Cancer Mabe Flashcards
1
Q
cancer median age of dx
A
67 years
2
Q
T/F: Cancer mortality is falling
A
True
3
Q
what is a neoplasm? malignant or non?
A
new growth, malignant or non
4
Q
what is a tumor? malignant or non?
A
lump or swelling, malignant or non
5
Q
what is cancer?
A
any malignant neoplasm
6
Q
what is hyperplasia?
A
increase in organ or tissue size, increase in # of cells
7
Q
what is a metaplasia?
A
substitution of one type of adult tissue to another, adaptive
8
Q
what is a dysplasia?
A
loss of normal architecture from an abnormal proliferation of cells (rapid growth)
9
Q
what is an anaplasia?
A
loss of structural differentiation, cells going to an earlier phase
10
Q
anaplasia commonly happens in what
A
tumors
11
Q
malignant neoplasm of squamous epithelial cell origin?
A
carcinoma
12
Q
what is a benign carcinoma called
A
papilloma
13
Q
malignant neoplasm derived from glandular tissue
A
adenocarcinoma
14
Q
what is a benign adenocarcinoma
A
adenoma
15
Q
colorectal cancer is a form of what
A
adenocarcinoma
15
Q
malignnat neoplasm of bone, muscle, fat
A
sarcoma
16
Q
malignant neoplasm of blood tissue
A
lymphoma / leukemia
17
Q
cancer of melanocytes in skin or eye
A
melanoma
18
Q
malignancies in precursor cells, common in children
A
blastoma
19
Q
germ cell neoplasm made of several differentiated cells
A
teratoma
20
Q
leukemia types
A
myeloid and lymphocytic
21
Q
leukemia is a cancer of what types of blood cells?
A
white
22
Q
TNM staging : T
A
primary tumor - somewhere not in lymph node
number = size
23
Q
TNM staging: N
A
lymph node number
24
TNM staging: M
distant metastasis
25
abnormal cells only present in the layer they were developed in
in situ
26
cancer only in organ it began in
localized
27
cancer spread beyond primary site to nearby nodes tissues or organs
regional
28
numerical staging of cancer (0-IV) stage 0
no sign of local invasion
29
numerical staging of cancer I
microscopic invasion
30
numerical staging of cancer II and III
II - 4-9 lymph nodes
III - 10+ lymph nodes
31
32
numerical staging of cancer stage IV
distant metastases
33
tumor grade is ____
description assigned by pathologist
34
well differentiated means
resembles normal tissue
35
G1
well differentiated (low grade)
36
G2
moderately differentiated (intermediate grade)
37
G3
poorly differentiated (high grade)
38
G4
undifferentiated (high grade)
39
three characteristics of cancer
uncontrolled cell growth
tissue invasion
metastasis
40
T/F: growth of the primary tumor is life threatening
no usually primary not lethal it's when it moves out
41
what is a proto-oncogene?
a gene that could be capable of causing cancer but is healthy right now
42
what is an oncogene?
mutated form of proto-oncogene that could cause cancer
ex. RSV encodes v-Src an oncogene
43
what is a tumor suppressor?
regulated cell division and growth, could be genetic
ex. RB-1 in retinoblastoma
44
what is the 2 hit hypothesis
in retinoblastoma, if homozygous for RB-1 will get it and if heterozygous increased risk for family history
45
RB-1 is a _____
tumor suppressor
46
v-Src is what
oncogene
47
p16 is what
tumor suppressor
48
does one mutation cause cancer?
often not enough to cause cancer on its own
49
T/F: tumors of the same classification often have a unifying genetic driver
F: usually don't, except 100% CML pts have bcr-abl translocation
50
BCRA1 and BCRA2 are
tumor suppressors
51
BRCA 1 and 2 mutations commonly lead to what cancers?
breast and prostate (mainly breast)
52
BRCA inhibitors in breast cancer increase suseptibility to what
PARP inhibitors
53
what does PARP do?
repairs DNA
54
what does a PARP inhibitor do?
traps the PARP to DNA so it can't uncouple
55
5 year survival rates with chemo
69%
56
which cancers does chemo not really work
lung, brain, pancreatic
57
G0/1
cell contents duplicated except chromosomes
assembling building blocks for division
58
S
chromosomes duplicate (DNA)
59
G2
cell double checks the chromosomes for error and makes repairs, assembling machinery for chromosome segregation
60
cell cycle clock driven by what?
cyclins
61
R point happens when and does what?
restriction, decides if cell should enter cycle or not
62
G1 to S decision
is DNA repaired?
do we have the building blocks?
is there a go signal?
63
S to G2 decision
has the genome been replicated?
are there errors?
64
G2 to M decision?
have the sister chromatids been seperated?
has the machinery required for chromosome segregation and cytokinesis been assembled?
65
p53 oncogene or tumor suppressor?
tumor suppressor
66
p16 oncogene or tumor suppressor?
tumor suppressor
67
Kras oncogene or tumor suppressor?
oncogene
68
Rb1 oncogene or tumor suppressor?
tumor suppressors
69
PI3K oncogene or tumor suppressors?
oncogene
70
what does cyclin d and CDK 4 / 6 Do
phosphorylate Rb1 and keep cell cycle going
71
drug class palbociclib
CDK 4/6 inhibitor
72
palbociclib approved for what
BRCA 1 / 2 mutations
73
what phase does palbociclib block
G1
74
most active testosterone ?
DHT
75
uses of glucocorticoids in cancer
anti cancer effect: blood
palliative care
reduce hypersensitivity reactions (adverse effects)
76
glucocorticoids can be anti cancer for which three cancers?
lymphomas
pediatric ALL
multiple myeloma
77
primary targets of hormone therapies men and women
estradiol
DHT
78
steroid hormones bind receptor where and do what?
in cytosol, activate genes in nucleus
79
which type of estrogen receptor better for hormonal therapy?
ER+, more differentiated
80
what percent ER concentration is considered +?
10%
81
4 types of breast cancer
ER +
HER2
BRCA
Claudin-low
82
who would we give tamoxifen to?
ER+
not CYP2D6 poor metabolizers
83
tamoxifen agonist effect locations?
bone and endometrium
84
tamoxifen antagonist effects locations?
breast and brain
85
tamoxifen agonist effects
bone density preservation in post menopausal women
increase endometrial cancer risk
86
tamoxifen antagonist effects
hot flashes
blocks breast cancer prolif
87
is tamoxifen useful in pre menopause or post
both
88
how does raloxifine differ from tamoxifen?
no endometrial hyperplasia
89
fulvestrant MOA
SERD, full antagonist
90
elacestratnt MOA
partial agonist at low doses, SERD
91
elacestrant advantage
PO dosing vs IM fulvestrant
92
when to use SERD?
when metastatic progression on other antiestrogen therapy
93
what does aromatase do
androgens to estrogens
removes methyl
94
where is source of estrone located in postmenopausal women?
adipocytes
95
are aromatase inhibitors used in pre, post, or both?
post menopausal
96
non steroidal aromatase inhibitors?
anastrazole and letrozole
97
are anastrazole and letrozole competitive or non?
competitivve
98
anastrazole and letrozole when to give
first line or 3-5 years after tamoxifen
99
anastrazole and letrozole side effect
bone loss
100
steroidal aromatase inhibitor
exemestane
101
exemestane MOA
looks like androstenedione and irreversibly binds aromatase so aromatase can't convert anything else
102
LH can activate what
Chol-scc
103
FSH can activate whta
aromatase
104
GnRH dosage form
depot subq
105
what is the estrogen flare
when we first give GnRH analog we get a surge of LH and FSH which increases steroid hormone levels
after 3-4 weeks we get inhibititon
106
GnRH analogs
leuprolide acetate
goserelin
triptorelin
107
GnRH indication
premenopausal breast cancer
108
long term GnRH side effects
hot flashes
sexual dysfunction
109
what happens in prostate cancer
testosterone rapidly converted to DHT via 5 alpha reductase
110
AR in cytoplasm is translocated to nucleus
111
PSA level of what is high
>6.5 ng/mL
112
what is a chemical castration
GnRH analog
113
GnRH antagonists and advantage
-relix
degarelix, relugolix
no flare
114
what is abiraterone
17 hydroxylase and 17, 20 lyase inhibitor
increase in choleseterol levels
115
AR antagonists
-lutamides
enzulutamide, apalutimidie, darolutimide
116
are 5 alpha reductase inhibitors reccomended in prostate cancer?
no
