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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
Were discovered as genes mutated in inherited cancer syndromes (e.g. Ptc1 in medulloblastoma)
Tumor suppressor genes
26
Loss-of-function mutations inactivate
Tumor suppressor protein
27
Are recessive, meaning both functional copies must be lost to cause a cell to become cancerous
Tumor suppressor genes
28
In pedigrees, tumor suppressor gene mutations appear
Dominant (even though they are actually recessive)
29
Caretaker genes prevent or repair DNA damage, what are three examples?
1. ) MLH 2. ) ERCC1 3. ) BRCA-1/2
30
Gatekeeper genes restrict cell division. What are the two most important?
1. ) Rb | 2. ) p53
31
Inhibits the G1/S transition by inhibiting E2F
Rb
32
Halts cell division or initiates apoptosis in response to DNA damage or other stress
p53
33
Mutations in caretaker genes cause
Familial cancer syndromes
34
Mutations in MLH cause lynch syndrome which is associated with defects in which repair pathway?
Mismatch repair
35
Mutations in ERCC1 result in Xeroderma pigmentosum. This is associated with defects in which repair pathway?
NER
36
Mutations in BRCA-1/2 result in familial breast/ovarian cancer. This is associated with defects in which repair pathway?
Double-strand break repair
37
Loss of function mutations in Rb cause retinoblastoma. What are the two forms of the disease?
1. ) Sporadic retinoblastoma | 2) Familial (inherited) retinoblastoma
38
Single tumors in one eye of one person in a family
Sporadic retinoblastoma
39
Tumors are often bilateral and often multiple family members are affected
Familial retinoblastoma
40
Which occurs at a younger age on average, familial or sporadic retinoblastoma?
Familial
41
In retinoblastoma, the tumor replaces the retina. As a result, the pupil appears
White
42
Follow the curve expected if two events are required for tumor formation
Unilateral Rb tumors
43
Follow the curve expected if only one event is required for tumor formation
Bi-lateral Rb tumors
44
How many mutations are required to acquire sporadic Rb?
Two (because it is a recessive disease)
45
How many mutations are required to acquire familial Rb?
One
46
If one defective copy of a tumor suppressor gene is inherited, it is likely that the second copy will be inactivated. This is called
Loss of Heterozygosity (LOH)
47
Loss of p53 renders cancer cells immune to
Apoptosis
48
The most commonly mutated protein in human cancers
p53
49
p53 stimulates transcription of
1. ) Cdk inhibitors | 2. ) pro-apoptotic proteins
50
Intrinsically unstable, but is stabilized in response to DNA damage
p53
51
p14ARF (ARF = alternate reading frame) stabilizes
p53
52
p53 is stabilized by ARF and destabilized by
MDM2
53
ARF binds MDM2 and frees p53. Thus, as far as cell death is concerned, ARF is considered to be
Pro-apoptotic
54
Cell stress activates a p53 modification that blocks
MDM2 binding
55
In un-stressed cells, p53 is destroyed by - a ubiquitin ligase - anti-apoptotic
MDM2
56
p53 has no defined tertiary structure unless it is bound to
DNA
57
Destabilize p53's DNA binding domain, blocking its apoptotic activity
Oncogenic mutations
58
A gene that can cause cancer when activated or expressed
Oncogene
59
A normal gene that can turn into an oncogene as a result of mutations or increased expression
Proto-oncogene
60
Discovered in retroviruses, which insert a DNA copy of its genome into host-cell DNA
Oncogenes
61
Viral oncogenes are originally derived from the genome of the
Host cell
62
Lead to continuous (constitutive) activity of the protein, unaffected by normal regulatory mutations -gain of function mutations
Oncogenic mutations
63
Gain-of-function mutations show which type of heredity?
Dominant
64
Family of tyrosine kinase proteins with SH2 domains that transduce signaling through various Protein Kinase receptors
Src (c-Src is a proto-oncogene)
65
NF1 (a ras-GAP), Cdk inhibitor, and Rb are all considered to be
Tumor suppressor proteins
66
The mTOR pathway is frequently mutated in
Tumors
67
Promotes cell growth downstream of growth-factors -a proto-oncogene
mTOR pathway
68
What is the kinase that converts PIP2 to PIP3?
PI3K
69
What is the phosphatase that converts PIP3 back to PIP2
PTEN
70
A protein kinase activated in the presence of PIP3 that phosphorylates and inhibits TSC
AKT (PKB)
71
An inhibitor of mTOR -mutations cause tuberous sclerosis in CNS, kidney, heart, and lung
TSC
72
A protein kinase that phosphorylates multiple targets to promote protein synthesis and cell growth
mTOR
73
What are three examples of activation of oncogenes?
1. ) c-myc 2. ) c-abl 3. ) c-ras
74
Promotes expression of about 15% of human genes -Activated by overproduction
c-myc
75
Genetic change allows self-activation so normal regulatory stimuli are no longer required
c-abl
76
Mutations prevent inactivtion
c-ras
77
In some tumors, the number of gene copies of c-myc is
Increased (gene amplification)
78
Increase expression of c-myc can also be the result of a
Chromosomal translocation
79
If copies of c-myc remain in the chromosome, they form a -whole chromosome glows in FISH
Homogenously-staining region (HSR)
80
In c-myc amplification, the c-myc genes may also be found outside of the chromosome in tiny
double-minute chromosomes
81
When chromosomes break and rejoin crosswise
Translocation
82
Alterson transcriptional control of c-myc by placing the gene under the control of a powerful promoter
Translocation of c-myc
83
A tumor of B lymphocytes that results from c-myc activation
Burkitt Lymphoma
84
In Burkitt lymphoma, the transcription of antibody genes is driven by powerful
B-cell enhancers
85
When translocations put c-myc under control of an antibodygene enhancer and the c-myc gene is transcribed at many times the normal rate
Burkitt Lymphoma
86
Results from a a translocation which results in constitutive activity of the protein kinase c-abl
Chronic Myelogenous leukemia (CML)
87
The karyotype of Chronic Myelogenous leukemia (CML) shows a chromosome known as the
"Philadelphia Chromosome"
88
In CML, there is a reciprocal translocation between -results in 1 large chromosome and 1 "Philadelphia chromosome"
Chr9 and Chr22
89
One of the most frequently altered proteins in human tumors
Ras
90
Binds guanine nucleotides - Active when GTP is bound - Inactive when GDP is bound
Ras
91
Ras has slow intrinsic GTPase activity that is stimulated by
GAPs
92
A ras-GAP in which mutations result in neurofibromatosis (tumors of peripheral nerves)
NF1 protein
93
What are 4 examples of proteins containing ras homology domain?
1. ) Translation factors 2. ) Large G-proteins 3. ) Dynamins 4. ) Myosin and Kinesin
94
Translation factors such as the aminoacyl-tRNA binding to ribosomes and the translocation of peptidyl-tRNA contain
Ras homology
95
Transduce signals from 7-α-helix receptors
Large G-proteins
96
Proteins that function in the budding of membrane vesicles
Dynamins
97
Most oncogenic mutations in Ras are amino acid substitutions at which two positions?
gly-12/13 and gln-61
98
If mutations in many genes are required to initiate cancer, how can a single drug with presumably a single cellular target block cancer progression?
"oncogene addiction" i.e. some tumors come to rely on one dominant oncogene, which can then be targeted by drugs

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