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PHRM 864 > Cancer Mabe > Flashcards

Cancer Mabe Flashcards

1
Q

cancer median age of dx

A

67 years

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2
Q

T/F: Cancer mortality is falling

A

True

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3
Q

what is a neoplasm? malignant or non?

A

new growth, malignant or non

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4
Q

what is a tumor? malignant or non?

A

lump or swelling, malignant or non

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5
Q

what is cancer?

A

any malignant neoplasm

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6
Q

what is hyperplasia?

A

increase in organ or tissue size, increase in # of cells

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7
Q

what is a metaplasia?

A

substitution of one type of adult tissue to another, adaptive

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8
Q

what is a dysplasia?

A

loss of normal architecture from an abnormal proliferation of cells (rapid growth)

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9
Q

what is an anaplasia?

A

loss of structural differentiation, cells going to an earlier phase

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10
Q

anaplasia commonly happens in what

A

tumors

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11
Q

malignant neoplasm of squamous epithelial cell origin?

A

carcinoma

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12
Q

what is a benign carcinoma called

A

papilloma

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13
Q

malignant neoplasm derived from glandular tissue

A

adenocarcinoma

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14
Q

what is a benign adenocarcinoma

A

adenoma

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15
Q

colorectal cancer is a form of what

A

adenocarcinoma

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15
Q

malignnat neoplasm of bone, muscle, fat

A

sarcoma

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16
Q

malignant neoplasm of blood tissue

A

lymphoma / leukemia

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17
Q

cancer of melanocytes in skin or eye

A

melanoma

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18
Q

malignancies in precursor cells, common in children

A

blastoma

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19
Q

germ cell neoplasm made of several differentiated cells

A

teratoma

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20
Q

leukemia types

A

myeloid and lymphocytic

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21
Q

leukemia is a cancer of what types of blood cells?

A

white

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22
Q

TNM staging : T

A

primary tumor - somewhere not in lymph node
number = size

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23
Q

TNM staging: N

A

lymph node number

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24
Q

TNM staging: M

A

distant metastasis

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25
Q

abnormal cells only present in the layer they were developed in

A

in situ

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26
Q

cancer only in organ it began in

A

localized

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27
Q

cancer spread beyond primary site to nearby nodes tissues or organs

A

regional

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28
Q

numerical staging of cancer (0-IV) stage 0

A

no sign of local invasion

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29
Q

numerical staging of cancer I

A

microscopic invasion

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30
Q

numerical staging of cancer II and III

A

II - 4-9 lymph nodes
III - 10+ lymph nodes

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31
Q
A
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32
Q

numerical staging of cancer stage IV

A

distant metastases

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33
Q

tumor grade is ____

A

description assigned by pathologist

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34
Q

well differentiated means

A

resembles normal tissue

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35
Q

G1

A

well differentiated (low grade)

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36
Q

G2

A

moderately differentiated (intermediate grade)

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37
Q

G3

A

poorly differentiated (high grade)

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38
Q

G4

A

undifferentiated (high grade)

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39
Q

three characteristics of cancer

A

uncontrolled cell growth
tissue invasion
metastasis

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40
Q

T/F: growth of the primary tumor is life threatening

A

no usually primary not lethal it’s when it moves out

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41
Q

what is a proto-oncogene?

A

a gene that could be capable of causing cancer but is healthy right now

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42
Q

what is an oncogene?

A

mutated form of proto-oncogene that could cause cancer
ex. RSV encodes v-Src an oncogene

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43
Q

what is a tumor suppressor?

A

regulated cell division and growth, could be genetic
ex. RB-1 in retinoblastoma

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44
Q

what is the 2 hit hypothesis

A

in retinoblastoma, if homozygous for RB-1 will get it and if heterozygous increased risk for family history

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45
Q

RB-1 is a _____

A

tumor suppressor

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46
Q

v-Src is what

47
Q

p16 is what

A

tumor suppressor

48
Q

does one mutation cause cancer?

A

often not enough to cause cancer on its own

49
Q

T/F: tumors of the same classification often have a unifying genetic driver

A

F: usually don’t, except 100% CML pts have bcr-abl translocation

50
Q

BCRA1 and BCRA2 are

A

tumor suppressors

51
Q

BRCA 1 and 2 mutations commonly lead to what cancers?

A

breast and prostate (mainly breast)

52
Q

BRCA inhibitors in breast cancer increase suseptibility to what

A

PARP inhibitors

53
Q

what does PARP do?

A

repairs DNA

54
Q

what does a PARP inhibitor do?

A

traps the PARP to DNA so it can’t uncouple

55
Q

5 year survival rates with chemo

56
Q

which cancers does chemo not really work

A

lung, brain, pancreatic

57
Q

G0/1

A

cell contents duplicated except chromosomes
assembling building blocks for division

58
Q

S

A

chromosomes duplicate (DNA)

59
Q

G2

A

cell double checks the chromosomes for error and makes repairs, assembling machinery for chromosome segregation

60
Q

cell cycle clock driven by what?

61
Q

R point happens when and does what?

A

restriction, decides if cell should enter cycle or not

62
Q

G1 to S decision

A

is DNA repaired?
do we have the building blocks?
is there a go signal?

63
Q

S to G2 decision

A

has the genome been replicated?
are there errors?

64
Q

G2 to M decision?

A

have the sister chromatids been seperated?
has the machinery required for chromosome segregation and cytokinesis been assembled?

65
Q

p53 oncogene or tumor suppressor?

A

tumor suppressor

66
Q

p16 oncogene or tumor suppressor?

A

tumor suppressor

67
Q

Kras oncogene or tumor suppressor?

68
Q

Rb1 oncogene or tumor suppressor?

A

tumor suppressors

69
Q

PI3K oncogene or tumor suppressors?

70
Q

what does cyclin d and CDK 4 / 6 Do

A

phosphorylate Rb1 and keep cell cycle going

71
Q

drug class palbociclib

A

CDK 4/6 inhibitor

72
Q

palbociclib approved for what

A

BRCA 1 / 2 mutations

73
Q

what phase does palbociclib block

74
Q

most active testosterone ?

75
Q

uses of glucocorticoids in cancer

A

anti cancer effect: blood
palliative care
reduce hypersensitivity reactions (adverse effects)

76
Q

glucocorticoids can be anti cancer for which three cancers?

A

lymphomas
pediatric ALL
multiple myeloma

77
Q

primary targets of hormone therapies men and women

A

estradiol
DHT

78
Q

steroid hormones bind receptor where and do what?

A

in cytosol, activate genes in nucleus

79
Q

which type of estrogen receptor better for hormonal therapy?

A

ER+, more differentiated

80
Q

what percent ER concentration is considered +?

81
Q

4 types of breast cancer

A

ER +
HER2
BRCA
Claudin-low

82
Q

who would we give tamoxifen to?

A

ER+
not CYP2D6 poor metabolizers

83
Q

tamoxifen agonist effect locations?

A

bone and endometrium

84
Q

tamoxifen antagonist effects locations?

A

breast and brain

85
Q

tamoxifen agonist effects

A

bone density preservation in post menopausal women
increase endometrial cancer risk

86
Q

tamoxifen antagonist effects

A

hot flashes
blocks breast cancer prolif

87
Q

is tamoxifen useful in pre menopause or post

88
Q

how does raloxifine differ from tamoxifen?

A

no endometrial hyperplasia

89
Q

fulvestrant MOA

A

SERD, full antagonist

90
Q

elacestratnt MOA

A

partial agonist at low doses, SERD

91
Q

elacestrant advantage

A

PO dosing vs IM fulvestrant

92
Q

when to use SERD?

A

when metastatic progression on other antiestrogen therapy

93
Q

what does aromatase do

A

androgens to estrogens
removes methyl

94
Q

where is source of estrone located in postmenopausal women?

A

adipocytes

95
Q

are aromatase inhibitors used in pre, post, or both?

A

post menopausal

96
Q

non steroidal aromatase inhibitors?

A

anastrazole and letrozole

97
Q

are anastrazole and letrozole competitive or non?

A

competitivve

98
Q

anastrazole and letrozole when to give

A

first line or 3-5 years after tamoxifen

99
Q

anastrazole and letrozole side effect

100
Q

steroidal aromatase inhibitor

A

exemestane

101
Q

exemestane MOA

A

looks like androstenedione and irreversibly binds aromatase so aromatase can’t convert anything else

102
Q

LH can activate what

103
Q

FSH can activate whta

104
Q

GnRH dosage form

A

depot subq

105
Q

what is the estrogen flare

A

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
Q

GnRH analogs

A

leuprolide acetate
goserelin
triptorelin

107
Q

GnRH indication

A

premenopausal breast cancer

108
Q

long term GnRH side effects

A

hot flashes
sexual dysfunction

109
Q

what happens in prostate cancer

A

testosterone rapidly converted to DHT via 5 alpha reductase

110
Q

AR in cytoplasm is translocated to nucleus

111
Q

PSA level of what is high

A

> 6.5 ng/mL

112
Q

what is a chemical castration

A

GnRH analog

113
Q

GnRH antagonists and advantage

A

-relix
degarelix, relugolix
no flare

114
Q

what is abiraterone

A

17 hydroxylase and 17, 20 lyase inhibitor
increase in choleseterol levels

115
Q

AR antagonists

A

-lutamides
enzulutamide, apalutimidie, darolutimide

116
Q

are 5 alpha reductase inhibitors reccomended in prostate cancer?

PHRM 864 (28 decks)

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