Lecture 38 Genetics of Cancer oncogenes and Tumor Suppressors Flashcards

1
Q

What does chromosomal translocation lead to?

A
  • production of protein product that shouldn’t exist
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2
Q

What is a chronic mylogenous leukemia?

A
  • bone marrow produces excessive amounts of abnormal granulocytes at the expense of other healthy white blood cells.
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3
Q

Why was Philadelphia chromosome named as such?

A
  • because it was discovered in a Philadelphia lab
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4
Q

When we extract DNA from blood where do we get it from?

A
  • white blood cells because RBC’s don’t have a nucleus
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5
Q

Is a single mutation enough to cause cancer?

A
  • no you need a second hit
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6
Q

Is cancer or tumor formation somatic?

A
  • yes it is a somatic event involving other mutations and environmental factors
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7
Q

Do most inherited mutations associated with cancer affect a persons risk for developing cancer?

A
  • Yes
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8
Q

Does tumor growth start with multiple cells?

A
  • no it starts with a single cell
  • tumor growth and progression generally involves multiple, successive rounds of genetic changes with the end result of natural selection of a clonal cell that produces a tumor or cancer
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9
Q

Do tumors only arise from an increase in cell division?

A
  • no they can arise from decreased cell apoptosis
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10
Q

Can you develop a tumor while having normal cell division?

A
  • yes if the cell is not having normal apoptosis
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11
Q

A tumor resulting from genetic gene inactivation would come from?

A
  • a nucleotide change
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12
Q

What is an epigenetic change that leads to tumors?

A
  • a change outside of DNA sequence that regulates the gene

- such as an inhibitor being eleminated

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13
Q

Do common variants of a single nucleotide have a high risk of cancer?

A
  • no they have a low risk
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14
Q

Do mutations in the BRCA1/BRCA2 that are rare variants and high penetrance increase risk of cancer?

A
  • yes
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15
Q

What type of cancer has BRCA1/BRCA2 been linked to?

A
  • many types
  • breast
  • ovarian
  • lymphatic
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16
Q

What are malignant tumors classified by?

A
  • their cell type from which they originated
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17
Q

Carcinomas come from what type of tissue?

A
  • epithelial cells
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18
Q

Sarcomas arise from what type of tissue?

A
  • connective tissue or muscle cells
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19
Q

Leukemia’s derive from ___ blood cells and their precursors?

A
  • white blood cells
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20
Q

What are the precursors of white blood cells?

A
  • hematopoietic cells
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21
Q

Where do lymphomas derive from?

A
  • lymphatic tissue
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22
Q

Where do gliomas derive from?

A
  • glial cells in the CNS
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23
Q

What are adenomas?

A
  • benign epithelial tumors with glandular organization
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24
Q

What are chondromas?

A
  • benign tumors that arise from cartilage
25
Q

What is a characteristic of benign tumors?

A
  • they are contained within the tissue where they originated
26
Q

How can you differenciate a malignant tumor from a benign?

A
  • a malignant tumor develops invasiveness and can grow to distal sites outside of the tissue where it originated from
27
Q

Is a high grade intraepithelial neoplasia benign or malignant?

A
  • it is still considered benign because it has not escaped the original tissue
28
Q

What type of cancer can tobacco lead to?

A
  • lung, kidney and bladder
29
Q

What type of cancer can a diet low in vegetables and high in salt lead to?

A
  • stomach

- esophagous

30
Q

What type of cancer can a high fat low fiber, fried and broiled food diet lead to?

A
  • bowel
  • pancreas
  • prostate
  • breast
31
Q

What can alcohol and tobacco lead to?

A
  • throat and mouth cancer
32
Q

Why do chemotherapy and other cancer treatment target stem cells?

A
  • because stem cells grow very slow but they produce progeny that produce tumors
  • chemo is trying to eliminate stem cells
33
Q

What do mutations to a transit amplifying cell or normal cell lead to?

A
  • a malignant cancer stem cell that continues to grow and produce other cancer cells
34
Q

Can tumors live without a blood supply?

A
  • no they need angiogenesis to grow and that is why they produce VEGF
  • they are very self sufficient
35
Q

Do external anti proliferative signals effect cancer cells?

A
  • no they are resistant to anti growth signals
36
Q

Are cancer cells prone to apoptosis?

A
  • no they dont die
37
Q

Do cancer cells use the same regulator mechanisms of normal cells?

A
  • no thats why they grow so quickly and uncontrolled
38
Q

Are cancer cells genetically stable?

A
  • no they are very unstable because they dont use normal regulatory mechanisms
  • will produce new cells despite environment or DNA damage
39
Q

What are the main classifications of cancer genes?

A
  • genes that normally inhibit cellular proliferation
  • genes that activate proliferation
  • genes that participate in DNA repair
40
Q

what are oncogenes?

A
  • they are mutated forms of certain normal genes called pro-oncogenes
  • oncogenes continue to divide
41
Q

What are tumor suppressor genes?

A
  • these are genes that slow down cell division, repair DNA mistakes, or tell cells when to die
  • mutations in these genes leads to uncontrolled growth
42
Q

What is an important distinction between oncogenes and tumor suppressor genes?

A
  • oncogenes are turned on and continuously divide

- tumor suppressor genes are turned off and can no longer inhibit growth

43
Q

What was alfred knudsons original hypothesis?

A
  • that a person needed to acquire two mutant copies of the Rb gene
44
Q

How would somone acquire two copies of the mutant gene?

A
  • one germline mutation inherited from one parent and then a somatic second mutation/event in the normal allele
45
Q

What is the normal Rb protein function?

A
  • to put a break on the cell cycle progession
46
Q

What is inherited from parents with a mutant allele?

A
  • a strong predisposition to develop a tumor
47
Q

How does p16 function?

A
  • binds to Cdk 4 and inhibits cyclin D from binding
48
Q

When does p16 decide to bind to the cdk complex and stop cell proliferation?

A
  • when there is stress in the cellular environment
49
Q

What are factors that halt cell division and stimulate p53?

A
  • hyperproliferative signals
  • DNA damage
  • Telomere shortening
  • Hypoxia
50
Q

What does p53 do when it is function correctly?

A
  • cell cycle arrest
  • senescence
  • apoptosis
  • all these things prevent further cell production
51
Q

What does a mutation in the apc and Wnt b catenin pathway lead to?

A
  • unligand activated signaling which leads to colon cancer
52
Q

What is Wnt?

A
  • wnt is a ligant that binds to a membrane receptor and induces cell signaling
53
Q

Are virus genomes found in the form of DNA or RNA?

A
  • both
54
Q

Are virus genomes double stranded or single?

A
  • both
55
Q

Are virus genomes linear or circular?

A
  • both
56
Q

How many human cancers develop from virus genomes?

A
  • 15%
57
Q

What was the first viral oncogene identified?

A
  • Avian Rous Sarcoma Virus (RSV)
58
Q

What are the mutations usually found in when dealing with RNA viruses?

A
  • oncogenes/protoncogenes

- mitotic signal transduction pathways

59
Q

What mutations do DNA tumor viruses normally have?

A
  • mutations in tumor suppressor genes that affect cell cycle regulation