Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Reproduction Pharmacology > Treatment of Breast & Endometrial Cancer > Flashcards

Treatment of Breast & Endometrial Cancer Flashcards

1
Q

Aromatase Inhibitors Drugs:

A

Anastrozole
Letrozole
Exemestane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

SERDs & SERMs Drugs:

A

Raloxifene
Tamoxifen
Toremifene
Fulvestrant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

HER-2/neu Antibodies Drugs:

A

Pertuzumab
Trastuzumab
Ado-Trastuzumab Emtasine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

TKI Drugs:

A

Lapatinib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

GnRH Agonist Drugs:

A

Goserelin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

mTOR Inhibitor Drugs:

A

Everolimus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

BRCA1 & BRCA2 Function:

A

Tumor suppressors involved in repair of double strand breaks.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

PIK3CA Function:

A

Catalytic subunit of PI3 kinase; key signal transduction enzyme involved in cellular growth, survival and insulin signaling.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

TP53 Function:

A

Tumor suppressor; key regulator of cell cycle, DNA repair, apoptosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

GATA3 Function:

A

Transcription factor which regulates luminal epithelial cell differentiation in the mammary gland.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

MAP3K1 Function:

A

Kinase that activates ERK and JNK kinase pathways.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

MLL3 Function:

A

Histone-lysine N-methyltransferase involved in transcriptional co-activation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Options for Mutant BRCA1/2 Carriers Prophylactic

A

Mastectomy and bilateral salpingo-oophorectomy (BSO) in order to decrease the risk of breast and ovarian cancer.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Bilateral mastectomy decreases breast cancer risk by?

A

90%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Options for Mutant BRCA1/2 Carriers Chemoprevention?

A

tamoxifen or raloxifene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Prospective study indicates 50% reduction in risk for BRCA2 mutation carriers but no effect for BRCA1 carriers. Why?

A
  • 60-75% BRCA2-tumors are ER+

* 70-90% of BRCA1-tumors are ER-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Clinical features that warrant referral for genetic

testing for BRCA1/2 mutations?

A
  • Early-onset breast cancer, (< age 50 or 45)
  • Ovarian, fallopian tube or primary peritoneal cancer
  • Individuals with 2 or more primary breast cancers, or breast & ovarian cancer in the same individual
  • Male breast cancer
  • 2 or more individuals in the family with breast and/or ovarian cancer
  • Ashkenazi Jewish ancestry
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

A significant number of patients with ER- or PR-positive tumors

A

Respond to hormonal therapy. Clinically response in 8 to 12 weeks to detect.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Anti-estrogen therapy includes:

A

Selective Estrogen Receptor Downregulators (SERDs)
Selective Estrogen Receptor Modulators (SERMs)
Aromatase Inhibitors (AI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Fulvestrant Mechanism:

A

Pure antagonist; no estrogenic actions.

Impaired dimerization, increased turnover, disrupted nuclear localization, degradation leading to decrease ER levels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Fulvestrant used in treatment for?

A

For ER+ metastatic BC in PM women with disease

progression following anti-estrogen therapy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Fulvestrant
Administer:
Metabolism:
Side Effects:

A 
Monthly IM: sustained plasma levels
Hepatic metabolism; no drug interactions
Adverse effects – PM symptoms
– Nausea, asthenia, pain, vasodilation (hot flashes),
& headache
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Fulvestrant Failure of therapy

A

Estrogen-independent cell growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Tamoxifen & Raloxifene Mechanism:

A

ER agonist/antagonist
– Location of ER subtypes (α and β)
– Estrogen effect on bone
– Anti-estrogen effect on mammary tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Tamoxifen Dosage:

A

Daily PO [Tam]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Raloxifene Doseage:

A

Monthly IM [Ral]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Tamoxifen & Raloxifene Effects:

A

– Decrease bone metabolism (Increase bone mineral density)

– Decrease serum cholesterol, LDL, lipoproteins, and Increase apolipoprotein-A1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Tamoxifen & Raloxifene High dosage causes?

A

– Retinal degeneration at high doses

– Teratogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Tamoxifen BBW:

A 
Endometrial hypertrophy, vaginal bleeding, endometrial cancer.
Thromboembolic disease (DVT or PE), Stroke.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Raloxifene BBW

A

Thromboembolic disease (DVT or PE), Stroke.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Toremifene Mechanism:

A

Derivative of tamoxifen with antiestrogenic properties.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Toremifene Dosage:

A

PO Daily; CYP3A4 metabolism (no active products)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Toremifene Side effects & CI:

A
  • Teratogen
  • Similar adverse effects – except prolongs QT interval. Avoid in pre-existing condition & with 3A4 inhibitors
  • NO other BBWs BUT recommended avoid with Hx of: Endometrial cancer/hyperplasia, Thromboembolic disease
34
Q

AIs: Mechanism: Anastrozole & Letrozole

A

Non-steroidal – reversible inhibitor

35
Q

AIs: Mechanism: Exemestan

A

Steroidal - irreversible inhibitor

36
Q

AI: Anastrozole, Letrozole, & Exemestan
Dosage:

A

Daily oral: hepatic metabolism

37
Q

AI: Anastrozole, Letrozole, & Exemestan

Side Effects:

A

• Hot flashes, nausea, hair thinning
No effect on adrenal steroids, thyroid & other hormones.
• More arthralgia & diarrhea but fewer gynecologic symptoms than tamoxifen

38
Q

The American Society of Clinical Oncology recommends that all postmenopausal women with hormone receptor positive early breast cancer?

A

Receive adjuvant aromatase inhibitor therapy.

39
Q

Aromatase Therapy Options include:

A

5 years of an aromatase inhibitor or sequential therapy with 2—3 years or 5 years of tamoxifen followed by 2—3 years or 5 years of an aromatase inhibitor.

40
Q

Adjuvant Tamoxifen: Longer Against Shorter (ATLAS) trial Findings?

A

Benefit of reduced breast cancer recurrence & mortality with 10 yrs of adjuvant tamoxifen vs. 5 yrs out weighs increase risk of endometrial cancer (in PM women).

41
Q

Testing Guides for HER2 Therapy Which tests?

A

Immunohistochemistry (IHC) or in situ hybridization (ISH) assay.

42
Q

Testing Guides for HER2 Therapy Test Results:

A

A positive test is IHC 3+ or ISH positive, equivocal is IHC 2+ or ISH equivocal, and negative is IHC 1+ or IHC 0 or ISH negative

43
Q

Testing Guides for HER2 Therapy When to test?

A

Must request testing for every primary invasive cancer (and on the metastatic site if stage IV)
– Should recommend targeted therapy if the test is positive
• Must delay treatment decision if initial test result is equivocal
– Must not recommend targeted therapy after negative tests
• May consider HER2-targeted therapy if a test result remains equivocal, even after reflex testing with an alternative assay.

44
Q

Her-2/neu: Drugs

A

Pertuzumab, Trastuzumab, & Ado-Trastuzumab

45
Q

Pertuzumab Mechanism:

A

A monoclonal antibody “HER dimerization inhibitors” by binding to HER2, it inhibits the dimerization of HER2 with other HER receptors.

46
Q

Trastuzumab Mechanism:

A

is a monoclonal antibody that interferes with the HER2/neu receptor.

47
Q

Ado-Trastuzumab Mechanism:

A

An antibody-drug conjugate consisting of the monoclonal antibody trastuzumab (Herceptin) linked to the cytotoxic agent mertansine. Because the monoclonal antibody targets HER2, and HER2 is only over-expressed in cancer cells, the conjugate delivers the toxin specifically to tumor cells.

48
Q

Pertuzumab, Trastuzumab

Dosage:

A

IV Q21D: long half-lives

49
Q

Pertuzumab, Trastuzumab

Reaction:

A

Caution; hypersensitivity reactions with initial dose

50
Q

Pertuzumab, Trastuzumab

Common Adverse Effects:

A

GI upset, asthenia, blood dyscrasias, fatigue

51
Q

Pertuzumab

Unique AE:

A

Alopecia, loss of appetite

Increase LVEF, neutropenia & leukopenia.

52
Q

Trastuzumab

Unique AE:

A

Peripheral edema, rash, weight gain, dizziness, URTIs, pharyngitis, fatigue
Cardiomyopathy & HF, renal failure, hepatotoxicity, pneumonia & respiratory failure

53
Q

Pertuzumab BBWs

54
Q

Trastuzumab BBWs

A 
Cardiomyopathy 
Infusion reactions
Pregnancy
Respiratory distress syndrome*
Respiratory insufficiency*
*Sequelae of infusion reactions
55
Q

Ado-Trastuzumab BBWs

A

Heart failure
Hepatic disease
Pregnancy
Ventricular dysfunction

56
Q

Lapatinib Mechanism:

A

Dual tyrosine kinase inhibitor which interrupts the HER2/neu and epidermal growth factor receptor (EGFR) pathways.

57
Q

Lapatinib Metabolism:

A

Extensive hepatic metabolism; CYP3A4 & 5
• Liver disease or dysfunction will lead to increase levels & persistence
• Elevates LFTs; routine monitoring required

58
Q

Lapatinib Common AE:

A

GI issues toxicity, anemia & thrombocytopenia, hand-foot syndrome, rash pain, headache, backache.

59
Q

Lapatinib Serious AE:

A

Interstitial lung disease/pneumonitis; QT prolongation.

60
Q

Hormonally-responsive tumors Mechanism:

A

Down-regulation of the GnRH receptor on the pituitary gland and ultimately decreased production of FSH and LH. Serum levels of estradiol consequently fall to post-menopausal levels in 2-4 weeks.

61
Q

Goserelin Mechanism:

A

GnRH agonist

62
Q

Goserelin Administered:

A

SC injection q 28d in upper abdominal wall

63
Q

Goserelin Side Effects:

A

(hypo-estrogenic action) Amenorrhea, hot flashes, decrease libido , vaginal dryness, emotional lability, depression, sweating, and gynecomastia. Also headache, N/V, peripheral edema, lethargy & anorexia

64
Q

Goserelin Bone effects:

A

Decrease bone density, osteopenia/osteoporosis.

65
Q

Everolimus Mechanis:

A

mTOR regulates cell proliferation, angiogenesis, and cell metabolism by activating or inhibiting protein synthesis upon receipt of appropriate biochemical signals.
Drug binds to FKBP-12 & forms a 3-way complex with mTOR that blocks protein action & downstream consequences.

66
Q

Everolimus Used in advanced:

A

ER +ve, HER-2 –ve tumors, with exemestane

67
Q

Everolimus Inhibitor:

A

CYP3A4 & P-gp substrate; 3A4, 2D6 inhibitor & P-gp inhibitor

68
Q

Everolimus Side Effects

A

• Non-infectious pneumonitis – sometimes fatal
• Blood dyscrasias, hyperglycemia, hyperlipidemia,
hypertriglyceridemia, & elevated creatinine - liver enzymes
• N/V, diarrhea, pain, constipation

69
Q

Everolimus BBW:

A

Risk of opportunistic infections – neoplasia; lymphoma/SCC

70
Q

Triple Negative Breast Ca Excision of primary tumor & lymph nodes is standard practice for?

A

Early stage disease

71
Q

Triple Negative Breast Ca Drugs and/or radiation are utilized in an?

A

Adjuvant role to prevent recurrence of disease or a neoadjuvant role prior to excision

72
Q

Advanced tumor - metastatic disease - triple negative breast cancer (TNBC; estrogen receptor –ve, progesterone receptor –ve & HER-2/neu –ve)
TREATMENT:

A

Systemic treatment with conventional chemotherapeutic agents is the norm

73
Q

PR+ in primary breast cancers =

A

Favorable prognosis
More differentiated, less invasive phenotype
PR+ is also predictive of better overall survival

74
Q

Loss of PR in ER+ tumors is associated with?

A

A more aggressive tumor phenotype, reduced responsiveness to endocrine therapies, & a shorter overall survival.

75
Q

Menopausal hormone therapy: A combination of estrogen and progestin [Prempro] was associated with?

A

A 28% increased risk of invasive breast cancer.

76
Q

Menopausal hormone therapy: Estrogen alone was associated with a significant?

A

(21%) reduction in breast cancer.

77
Q

Drugs for Endometrial Cancer

A

Medroxyprogesterone

Megestrol

78
Q

Medroxyprogesterone Mechanism:

A

A progestin contraceptive: Bind to progestin receptors & block GnRH release.

79
Q

Medroxyprogesterone Side Effects:

A

Amenorrhea, edema, anorexia, weakness

80
Q

Megestrol Mechanism:

A

Synthetic oral progestin: Suppresses pituitary LH release & enhances estrogen degradation. Promotes differentiation/maintenance of endometrial tissue.

81
Q

Megestrol Side Effects:

A

Weight gain (increased appetite), hot flashes, malaise, asthenia, lethargy, sweating (diaphoresis) & rash (unspecified)

82
Q

Megestrol Adverse Effects:

A

Thrombophlebitis, thrombo- or pulmonary-embolism

Reproduction Pharmacology (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions