BREAST, PROSTATE CANCER Flashcards
WHAT ROLE DO THE BRCA GENES PLAY NORMALLY AND IN CANCER?
NORMALLY SUPPRESS TUMOR GROWTH
MUTATIONS WILL PREVENT CELL REPAIR AND INCREASE BREAST CANCER INCIDENCE
WHAT IS THE MARKER THAT IS TARGETED IN BREAST CANCER TREATMENT
HER2/NEU RECEPTOR
HOW LONG ARE HORMONE-SENSITIVE CANCERS TYPICALLY TREATED FOR
5-10 YEARS TO SUPPRESS CANCER RECURRENCE
WHAT DETERMINES THE DECISION OF HORMONE TREATMENT
MENOPAUSAL STATUS
FOR HORMONE SENSITIVE CANCERS, WHAT IS USED FOR PREMENOPAUSAL WOMEN VS POST MENOPAUSAL WOMEN AND WHY?
POST MENOPAUSE - AROMATASE INHIBITORS SINCE MOST ESTROGEN IS MADE FROM CONVERSION OF ANDROGENS. THIS WOULD NOT BE EFFECTIVE IN PREMENOPAUSAL SINCE MOST ESTROGEN PRODUCTION IS FROM THE OVARIES.
PREMENOPAUSE - TAMOXIFEN WHICH BINDS TO ESTROGEN RECEPTORS ON TUMORS
SELECTIVE ESTROGEN RECEPTOR MODULATOR (SERM) AGENT
TAMOXIFEN, RALOXIFENE
ESTROGEN ANTAGONIST
AROMATASE INHIBITORS
ANASTRAZOLE
PREVENT THE CONVERSION OF ANDROGENS TO ESTROGENS
WHY WOULD A PATIENT BE PUT ON GnRH AGONSTS?
WILL PUT A PREMENOPAUSAL WOMAN INTO MENOPAUSE TO SUPPRESS OVARIAN E2 PRODUCTION, MAKING AROMATASE INHIBITORS A REASONABLE TREATMENT OPTION
WHICH CHEMO AGENTS ARE THE PREFERRED IN COMBINATION WITH HORMONE TREATMENT FOR METASTATIC BREAST CANCER
CDK4/6 INHIBITORS
mTOR INHIBITOR EVEROLIMUS
TAMOXIFEN IS A PRODRUG CONVERTED BY WHICH ENZYME?
CYP2D6
TAMOXIFEN SIDE EFFECTS
HOT FLASHES/NIGHT SWEATS, VAGINAL BLEEDING/SPOTTING, DISCHARGE/DRYNESS/PRURITUS, ↓ LIBIDO
↓BONE DENSITY IN PREMENOPAUSE WOMEN
TAMOXIFENE CAN CAUSE HOT FLASHES AND NIGHT SWEATS. HOW IS THIS MANAGED?
CANNOT USE ESTROGENS (NORMAL THERAPY)
CANNOT USE FLUOXETINE OR PAROXETINE SINCE CYP2D6 INHIBITORS
VENLAFAXINE IS THE PREFERRED
WHEN IS RALOXIFENE USED?
BREAST CANCER PROPHYLAXIS
ALSO INCREASES BONE DENSITY AND IS INDICATED FOR OSTEOPOROSIS PREVENTION AND TREATMENT IN SELECT POST MENOPAUSAL WOMEN WHO ALSO NEED BREAST CANCER PREVENTION
SERM BOXED WARNINGS
RISK OF UTERINE OR ENDOMETRIAL CANCER
THROMBOEMBOLIC EVENTS
FULVESTRANT, WHAT IS THIS?
SELECTIVE ESTROGEN RECEPTOR DEGRADER (SERD)
AN OPTION WHEN SERM CANNOT BE USED
FULVESTRANT FORMULATION
IM INJECTION
FULVESTRANT SIDE EFFECTS
↑LFT
INJECTION SITE PAIN
HOT FLASHES
ANASTRAZOLE CONCERNS
HIGHER RISK OF OSTEOPOROSIS
HIGHER CVD RISK COMPARED TO SERMS
ANASTRAZOLE CONTRAINDICATION
PREGNANCY
ANASTRAZOLE SIDE EFFECTS
HOT FLASHES/NIGHT SWEATS
ARTHRALGIA/MYALGIAS
CDK4/6 INHIBITORS
PALBOCICLIB
ABEMACICLIB
RIBOCICLIB
WHAT IS PRODUCED AT INCREASED LEVELS IN PROSTATE CANCER
PROSTATE SPECIFIC ANTIGEN (PSA)
WHAT IS THE HORMONAL THERAPY IN PROSTATE CANCER
TESTOSTERONE AND ACTIVE METABOLITE DHT
WHAT IS THE HORMONAL TREATMENT IN PROSTATE CANCER CALLED?
ANDROGEN DEPRIVATION THERAPY (ADT) OR
CHEMICAL CASTRATION
WHAT ARE THE ADVERSE EFFECTS OF ADT
IMPOTENCE
WEAKNESS
HOT FLASES
LOSS OF BONE DENSITY
WHAT AGENTS ARE USED IN ADT
GnRH ANTAGONIST ALONE OR
GnRH AGONIST WITH AN ANTIANDROGEN
HOW DO GnRH AGONISTS WORK IN PROSTATE CANCER?
WORK BY USING THE NEGATIVE FEEDBACK LOOP
↑ LHRH/GnRH WHICH WILL INITIALLY ↑TESTOSTERONE, THEN WILL ↓TESTOERONE
INITIAL SURGE CAN CAUSE A TUMOR FLARE, SO AN ANTIANDROGEN IS GIVEN TO PREVENT THE FLARE
GnRH AGONIST AGENTS
LEUPROLIDE
GOSRELIN
GnRH AGONIST CONCERNS
↓BONE DENSITY; SHOULD SUPPLEMENT WITH CA/VIT D
GnRH AGONIST SIDE EFFECTS
HOT FLASHES
IMPOTENCE
GYNECOMASTIA
BONE PAIN
GnRH ANTAGONIST MOA
↓GnRH/LHRH = ↓TESTOSTERONE WITHOUT THE INITIAL SURGE
GnRH ANTAGONIST AGENTS
DEGARELIX
RELUGOLIX
GnRH CONCRENS
OSTEOPOROSIS RISK
ANTIANDROGEN 1ST GEN AGENTS
BICALUTAMIDE
FLUTAMIDE
NILUTAMIDE
ANTIANDROGEN 2ND GEN AGENTS
APALUTAMIDE
DAROLUTAMIDE
ENZALUTAMIDE
ANDROGEN BIOSYNTHESIS INHIBITOR MOA
INTERFERES WITH SPECIFIC CYP ENZYMES INVOLVED IN STEROID SYNTHESIS IN THE TESTES TO ↓TESTOSTERONE PRODUCTION
COMMON CHEMO REGIMEN FOR BREAST CANCER
AC REGIMEN
CYCLOPHOSPHAMIDE + ANTHRACYCLINE (DOXARUBICIN)
