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CA Flashcards

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
Q

What is the protein involved in neurofibromatosis? Symptoms?

A

Neurofibromin

CA cells around neuronal sheaths

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26
Q

What is the cause of HBOC syndrome? Is this a recessive or dominant trait?

A

Mutation in BRCA1 and BRCA2 genes.

Dominant

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27
Q

What are the BRCA genes used for?

A

Encoding proteins that repair double stranded DNA breaks

Also involved in E3 ubiuitin ligase

28
Q

What are the two ways CA can develop from epigentic changes?

A

Silencing a gene (increased methylation)

Increasing the transcription of a gene (loss of methylation)

29
Q

Why do cancer cells produce excess telomerases?

A

To avoid the inevitable breakage/fusion/bridge cycles that occur in somatic cells

30
Q

What is the function of HIF-1aB?

A

An oxygen sensitive transcription factor that activates vascular endothelial growth facto (VEGF)

31
Q

What is VEGF?

A

A protein stimulated by HIF-1aB that promotes the development of an angiogenic gradient, and thus new blood vessels

32
Q

What is the signal for HIF-1aB to activate?

A

Hypoxia

Oxygen causes a P-hydroxylase to ubiquinate HIF-1AB

33
Q

What is the function of E-adherin?

A

Hold epithelial cells together

34
Q

What is the function of MMPs (matrix metalloproteases) in tumor cell metatasis?

A

Break down basement membrane holding the tumor cell down

35
Q

What are the two chemical in the ECM that generate signals that stimulate the migration of tumor cells?

A

Collagen IV and laminin

36
Q

What is the process by which tumor cells enter the circulation?

A

intravasation

37
Q

What is extravasation?

A

The process by which tumor cells exit the bloodstream

38
Q

What is FAP (familial adenomatous polypsis)?

A

Inherited condition where people develop thousands of adenomatous polyps in their colon.

39
Q

If FAP is left untreated, what develops?

A

Colorectal carcinoma

40
Q

What is the treatment for FAP?

A

Prophylactic colectomy

41
Q

What gene is responsible for FAP?

A

APC-a tumor suppressor gene

42
Q

The signal that APC regulates comes through what pathway?

A

WNT pathway

43
Q

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?

A

Beta-catenin

44
Q

What is the function of beta-catenin?

A

increases the transcription of Myc and cyclin D

45
Q

Is FAP a dominant or recessive disorder?

46
Q

What will happen if the second FAP allele is mutated?

A

Ras mutates to onconic Ras

p53 inactivation

47
Q

How does the loss of APC lead to genomic mutations?

A

It plays a role in ensuring microtubles attach to the kinetichore of chromosomes

48
Q

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?

A

MLH1 or MSH2

49
Q

What is the function of the MSH2 protein?

A

Recognizes mismatches in DNA

50
Q

What is the function of the MLH1 protein?

A

Repair DNA mismatch errors

51
Q

What is microstaellite instability? What disease is it found in?

A

The propensity of microsatellite repeats to mutate

HNPCC

52
Q

What is chronic myeloid leukemia?

A

CA that is the result of translocation of chromosomes 9 and 22.

53
Q

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?

A

BCR and ABL1

a Bcr-Abl tyrosine kinase

54
Q

What is the action of the Bcr-Abl tyrosine kinase in Chronic myeloid leukemia?

A

Phosphorylates many target cells, potentially stimulating cell division–particularly in WBCs

55
Q

What is the philidelphia chromosome? What disease is it a part of?

A

Combination of chromosome 9 and 22

Chronic myeloid leukemia

56
Q

What are imatinib mesylate (Gleevec), dasatinib (Sprycel), and nilotinib (Tasigna) used for? What is their mechanism of action?

A

Used in chronic myeloid leukemia

Inhibits the activity of Bcr-Abl tyrosine kinase

57
Q

What is the function of trastuzumab (Herceptin)?

A

It is a monoclonal antibody that inhibits HER2/Neu in breast CA

58
Q

What happens to the ErbB1 to turn it into an onoprotein?

A

Loss of the ligand binding domain

59
Q

What happens to the HER2 (Neu) receptor to turn it into an oncoprotein?

A

Dimerization

60
Q

What is the change in c-Myc that makes it oncogenic?

A

More stable

61
Q

What is the change in c-fos that makes it oncogenic?

A

More stable

62
Q

What is the chromosomal change in Burkitt’s lymphoma?

A

c-Myc gene is translocated from chromosome 8 to chromosome 14

63
Q

Are oncogenes usually dominant or recessive genes?

64
Q

Are tumor suppressor genes usually dominant or recessive genes?

65
Q

What is the gene that encodes p53?

Enzymes (24 decks)

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