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Bio of Cancer > Exam 3 > Flashcards

Exam 3 Flashcards

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1
Q

what is the progression of tumors

A

normal –> hyperplasia –> dysplasia –> neoplasia –> metastasis

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2
Q

hyperplasia is characterized increases in what

A

GF and transcription factors

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3
Q

what is more influential for carcinogens to cause cancer

A

cumulative exposure rather than age

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4
Q

what could decrease cancer incidences

A

removal of potentially cancerous cells

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5
Q

give an example of decreasing cancer incidence by removing cancerous cells

A

removing polyps in colorectal cancer

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6
Q

give an example of cumulative exposure to a carcinogen that is linked to cancer

A

cancer related to smoking is parallel to the average number of ppl smoking 30 years later

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7
Q

give two examples of tumor progression

A

colorectal cancer can be stopped by removing polyps

pancreatic cancer is one of the most orderly cancers

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8
Q

explain what colonal succession means

A

one cell obtains a proliferative mutations that takes over an area. The pattern continues to make growths and allows for treatment resistance

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9
Q

are tumor stem cells real stem cells? Explain

A

no because relatively few cells from a tumor can form a new one

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10
Q

explain clonal diversification in tumors

A

cells mutate indifferent ways and form multiple parallel clonal expansions that may be benign or cancerous

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11
Q

What is comparative genomic hybridization (CGH)

A

gives an idea for reason behind duplications or deletions

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12
Q

How does comparatice genomic hybridization work

A

hybridize DNA from normal tissues and from cancerous tissues and label them differently. if things in clone not in tumor= deletion. if things in higher levels in clone= amplification

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13
Q

how many mutations does transformation require

A

more than 1

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14
Q

what does the k-ras oncogene do

A

gives hyperplasia

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15
Q

what are the four key pathways to alter to make cancer and what do they affect

A

Ras- mitogenic signaling and cell cycle
pRB- eliminates suppression of cell cycle
p53- disrupts apoptosis
telomeres- stablize for immortality

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16
Q

what are some toxic/mitogenic agents that can act as tumor progressors

A

ethanol, inflammation, hormone fluctuations such as the menstrual cycle

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17
Q

how does inflammation lead to tumors

A

preserves stressed and damaged cells

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18
Q

what is NSAID

A

non-steroidal anti-inflammatory drugs

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19
Q

how can NSAID decrease colorectal cancer

A

decreases inflammation

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20
Q

what happens when TNF-alpha is inhibited to release NF-KB

A

TNF-alpha leads to more inflammation

cyclin D1 and Myc lead to mitogenesis

anti-apoptotic genes

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21
Q

What does TUNEL assay do

A

looks for chromosomal ends

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22
Q

What does PCNA staining do

A

looks for proliferating cells

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23
Q

What does enabling COX-2 do

A

leads to prostaglandin productions which causes loss of contact inhibition, independent proliferation, and increased cell proliferation

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24
Q

What does LT inhibit

A

pRB and P53

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25
Q

What happens when pRB is transformed

A

resistance to growth inhibition

immortilization

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26
Q

What happens when p53 is transformed

A

resistance to growth inhibition

apoptosis evasion

immortilization

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27
Q

What happens when sT is transformed

A

mitogenic independence

metastasis

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28
Q

What happens when hTERT is transformed

A

immortilization

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29
Q

What happens when Ras is transformed

A

apoptosis evasion
mitogenic independence
angiogenesis
metastasis

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30
Q

characteristics of transit-amplifying cells

A

divide the most

turn into differentiated cells

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31
Q

characteristics of stem cells

A

rarely divide
kept safe deep in the tissues covered in vili and mucous
when divide make one stem cell and one transit amplifying cell

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32
Q

ways to limit mutations in stem cells

A

apoptotic hair trigger
highly active MDR proteins that pump bad tings out
asymmetric strand allocation

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33
Q

how does asymmetric strand allocation work

A

preserve original DNA strand to serve as template for stem cell then use nonconserved strand for transit ampmlifying cells

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34
Q

what happens if we lose a stem cell

A

symmetric division– make two stem cells, one with conserved and one with non-conserved and then non picks up a cons. and then divides as normal

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35
Q

what is mismatch repair

A

the DNA polymerase degrades and renews the strand nucleotides

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36
Q

What are ways DNA proofreads itself

A

if theres a wrong nucleotide a buldge occurs becuase it won’t connect

DNA polymerase is constantly doubling back to check its work

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37
Q

What are two types of damage that can occur when not replicating

A

endogenous and exogenous

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38
Q

what are examples of endogenous damage

A

depurination
depyrimidation
deamination
ROS

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39
Q

what is depurination

A

endogenous

loss of a purine (G or A)

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40
Q

What is depyrimidinaiton

A

loss of a pyrimidine (C or T)

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41
Q

Which is more common depurination or depyrimidination

A

depurination

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42
Q

What is deamination

A

loss of an amine

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43
Q

what is ROS

A

oxidizes bases

DNA breaks causing abasic sites

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44
Q

What are examples of Exogenous DNA damage

A

x-rays
UV-radiation
Chemical agents
Liver decontammination

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45
Q

What are ways X-rays damage DNA

A

breaks sugar phosphate backbone

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46
Q

what are ways UV-rays damage DNA

A

creates pyrimidine dimers

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47
Q

What are ways chemicals damage DNA and give an example

A

Mustard gas, benzo(a)pyrine
alter pairing
attach methyl groups to bases

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48
Q

how does benzo(a)pyrine damage DNA

A

cytochrome p450 tried to break it down and if it doesn’t then it makes it more toxic and forms an adduct

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49
Q

What are adducts in DNA damage

A

they prevent DNA nucleotides from pairing normally

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50
Q

What are some DNA damages that are seen in cancer

A

transversion

transiton

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51
Q

What is transversion

A

switching purine with a pyrimidine

52
Q

What is transition

A

Switching purine with a dif purine or a pyrimidine with a dif pyrimidine

53
Q

What are some ways to protect DNA

A

physical protection shields, scavenging for ROS, inactive electrophilic compounds

54
Q

what is a way to physically protect DNA

A

depositing melanin into keratinocytes

55
Q

What are ways to repair DNA

A 
direct repair
base excision repair
nucleotide excision repair
error-prone repair
BRCA1 and 2 proteins
56
Q

How does Direct repair work

A

direct removal of ethyl group by MGMT

57
Q

How does base excision repair work

A

excision of altered base which can then be repaired individually or with a new strand segment

58
Q

how does nucleotide excision repair work

A

DNA is cut out and a new stand is synthesized

59
Q

explain short vs long patch repair

A

short puts in a new pair

long makes a new strand

60
Q

how do BRCA 1 and 2 proteins work to repair DNA

A

plays a role in dsDNA break repairs at replication forks

61
Q

What is aneuploidy

A

missing or extra chromosomes

62
Q

what is CIN and what cancer is it seen in

A

chromosomal instability has a lot of aneuploidy

Breast Cancer

63
Q

what is MIN and what cancer is it seen in

A

microsatellite instability has little aneuploidy

colorectal cancer

64
Q

what is heterotypic signaling

A

one cell type tells another what to do

65
Q

tumors are mostly made up of what type of cell

A

stromal cells

66
Q

stromal support is essential for which type of tumors

A

carcinomas

67
Q

explain the epithelial to mesenchymal transition

A

cells turn motile to cover the wound but then don’t go through mesenchymal to epithelial transition so then there are changes in the cytoskeleton

68
Q

why are firboblasts important in cancer

A

they produce response proteins and make it more likely that the cancer will metastasize

69
Q

how are tumor vessels different from normal ones

A

large, unorganized, leaky

70
Q

How do leaky vessels affect tumors

A

they create heard lumps from the plasma leaking out and fibrin bundles

71
Q

how do macrophages contribute to tumorigenesis

A

in hypoxic conditions they produce lots of VEGF and IL-8 which then form new blood vessels

supply EGF for proliferation

secrete proteases to disrupt the ECM

72
Q

what recruits macrophages for tumors

A

production of CSF-1 and PDGF

73
Q

what happens if tumors can’t get a blood supply

A

they go through necrosis

74
Q

What is the angiogenesis switch

A

induces blood vessel growth at will

75
Q

how are malignancy and microvessel density related

A

greater density give more blood supply to tumors and therefore lowers survival rate

76
Q

What is the thrombospondin-1 pathway

A

controls formation of new blood vessels to maintain order

new blood cells are targeting by Fas die but mature endothelial cell don’t produce Fas receptor so they don’t die

77
Q

neoangiogenesis

A

mechanism cancer uses for creation of new blood vessels to supply growths

78
Q

how can we target neoangiogenesis

A

treat with Avastin antibody that attacks VEGF

VEGF receptor inhibitors

Attack stromal cells

79
Q

define intravasion

A

cancer cells invade blood vessels

80
Q

define extravasion

A

the cancer cell gets stuck somewhere and moves out of the blood stream

81
Q

explain the process of metastasis

A

intravasion, extravasion, micrometastasis, macrometastasis

82
Q

How do EMT and E-Cadherin enable carcinoma cell invasiveness

A

overexpression of transc. factors can induce EMT without E-cad. E-cad get replaced with N-cad and allows epi cells to talk to stromal cells

83
Q

What does TGF-Beta do

A

stops the progression of the cell cycle

84
Q

What happens when TGF-Beta is present in a cell

A

the cells undergo EMT and suppress expression of E-cad and express vimentin

85
Q

how do macrophages assist in stromal signals causing EMT

A

allow cells to gain access to blood vessels by degrading ECM

86
Q

What happens when MT-1-MMP is expressed by cancer cells

A

degrades the basement membrane to invade he stroma deeper and frees up GFs

87
Q

What is cell motility controlled by

A

Ras-like GTPases

88
Q

how are filopodia and lemelipodia formed on cells

A

Ral-GEF activating Cdc42 forms filopodia

Ral-GEF activating Rac forms lemelipodia

89
Q

how can you tell cancer is spreading by looking at the lymph nodes

A

look at sentinal node where tumor lymph drains because would shoe the cancer first

90
Q

Where does prostate cancer usually move to

A

bone marrow, lungs

91
Q

Where does colon cancer usually move to

A

liver, lungs

92
Q

where does breast cancer usually move to

A

lungs, bone marrow

93
Q

where does pancreatic cancer usually move to

A

liver, lungs

94
Q

what do osteoblasts do

A

create bone

95
Q

what do osteoclasts do

A

break down bone

96
Q

Explain how osteoblasts balance bone degradation and growth

A

osteob creates RANKL protein to activate osteoclasts

osteob also creates OPG which inhibits RANKL

97
Q

How does breast cancer metastasize to bone marrow

A

can produce PTHrP which tells osteob to produce RANKL and produce more osteoc

98
Q

list metastasis suppressor genes and what they suppress

A

NM23 regulates MAPK cascade for cell proliferation and growth

E-cadherin stabalizes cell-cell contact in epithelial cells to prevent EMT and keep them in contact with each other

RhoGD1-2 supresses Rho proteins to reduce cell mobility

99
Q

what do T-cell receptors bind to

A

major historeceptor proteins

100
Q

What is the humoral immune response

A

generates soluble antibodies to bind invaders

helps keep invaders out of cell and targets them for degredation

101
Q

how do macrophages help the humoral immune response

A

antigens bind to various domains to notify macrophages to endocytase

102
Q

explain the cellular immune response

A

develop specialized cytotoxic cells that attack cell displaying certain antigens

Tcells and CTLs

103
Q

what do T cells do

A

directly attack target cell

104
Q

what do Cytotoxic T lymphocytes do

A

help trigger apoptosis in cell

105
Q

Explain the adaptive immune response

A

requires previous exposure to antigen

MHC class 1 and 2 targeted by T cells

106
Q

What is the difference between MHC-c1 and MHC-c2

A

c1 display proteins that are being made in the cell and are looked at by CTLs

c2 display oligopeptides and are displayed by dendritic cells or macrophages and are looked at by T helper cells

107
Q

How to CTLs kill

A

secrete perforin to put holes in the membrane to allow granzyme to enter the cell

secrete death ligand FasL

108
Q

Explain the innate immune response

A

no prior exposure, automatically recognize abnormal things

NK cells

109
Q

how do NK cells work

A

recognize cells with low MHC-c1 expression and attacks them

secretes IFN-y to recruit other immunocytes to the area such as B-cells

110
Q

How do regulatory Tcells work

A

express specific TCRs to stop activation of Tcells

release TGF-B and IL-10 to kill other T lmphocytes and block CTLs actions

111
Q

What do we use to know when T cells should kill something or not

A

regulatory T cells

112
Q

what are some cancers not associated with infectious agents

A

breast, prostate, colon, rectum, ovary, lung

113
Q

what are some cancers associated with infectious agents

A

(non)Hodkins lymphoma, liver, Kaposi’s sarcoma

114
Q

How do cells distinguish neoplastic cells from normal cells

A

look at what is expressed on the MHC-c1

115
Q

How do tumors evade detection of immune response

A 
repress expression of MHC-1
Hide stress/repress NKG2D ligands
innactivate immunocytes that target cancer cells
avoid apoptosis
lose B2-microglobulin or TAP proteins
block eat me signal
116
Q

What are the proteins that signal eat me or dont eat me

A

eat me- calreticulin

dont eat me- CD47

117
Q

What are some Tumor cell counterattacks

A

become resistant to FasL mediated apoptosis

produce IL-10 or TGF-B that are kill lymphocytes

recruit TregS

118
Q

ways to use the immune system to kill cancer

A

passive immunization

adaptive immune response

stimulate response or inhibit suppression

119
Q

Ways to use passive immunization to kill cancer and examples

A

supply body with antibodies- herceptin for Breast Cancer

Treat B cells with monoclonal antibodies– retuxan for Burkitt’s

120
Q

ways to use adaptive immune response to kills cancer and give an example

A

preload dendritic cells with antigen– provenge for prostate cancer

121
Q

ways to stimulate a response or inhibit supression to kill cancer

A

enhance antigen presentation by dendritic cells

block immunologic checkpoints

enhance activity of tumor-specific Tcells at metastasis site

122
Q

what are electrophilic compounds

A

things that can react witht the bases to cause oxidative damage or adducts

123
Q

What inactivates electrophilic compounds

A

glutathione

124
Q

activators of the angiogenic switch

A

VEGF, FGF

125
Q

inhibitors of the angiogenic switch

A

Thrombospondin 1,

ECM proteins

Bio of Cancer (4 decks)

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