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pathophysiology > tumor suppressors > Flashcards

tumor suppressors Flashcards

1
Q

unlike oncogenes, tumor suppressors

A

have to be turned “down” or “off” to contribute to cancer spread

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2
Q

the tumor suppressor genes and their resulting proteins usually

A

prevent tumorigenesis

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3
Q

tumor suppressor genes

A

are actual genes

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4
Q

tumor supressor proteins

A

are the resulting proteins

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5
Q

tumor suppressor genes usually follow

A

“two-hit hypothesis”

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6
Q

_____ copies of tumor suppressor genes usually

A

both copies of the genes usually have to be faulty for cancers to develop, recessivee?

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7
Q

BRCA is a

A

tumor suppressor gene

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8
Q

mutation to BRCA is said to be passed down

A

in a dominant fashion

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9
Q

why is BRCA mutations passed down in a dominant fashion

A

one copy is already “out”, people are a single mutation away from developing cancer

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10
Q

how can tumor suppressor genes be turned down or off

A

chromosomal translocation, error with regulation, chromosomal deletion

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11
Q

chromosomal translocation (tumor suppressors)

A

moves the gene to a different part of the chromosome where it’s experienced less

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12
Q

error with regulation (tumor suppressor)

A

activator protein is deformed and never turns gene “on” or operator/promoter sequence is mutated

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13
Q

how can tumor suppressor proteins be turned “down” or “off”

A

hypomorphic or amorphic mutation

error with on/off switch

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14
Q

hypomorphic or amorphic mutation ( tumor suppressor proteins)

A

causes damaged proteins

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15
Q

error with on/off switch (tumor suppressor genes)

A

kinase, phosphatase or other “on/off” switch fails to turn protein on

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16
Q

examples’ tumor suppressors

A

p53
Rb
VHL

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17
Q

what gene codes for p53

A

TP53

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18
Q

where is TP53 located

A

on chromosome 11

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19
Q

what is p53 known as

A

the guardian of the genome

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20
Q

what is the primary job of p53

A

halt the cell cycle if DNA damage is detected

begin apoptosis cascade if the DNA damage is not fixed

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21
Q

what is the Knudson Hypothesis

A

the idea that cancer comes from a gradual accrual of mutations in various oncogenes and tumor suppressor genes

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22
Q

so basically the knudson hypothesis is saying…

A

we need to activate all 6 hallmarks

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23
Q

with p53 preventing DNA damage (mutations) then»»>

A

we shouldn’t ever satisfy the Knudson Hypothesis

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24
Q

p53 is best regulated by what

A

another protein called mdm2

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25
Q

what does mdm2 do

A

indirectly activates p53

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26
Q

in response to DNA damage, mdm2 will

A

unbind from p53, setting it free

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27
Q

p53 serves as an ____ for many

A

serves as an activator for many genes

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28
Q

what genes does p53 serve as an activator for

A

p21
BAX
BBC3

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29
Q

what does p21 do

A

halts the cell cycle

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30
Q

BAX function

A

cause apoptosis if BCL-2 does not block it

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31
Q

BBC3 function

A

codes for BCL-2 binding complex 3,

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32
Q

BCL-2 binding complex 3 function

A

blocks BCL-2 and helps cause apoptosis

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33
Q

who’s paradox?????

A

PETO’s :O

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34
Q

what is Peto’s Paradox

A

if an organism has more cells, its chances of getting cancer should be higher

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35
Q

elephants have more cells than us, why do they hardly ever get cancer

A

they have 40 copies of the TP53 gene, humans have 2

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36
Q

why have humans not evolved to have extra copies of p53

A

Rats w/ artificially high amounts of p53 tend to exhibit senescence faster than those with normal amounts

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37
Q

senescence

A

aging

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38
Q

what hallmark would the p53 pathway be

A

evading growth suppressors

resisting cell death

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39
Q

Rb gene codes for

A

Rb protein

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40
Q

Rb protein is a

A

pocket protein

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41
Q

pocket protein

A

has a pocket where another protein can bind perfectly

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42
Q

Rb sends a signal to

A

to stop the cell cycle between the G1 phase and the S phase UNLESS

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43
Q

b perpetually sends a signal to stop the cell cycle between the G1 phase and the S phase unless what???

A

its pocket has been filled with a specific molecule not normally present in the cell

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44
Q

G1 and S

A

G1 is organelles duplicated

S is chromosomes duplicated

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45
Q

a cell may only progress to the next phase of mitosis if

A

Rb stops sending its signal

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46
Q

in cancer, Rb is

A

often faulty and fails to deliver its signal

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47
Q

when Rb dosen’t work properly

A

cells may progress from G1 to S phase whenever they want

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48
Q

which hallmark is the Rb pathway

A

Evading growth suppressors

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49
Q

VHL stands for

A

von Hippel-Lindau protein

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50
Q

VHL acts as an

A

E3 ubiquitin ligase

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51
Q

what does an E3 ubiquitin ligase do

A

attaches ubiquitin molecules to proteins, signaling that they need to be destroyed

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52
Q

what does VHL do????

A

ubiquitinates the HIF protein family

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53
Q

does HIF stand foe

A

hypoxia inducible factor

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54
Q

HIF proteins are

A

activators for many different genes that are all linked to angiogenesis

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55
Q

angiogenesis

A

the formation of blood vessels

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56
Q

In cancer, VHL is

A

absent, and HIF is constantly present

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57
Q

if HIF is constantly present

A

it allows cancerous tumors to grow new blood vessels as needed

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58
Q

what hallmark is the VHL pathway

A

inducing angiogenesis

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59
Q

neoplasia

A

any new growth, often synonymous with a tumor

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60
Q

tumors are classified based on

A

the type of cell that becomes cancerous

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61
Q

the two big categories of cancer classification

A

sarcoma carcinoma

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62
Q

suffix for cancer

A

oma

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63
Q

cancer prefix

A

make quizlet

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64
Q

how many specialized cell types in the body

A

2990

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65
Q

all specialized cells are derived from

A

the zygote formed when a mother’s egg meets a father’s sperm

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66
Q

cell differentiation

A

a cell growing up and deciding what it wants to be

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67
Q

cell differentiation is usually

A

irreversible

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68
Q

what is the self-renewal of a stem cell

A

one cell grows up, the other remains a stem cell

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69
Q

what are stem cells

A

cells that undergo self renewal

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70
Q

types of stem cells

A

totipotent stem cells

pluripotent stem cells

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71
Q

totipotent stem cells

A

can grow up to become anything

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72
Q

totipotent stem cells only truly exist…

A

in zygotes/ very early in development

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73
Q

pluripotent stem cells

A

can grow up to become several things, but not all things

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74
Q

there are many pluripotent stem cells…..

A

in a full-grown body

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75
Q

progenitor cells

A

they are no longer stem cell

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76
Q

do progenitor cells self-renew

A

no, although some still divide, they can still become many different things when they grow up

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77
Q

differentiated cells

A

cells that are all grown up

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78
Q

rule of thumb for cancer and stem cells

A

the more grown up a cancer cell is, the less severe the cancer will be

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79
Q

embryonic stem cells can spit to become a cell in what 3 categories

A

mesoderm
endoderm
ectoderm

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80
Q

another name for sarcomas

A

sarcomata

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81
Q

sarcomas are

A

very rare types of cancer

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82
Q

about how many new cases of sarcomas in the US every year

A

15k

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83
Q

sarcomas affect..

A

cells of mesodermal origin

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84
Q

example of cells of mesodermal origin that sarcomas affect

A

fat, muscle, cartilage, lymph and bone cellls

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85
Q

where is blood created

A

inside of bone

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86
Q

blood cancers are considered

A

“sub-types” of sarcoma

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87
Q

examples of blood cancers that are subtypes of sarcomas

A

leukemia, lymphoma, myeloma

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88
Q

sarcomas are nearly

A

nearly always malignant , can often happen in people under age 50

89
Q

in a stromal cell sarcoma

A

tumor begins forming in the middle of a busy structure, as opposed to the edge

90
Q

what is a carcinoma

A

a type of cancer that affects cells of endothermal or ectothermal origin

91
Q

most carcinomas end uo affcecting

A

epithelia

92
Q

carcinomas are much more

A

much more common than sarcomas

93
Q

can carcinomas sometimes be benign

A

yes, although they are often not

94
Q

carcinomas occur mostly in who

A

people above the age of 50

95
Q

function of epithelial tissues

A

surround all organs and serve as a coating

96
Q

epithelia cells regenerate

A

from bottom to top and cells quickly “grow up” as they reach the surface

97
Q

epithelial tissues come in

A

many shapes and sizes

98
Q

looking at a picture of a carcinoma

A

cells don’t mature and flatten out as they reach the surface

99
Q

when carcinomas are small and limited to the epithelial layer

A

they are cancer in-situ

100
Q

origin of carcinomas and sarcomas

A

carcinomas: epithelium
sarcomas: connective tissues

101
Q

both carcinomas and sarcomas are

A

malignant

102
Q

frequency of carcinomas and sarcomas

A

carcinoma: common
sarcoma: rare

103
Q

preferred route of metastasis carcinoma, sarcoma

A

carcinoma: lymph
sarcoma: blood

104
Q

Are carcinomas in the in situ phase

A

yes

105
Q

are sarcomas in the in situ phase

A

no

106
Q

stage 0

A

Very early cancer mass contained entirely within its tissue. Also called “cancer in situ”

107
Q

stage 1

A

Cancer contained within one area, often can be surgically removed

108
Q

stage 2

A

Cancer “early locally advanced”. It has begun spreading to nearby lymph nodes.

109
Q

stage 3

A

Cancer “late locally advanced”. It has spread more to the nearby area.

110
Q

the difference between types 2 and 3

A

depends on the cancer type

111
Q

stage 4

A

cancer has metastasize to other organs or parts of the body

112
Q

many cancers are also staged using the

A

TNM

113
Q

TNM

A

tumor, node, metastasis system

114
Q

sample TNM notation

A

T3N1Mx

115
Q

T in TNM

A

stands for the size of the tissue and how many foreign tissues it has invaded

116
Q

T number varies from what in TNM

A

0 (smallest) to 4 (biggest)

117
Q

if the size of a tumor is unknown or can’t be determined (TNM)

A

Tx

118
Q

the classification of T changes

A

the type of cancer and which tissues surround the area

119
Q

N in TNM

A

stands for the extent of the spread to the lymph nodes

120
Q

codes for N in TNM

A

x-can’t tell
0-none
1-in very local lymph nodes
2/3-in far away lymph nodes

121
Q

what is the lymph system

A

a series of lymph vessels and lymph nodes

122
Q

the lymph system does what

A

serves as a place to store and filter interstitial fluids

123
Q

The nymph nodes are more _____ than _____

A

loose, than blood vessels

124
Q

it is much easier for cancer cells to

A

enter lymph nodes than blood vessels

125
Q

M in TNM

A

stands for metastasis

126
Q

numbers of M in TNM

A

M1
M0
Mx

127
Q

M1

A

if there is metastasis in other organs

128
Q

M0

A

if there is not metastasis in other organs

129
Q

Mx

A

if you cannot tell if there is metastasis or not

130
Q

what are the common cancer treatment

A

radiation
surgery
chemotherapy

131
Q

radiation

A

using waves of radiation focused on the tumor

132
Q

radiation is like

A

burning things with a magnifying glass

133
Q

surgery

A

physically cutting out the tumor and surrounding tissue

134
Q

chemotherapy

A

medication that stop mitosis of cells, generally affects all cells of body

135
Q

pros of radiation

A
  • safety for patient
  • kills large proportion of cancer cells
  • can relieve mass effect by shrinking tumor
  • preserves organ
136
Q

why does radiation have safety for the patient

A

only targets a very small area

137
Q

what is mass effect

A

tumor pushes on surrounding tissue

138
Q

cons to radiation

A
  • damages surrounding tissue
  • misses hidden metastases
  • inconvenient (many doses for many months)
  • increase the healing time in surgeries
139
Q

pros to surgery

A
  • can decrease mass effect
  • can completely cure patient if whole tumor is removed
  • convenient: (1 day surgery))
  • ability to biopsy and test tissue
140
Q

cons to surgery

A
  • tough to kill microscopic disease
  • does not target metastases
  • risk of secondary infection
  • patients must be able to tolerate anesthesia
  • loss of a part or all of an organ
141
Q

why is it tough to kill microscopic disease using surgery

A

one leftover cell can cause regeneration

142
Q

pros of chemotherapy

A
  • can kill cells in the entire body
  • preserves organ
  • patient-specific tailored treatment
143
Q

can chemo kill metastases

A

yes

144
Q

cons to chemotherapy

A
  • usually can’t kill cancer alone
  • inconvenient
  • kills cells in random distribution
  • systemic toxicity
145
Q

chemo must be

A

coupled with radiation or surgery

146
Q

why is chemo inconvenient

A

many doses over long time

147
Q

why does chemo have systemic toxicity

A

affects all cells

148
Q

what are the six hall marks

A
  • proliferative signaling
  • evading growth suppressors
  • resisting cell death
  • enabling replicative immortality
  • inducing angiogenisis
  • activating angiogenesis
149
Q

to be cancerous must undergo…

A

some genetic changes that it to show each of the hallmarks of cancer

150
Q

the genetic changes that cause cancer that occur on or around genes are sorted into what 2 categories

A

oncogenes and tumor suppressor genes

151
Q

oncogene

A

gene that has the power to cause cancer when turned “on” or “up”

152
Q

oncoprotein

A

the protein coded for by an oncogene

153
Q

oncogenes and oncoproteins usually

A

don’t cause cancer, only do when there is some kind of mutation

154
Q

before they mutate, oncogenes are called

A

proto-oncogenes

155
Q

how can proto-oncogenes be activated

A

gene duplication , error with regulatory protein, error with regulatory DNA , chromosomal translocation

156
Q

gene duplication (proto-onco)

A

the gene is accidentally copied, resulting in more expression of the protein

157
Q

result of gene duplication (proto-onco)

A

genes have an extra copy and will expressed at higher rates

158
Q

error with regulatory protein (proto-onco)

A

the protein that would turn a gene off can no longer do so

159
Q

(thinking of regulation) almost all genes have

A

promoters and operator just upstream of the gene

160
Q

upstream

A

in front

161
Q

example of a promoter

A

where RNA polymerase binds to turn DNA into mRNA

162
Q

example of an operator

A

where regulatory proteins bind to alter expression of the gene

163
Q

activators

A

turn expression up

164
Q

repressor

A

turn expression down

165
Q

so with an error with regulatory protein…. there is a

A

repressor that does not work

166
Q

error with regulatory DNA (prot-onco)

A

the DNA in the operato mutates so that regulatory proteins cannot bind there anymore

167
Q

chromosomal translocation (proto-onco)

A

the gene “moves” during DNA replication and has a new operator

168
Q

things that causes the activation of oncoproteins

A

hypermorphic mutation
failure of on/off switch
failure of ubiquitination

169
Q

hypermorphic mutation (proto-onco)

A

mutation in protein structure makes it work faster

170
Q

failure of on/off switch

A

kinase, phosphatase, or other on/ off switch fails to turn off oncoprotein

171
Q

failure of ubiquitination

A

failure to destroy a protein leads to higher levels of them

172
Q

examples of oncogenes

A

RAS
BCL-2
Telomerase

173
Q

ubiquitination is the

A

systematic and selective destruction of a protein

174
Q

RAS genes have over

A

150 products

175
Q

the most common RAS genes are

A

H-ras, N-ras, K-ras

176
Q

H-ras is found on

A

chromosome 11

177
Q

N-ras is found on

A

chromosome 1

178
Q

K-ras is found on

A

chromosome 12

179
Q

each one of the RAS genes is responsible for

A

turning on or off various proteins that turn on proteins,

180
Q

RAS genes are one of first steps starts a cascade

A

that will ultimately turn on genes that often lead to more cell division

181
Q

RAS proteins themslves can be

A

turned on of off

182
Q

mutant RAS is found in

A

30% of cancer, 90% of pancreatic cancers

183
Q

each RAS protein can be turned “on” or “off” by a system v

A

very similar to phosphorylation

184
Q

in the case of RAS proteins being turned on or off, RAS proteins will either be bound to

A

GDP

GTP

185
Q

GDP

A

guanidine diphosphate

186
Q

when RAS proteins binds to GDP

A

it will be off

187
Q

GTP

A

guanidine triphosphate

188
Q

when RAS proteins binds to GTP

A

it will be on

189
Q

RAS proteins are almost always located

A

very close to a receptor protein on a cell’s membrane

190
Q

when a receptor protein on the cell membrane is activated by RAS

A

a cascade will cause a GDP to be removed from RAS and a GTP to be added to it, causing RAS to become active

191
Q

when other things happen, RAS is turned off by having

A

the third phosphate group cut off ( becomes GDP)

192
Q

while all 150 RAS proteins are somewhat different

A

the begininng amino acid sequences are the same

193
Q

Almost all mutations affecting the ____codon of any RAS protein have

A

affecting the 61st codon, have been shown to inhibit the conversion of GTP to GDP

194
Q

mutations to RAS proteins inhibiting the conversion of GTP to GPD causes

A

the RAS proteins to be always on and cells are always told to grow `

195
Q

RAS would be an example of which of the 6 hallmarks

A

proliferative signalling

196
Q

BCL-2 is

A

a protein involved in the apoptosis pathway

197
Q

BCl-2 usually works to

A

PREVNT apoptosis

198
Q

in some cases, BCL-2

A

is turned up too high, which stops p53 and its friends form initiating apoptosis

199
Q

when BCL-2 stops p53 and friends from iniitiating apoptosis

A

allows cancerous cells to proliferate

200
Q

shutting off the overexpression of BCL-2 is crucial to

A

helping anti-cancer medications work, so we can let to body cure itself by committing apoptosis instead f killing it ourselves

201
Q

genasense

A

an antisense drug

202
Q

genasense is

A

perfectly complementary to mRNA strand that carries instructions to produce BCL-2

203
Q

soooo genasense can

A

stop ribosomes from reading the mRNA and making the protein

204
Q

which hallmark is the BCL-2 . protein

A

Resisting cell death

205
Q

Every chromomsome has a

A

'’cap’’ on both end of the same 6 bases

206
Q

every chromomsome has a “cap” on both ends of which of the same bases

A

TTAGGG

207
Q

TTAGGG are repeated how many times

A

2500 times per chromosome in new cells

208
Q

each time a chromosome replicates and the cell divides

A

part of the telomere is lost and the chromosome shortens

209
Q

after the telomere is entirely lost…..

A

chromosome replication and cells division stops completely

210
Q

Hayflick limit was by

A

Leonard Hayflick in the 1960s

211
Q

what did Hayflick discover

A

that human cells are only capable of replicating a certain number of times

212
Q

human cells can only replicate about how many times

A

50-70

213
Q

telomerase is an enzyme

A

that lengthens the telomeres

214
Q

telomerase is almost

A

almost always off in somatic human cells,

215
Q

exception of a new cell types where telomerase is off

A

stem cells, white blood cells, sperm cells, skin cells, etc

216
Q

does every cell have the gene to make telomerase

A

yes

217
Q

why is telomerase considered an oncoprotein

A

because without it, cancer cells would have a limited number of replications because they couldn’t replicate anymore

218
Q

what hallmark is the telomerase pathway

A

enabling replicative immortality

pathophysiology (24 decks)

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