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PMCOL 303 > Carcinogenesis > Flashcards

Carcinogenesis Flashcards

1
Q

what are the 3 most common types of cancer

A

lung breast and colorectal

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2
Q

what is non neoplastic growth

A

a normal reaction to some stimulus

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3
Q

what are 2 types of non neoplastic growth

A

hypertrophy and hyperplasia

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4
Q

What is hyperplasia

A

overgrowth, the enlargement of an organ or tissue caused by an increase in the reproduction rate of its cells, often as an initial stage in the development of cancer.

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5
Q

how can you cause regression of the lesion with non neoplastic growth

A

remove the stimulus

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6
Q

what is neoplasm

A

a new and abnormal growth of tissue in some part of the body

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7
Q

what 3 things characterize cancer

A

proliferation, anaplastic and metastasize

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8
Q

what is proliferation

A

rapid growth

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9
Q

what is anaplastic

A

less specialized cells (lost their mature or specialized features)

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10
Q

What is metastasize

A

when the cells spread throughout to new sites

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11
Q

what is neoplasia

A

new growth, refers to the process of abnormal cell proliferation which results in a structure known as neoplasm (the formation or presence of a new, abnormal growth of tissue)

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12
Q

what is a neoplasm

A

a tumor, a new and abnormal growth of tissue in some part of the body, especially as a characteristic of cancer

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13
Q

what is a main difference with neoplastic and non-neoplastic growth

A

Neoplastic cells tend to be monoclonal, Non-neoplastic proliferations have cells that are polyclonal in origin.

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14
Q

what is monoclonality

A

tumor derived from a single cell

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15
Q

what is polyclonal tumor

A

multiple diff cells can produce tumor cells

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16
Q

what can cause a polyclonal tumor

A

like a bad chemical hits multiple cells and they get mutated and lead to the same outcome (doesn’t have to be the same mutation, just abnormal growth

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17
Q

how fast do bening tumors grow

A

slow

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18
Q

what do benign tumors do and not do

A

displace rather than destroy

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19
Q

where do benign tumors go

A

no where, they just stay in one place

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20
Q

can benign tumors kill you

A

no

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21
Q

what can happen to a bening tumor

A

it can promote vessel growth to become vascularized

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22
Q

what can happen once a tumor gets vascularized

A

it can detach, invade circulation and lymph

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23
Q

what can happen once a tumor detaches, invades circulation and lymph

A

it can take over and expand quickly

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24
Q

when do you call a tumor cancer

A

once its can detach and start spreading

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25
Q

do malignant tumors kill

A

yes

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26
Q

what are 2 ways malignant tumors spread

A 
direct invasion (neighbor)
metastasis
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27
Q

what kind of differentiation do benign tumors have

A

well differentiated, looks more like the tissue of origin

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28
Q

what kind of differentiation do malignant tumors have

A

less differentiated, anaplastic

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29
Q

what rate of growth in benign tumors have

A

slow

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30
Q

what rate of growth in malignant tumors have

A

faster usually

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31
Q

what local invasion do benign tumors have

A

none! dont leave capsule or site of origin

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32
Q

what local invasion do malignant tumors have

A

invasive and early on

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33
Q

do malignant tumors metastasize

A

yes

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34
Q

do benign tumors metastasize

A

never

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35
Q

do benign tumors necrosis

A

uncommon

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36
Q

do malignant tumors necrosis + why

A

common because outgrowth of blood supply, but much blood in the middle of the cell clumps

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37
Q

what is the cytology of malignant tumors

A
  • pleomorphic
  • hyperchromatic nucleui
  • high nuc/cyt ratio
  • abnormal mitosis
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38
Q

what does pleomorphic mean

A

they vary in size and shape

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39
Q

do neoplastic cells have differentiation

A

no it is lost, they are no longer specialized

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40
Q

what is a hallmark of transformation with cancer

A

anaplasia where there is primitive disordered cell morphology

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41
Q

are benign tumors differentiated

A

yes, well

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42
Q

are malignant tumors differentiated

A

they range from well to undifferentiated

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43
Q

what is 1 work to describe neoplasm

A

tumor

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44
Q

what is 1 work to describe malignant neoplasm

A

cancer

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45
Q

what is 1 work to describe tumor

A

neoplasm

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46
Q

what is 1 work to describe cancer

A

malignant neoplasm

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47
Q

what are 2 steps between normal cells and cancer cells

A

hyperplasia(new cells growing) and dysplasia (function and morphology change)

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48
Q

what is the diff with genotoxic and nongenotoxic cancer

A

genotoxic: a chemical capable of producing cancer by directly altering the genetic material of target cells
non-genotoxic: chemical capable of producing cancer by some secondary mechanism not related to direct gene damage

49
Q

what is genotoxic

A

a chemical capable of producing cancer by directly altering the genetic material of target cells

50
Q

what is non genotoxic

A

chemical capable of producing cancer by some secondary mechanism not related to direct gene damage

51
Q

what are the 3 main cancer stages *

A

Initiation
Promotion
Progression

52
Q

what happens in Initiation

A
  • DNA mod, mutation, genotoxic
  • one dividion can lock in mutation to make it non reversible mutation
  • modification not enough to produce cancer
53
Q

what happens in Promotion

A
  • non direct DNA mod or mutation, non genotoxic
  • multiple cell divisions necessary, clonoal expansion
  • reversible, apoptosis, threshold
  • lots of treatments needed to stop the growth
  • proliferation
54
Q

what happens in Progression

A
  • DNA mod, genotoxic event, mutation, chromosome disarrangement
  • irreversible, goes from neoplasia to malignant
  • # of treatments unknown
55
Q

is initiation reversible

A

no

56
Q

is promotion reversible

A

yes

57
Q

is progression reversible

A

no

58
Q

what are the 2 main umbrella terms for what can cause cancer

A

gene or enviro

59
Q

what are the 3 largest causes of cancer

A

diet, tobacco, infections

60
Q

what are 2 main groups of genotoxic carcinogens

A

direct acting and indirect acting

61
Q

what are 2 main gene changes that can happen

A

DNA damage (direct) or epigenetic

62
Q

what are 5 examples of DNA damage

A

ss break, ds break, insertion, deletion, interstrand cross link

63
Q

what are 5 examples of damaging agents to DNA

A

x rays, UV light, ROS, replication errors, xenobiotics (alkylatinf agents, hydrocarbons, polycyclic aromatics, anti-tumor drugs)

64
Q

what are 4 consequences of DNA damage

A

cell cycle arrest, apoptosis, cancer and aging

65
Q

what is an example of epigenetic changes that could effect cancer

A

Diff chemicals interfere with epigenetic changes, like increased or decreased cell proliferation

66
Q

what activates the AHR receptor

A

dioxin

67
Q

what happens when the AHR receptor is activated

A

it leads to increased CYP 1 transcription

68
Q

what is an example of bioactivation

A

AHR receptor is activated, it leads to increased CYP 1 transcription, increasing metabolism enzymes which can make compounds genotoxic

69
Q

what is an example of something that becomes more toxic with metabolism

A

benzeo(a)pyrene, which can get extra epoxide to be resistant to hydrolation, leading to tumors

70
Q

what is benzeo(a)pyrene

A

polyaromatic hydrocarbon

71
Q

what are the 6 hallmarks of cancner cells

A
  • self sufficiency in growth signals
  • insensitivity to anti growth signals
  • evading apoptosis
  • limitless replicative potential
  • sustained angiogenesis
  • tissue invasion and metastasis
72
Q

explain: self sufficiency in growth signals

A

all normal cells require extrinsic factors produced by other cells, but not cancer cells

73
Q

how do cancer cells achieve self sufficiency in growth signals (5)

A
  • prolonged ligand-induced signalling
  • increase sensitivity
  • express new receptors
  • make own growth factors
  • signal in absense of ligand
74
Q

how do cancer cells prolonged ligand-induced signalling

A

decreased degradation, turn off negative regulator

75
Q

what are 2 important genes in cancer

A

oncogene and tumor supressor gene

76
Q

what is oncogene

A

a gene when mutated, amplified or activated, promotes unregulated cell growth gain-of-function (always “ON”)

77
Q

what is tumor suppressor gene

A

a gene when mutated or inactivated will release cell cycle inhibition, loss of function

78
Q

what is an example of an oncogene

A

ras

79
Q

what is an example of an tumor suppressor gene

A

Rb and p53

80
Q

where are the cell cycle checkpoints

A

between G1 and S, and inside mitosis

81
Q

what does RAS do normally and how

A

it is activated by receptors to exchange GDP to GTP

82
Q

what happens to mutant forms of RAS

A

they are not inactivated (always on)

83
Q

what % of all cancers have RAS mutation

A

15-20%

84
Q

what happens usually in normal cells (not cancer cells that insensitivity to anti growth signals)

A

-most cells in G0 with growth inhibitory proteins in extracellular space

85
Q

which stage are most cells in

A

G0

86
Q

what inhibits further cell growth

A

terminal differentiation, growth inhibitory proteins

87
Q

what can produce cell cycle arrest

A

oncogene expression

88
Q

what is another name for tumor suppressor genes

A

antiproliferative genes

89
Q

what are 3 examples of antiproliferative genes

A

retinoblastoma protein
Rb
p53

90
Q

what does retinoblastoma protein do

A

normally keeps cell in G0 (suppressor)

91
Q

what is cell cycle arrest

A

the cell is no longer involved in the processes surrounding duplication and division

92
Q

what are 2 cancers that Rb mutations are common in

A

retinoblastomas, small cell lung cancers (80%)

93
Q

what is the main role of Rb

A

antiproliferative

94
Q

what is the main role of p53

A

antiproliferative

95
Q

what is the main role of retinoblastoma protein

A

antiproliferative

96
Q

what % of cancers have p53 mutation

A

50-75%

97
Q

what are 3 ways that cancer cells avoid apoptosis

A
  • decoy death receptors
  • mutations in intracellular proteins that monitor DNA damage(p53)
  • increased expression of various anti-apoptotic proteins (bcl-2)
98
Q

what is necrosis role in cancer (evading apoptosis)

A

evidence might do more damage by recruiting tumor promoting inflammatory cells that bring growth stimulating factors

99
Q

what are 2 examples of ways that cells do cell death

A

necrosis and autophagy

100
Q

what is autophagy

A

Activate mechanism to remove organelles or proteins they don’t need to survive - cancer cells is activated during starvation

101
Q

what are 2 ways that cancer cells do limitless proliferative capacity

A

avoid replicative senescence and avoid crisis

102
Q

what are 2 ways that cancer cells avoid replicative senescence

A
  • mutate p53/Rb can extend lifespan

- rare mutations lead to immortalization

103
Q

how do cancer cells avoid massive death and chromosomal (karyotypic) disrray

A

activate telomerase (adds nucleotides at the end of the chromosomes)

104
Q

how do tumors increase blood flow + how does it work

A

activate VEGF–> signal endothelial cell proliferation and growth of blood vessels

105
Q

what are the center of tumors usually like and why

A

necrotic because oxygen cannot reach, angiogenesis does not keep up

106
Q

what is the warburg effect

A

most cancer cells produce energy by glycolysis due to lack of oxygen

107
Q

what about cancer kills you

A

metastasis, not the primary tumor

108
Q

whata re 2 things that metastatic cells must be able to do

A

enter and leave the bloodstream and to survive in an ectopic location

109
Q

what is the underlying mechanism of tissue invasion and metastasis

A

unknown, succession of cell changes… lots of things

110
Q

what are 2 new emerging cancer hallmarks

A

deregulating cellular energetics, avoiding immune destruction

111
Q

what are 2 new enabling cancer characteristics

A

genome instability and mutation, tumor promoting inflammation

112
Q

are tumors complex tissues

A

yes - like their own organs, with some diff cell types, microenvironments and vasculature

113
Q

what are 3 environmental DNA damaging agents

A

chemicals, radiation, viruses

114
Q

what are 2 genes that mutations in can cause cancer

A

genes affected DNA repair and cell growth or apoptosis

115
Q

what happens once there are mutations in genome of somatic cells (3)

A

inactivation of growth promoting oncogenes, inactivation of tumor suppressor genes, alterations in genes that regulat apoptosis

116
Q

what 2 things lead to clone expansion

A

unregulated cell proliferation and decreases apoptosis

117
Q

what 3 things make clone expansion lead to tumor progression and malignant neoplasm

A

additional mutations, angiogenesis, escape from immunity

118
Q

what is the total cell-cell cycle time with cancer

A

typically normal (cancer cells do not grow or divide faster than normal cells, lack of control of cell growth, so that they keep on growing without limit, even if slowly)

PMCOL 303 (25 decks)

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