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BMS > Cancer > Flashcards

Cancer Flashcards

1
Q

A disease in which a single cell escapes normal control over growth and division, and proliferates without limit

A

Cancer

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2
Q

Any abnormal new growth of cells

-Can compete with normal cells for nutrients

A

Tumor or Neoplasm

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3
Q

Tumors (neoplasms) can be either

A

Benign or Malignant

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4
Q

Non-cancerous tumor. It is localized and does not spread

-can cause secondary problems

A

Benign tumor

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5
Q

Cancerous tumors that resist treatmens, can spread to other parts of the body, and may recur after removal

A

Malignant Tumor

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6
Q

Most cancer-causing mutations are

-occur post fertilization

A

Somatic

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7
Q

Mutagens are mostly environmental. The most important are

A

Smoking and Viral infections

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8
Q

What are two common viral causes of cancer, which are responsible for 30-50% of worldwide cancer cases?

A

Human papilloma and Hepatitis B and C

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9
Q

Multiple mutations are required to cause

A

Cancer

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10
Q

Typically about a dozen signal-transduction pathways are altered in a

A

Tumor cell

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11
Q

Lose the ability to respond to ECM and neighboring cell signals

A

Cancer cells

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12
Q

Normal cells will cease division when they come into contact with neighboring cells. This is called

A

Contact inhibition

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13
Q

Normal cells do not survive or divide in the absence of signals from the

A

Extracellular matrix

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14
Q

Are immune to contact inhibition

A

Cancer cells

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15
Q

In cancer cells, detachment from other cells and invasion of neighboring tissue is promoted by

A

Loss of cadherins

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16
Q

Not dependent on signals from the ECM for cell division

A

Cancer cells

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17
Q

Cancer cells secrete metalloproteases that degrade the ECM and facilitate

A

Tissue invasion

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18
Q

Mutations in which three classes of genes underlie most cancers?

A
  1. ) Caretaker genes
  2. ) Gatekeeper genes
  3. ) Oncogenes
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19
Q

Its products prevent or repair damage to DNA

A

Caretaker genes

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20
Q

Is not oncogenic itself, but promotes further genetic change/increases chance

A

Loss of caretaker protein function

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21
Q

Its products restrain cell division or induce apoptosis if cells initiate division when they should not

A

Gatekeeper genes

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22
Q

Loss of gatekeeper protein allows

A

Uncontrolled proliferation

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23
Q

Its products promote cell growth and division

A

Oncogenes

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24
Q

Mutations in these genes do not inactivate their proteins, but cause loss of normal control, so that continuous activity drives cell division

A

Oncogenes

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25
Q

Were discovered as genes mutated in inherited cancer syndromes (e.g. Ptc1 in medulloblastoma)

A

Tumor suppressor genes

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26
Q

Loss-of-function mutations inactivate

A

Tumor suppressor protein

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27
Q

Are recessive, meaning both functional copies must be lost to cause a cell to become cancerous

A

Tumor suppressor genes

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28
Q

In pedigrees, tumor suppressor gene mutations appear

A

Dominant (even though they are actually recessive)

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29
Q

Caretaker genes prevent or repair DNA damage, what are three examples?

A
  1. ) MLH
  2. ) ERCC1
  3. ) BRCA-1/2
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30
Q

Gatekeeper genes restrict cell division. What are the two most important?

A
  1. ) Rb

2. ) p53

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31
Q

Inhibits the G1/S transition by inhibiting E2F

A

Rb

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32
Q

Halts cell division or initiates apoptosis in response to DNA damage or other stress

A

p53

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33
Q

Mutations in caretaker genes cause

A

Familial cancer syndromes

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34
Q

Mutations in MLH cause lynch syndrome which is associated with defects in which repair pathway?

A

Mismatch repair

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35
Q

Mutations in ERCC1 result in Xeroderma pigmentosum. This is associated with defects in which repair pathway?

A

NER

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36
Q

Mutations in BRCA-1/2 result in familial breast/ovarian cancer. This is associated with defects in which repair pathway?

A

Double-strand break repair

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37
Q

Loss of function mutations in Rb cause retinoblastoma. What are the two forms of the disease?

A
  1. ) Sporadic retinoblastoma

2) Familial (inherited) retinoblastoma

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38
Q

Single tumors in one eye of one person in a family

A

Sporadic retinoblastoma

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39
Q

Tumors are often bilateral and often multiple family members are affected

A

Familial retinoblastoma

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40
Q

Which occurs at a younger age on average, familial or sporadic retinoblastoma?

41
Q

In retinoblastoma, the tumor replaces the retina. As a result, the pupil appears

42
Q

Follow the curve expected if two events are required for tumor formation

A

Unilateral Rb tumors

43
Q

Follow the curve expected if only one event is required for tumor formation

A

Bi-lateral Rb tumors

44
Q

How many mutations are required to acquire sporadic Rb?

A

Two (because it is a recessive disease)

45
Q

How many mutations are required to acquire familial Rb?

46
Q

If one defective copy of a tumor suppressor gene is inherited, it is likely that the second copy will be inactivated. This is called

A

Loss of Heterozygosity (LOH)

47
Q

Loss of p53 renders cancer cells immune to

48
Q

The most commonly mutated protein in human cancers

49
Q

p53 stimulates transcription of

A
  1. ) Cdk inhibitors

2. ) pro-apoptotic proteins

50
Q

Intrinsically unstable, but is stabilized in response to DNA damage

51
Q

p14ARF (ARF = alternate reading frame) stabilizes

52
Q

p53 is stabilized by ARF and destabilized by

53
Q

ARF binds MDM2 and frees p53. Thus, as far as cell death is concerned, ARF is considered to be

A

Pro-apoptotic

54
Q

Cell stress activates a p53 modification that blocks

A

MDM2 binding

55
Q

In un-stressed cells, p53 is destroyed by

  • a ubiquitin ligase
  • anti-apoptotic
56
Q

p53 has no defined tertiary structure unless it is bound to

57
Q

Destabilize p53’s DNA binding domain, blocking its apoptotic activity

A

Oncogenic mutations

58
Q

A gene that can cause cancer when activated or expressed

59
Q

A normal gene that can turn into an oncogene as a result of mutations or increased expression

A

Proto-oncogene

60
Q

Discovered in retroviruses, which insert a DNA copy of its genome into host-cell DNA

61
Q

Viral oncogenes are originally derived from the genome of the

62
Q

Lead to continuous (constitutive) activity of the protein, unaffected by normal regulatory mutations

-gain of function mutations

A

Oncogenic mutations

63
Q

Gain-of-function mutations show which type of heredity?

64
Q

Family of tyrosine kinase proteins with SH2 domains that transduce signaling through various Protein Kinase receptors

A

Src (c-Src is a proto-oncogene)

65
Q

NF1 (a ras-GAP), Cdk inhibitor, and Rb are all considered to be

A

Tumor suppressor proteins

66
Q

The mTOR pathway is frequently mutated in

67
Q

Promotes cell growth downstream of growth-factors

-a proto-oncogene

A

mTOR pathway

68
Q

What is the kinase that converts PIP2 to PIP3?

69
Q

What is the phosphatase that converts PIP3 back to PIP2

70
Q

A protein kinase activated in the presence of PIP3 that phosphorylates and inhibits TSC

71
Q

An inhibitor of mTOR

-mutations cause tuberous sclerosis in CNS, kidney, heart, and lung

72
Q

A protein kinase that phosphorylates multiple targets to promote protein synthesis and cell growth

73
Q

What are three examples of activation of oncogenes?

A
  1. ) c-myc
  2. ) c-abl
  3. ) c-ras
74
Q

Promotes expression of about 15% of human genes

-Activated by overproduction

75
Q

Genetic change allows self-activation so normal regulatory stimuli are no longer required

76
Q

Mutations prevent inactivtion

77
Q

In some tumors, the number of gene copies of c-myc is

A

Increased (gene amplification)

78
Q

Increase expression of c-myc can also be the result of a

A

Chromosomal translocation

79
Q

If copies of c-myc remain in the chromosome, they form a

-whole chromosome glows in FISH

A

Homogenously-staining region (HSR)

80
Q

In c-myc amplification, the c-myc genes may also be found outside of the chromosome in tiny

A

double-minute chromosomes

81
Q

When chromosomes break and rejoin crosswise

A

Translocation

82
Q

Alterson transcriptional control of c-myc by placing the gene under the control of a powerful promoter

A

Translocation of c-myc

83
Q

A tumor of B lymphocytes that results from c-myc activation

A

Burkitt Lymphoma

84
Q

In Burkitt lymphoma, the transcription of antibody genes is driven by powerful

A

B-cell enhancers

85
Q

When translocations put c-myc under control of an antibodygene enhancer and the c-myc gene is transcribed at many times the normal rate

A

Burkitt Lymphoma

86
Q

Results from a a translocation which results in constitutive activity of the protein kinase c-abl

A

Chronic Myelogenous leukemia (CML)

87
Q

The karyotype of Chronic Myelogenous leukemia (CML) shows a chromosome known as the

A

“Philadelphia Chromosome”

88
Q

In CML, there is a reciprocal translocation between

-results in 1 large chromosome and 1 “Philadelphia chromosome”

A

Chr9 and Chr22

89
Q

One of the most frequently altered proteins in human tumors

90
Q

Binds guanine nucleotides

  • Active when GTP is bound
  • Inactive when GDP is bound
91
Q

Ras has slow intrinsic GTPase activity that is stimulated by

92
Q

A ras-GAP in which mutations result in neurofibromatosis (tumors of peripheral nerves)

A

NF1 protein

93
Q

What are 4 examples of proteins containing ras homology domain?

A
  1. ) Translation factors
  2. ) Large G-proteins
  3. ) Dynamins
  4. ) Myosin and Kinesin
94
Q

Translation factors such as the aminoacyl-tRNA binding to ribosomes and the translocation of peptidyl-tRNA contain

A

Ras homology

95
Q

Transduce signals from 7-α-helix receptors

A

Large G-proteins

96
Q

Proteins that function in the budding of membrane vesicles

97
Q

Most oncogenic mutations in Ras are amino acid substitutions at which two positions?

A

gly-12/13 and gln-61

98
Q

If mutations in many genes are required to initiate cancer, how can a single drug with presumably a single cellular target block cancer progression?

A

“oncogene addiction” i.e. some tumors come to rely on one dominant oncogene, which can then be targeted by drugs

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