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CA Flashcards

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1
Q

What are the three types of genes that CA cells change?

A
  1. proto onco genes
  2. Tumor suppressor genes
  3. caretaker genes
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2
Q

What is the mutational function of protoonco genes?

A

Converted to oncogenes that increase cell division

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3
Q

What is the mutational function of Tumor suppressor genes?

A

Will not turn off cell growth

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4
Q

What is the mutational function of Caretaker genes?

A

Do not prevent/repair DNA mutations

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5
Q

What are the 6 traits that a cell must obtain in order to become metastatic CA?

A
  1. self sufficiency in growth
  2. Insensitivity to antigrowth signals
  3. Evading apoptosis
  4. Limitless replicative potential
  5. Sustained angiogenesis
  6. Tissue invasion and metastasis
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6
Q

True or false: conversion of a proto-onco gene to an oncogene changes the activity of the protein itself

A

False- only results in excess production of the protein, or disrupts the normal control of the proteins function

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7
Q

The receptor for epidermal growth factor, which is a tyrosine kinase, is called what?

A

ErbB1 or HER2

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8
Q

What type of cascade does EGF act through?

A

MAP kinase cascade

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9
Q

How does ErbB1 become mutated?

A

remove the signal receptor

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10
Q

How does HER2 become mutated?

A

Dimerization in the absence of ligand due to changes in the plasma membrane spanning portion

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11
Q

How is Ras mutated?

A

point changes in amino acids leads to constant activation

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12
Q

How are c-Fos and c-Myc mutated?

A

Stabilization

Normally they are unstable. DNA changes = stabilization

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13
Q

What is Burkitt’s lymphoma?

A

Increased in Myc activity

translocation of Myc from chromosome 8 to chromosome 14= incrased transcription

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14
Q

In general, are oncogenes on dominant alleles or recessive allele?

A

Dominant

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15
Q

In general, are tumor suppressor genes on dominant alleles or recessive allele?

A

Recessive

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16
Q

What needs to happen in the “two hit” model of CA proliferation in tumor suppressor gene for CA to develop?

A

Need one somatic mutation to develop CA cells

(Since tumor suppression genes are typically recessive genes, individuals can be carriers for mutant suppressor genes. Thus only a single allele needs to be mutated)

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17
Q

What is retinoblastoma?

A

CA caused by a mutation of the Rb protein gene, causing no Rb to be produced.

(note that this is a recessive allele in herditary form. Somatic form do not inherit any mutated allele.
Also, recall how Rb inhibits E2F)

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18
Q

What is the protein that associates with p53, makes it likely to be ubiquinated, and therefore likely to be degraded by proteosome?

A

Mdm2

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19
Q

What happens when p53 is phosphorylated by ATM or ATR? What molecule does p53 increase?

A

Stabilized

p21^CIP1

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20
Q

What is the most common genetic alteration in human CAs?

A

Mutations in p53

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21
Q

p53 is a homotetramer. How does this fact contribute to how mutations in the gene for p53 lead to cancer?

A

Makes it a dominant type of mutation

a mutation will lead to incorrect protein in all tetramers since they are all the same

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22
Q

What is Li-Fraumeni syndrome? What causes it?

A

Disease characterized by a propensity to develop a wide variety of tumors.
A mutation in the p53 allele.

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23
Q

HPV produces two proteins called what? What two proteins do they suppress?

A

E6 and E7

Both repress Rb, and p53

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24
Q

What causes neurofibromatosis?

A

Recessive gene mutation in NF1 that result in changes in neurofibromin

(neurofibromin functions to accelerate Ras hydrolysis–mutation= prolonged Ras)

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25
What is the protein involved in neurofibromatosis? Symptoms?
Neurofibromin | CA cells around neuronal sheaths
26
What is the cause of HBOC syndrome? Is this a recessive or dominant trait?
Mutation in BRCA1 and BRCA2 genes. | Dominant
27
What are the BRCA genes used for?
Encoding proteins that repair double stranded DNA breaks Also involved in E3 ubiuitin ligase
28
What are the two ways CA can develop from epigentic changes?
Silencing a gene (increased methylation) | Increasing the transcription of a gene (loss of methylation)
29
Why do cancer cells produce excess telomerases?
To avoid the inevitable breakage/fusion/bridge cycles that occur in somatic cells
30
What is the function of HIF-1aB?
An oxygen sensitive transcription factor that activates vascular endothelial growth facto (VEGF)
31
What is VEGF?
A protein stimulated by HIF-1aB that promotes the development of an angiogenic gradient, and thus new blood vessels
32
What is the signal for HIF-1aB to activate?
Hypoxia | Oxygen causes a P-hydroxylase to ubiquinate HIF-1AB
33
What is the function of E-adherin?
Hold epithelial cells together
34
What is the function of MMPs (matrix metalloproteases) in tumor cell metatasis?
Break down basement membrane holding the tumor cell down
35
What are the two chemical in the ECM that generate signals that stimulate the migration of tumor cells?
Collagen IV and laminin
36
What is the process by which tumor cells enter the circulation?
intravasation
37
What is extravasation?
The process by which tumor cells exit the bloodstream
38
What is FAP (familial adenomatous polypsis)?
Inherited condition where people develop thousands of adenomatous polyps in their colon.
39
If FAP is left untreated, what develops?
Colorectal carcinoma
40
What is the treatment for FAP?
Prophylactic colectomy
41
What gene is responsible for FAP?
APC-a tumor suppressor gene
42
The signal that APC regulates comes through what pathway?
WNT pathway
43
Which protein in the WNT pathway forms a "destruction complex" along with APC and other proteins to destroy itself when there is no WNT signals?
Beta-catenin
44
What is the function of beta-catenin?
increases the transcription of Myc and cyclin D
45
Is FAP a dominant or recessive disorder?
Recessive
46
What will happen if the second FAP allele is mutated?
Ras mutates to onconic Ras | p53 inactivation
47
How does the loss of APC lead to genomic mutations?
It plays a role in ensuring microtubles attach to the kinetichore of chromosomes
48
HNPCC is the result of a mutation in the DNA mismatch repair mechanism, leading to the formation of colorectal cancer. Which genes are mainly impacted?
MLH1 or MSH2
49
What is the function of the MSH2 protein?
Recognizes mismatches in DNA
50
What is the function of the MLH1 protein?
Repair DNA mismatch errors
51
What is microstaellite instability? What disease is it found in?
The propensity of microsatellite repeats to mutate | HNPCC
52
What is chronic myeloid leukemia?
CA that is the result of translocation of chromosomes 9 and 22.
53
The translocation of chromosomes 9 and 22 in chronic myeloid leukemia results in the fusion of what two genes? What protein does this combined gene produce?
BCR and ABL1 | a Bcr-Abl tyrosine kinase
54
What is the action of the Bcr-Abl tyrosine kinase in Chronic myeloid leukemia?
Phosphorylates many target cells, potentially stimulating cell division--particularly in WBCs
55
What is the philidelphia chromosome? What disease is it a part of?
Combination of chromosome 9 and 22 | Chronic myeloid leukemia
56
What are imatinib mesylate (Gleevec), dasatinib (Sprycel), and nilotinib (Tasigna) used for? What is their mechanism of action?
Used in chronic myeloid leukemia | Inhibits the activity of Bcr-Abl tyrosine kinase
57
What is the function of trastuzumab (Herceptin)?
It is a monoclonal antibody that inhibits HER2/Neu in breast CA
58
What happens to the ErbB1 to turn it into an onoprotein?
Loss of the ligand binding domain
59
What happens to the HER2 (Neu) receptor to turn it into an oncoprotein?
Dimerization
60
What is the change in c-Myc that makes it oncogenic?
More stable
61
What is the change in c-fos that makes it oncogenic?
More stable
62
What is the chromosomal change in Burkitt's lymphoma?
c-Myc gene is translocated from chromosome 8 to chromosome 14
63
Are oncogenes usually dominant or recessive genes?
Dominant
64
Are tumor suppressor genes usually dominant or recessive genes?
Recessive
65
What is the gene that encodes p53?
TP53

Enzymes (24 decks)

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