relation to VEGF?

A

They move in an upwards concentration gradient towards the source of the VEGF.

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21
Q

What is the effect of new vessels wrapping around the tumour?

A

They provide the tumour with oxygen and nutrients.

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22
Q

What do new vessels bind to?

A

They bind to VEGFR on endothelial cells.

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23
Q

What is a characteristic of new vessels compared to normal blood vessels?

A

They don’t have the structure and regulation of normal blood vessels.

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24
Q

What is the structure of new vessels?

A

They have a disorganised vascular structure.

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25
What is the condition of inter-endothelial cell junctions in new vessels?
They have low inter-endothelial cell junctions, which are leaky.
26
What is the pericyte coverage like in new vessels?
They have low pericyte coverage.
27
What is the permeability of new microvasculature?
They have increased microvasculature permeability (leakiness).
28
What is the integrity of new vessels?
They are low integrity vessels and can collapse easily.
29
What happens if a new vessel breaks down?
The tumour will just grow another one.
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What is the balance in angiogenesis?
The balance of activators of angiogenesis and inhibitors.
32
What are endogenous inhibitors?
Endogenous inhibitors are normally slightly more prevalent than activators.
33
What happens when we get a wound regarding angiogenesis?
We upregulate our activators temporarily to switch on angiogenesis for growth, then switch it off again by upregulating more inhibitors.
34
What role do tumour suppressor proteins play in angiogenesis?
Tumour suppressor proteins upregulate anti-angiogenesis factors to suppress angiogenesis.
35
What occurs in cancers regarding p53 and angiogenesis?
In cancers, there is a downregulation (loss of function) of p53, which cannot downregulate the activators, leading to a surge of angiogenic activators.
36
What is the correlation between increased angiogenesis and patient prognosis?
Increased angiogenesis correlates to worse prognosis for the patient, as the tumour grows faster and there is an increased risk of spreading around the body.
37
What is Bevacizumab?
Bevacizumab (Avastin) is an anti-VEGFA antibody.
38
What is Ramucirumab?
Ramucirumab is an anti-VEGFR-2 antibody.
39
What is Aflibercept?
Aflibercept (Zaltrap) is a decoy receptor that binds to VEGF-A and VEGF-B.
40
What are Sorafenib and Sunitinib?
Sorafenib and Sunitinib are multi-kinase inhibitors.
41
What is the function of Thalidomide and its analogues?
Thalidomide and analogues inhibit phosphorylation of AKT, crucial for downstream signaling of various growth factors.
42
Why do they sample lymph nodes around a tumour?
They sample lymph nodes because if something breaks off from the main tumour mass, it might enter the bloodstream or drain into the lymphatics that pass through the lymph nodes.
43
What is the role of lymph nodes in relation to tumours?
Lymph nodes are where immune cells are located, and they can be a pathway for tumour cells to spread throughout the body.
44
How do tumour cells spread through the body?
Tumour cells can be carried around the body through the lymphatics once they enter this system.
45
Why do tumour cells tend to penetrate lymphatics easier?
Tumour cells tend to penetrate lymphatics easier, indicating that if they are located in the lymphatics, they may have already broken away from the localized area.
46
Describe the metastatic cascade
The metastatic cascade 1. Primary tumour growth (proliferation) 2. Angiogenesis 3. Detachment and invasion into the surrounding tissue towards the vessels and enter the blood vessels 4. Intravasation into lymphatics/ capillaries 5. Survival in the circulation 6. Arrest in new/ secondary organ (small capillaries, adhesion to vessel wall) 7. Extravasation into the secondary tissue 8. Establishment of microenvironment - death - dormant - proliferating
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Where do the majority of life-threatening cancers occur?
The great majority of life-threatening cancers occur in epithelial tissues.
49
What must carcinoma cells undergo to acquire motility and invasiveness?
Carcinoma cells must change their phenotype from a more epithelial to mesenchymal phenotype through EMT (epithelial to mesenchymal transition) in stem cells.
50
What are the characteristics of epithelial cells?
Epithelial cells have cytokeratin expression, adherence junctions (E-cadherin), epithelial cell polarization, and epithelial markers such as E-cadherin and b-catenin.
51
What are the characteristics of mesenchymal cells?
Mesenchymal cells have a fibroblast-like shape, increased motility and invasiveness, secretion of proteases (MMPs), and mesenchymal markers such as N-cadherin and vimentin.
52
What stimulates the transition from epithelial to mesenchymal phenotype?
The transition is stimulated by autocrine and paracrine signals from the tumor microenvironment (TME), e.g., TGF-beta.
53
What are the two types of macrophages in the tumour microenvironment?
M1 - proinflammatory, antitumour ## Footnote M2 - less inflammatory and very pro tumour
54
What is the desired activation of macrophages in cancer treatment?
Want to have lots of M1 activation - to reactivate our immune cells
55
What role do cancer-associated fibroblasts play in cancer progression?
They secrete factors that drive EMT, digest the extracellular matrix, and allow cancer cells to escape.
56
What are cancer cells?
Cells that can divide uncontrollably and have the potential to invade other tissues.
57
What are cancer stem cells?
A subset of cancer cells that have the ability to self-renew and drive tumorigenesis.
58
What is the role of myeloid-derived suppressor cells (MDSCs) in the pre-metastatic niche?
MDSCs prepare the pre-metastatic niche by promoting compatible adhesion molecules on endothelial cells, appropriate growth factors, ECM, selective chemotaxis, and physical features.
59
What happens to secondary tumors when the primary tumor is removed?
Sometimes the secondary tumor shrinks, but in other cases, it can do better.
60
What are MMPIs and their limitations?
MMPIs, like the 1st gen Marimastat, have poor efficacy, high toxicity, and lack specificity, though there is potential for alpha-MMP.
61
What is the purpose of MMPIs in targeting metastasis?
MMPIs aim to stop the digestion of the extracellular matrix to prevent migration into and out of blood vessels.
62
What is cabozantinib used for?
Cabozantinib is a VEGFR/MET inhibitor targeting the epithelial-mesenchymal transition (EMT) receptor.
63
What is the focus of targeting metastatic recolonization?
The focus is on dormant disseminated micrometastatic tumor cells (DTCs), which can be reactivated by fibrosis.
64
What is Pamrevlumab used for?
Pamrevlumab is being tested as an anti-fibrotic antibody to prevent reactivation of dormant DTCs.
65
How do metastases to bone affect RANKL?
Metastases to bone can upregulate RANKL, activating osteoclasts and causing bone resorption.
66
What is Denosumab?
Denosumab is an alpha-RANKL that targets bone resorption.

SL32113 - Molecular Biology (7 decks)

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