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Reproductive > Hormonally responsive cancers > Flashcards

Hormonally responsive cancers Flashcards

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
Q

side effects of Fulvestrant

A

PM symptoms

  • VMS
  • irritability
  • N/V
  • ASthenia
  • pain
  • HA
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26
Q

failure of therapy with SERMS and SERDs

A

estrogen independent cell growth

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27
Q

Effects of SERMS in woman body

A

estrogenic effects on bones, anti-estrogenic signalling effects on the breast tissue

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28
Q

ROAdministration for SERMS

A

daily PO=tamoxifene

monthlY IM=Raloxifen

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29
Q

BBW for tamoxifen only

A

Endometrial hypertrophy, Vaginal bleeding, Endometrial Cancer

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30
Q

bbw for Tam and Ral BOTH

A

thromboembolic disease (DVT or PE), Stroke

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31
Q

other outcomes of SERM use

A 
dec. bone metabolism
inc density of bone
impove lipid profile
retinal degen. at high dose
teratogenic*****
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32
Q

safer, more convenient serm

A

raloxifen

33
Q

BBW for toremifene

A

Prolongs QT

*therfore avoid with other 3A4 inihibitors

34
Q

all SERMS are

A

teratogens

35
Q

avoid toremifine if hx of

A

endometrial cancer/hyperplasia

thromboembolic disease,

36
Q

what determines if SERM will be antag or agonistic in given tissue

A

whether it binds co-activators upon dimerization in nucleus or co-repressors (though histone deacetylase 1)

37
Q

concern for tamoxifene

A

poor metabolizers (defective CYP2d6) will not produce as much of the MORE HIGHLY active offspring product 4OH tamoxifen–> less effective

38
Q

cyp involved in tamoxifen administration and efficacy

A

CYP2D6

39
Q

MOA for aromatase inhibitors

A

Block CYP19A1 mediated prodcution of estrone (fat) and estradiol, thereby starving the tumor cell of continued proliferation signal

40
Q

Steroidal aromatase inhibitor

A

exemestane

–>irreversible inhibitor

41
Q

Non-Steroidal Aromatase inhibitor

A

Anastrazole, Letrozole

–>reversible inhibition

42
Q

side effects of aromatase inhibitors

A

menopause symptoms

  • less gyn symptoms that tamoxifen
  • new research says tamoxifene for 10 years is better
43
Q

how to test for Her2 Neu overespression

A

ISH or IHC

44
Q

MOA for trastuzumab

A

bind Juxtaglomerular regio of extracellular HER2 domain

45
Q

MOA for Pertuzumab

A

binds EC dimerization domain (subdomain II)–>inhibits Her2 from dimerizing with Her3 and her4

46
Q

Trasztuzumab DM1 MOA

A

bind to receptor and is internalized…then thioester-linked chemotherapeutic agent acts on microtubules

47
Q

MOA for lapatinib

A

TKI, BINDS intracellularly and inhibits HER1/2 by binding to ErbB1 and ErbB2 receptors and comepting with ATP

48
Q

linker-cytotoxic combination used in Her2+ breast CA’s

A

Ado-Trastuzumab-AKA Kadcyla-AKA TDM1

trastuzumab +emantsine (cytotoxic) microtubule inhibitor-makes up T-DM1

49
Q

mab with cardiopulmonary , reno-heaptic AE’s

A

trastuzumab

50
Q

BBW for Trastuzumab

A 
Cardiomyopathy
Infusion reactions
Pregnancy
Respiratory Distress Syndrome
Respiratory insufficiency
(RDS and RIS can eb sequelae of infusion rxns)
51
Q

BBW for pertuzumab

A

pregnancy

52
Q

BBW for Ado-Trastuzumab

A

Heart failure
hepatic disease
pregnancy
ventricular dysfunction

53
Q

BBW for Lapatanib

A

Liver Disease-will increase persistence

54
Q

hand-foot syndrome, rash, GI issue are seen with which agent

A

lapatinib-. Small Molecule TKI

55
Q

serious AE’s seen with Lapatinib

A

intersitial lung disease/pneumonitis, QT prolongation

*cannot use with drugs hosting similar side effects

56
Q

high levels of sex steroid inhibits

A

FSH LH release from AP–> thus less estrogen mad in the ovaries

57
Q

continueal drug stimulation of GnRH receptors in the anterior pituitary –>results in

A

receptor downregulation-> less FSH and Lh secreted

58
Q

how long does it take for GnRH agonsit to work

A

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
Q

GnRH agonist

A

Goserelin

60
Q

AE’s with goserelin

A

PM symptoms->tough on bones esp.

61
Q

MTOR inhibitors work via what mechanism

A

binf to FKBP12 and forma a three way complex with mTOR that blocks protein action and downstream conseuquences

62
Q

mTOR signalling in viv does what

A

angiogenesis
Proliferation
Cell metabolism

63
Q

BBW for Everolimus (mTOR inhibitor)

A

risk of opportunisitic infections-NEOPLASIA, SCC/LYMPHOMA

*THIS SHIT IS AN IMMUNUPRESSANT

64
Q

when is everolimus emplyed

A

Advances ER+, Her2-ve tumors with EXEMESTANE (STEROIDIAL)

65
Q

STANDARD OF CARE FOR TNBC’S

A

EXCISION OR PRIMARY TUMOR AND ADJACENT LYMPH NODES

*IF ADVANCES-CYTOTOXIC THERAPY

66
Q

ADJUVANT

A

TO PREVENT RECURRANCE

67
Q

NEOADJUVANT

A

TO SHRINK AND IMPROVE SURGICAL OUTCOMES

68
Q

DO ALL PATIENTS WITH TNBC REQUIRE ADJUVANT THERAPY?

A

NOPE–> LOOK AT TNM STAGING
(LN+-ADJUVANT
LN- AND >1CM) FOR SURE

69
Q

AE OF DOXORUBICIN

A

cardiomyopathy

70
Q

standard adjuvant care of BC with either poor signature or, LN + or LN-ve and greater than Icm

A

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
Q

Progesterone signalling is now known to be controlled by

A

controlled both by the process of SUMOylation ( a form of ubiquitination) and by post-translational phosphorylation on as many as 10 sites.

72
Q

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)

A

stimulates cyclical proliferation of the mature breast epithelium and activates mammary stem cell pools or occult tumor initiating cells

73
Q

worse prognosis PR + or negative

A

negative

74
Q

PR late in disease contributes to tumor progression in that…

A

PR signalling pathways naturally/unatrually supress tumor invasion and mets through maintaining epithelial cell phenotype and imeding the EMT

75
Q

sum up PR in breast cancer

A

enhances proliferation of PR- cells in a paracrine fashion, then late impede EMT

76
Q

CEE + MPA=

A

increased risk of invasive breast cancer

77
Q

CEE ALONE=

A

21% decrease in BC

78
Q

Drugs for endometrial cancer

A

Medoxyprogesterone (progestin) “Depo-Provera”

Megestrol-synthetic oral progestin

Reproductive (9 decks)

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