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NYCC Physiopathology > Molecular Biology of Neoplasias > Flashcards

Molecular Biology of Neoplasias Flashcards

1
Q

Most cells in the human body are in what phase of mitosis?

A

G0 (quiescent/not dividing)

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2
Q

What is the molecular etiology of neoplasia?

A

Genetic mutation

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3
Q

All gene mutations cause cancer (TRUE/FALSE)?

A

FALSE

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4
Q

What are genetic mutations?

A

Alterations in nuclear DNA sequences

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5
Q

Most mutations are repaired (TRUE/FALSE)?

A

TRUE

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6
Q

What non-repaired genes will give rise to neoplasia?

A

Genes that control cell growth, division, and differentiation

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7
Q

What are examples of DNA mutations?

A

Point mutations
Chromosomal translocation
Gene amplification

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8
Q

What is the minimum range of mutations that must occur for a cancer to manifest?

A

6-12 mutations

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9
Q

What is a DNA point mutation?

A

Changes in DNA affecting just one nucleotide causing a specific “base-pair” mismatch

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10
Q

What is chromosomal translocation?

A

When genetic material is swapped with another chromosome and genes are added or removed

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11
Q

What is gene amplification?

A

When a promoter sequence causes overexpression of growth factor genes or gene duplication occurs via virus infection

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12
Q

What are examples of environmental mutagens that can cause a genetic mutation?

A

Chemical carcinogens
Radiation
Dietary carcinogens
Tobacco smoke

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13
Q

What are the two primary examples of genetic mutations arising from normal cell metabolism?

A

Free radical-induced mutations
Spontaneous errors in DNA replication & repair

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14
Q

Neoplasms are the result of ____ genetic damage that is acquired or inherited?

A

Non-lethal

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15
Q

What normal regulatory genes are principal targets of genetic damage?

A

Proto-oncogenes (growth promoting genes)
Anti-oncogenes (growth inhibiting or cancer suppressor genes)
Genes regulating apoptosis
Genes regulating DNA repair

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16
Q

What is the “gas pedal” gene for mitosis?

A

Proto-oncogenes

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17
Q

What is the “brake pedal” gene for mitosis?

A

Anti-oncogenes

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18
Q

What are anti-oncogenes also known as?

A

Cancer suppressor or growth-inhibiting genes

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19
Q

oncogenes encode proteins called ____, which resemble normal products of ____

A

onco-proteins
proto-oncogenes

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20
Q

name 2 differences between onco-proteins and products of proto-oncogenes

A
  • onco-proteins do not have important regulatory functions
  • onco-protein production in transformed cell does not depend on growth factors or other external signals
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21
Q

If a prefix is given to a proto-oncogene it is considered oncogenic (TRUE/FALSE)?

A

TRUE

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22
Q

What does the prefix “V” indicate in front of a gene?

A

Viral mutation etiology

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23
Q

What does the prefix “C” indicate in front of a gene?

A

Cellular mutation etiology

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24
Q

What gene codes for platelet derived growth factor (PDGF)?

A

Sis

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25
Q

What are examples of genes that code for receptors?

A

Ret
Erb
Her2/neu

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26
Q

What gene codes for the estrogen receptor?

A

Her2/neu

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27
Q

What is an example of a gene that codes for G proteins?

A

Ras

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28
Q

What do G proteins require for movement?

A

GTP

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29
Q

What proteins trigger mitosis?

A

Nuclear regulatory proteins

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30
Q

What are examples of genes that code for nuclear regulatory proteins?

A

Myc
Jun
Fos

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31
Q

Mutation of proto-oncogenes all have different effects based on what is mutated (TRUE/FALSE)?

A

FALSE (result in cell division)

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32
Q

What are oncogenes?

A

Mutations of naturally occurring proto-oncogenes that promote neoplastic growth

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33
Q

What are Proto-oncogenes?

A

Cellular genes that promote normal growth and differentiation and are the gas pedal for mitosis

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34
Q

Name 4 classes of oncogenes

A

Growth factors
Growth factor receptors
Signal transduction proteins
Nuclear regulatory proteins

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35
Q

What results from mutations of genes that code for growth factors?

A

renders protein products oncogenic either by overexpression or increased binding capacity

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36
Q

what are growth factor receptors? what does normal receptor binding by growth factor result in?

A
  • transmembrane proteins with an external ligand binding domain & a cytoplasmic tyrosine kinase domain
  • results in transient activation of tyrosine kinase activity = transient second messenger activity
37
Q

how do oncogenic growth factor receptors differ from normal?

A

over-expressed or demonstrate persistent activation of enzyme activity = continuous mitogenic signals to cell

38
Q

name 3 examples of oncogenic growth factor receptors

A

ret
erb
Her2/neu

39
Q

What will mutation of the ret gene result in?

A

Continuous activation of growth factor receptors not requiring a binding to trigger

40
Q

What will mutation of the erb gene result in?

A

Overexpression of growth factor receptors (more receptors)

41
Q

What will mutation of the Her2/neu gene result in?

A
  • Overactivation of estrogen receptors
  • increased sensitivity
42
Q

What proto-oncogene is chiefly mutated in breast adenocarcinoma?

A

Her2/neu

43
Q

name an example of membrane associated signal transduction proteins

A

ras (G-protein family)

44
Q

how does a ras mutation contribute to neoplasia?

A

maintains ras protein in activated state

45
Q

What are nuclear regulatory proteins?

A

Proteins localized in the nucleus of a cell which bind to DNA and activate transcription of proto-oncogenes

46
Q

What is the “One-Hit hypothesis”?

A

Theory that proto-oncogenes only need to mutate one of their two copies to get an oncogenic effect

47
Q

What are the two primary functions of anti-oncogenes (tumor suppressor genes)?

A

Cell cycle arrest and DNA repair

48
Q

What is the “Two-Hit hypothesis”?

A

Theory that anti-oncogenes require mutations of both alleles in order to get an oncogenic effect

49
Q

Proto-oncogene mutation obeys the (One hit/Two hit) hypothesis?

A

One hit

50
Q

Anti-oncogene mutation obeys the (One hit/Two hit) hypothesis?

A

Two hit

51
Q

At what step(s) of signal transduction can a mutation occur?

A

any step

52
Q

What are examples of common tumor suppressor genes?

A

RB
P53
BRCA1
BRCA2
NFx
WTx
DCC
APC

53
Q

What gene is often mutated in retinoblastoma and osteosarcoma presentations?

A

RB

54
Q

What was the first tumor suppressor gene discovered?

A

RB

55
Q

What tumor suppressor gene is most commonly mutated in most cancer presentations?

A

P53

56
Q

How many copies of P53 are in the human body?

A

Two

57
Q

What is Li Fraumeni Syndrome?

A

Congenital loss of both P53 genes leading to spontaneous tumor production throughout the body

58
Q

What tumor suppressor gene is commonly mutated in breast carcinoma?

A

BRCA

59
Q

What does the NFx gene stand for?

A

Neurofibromatosis

60
Q

What are the primary symptoms of neurofibromatosis?

A

‘Cafe au lait’ spotting on the body
Large kyphoscoliosis
Fibroid tumors throughout the body

61
Q

Patient presents with thoracic back pain. A large kyphosis is visualized. Radiograph shows severe kyphoscoliosis and numerous fibroids throughout the body. The patient complained recently of numerous “spots” on their body? What is the likely diagnosis? What gene has likely undergone a mutation?

A
  • Neurofibromatosis
  • mutation of NFx gene
62
Q

What does the gene WTx stand for?

A

Wilm’s tumor

63
Q

What is a Wilm’s tumor?

A

Tumor caused by pediatric kidney carcinoma (childhood nephroblastoma) bilaterally from a WTx gene mutation

64
Q

What does the gene DCC stand for?

A

Deleted in colon carcinoma

65
Q

What tumor suppressor gene is the exception to the two hit hypothesis? Why?

A

APC because both copies of the gene must be fully functional for full defense to occur
(only need to mutate one copy)

66
Q

What will the mutation of one of the two APC genes often present as?

A

Solitary polyps in the area of the mutated gene on the colon

67
Q

What condition will result from an APC gene mutation?

A

Adenomatous polyposis coli

68
Q

What is a somatic mutation?

A
  • Mutation during cell division that has occurred after conception
  • disease process presents later in life
69
Q

What is a germline mutation?

A
  • Mutation during cell division that has occurred prior to conception in the gamete stages
  • disease process presents earlier in life
70
Q

when does manifestation of inherited retinoblastoma occur?

A

childhood

71
Q

when does manifestation of sporatic retinoblastoma occur?

A

adulthood/older

72
Q

Inherited neoplasms involve a germline mutation and then a somatic mutation (TRUE/FALSE)?

A

TRUE

73
Q

Sporadic neoplasms involve two somatic mutations (TRUE/FALSE)?

A

TRUE

74
Q

What occurs at the chromosomal level in a patient with inherited retinoblastoma?

A

Germline mutation of chromosome 13 followed by a somatic mutation

75
Q

What occurs at the chromosomal level in a patient with sporadic retinoblastoma?

A

One somatic mutation followed by another somatic mutation

76
Q

P53 assists in DNA repair by causing ____ and ____?

A

Cell cycle (G1) arrest, inducing DNA repair genes

77
Q

what happens when there is homozygous loss of p53?

A
  • DNA damage goes un-repaired
  • mutations become permanent in dividing cells (free to acquire mutations without repair)
78
Q

What are examples of genes that regulate apoptosis?

A

Bcl-2
Bax

79
Q

What is an example of an anti-apoptotic gene?

A

Bcl-2

80
Q

What is an example of a pro-apoptotic gene?

A

Bax

81
Q

What gene is triggered by p53 when genes are not repairable?

A

Bax

82
Q

What gene is often overexpressed in a patient with malignant lymphoma?

A

Bcl-2

83
Q

What gene is activated in higher amounts with infectious mononucleosis?

A

Bcl-2

84
Q

What gene causes apoptosis directly?

A

Bax

85
Q

What gene opposes apoptosis directly?

A

Bcl-2

86
Q

deletion of the bax gene can lead to ____

A

malignancy
(can’t do apoptosis, mutated cells survive)

87
Q

What is telomerase?

A

An enzyme which prevents chromosome shortening by adding nucleotides

88
Q

what is the reason for the eventual fate of cell death in somatic cells?

A

somatic cells lack telemorase

NYCC Physiopathology (28 decks)

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