Cancer 1 Flashcards
1
Q
what is cancer
A
cell that has quiet mutations that give it proliferation or survival advantage over surrounding cells
2
Q
what two things happen in cancer
A
exessive signaling for survival
exessive signaling for cell proliferation
3
Q
how many mutations have to happen for cell to become cacner
A
multiple
4
Q
difference b/w tumor and cancer
A
tumors can be malignant or benign
malignant tumors can invade
5
Q
what is carcinogen
A
anything that induces mutations in germiline
6
Q
what is mutated in leukemia
A
cell that became cancerous is a blood cell
7
Q
what are 4 general classifications for leuekmia
A
myloid lymphoid or lymphoid lineage
acute or chronic
8
Q
what is acute leukemia
A
rapid progression, few months survival
9
Q
B cell ALL
A
b lineage, acute eukemia
10
Q
what is a carcinoma
A
cell type that became cancerous was epithelial cells
11
Q
what is the most common type of cancer that affect human
A
carcinoma
12
Q
adenocarcinoma
A
secretory cell became cancerous
13
Q
squamous cell carcinoma is rare?
A
no ,very common
14
Q
sarcoma is what
A
cell that became cancerous is from connective tissue
15
Q
osteosarcoma
A
osteocyte or osteoblast had mutation
16
Q
chondrosarcoma
A
cartilage mutation
17
Q
leimoysarcoma
A
muscle cell became cancerous
18
Q
are sarcomas rare
A
yes
19
Q
lymphomas
A
cell that becomes cancerous is cell of lymphoid lineage
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
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
22
Q
what is second leading cause of death
A
cancer
23
Q
what is incidence
A
number of new disease cases/year
24
Q
what is prevalence
A
total number of diseae cases
25
what is most common cancer for male
prostate
26
what is most common cancer for female
breast cancer
27
50% of tumor are not diagnosed until when
they are already metastic, harder to treat when they have already spread
28
non-melanoma skin cancer are how common
most common kind of cancer
29
why are non-melanoma skin cancers not listed as most common cancer
b/c they are so easy to treat and diagnosed so early
30
the actual number one cancer affecting males is
NMSC
31
BCC is what
basal cell carinoma
32
what is the chance of dying from cancer
1 in 4
33
compared to diagnosis what is death rate
not a high death rate compared to diagnosis
34
why is lung cancer more likely to kill you than prostate and breast
a lot more awareness for breast and prostate, we can screen for breast and prostate but don't have screening methods for lung cancer.
35
look at graph comparing incidence and moratlity for cancer slide 12
lung cancer mortality almost as high as incidence
36
where is skin cancer most common (what country)
australia
37
where is lowest risk of skin cancer (what country)
japan
38
what are 4 stage of cell cycle
G1 S G2 mitotic phase
39
what are preparation phases of cell cycle
G1 S G2
40
G1 S and G2 are part of what phase
interphase
41
proto-oncogene is what
wild type version of gene
42
what is oncogene
gene that has mutation
43
oncogene normally promotes what
cell proliferation
44
in cancer what happens to oncogene
activating mutation in oncogene and cell proliferates too much
45
EGFR stands for what
epidermal growth factor receptor
46
EGFR is an example of what
proto-oncogene
47
what does oncogene normally promote?
normally promotes cell proliferation
48
if oncogene is activated it will cause what
tumor
49
what are main genes mutated in cancer
tumor suppressor gene and oncogene
50
in cancer what happens to tumor suppressor gene
loss of function of mutation of tumor suppressor gene
51
What is TP53
tumor suppressor gene
52
what is function of TP53
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
53
if DNA damage doesn't get repaired what does TP53 do
induce apoptosis
54
what does Rb stand for
retinoblastoma
55
what is Rb
tumour suppressor gene
56
what is function of Rb
if phosphorylated it inhibits G1 → S
57
draw out p53 and Rb cell cycle regulation
slide 19
58
if its stimulating pathway
oncogene
59
if it blocks pathway
tumor supressor gene
60
what is external signal
growth factor
61
growth factor binds and activates what
growth factor receptor
62
RAS activates what
other kinases
63
MAP kinase activation results in activation of what
MYC
64
after activation of MYC it transcribes what
cyclin D
65
what is MYC
transcription factor
66
cell cycle is controlled by what
cyclins and kinases
67
kinases controlling cell cycle called what
cyclin dependent kinase (CDK)
68
what does CDK stand for
cyclin dependent kinase
69
kinase is not active without what
it's particular cyclin
70
When Rb is not phorphorylated what does Rb bind to
it is bound to E2F
71
what does Rb inhibit
E2F
72
What is E2F
Transcription factor
73
cyclin E activates what kinase
CDK2
74
Active cyclin E/CDK2 does what to cell
pushes into S phase of cell cycle
75
p21 is what
inhibitor of cyclin D/CDK4
also inibits CDK2
can inhibit all CDK, can block at any stage of cell cycle
76
How is p21 activated
by p53
77
anything blocking cell cycle is what
tumor suppressor gene
78
are benign tumours invasive
no
79
describe cells in benign tumoursq
they still resemble the cell type they originate from
often small
don't invade surrounding tissues
don't spread to distant sites
80
what are problems that can happen from benign tumor
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
what are benign tumors likely to become invasive
polyps in colon
82
what is polyp
begnign tumor in colon
83
allepithelial cells are attached to what
basal lamina
84
in benign tumor describe location with basal lamina
still containted by basal lamina
85
describe relationship b/w malignant tumor and basal lamina
tumor invades out of basal lamina
86
in situ means what
hasn't spread anywhere
87
how is in situ carcinoma different from carcinoma
cells have invasive properties they just haven't invaded yet
88
where are primary cells from in colon-derived cancer cells in liver
colo-rectum
89
describe how cancer is monoclonal
all cells in tumor are all derived from same cell
90
heterogenous
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
why are cancer cells genetically unstable
they have mutatinos that prevent DNA repair, so mutations arent being fixed
92
anchorage independence
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
define avoid replicative senescence
avoid replicative senescence: cell that is going to stop dividing
94
avoid replicative senescence
there is a certain amount of time the cell will divide, cancer cells will never stop replicating
95
loss of contact inhibition
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
disregard signals for cell cycle control
lots of mutations
97
stimulate angiogenesis
tightly correlated to spread ometastisis
98
vegF
?
99
as tumors grow they stimualate angiogenesis
stimluate growth of their own blood supply
100
angiogensis and metastesis
they have own blood supply and can easily enter blood supply
101
can tumors be polyclonal
no
102
tumor clonality
tumor initiation from single cell that prliferates abnormally
103
Descrive X inactiation and monoclonal
all the cancer cells in female will have same X inactivation pattern b/c they originate from same cell
104
multiple myelomas
cancer of a plasma cell (differentiated B cell) - plasma secrete antibodies. translocations cause initiation of cancer
105
break point - see same initation breakpoint in every cancer cell (of same pt), why?
b/c that was the initiating even that caused tumor
106
what is philadelphia chromosome
translocation b/w chromosome 9 and 22
107
in beginning stages of cancer describe chromosomes
point mutations, lots of mutations, but not massive chromosomal abnormalities yet
108
later stages of cancer describe chromosomes
translocations and more chromosomal abnormalities
109
cancer cells get mutations where
all over
110
mutations cancer gets may or may not provide what
selective advantage for growth
111
the cells that have mutations in tumor suppressor and oncogenes have what
selective advantage, so this is why the cancer cells we see have this, they will proliferate and grow more
112
normally epithelial cells have to be attached to
basal lamina
113
do cancer cells have to be attached to basal lamina
no
114
put cells in soft agar and if its cancer cell what happens
it grows, doesn't need to be attached to basal lamina
115
wound that never heals
cancer cells don't stop growing when they are touching other cells
116
in normal cell describe telomeres and growth
short telomeres stop cell from dividing after certain amount of time
117
what expresses telomerase
stem cells
118
do somatic cells express telomeraes
no, just stem cells
119
what happens to telomeres in cancer
telomerase (gene that activates it is turned on) so they keep elongating their telomeres and can keep dividing
120
do cancer cells differentiate
no
121
why is lack of differentiation a problem in cancer
can't tell where cell came from, called anaplastic tumor
122
anaplastic tumor is what
so undifferentiated that they don't look like any other cell, can't tell where they came from
123
what happens to signaling pathway to kill cell in cancer
its lost
124
cancer cells lose ability to undergo what
apoptosis
125
after 1-2 milimeters in diameter the cells in middle get what
apoptoxic
126
What does VegF do?
VeF binds to receptors and proliferates proliferation and causes blood vessels to grow toward tumor
127
the cells in middle of tumor that die send out what signal
VegF
128
what is metastasis
spread of primary tumor to other sites of body
129
FDG is what
glucose analog - looks like glucose
| "Fudge Donuts Glucose"
130
cancer cells have changes in metabolism and do what to glucose
huge uptakes of glucose
131
PET scan and FDG
cancer cells uptake FDG and we can easily see cancer cells
132
What does ERB-B1/HER1 code for?
EGFR
133
What does ERB-B2/HER2 code for?
EGFR2
134
What does H-RAS code for?
GTPase
135
What does K-RAS code for?
GTPase
136
What does BCR-ABL code for?
TK
137
What does SRC code for?
TK
138
What does MYC code for?
TK
139
What does FOS code for?
TK
