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Hormonally responsive cancers Flashcards

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1
Q

name the aromatase inhibitors for breast cancer

A

anastrozole
exemestane
letrozole

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2
Q

name ther SERDS and SERMS for breast ca

A

raloxifene
tamoxifen
toremifene
fulvestrant

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3
Q

name the GnRH agonist for breast CA

A

gosorelin

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4
Q

name the Her-2/neu antibodies in breast ca

A

pertuzumab
trastuzumab (herceptin)
ado-trastuzumab
emtasine

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5
Q

name the TKI used in breast ca

A

lapatinib

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6
Q

mtor inhibitor useful in breast ca

A

everolimus

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7
Q

name the mutations common in breast CA

A

most common-PIK3ca and TP53
-BRCA1//2, GATA3, MAP3K1, MLL3
breast CA–>heterogenous accumulation of these thangs

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8
Q

consequence of BRCA1/2 mutations

A
  1. DNA strand breaks
  2. dysfunctional break repair
  3. uncontrolled cell cycling through abrogation of the normal checkpoint
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9
Q

BRCA1/2 tumors and EReceptor status

A

60-75% of BRCA2 tumors are ER +
ONLY 10-30% of BRCA1 tumors are ER +
(really says 70-90% are negative)

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10
Q

treatment options for BRCA1/2 + patients

A

prophyllactic mastectomy and BSO, SERM (only if BRCA2 will this have a 50% chance in reducing risk),

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11
Q

triple negative Breast CA’s treated with

A

conventional therapy-cytotoxic therapy-poor prognosis

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12
Q

ER+ tumors are driven by

A

estrogen

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13
Q

primary source of estrgoen pre-menopause

A

ovaries

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14
Q

tx of estrogen driven tumor before menopause

A

surgical removal of ovaries
>chemical castration with GnRH agonists/antagonists (block HP control)
>SERM (generally saves for Post Menopausal)

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15
Q

drugs generally saved for Post menopausal estrogen sensitive breast cancers

A

SERMS

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16
Q

source of Estrogen in post menopausal women

A

peripheral conversion of estrone in fat cells

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17
Q

drugs INEFFECTIVE after menopause

A

drugs targeting HP axis

GnRH agonist/atagonist

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18
Q

drug classes effective in Post Menopausal estrogen fed breast cancer

A
  1. SERMS
  2. SERDS
  3. Aromatase inhibitors
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19
Q

only two targets in ER + breast cancer for which agents currently exist

A

MTOR inhibition
EGFR/HER2-RTK action
Overall production of Estrogen

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20
Q

therapy failure with agents that target only classicla pathway

A

the cells are stil undergoing non-genomic actions carried out by estrogen (previously unrecognized)

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21
Q

will anti-estrogen therapy work on ER- or Pr+ tumors

A

yes-clinical response in 8-12 weeks

*average remission 6-12 months-sometimes many years

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22
Q

MOA for Fulvestrant

A

SERD
_binds ER but has bulk substrate which inibits dimerization in nucleus and signalling, achieves sustained down-regulation of EReceptors

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23
Q

Fulvestrant indicated for

A

Er+ METASTATIC breast CA in Post Menopausal women with DISEASE PROGRESION FOLLOWING ANTI-ESTROGEN THERAPY

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24
Q

inhibites receptoir dimerization in the nucleus leading to icnreased turnover and disruption of nuclear localization

A

Fulvestrant–> SERD

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25
side effects of Fulvestrant
PM symptoms - VMS - irritability - N/V - ASthenia - pain - HA
26
failure of therapy with SERMS and SERDs
estrogen independent cell growth
27
Effects of SERMS in woman body
estrogenic effects on bones, anti-estrogenic signalling effects on the breast tissue
28
ROAdministration for SERMS
daily PO=tamoxifene | monthlY IM=Raloxifen
29
BBW for tamoxifen only
Endometrial hypertrophy, Vaginal bleeding, Endometrial Cancer
30
bbw for Tam and Ral BOTH
thromboembolic disease (DVT or PE), Stroke
31
other outcomes of SERM use
``` dec. bone metabolism inc density of bone impove lipid profile retinal degen. at high dose teratogenic***** ```
32
safer, more convenient serm
raloxifen
33
BBW for toremifene
Prolongs QT | *therfore avoid with other 3A4 inihibitors
34
all SERMS are
teratogens
35
avoid toremifine if hx of
endometrial cancer/hyperplasia | thromboembolic disease,
36
what determines if SERM will be antag or agonistic in given tissue
whether it binds co-activators upon dimerization in nucleus or co-repressors (though histone deacetylase 1)
37
concern for tamoxifene
poor metabolizers (defective CYP2d6) will not produce as much of the MORE HIGHLY active offspring product 4OH tamoxifen--> less effective
38
cyp involved in tamoxifen administration and efficacy
CYP2D6
39
MOA for aromatase inhibitors
Block CYP19A1 mediated prodcution of estrone (fat) and estradiol, thereby starving the tumor cell of continued proliferation signal
40
Steroidal aromatase inhibitor
exemestane | -->irreversible inhibitor
41
Non-Steroidal Aromatase inhibitor
Anastrazole, Letrozole | -->reversible inhibition
42
side effects of aromatase inhibitors
menopause symptoms * less gyn symptoms that tamoxifen * new research says tamoxifene for 10 years is better
43
how to test for Her2 Neu overespression
ISH or IHC
44
MOA for trastuzumab
bind Juxtaglomerular regio of extracellular HER2 domain
45
MOA for Pertuzumab
binds EC dimerization domain (subdomain II)-->inhibits Her2 from dimerizing with Her3 and her4
46
Trasztuzumab DM1 MOA
bind to receptor and is internalized...then thioester-linked chemotherapeutic agent acts on microtubules
47
MOA for lapatinib
TKI, BINDS intracellularly and inhibits HER1/2 by binding to ErbB1 and ErbB2 receptors and comepting with ATP
48
linker-cytotoxic combination used in Her2+ breast CA's
Ado-Trastuzumab-AKA Kadcyla-AKA TDM1 trastuzumab +emantsine (cytotoxic) microtubule inhibitor-makes up T-DM1
49
mab with cardiopulmonary , reno-heaptic AE's
trastuzumab
50
BBW for Trastuzumab
``` Cardiomyopathy Infusion reactions Pregnancy Respiratory Distress Syndrome Respiratory insufficiency (RDS and RIS can eb sequelae of infusion rxns) ```
51
BBW for pertuzumab
pregnancy
52
BBW for Ado-Trastuzumab
Heart failure hepatic disease pregnancy ventricular dysfunction
53
BBW for Lapatanib
Liver Disease-will increase persistence
54
hand-foot syndrome, rash, GI issue are seen with which agent
lapatinib-. Small Molecule TKI
55
serious AE's seen with Lapatinib
intersitial lung disease/pneumonitis, QT prolongation | *cannot use with drugs hosting similar side effects
56
high levels of sex steroid inhibits
FSH LH release from AP--> thus less estrogen mad in the ovaries
57
continueal drug stimulation of GnRH receptors in the anterior pituitary -->results in
receptor downregulation-> less FSH and Lh secreted
58
how long does it take for GnRH agonsit to work
Estrogen levels fall to PM levels in 2-4 weeks--> can acutally cause disease flair prior to this downregulation Ex bone pain with mets, breast enlargement/tenderness
59
GnRH agonist
Goserelin
60
AE's with goserelin
PM symptoms->tough on bones esp.
61
MTOR inhibitors work via what mechanism
binf to FKBP12 and forma a three way complex with mTOR that blocks protein action and downstream conseuquences
62
mTOR signalling in viv does what
angiogenesis Proliferation Cell metabolism
63
BBW for Everolimus (mTOR inhibitor)
risk of opportunisitic infections-NEOPLASIA, SCC/LYMPHOMA | *THIS SHIT IS AN IMMUNUPRESSANT
64
when is everolimus emplyed
Advances ER+, Her2-ve tumors with EXEMESTANE (STEROIDIAL)
65
STANDARD OF CARE FOR TNBC'S
EXCISION OR PRIMARY TUMOR AND ADJACENT LYMPH NODES | *IF ADVANCES-CYTOTOXIC THERAPY
66
ADJUVANT
TO PREVENT RECURRANCE
67
NEOADJUVANT
TO SHRINK AND IMPROVE SURGICAL OUTCOMES
68
DO ALL PATIENTS WITH TNBC REQUIRE ADJUVANT THERAPY?
NOPE--> LOOK AT TNM STAGING (LN+-ADJUVANT LN- AND >1CM) FOR SURE
69
AE OF DOXORUBICIN
cardiomyopathy
70
standard adjuvant care of BC with either poor signature or, LN + or LN-ve and greater than Icm
ALL INVOLVE Doxorubicin (an anthrachyline--cumulative max dose) Doxorubicin-A Cyclophosphamide-C T=docetaxel Ca CAF, AC-t, TC, CAF *no evidecne any one regimine is better than the other
71
Progesterone signalling is now known to be controlled by
controlled both by the process of SUMOylation ( a form of ubiquitination) and by post-translational phosphorylation on as many as 10 sites.
72
PRogesterones role in breast cancer (present in about 40% of cells, however these effects are suspected to be paracrine because the cells responsive to Pr themselves are of non-proliferative potential)
stimulates cyclical proliferation of the mature breast epithelium and activates mammary stem cell pools or occult tumor initiating cells
73
worse prognosis PR + or negative
negative
74
PR late in disease contributes to tumor progression in that...
PR signalling pathways naturally/unatrually supress tumor invasion and mets through maintaining epithelial cell phenotype and imeding the EMT
75
sum up PR in breast cancer
enhances proliferation of PR- cells in a paracrine fashion, then late impede EMT
76
CEE + MPA=
increased risk of invasive breast cancer
77
CEE ALONE=
21% decrease in BC
78
Drugs for endometrial cancer
Medoxyprogesterone (progestin) "Depo-Provera" | Megestrol-synthetic oral progestin

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