Exam 2: Chapter 10 Angiogenesis and Metastasis Flashcards

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1
Q

Describe Angiogenesis.

A

It is the process where new blood vessels for from old ones.

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2
Q

Why is Angiogenesis a hallmark for cancer?

A

Tumors can only get bigger and spread by recruiting their own blood supply.

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3
Q

What are the 3 mechanisms that can trigger angiogenesis?

A
  1. Response to hypoxia
  2. Mutations in tumor suppressor gene (VHL) that regulates the hypoxia response
  3. Inflammation ( Wound Healing)
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4
Q

How does Angiogenesis occur?

A

Blood vessels are made of endothelial cells, new blood vessels are made as outgrowths from pre-existing vessels by cell division and migration.

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5
Q

What is HIF-1

A

It is a transcription factor that becomes activated when cells experience hypoxia.

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6
Q

What is VEGF?

A

It is the most potent angiogenic factor that is secreted by hypoxic cells.

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7
Q

What is VHL?

A

A tumor suppressor gene.

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8
Q

Why does a mutation in VHL cause cancer?

A

Loss of function means that it cant bind to HIF-1 so it remains permanently active and stimulates VEGF leading to increased cellular division and angiogenesis.

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9
Q

Describe Metastasis?

A

Cancer cells break free from the original tissue and then they penetrate surrounding tissues and enter the blood and lymph nodes.

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10
Q

What are Metalloproteinases?

A

Proteases that break up the extracellular matrix proteins that degrade the basal membrane and make space for the new blood vessel to form

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11
Q

Why do patients with primary colon cancer most frequently exhibit secondary tumors in the liver, whereas patients with primary kidney cancer most frequently exhibit secondary tumors in the lung.

A

The direct blood flow from the colon goes straight to the liver, while the blood flow from the kidney goes through the heart, directly connecting to the lungs. However, lung cancers can metastasize anywhere in the body.

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12
Q

Give one example of how EMT might make the treatment of cancer harder than expected, rather than easier

A

EMT is normally used in embryogenesis and wound healing. caner won’t need new mutations can just activate under the guise apart of the wound healing program. This will occur earlier than tumor progression is thought to be.

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13
Q

The EMT involves many molecular changes caused by a switch from epithelial to mesenchymal gene expression. Explain the significance of one molecular change by referring to a type of molecule or cell structure.

A

The receptor of HGF is called MET. These growth factors are also called scatter factor because it causes epithelial cells to become mobile and scatter. A key factor in the switch from EMT to MET if the loss of an epithelial cell to cell adhesion.

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14
Q

What is the new model of Metastasis?

A

Cancer cells reactivate a program of gene expression called EMT that is normally used in embryogenesis and wound healing

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15
Q

What are the triggers that activate EMT in caner cells?

A
  1. Wound healing response
  2. Growth factors like HGF and SF cause epithelial cells to become mobile and scatter
  3. Loss of an epithelial cell-cell adhesion molecule
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