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MCB II Block 1 > Cancer 1 > Flashcards

Cancer 1 Flashcards

1
Q

what is cancer

A

cell that has quiet mutations that give it proliferation or survival advantage over surrounding cells

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2
Q

what two things happen in cancer

A

exessive signaling for survival

exessive signaling for cell proliferation

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3
Q

how many mutations have to happen for cell to become cacner

A

multiple

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4
Q

difference b/w tumor and cancer

A

tumors can be malignant or benign

malignant tumors can invade

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5
Q

what is carcinogen

A

anything that induces mutations in germiline

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6
Q

what is mutated in leukemia

A

cell that became cancerous is a blood cell

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7
Q

what are 4 general classifications for leuekmia

A

myloid lymphoid or lymphoid lineage

acute or chronic

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8
Q

what is acute leukemia

A

rapid progression, few months survival

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9
Q

B cell ALL

A

b lineage, acute eukemia

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10
Q

what is a carcinoma

A

cell type that became cancerous was epithelial cells

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11
Q

what is the most common type of cancer that affect human

A

carcinoma

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12
Q

adenocarcinoma

A

secretory cell became cancerous

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13
Q

squamous cell carcinoma is rare?

A

no ,very common

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14
Q

sarcoma is what

A

cell that became cancerous is from connective tissue

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15
Q

osteosarcoma

A

osteocyte or osteoblast had mutation

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16
Q

chondrosarcoma

A

cartilage mutation

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17
Q

leimoysarcoma

A

muscle cell became cancerous

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18
Q

are sarcomas rare

A

yes

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19
Q

lymphomas

A

cell that becomes cancerous is cell of lymphoid lineage

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20
Q

difference b/w lymphoma and lyphoid leukemia

A

leukemia has high levels of circulation, lymphoma is solid mass, not so many circulating blood cells

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21
Q

neuroectodermal cancer

A

tumor of central or peripheral nervous system
neuro blastoma is common in childhood
it’s most common in children or young adults

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22
Q

what is second leading cause of death

A

cancer

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23
Q

what is incidence

A

number of new disease cases/year

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24
Q

what is prevalence

A

total number of diseae cases

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25
Q

what is most common cancer for male

A

prostate

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26
Q

what is most common cancer for female

A

breast cancer

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27
Q

50% of tumor are not diagnosed until when

A

they are already metastic, harder to treat when they have already spread

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28
Q

non-melanoma skin cancer are how common

A

most common kind of cancer

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29
Q

why are non-melanoma skin cancers not listed as most common cancer

A

b/c they are so easy to treat and diagnosed so early

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30
Q

the actual number one cancer affecting males is

A

NMSC

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31
Q

BCC is what

A

basal cell carinoma

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32
Q

what is the chance of dying from cancer

A

1 in 4

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33
Q

compared to diagnosis what is death rate

A

not a high death rate compared to diagnosis

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34
Q

why is lung cancer more likely to kill you than prostate and breast

A

a lot more awareness for breast and prostate, we can screen for breast and prostate but don’t have screening methods for lung cancer.

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35
Q

look at graph comparing incidence and moratlity for cancer slide 12

A

lung cancer mortality almost as high as incidence

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36
Q

where is skin cancer most common (what country)

A

australia

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37
Q

where is lowest risk of skin cancer (what country)

A

japan

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38
Q

what are 4 stage of cell cycle

A

G1 S G2 mitotic phase

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39
Q

what are preparation phases of cell cycle

A

G1 S G2

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40
Q

G1 S and G2 are part of what phase

A

interphase

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41
Q

proto-oncogene is what

A

wild type version of gene

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42
Q

what is oncogene

A

gene that has mutation

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43
Q

oncogene normally promotes what

A

cell proliferation

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44
Q

in cancer what happens to oncogene

A

activating mutation in oncogene and cell proliferates too much

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45
Q

EGFR stands for what

A

epidermal growth factor receptor

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46
Q

EGFR is an example of what

A

proto-oncogene

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47
Q

what does oncogene normally promote?

A

normally promotes cell proliferation

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48
Q

if oncogene is activated it will cause what

A

tumor

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49
Q

what are main genes mutated in cancer

A

tumor suppressor gene and oncogene

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50
Q

in cancer what happens to tumor suppressor gene

A

loss of function of mutation of tumor suppressor gene

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51
Q

What is TP53

A

tumor suppressor gene

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52
Q

what is function of TP53

A

activated if there is damage and cell shouldn’t go into S phase
arrests the cell cycle in G1 phase until damage is repaired
induces apoptosis if damage isn’t repaired
if there is hyperproliferation it can stop it

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53
Q

if DNA damage doesn’t get repaired what does TP53 do

A

induce apoptosis

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54
Q

what does Rb stand for

A

retinoblastoma

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55
Q

what is Rb

A

tumour suppressor gene

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56
Q

what is function of Rb

A

if phosphorylated it inhibits G1 → S

57
Q

draw out p53 and Rb cell cycle regulation

A

slide 19

58
Q

if its stimulating pathway

A

oncogene

59
Q

if it blocks pathway

A

tumor supressor gene

60
Q

what is external signal

A

growth factor

61
Q

growth factor binds and activates what

A

growth factor receptor

62
Q

RAS activates what

A

other kinases

63
Q

MAP kinase activation results in activation of what

A

MYC

64
Q

after activation of MYC it transcribes what

A

cyclin D

65
Q

what is MYC

A

transcription factor

66
Q

cell cycle is controlled by what

A

cyclins and kinases

67
Q

kinases controlling cell cycle called what

A

cyclin dependent kinase (CDK)

68
Q

what does CDK stand for

A

cyclin dependent kinase

69
Q

kinase is not active without what

A

it’s particular cyclin

70
Q

When Rb is not phorphorylated what does Rb bind to

A

it is bound to E2F

71
Q

what does Rb inhibit

A

E2F

72
Q

What is E2F

A

Transcription factor

73
Q

cyclin E activates what kinase

A

CDK2

74
Q

Active cyclin E/CDK2 does what to cell

A

pushes into S phase of cell cycle

75
Q

p21 is what

A

inhibitor of cyclin D/CDK4
also inibits CDK2
can inhibit all CDK, can block at any stage of cell cycle

76
Q

How is p21 activated

A

by p53

77
Q

anything blocking cell cycle is what

A

tumor suppressor gene

78
Q

are benign tumours invasive

A

no

79
Q

describe cells in benign tumoursq

A

they still resemble the cell type they originate from
often small
don’t invade surrounding tissues
don’t spread to distant sites

80
Q

what are problems that can happen from benign tumor

A

in brain, if large can cause a lot of neurological problems
in secretory cell like pituitary adenoma (carcinoma would be malignant) can cause secrtion large amounts of ACTH and can cause cushing’s disease

81
Q

what are benign tumors likely to become invasive

A

polyps in colon

82
Q

what is polyp

A

begnign tumor in colon

83
Q

allepithelial cells are attached to what

A

basal lamina

84
Q

in benign tumor describe location with basal lamina

A

still containted by basal lamina

85
Q

describe relationship b/w malignant tumor and basal lamina

A

tumor invades out of basal lamina

86
Q

in situ means what

A

hasn’t spread anywhere

87
Q

how is in situ carcinoma different from carcinoma

A

cells have invasive properties they just haven’t invaded yet

88
Q

where are primary cells from in colon-derived cancer cells in liver

A

colo-rectum

89
Q

describe how cancer is monoclonal

A

all cells in tumor are all derived from same cell

90
Q

heterogenous

A

different mutations b/w the cells b/c they are all proliferating rapidly and aquiring more mutations as they proliferate independent from each other

91
Q

why are cancer cells genetically unstable

A

they have mutatinos that prevent DNA repair, so mutations arent being fixed

92
Q

anchorage independence

A

normally epithelial cells attached to basal lamina
if they aren’t attached to basal lamina, normally signaling for apoptosis
cancer doesn’t need to be attached to anything, they can invade

93
Q

define avoid replicative senescence

A

avoid replicative senescence: cell that is going to stop dividing

94
Q

avoid replicative senescence

A

there is a certain amount of time the cell will divide, cancer cells will never stop replicating

95
Q

loss of contact inhibition

A

during wound healing, superificial wound at border of wound, cells will proliferate to heal until they touch each other. cancer cells won’t stop when they touch each other.

96
Q

disregard signals for cell cycle control

A

lots of mutations

97
Q

stimulate angiogenesis

A

tightly correlated to spread ometastisis

98
Q

vegF

A

?

99
Q

as tumors grow they stimualate angiogenesis

A

stimluate growth of their own blood supply

100
Q

angiogensis and metastesis

A

they have own blood supply and can easily enter blood supply

101
Q

can tumors be polyclonal

A

no

102
Q

tumor clonality

A

tumor initiation from single cell that prliferates abnormally

103
Q

Descrive X inactiation and monoclonal

A

all the cancer cells in female will have same X inactivation pattern b/c they originate from same cell

104
Q

multiple myelomas

A

cancer of a plasma cell (differentiated B cell) - plasma secrete antibodies. translocations cause initiation of cancer

105
Q

break point - see same initation breakpoint in every cancer cell (of same pt), why?

A

b/c that was the initiating even that caused tumor

106
Q

what is philadelphia chromosome

A

translocation b/w chromosome 9 and 22

107
Q

in beginning stages of cancer describe chromosomes

A

point mutations, lots of mutations, but not massive chromosomal abnormalities yet

108
Q

later stages of cancer describe chromosomes

A

translocations and more chromosomal abnormalities

109
Q

cancer cells get mutations where

A

all over

110
Q

mutations cancer gets may or may not provide what

A

selective advantage for growth

111
Q

the cells that have mutations in tumor suppressor and oncogenes have what

A

selective advantage, so this is why the cancer cells we see have this, they will proliferate and grow more

112
Q

normally epithelial cells have to be attached to

A

basal lamina

113
Q

do cancer cells have to be attached to basal lamina

A

no

114
Q

put cells in soft agar and if its cancer cell what happens

A

it grows, doesn’t need to be attached to basal lamina

115
Q

wound that never heals

A

cancer cells don’t stop growing when they are touching other cells

116
Q

in normal cell describe telomeres and growth

A

short telomeres stop cell from dividing after certain amount of time

117
Q

what expresses telomerase

A

stem cells

118
Q

do somatic cells express telomeraes

A

no, just stem cells

119
Q

what happens to telomeres in cancer

A

telomerase (gene that activates it is turned on) so they keep elongating their telomeres and can keep dividing

120
Q

do cancer cells differentiate

A

no

121
Q

why is lack of differentiation a problem in cancer

A

can’t tell where cell came from, called anaplastic tumor

122
Q

anaplastic tumor is what

A

so undifferentiated that they don’t look like any other cell, can’t tell where they came from

123
Q

what happens to signaling pathway to kill cell in cancer

A

its lost

124
Q

cancer cells lose ability to undergo what

A

apoptosis

125
Q

after 1-2 milimeters in diameter the cells in middle get what

A

apoptoxic

126
Q

What does VegF do?

A

VeF binds to receptors and proliferates proliferation and causes blood vessels to grow toward tumor

127
Q

the cells in middle of tumor that die send out what signal

A

VegF

128
Q

what is metastasis

A

spread of primary tumor to other sites of body

129
Q

FDG is what

A

glucose analog - looks like glucose

“Fudge Donuts Glucose”

130
Q

cancer cells have changes in metabolism and do what to glucose

A

huge uptakes of glucose

131
Q

PET scan and FDG

A

cancer cells uptake FDG and we can easily see cancer cells

132
Q

What does ERB-B1/HER1 code for?

A

EGFR

133
Q

What does ERB-B2/HER2 code for?

A

EGFR2

134
Q

What does H-RAS code for?

A

GTPase

135
Q

What does K-RAS code for?

A

GTPase

136
Q

What does BCR-ABL code for?

A

TK

137
Q

What does SRC code for?

A

TK

138
Q

What does MYC code for?

A

TK

139
Q

What does FOS code for?

A

TK

MCB II Block 1 (12 decks)

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