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ALERT: U.S. Boxed Warning
The FDA-approved labeling includes a boxed warning. See Warnings/Precautions section for a concise summary of this information. For verbatim wording of the boxed warning, consult the product labeling or www.fda.gov.
Pronunciation
(ta MOKS i fen)
Generic Available (U.S.)
Yes
Index Terms
Medication Guide
An FDA-approved patient medication guide, which is available with the product information and as follows, must be dispensed with this medication when used in females for breast cancer prevention or treatment of ductal carcinoma in situ:
Nolvadex®: http://www.fda.gov/downloads/Drugs/DrugSafety/ucm088661.pdf
Brand Names: Canada
Pharmacologic Category
Pharmacologic Category Synonyms
Use: Labeled Indications
Treatment of metastatic (female and male) breast cancer; adjuvant treatment of breast cancer after primary treatment with surgery and radiation; reduce risk of invasive breast cancer in women with ductal carcinoma in situ (DCIS) after surgery and radiation; reduce the incidence of breast cancer in women at high risk
Use: Unlabeled
Treatment of mastalgia, gynecomastia, ovarian cancer, endometrial cancer, uterine sarcoma, and desmoid tumors; risk reduction in women with Paget's disease of the breast (with DCIS or without associated cancer); induction of ovulation; treatment of precocious puberty in females, secondary to McCune-Albright syndrome
Pregnancy Risk Factor
D
Pregnancy Considerations
Animal studies have demonstrated fetal adverse effects and fetal loss. There have been reports of vaginal bleeding, birth defects and fetal loss in pregnant women. Tamoxifen use during pregnancy may have a potential long term risk to the fetus of a DES-like syndrome. For sexually-active women of childbearing age, initiate during menstruation (negative β-hCG immediately prior to initiation in women with irregular cycles). Tamoxifen may induce ovulation. Barrier or nonhormonal contraceptives are recommended. Pregnancy should be avoided during treatment and for 2 months after treatment has been discontinued.
Lactation
Excretion in breast milk unknown/not recommended
Breast-Feeding Considerations
It is not known if tamoxifen is excreted in breast milk, however, it has been shown to inhibit lactation. Due to the potential for adverse reactions, women taking tamoxifen should not breast-feed.
Contraindications
Hypersensitivity to tamoxifen or any component of the formulation; concurrent warfarin therapy or history of deep vein thrombosis or pulmonary embolism (when tamoxifen is used for cancer risk reduction in women at high risk for breast cancer and in women with DCIS)
Warnings/Precautions
Boxed warnings:
• Gynecologic effects/malignancies: See “Concerns related to adverse effects” below.
• Thromboembolic events: See “Concerns related to adverse effects” below.
Special handling:
• Hazardous agent: Use appropriate precautions for handling and disposal.
Concerns related to adverse effects:
• Bone marrow suppression: Thrombocytopenia and/or leukopenia may occur; neutropenia and pancytopenia have been reported rarely. Although the relationship to tamoxifen therapy is uncertain, rare hemorrhagic episodes have occurred in patients with significant thrombocytopenia.
• Gynecologic effects/malignancies: [U.S. Boxed Warning]: Tamoxifen use for breast cancer risk reduction in women at high-risk for breast cancer and in women with DCIS is associated with an increased incidence of uterine or endometrial cancers. Endometrial hyperplasia, polyps, endometriosis, uterine fibroids, and ovarian cysts have occurred. Amenorrhea and menstrual irregularities have been reported with tamoxifen use. Monitor and promptly evaluate any report of abnormal vaginal bleeding.
• Hepatotoxicity: Liver abnormalities such as cholestasis, fatty liver, hepatitis, and hepatic necrosis have occurred. Hepatocellular carcinomas have been reported in some studies; relationship to treatment is unclear.
• Ocular effects: Decreased visual acuity, retinal vein thrombosis, retinopathy, corneal changes, color perception changes and increased incidence of cataracts (and the need for cataract surgery) have been reported.
• Thromboembolic events: [U.S. Boxed Warning]: Serious and life-threatening events, including stroke and pulmonary emboli have occurred at an incidence greater than placebo during use for breast cancer risk reduction in women at high-risk for breast cancer and in women with DCIS; these events are rare, but require consideration in risk:benefit evaluation. In patients already diagnosed with breast cancer, the benefits of tamoxifen use are greater than the risks. An increased incidence of thromboembolic events has been associated with use; risk is increased with concomitant chemotherapy; use with caution in individuals with a history of thromboembolic events.
Disease-related concerns:
• Bone mineral density: Tamoxifen use may be associated with changes in bone mineral density (BMD) and the effects may be dependent upon menstrual status. In postmenopausal women, tamoxifen use is associated with a protective effect on bone mineral density (BMD), preventing loss of BMD which lasts over the 5-year treatment period. In premenopausal women, a decline (from baseline) in BMD mineral density has been observed in women who continued to menstruate; may be associated with an increased risk of fractures.
• Hyperlipidemia: Use with caution in patients with hyperlipidemias; infrequent postmarketing cases of hyperlipidemias have been reported.
• Metastatic breast cancer: Local disease flare and increased bone and tumor pain may occur; may be associated with (good) tumor response; onset is shortly after therapy initiation and usually resolves rapidly. In patients with bone metastasis, hypercalcemia has occurred usually within a few weeks of therapy initiation. Institute appropriate hypercalcemia management; discontinue if severe.
Concurrent drug therapy issues:
• High potential for interactions: Tamoxifen is associated with a high potential for drug interactions, including CYP- and Pgp-mediated interactions. Decreased efficacy and an increased risk of breast cancer recurrence has been reported with concurrent moderate or strong CYP2D6 inhibitors (Aubert, 2009; Dezentje, 2009).
• Selective serotonin reuptake inhibitors (SSRI): Concomitant use with select SSRIs may result in decreased tamoxifen efficacy. Strong CYP2D6 inhibitors (eg, fluoxetine, paroxetine) and moderate CYP2D6 inhibitors (eg, sertraline) are reported to interfere with transformation to the active metabolite endoxifen. Weak CYP2D6 inhibitors (eg, venlafaxine, citalopram) have minimal effect on the conversion to endoxifen (Jin, 2005; NCCN Breast Cancer Risk Reduction Guidelines v.2.2010); escitalopram is also a weak CYP2D6 inhibitor. In a retrospective analysis of breast cancer patients taking tamoxifen and SSRIs, concomitant use of paroxetine and tamoxifen was associated with an increased risk of death due to breast cancer (Kelly, 2010).
Special populations:
• CYP2D6 poor metabolizers: Lower plasma concentrations of endoxifen (active metabolite) have been observed in patients associated with reduced CYP2D6 activity (Jin, 2005) and may be associated with reduced efficacy.
Adverse Reactions
>10%:
Cardiovascular: Vasodilation (41%), flushing (33%), hypertension (11%), peripheral edema (11%)
Central nervous system: Mood changes (12% to 18%), pain (3% to 16%), depression (2% to 12%)
Dermatologic: Skin changes (6% to 19%), rash (13%)
Endocrine & metabolic: Hot flashes (3% to 80%), fluid retention (32%), altered menses (13% to 25%), amenorrhea (16%)
Gastrointestinal: Nausea (5% to 26%), weight loss (23%), vomiting (12%)
Genitourinary: Vaginal discharge (13% to 55%), vaginal bleeding (2% to 23%)
Neuromuscular & skeletal: Weakness (18%), arthritis (14%), arthralgia (11%)
Respiratory: Pharyngitis (14%)
Miscellaneous: Lymphedema (11%)
1% to 10%:
Cardiovascular: Chest pain (5%), venous thrombotic events (5%), edema (4%), cardiovascular ischemia (3%), angina (2%), deep venous thrombus (≤2%), MI (1%)
Central nervous system: Insomnia (9%), dizziness (8%), headache (8%), anxiety (6%), fatigue (4%)
Dermatologic: Alopecia (≤5%)
Endocrine & metabolic: Oligomenorrhea (9%), breast pain (6%), menstrual disorder (6%), breast neoplasm (5%), hypercholesterolemia (4%)
Gastrointestinal: Abdominal pain (9%), weight gain (9%), constipation (4% to 8%), diarrhea (7%), dyspepsia (6%), throat irritation (oral solution 5%), abdominal cramps (1%), anorexia (1%)
Genitourinary: Urinary tract infection (10%), leukorrhea (9%), vaginal hemorrhage (6%), vaginitis (5%), vulvovaginitis (5%), ovarian cyst (3%)
Hematologic: Thrombocytopenia (≤10%), anemia (5%)
Hepatic: AST increased (5%), serum bilirubin increased (2%)
Neuromuscular & skeletal: Back pain (10%), bone pain (6% to 10%), osteoporosis (7%), fracture (7%), arthrosis (5%), joint disorder (5%), myalgia (5%), paresthesia (5%), musculoskeletal pain (3%)
Ocular: Cataract (7%)
Renal: Serum creatinine increased (≤2%)
Respiratory: Cough (4% to 9%), dyspnea (8%), bronchitis (5%), sinusitis (5%)
Miscellaneous: Infection/sepsis (≤9%), diaphoresis (6%), flu-like syndrome (6%), cyst (5%), neoplasm (5%), allergic reaction (3%)
<1%, infrequent, or frequency not defined: Cholestasis, corneal changes, endometriosis, endometrial cancer, endometrial hyperplasia, endometrial polyps, fatty liver, hepatic necrosis, hepatitis, hypercalcemia, hyperlipidemia, lightheadedness, phlebitis, pruritus vulvae, pulmonary embolism, retinal vein thrombosis, retinopathy, second primary tumors, stroke, superficial phlebitis, taste disturbances, tumor pain and local disease flare (including increase in lesion size and erythema) during treatment of metastatic breast cancer (generally resolves with continuation), uterine fibroids, vaginal dryness
Postmarketing and/or case reports: Angioedema, bullous pemphigoid, erythema multiforme, hypersensitivity reactions, hypertriglyceridemia, impotence (males), interstitial pneumonitis, loss of libido (males), pancreatitis, Stevens-Johnson syndrome, visual color perception changes
Metabolism/Transport Effects
Substrate of CYP2A6 (minor), CYP2B6 (minor), CYP2C9 (major), CYP2D6 (major), CYP2E1 (minor), CYP3A4 (major); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential; Inhibits CYP2B6 (weak), CYP2C8 (moderate), CYP2C9 (weak), CYP3A4 (weak), P-glycoprotein
Drug Interactions
Abiraterone Acetate: May increase the serum concentration of CYP2D6 Substrates. Management: Avoid concurrent use of abiraterone with CYP2D6 substrates that have a narrow therapeutic index whenever possible. When concurrent use is not avoidable, monitor patients closely for signs/symptoms of toxicity. Risk D: Consider therapy modification
Aminoglutethimide: May increase the metabolism of Tamoxifen. Risk D: Consider therapy modification
Anastrozole: Tamoxifen may decrease the serum concentration of Anastrozole. Risk D: Consider therapy modification
ARIPiprazole: CYP3A4 Inhibitors (Weak) may increase the serum concentration of ARIPiprazole. Management: Monitor for increased aripiprazole systemic exposure/affects with concomitant use of a weak CYP3A4 inhibitor. Decrease aripiprazole dose to 25% of the usual dose in patients receiving both a CYP3A4 and a CYP2D6 inhibitor (regardless of potencies). Risk C: Monitor therapy
Colchicine: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Colchicine. Colchicine distribution into certain tissues (e.g., brain) may also be increased. Management: Colchicine is contraindicated in patients with impaired renal or hepatic function who are also receiving a p-glycoprotein inhibitor. In those with normal renal and hepatic function, reduce colchicine dose as directed. Risk D: Consider therapy modification
Conivaptan: May increase the serum concentration of CYP3A4 Substrates. Risk X: Avoid combination
CYP2C8 Substrates: CYP2C8 Inhibitors (Moderate) may decrease the metabolism of CYP2C8 Substrates. Risk C: Monitor therapy
CYP2C9 Inducers (Strong): May increase the metabolism of CYP2C9 Substrates. Risk C: Monitor therapy
CYP2C9 Inhibitors (Moderate): May decrease the metabolism of CYP2C9 Substrates. Risk C: Monitor therapy
CYP2C9 Inhibitors (Strong): May decrease the metabolism of CYP2C9 Substrates. Risk D: Consider therapy modification
CYP2D6 Inhibitors (Moderate): May decrease the metabolism of Tamoxifen. Specifically, CYP2D6 inhibitors may decrease the formation of highly potent active metabolites. Management: Consider alternatives with less of an inhibitory effect on CYP2D6 activity when possible. Risk D: Consider therapy modification
CYP2D6 Inhibitors (Strong): May decrease the metabolism of Tamoxifen. Specifically, strong CYP2D6 inhibitors may decrease the formation of highly potent active metabolites. Risk X: Avoid combination
CYP3A4 Inducers (Strong): May increase the metabolism of CYP3A4 Substrates. Risk C: Monitor therapy
CYP3A4 Inhibitors (Moderate): May decrease the metabolism of CYP3A4 Substrates. Risk C: Monitor therapy
CYP3A4 Inhibitors (Strong): May decrease the metabolism of CYP3A4 Substrates. Risk D: Consider therapy modification
Cyproterone: May decrease the serum concentration of CYP2E1 Substrates. Risk C: Monitor therapy
Dabigatran Etexilate: P-glycoprotein/ABCB1 Inhibitors may increase serum concentrations of the active metabolite(s) of Dabigatran Etexilate. Management: Dabigatran dose reductions may be needed. Specific recommendations vary considerably according to US vs Canadian labeling, specific P-gp inhibitor, renal function, and indication for dabigatran treatment. Refer to full monograph or dabigatran labeling. Risk D: Consider therapy modification
Darunavir: May increase the serum concentration of CYP2D6 Substrates. Risk C: Monitor therapy
Dasatinib: May increase the serum concentration of CYP3A4 Substrates. Risk C: Monitor therapy
Deferasirox: May decrease the serum concentration of CYP3A4 Substrates. Risk C: Monitor therapy
Everolimus: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Everolimus. Management: Everolimus dose reductions are required for patients being treated for subependymal giant cell astrocytoma or renal cell carcinoma. See prescribing information for specific dose adjustment and monitoring recommendations. Risk D: Consider therapy modification
Herbs (CYP3A4 Inducers): May increase the metabolism of CYP3A4 Substrates. Risk C: Monitor therapy
Ivacaftor: May increase the serum concentration of CYP3A4 Substrates. Risk C: Monitor therapy
Letrozole: Tamoxifen may decrease the serum concentration of Letrozole. Risk C: Monitor therapy
Peginterferon Alfa-2b: May decrease the serum concentration of CYP2C9 Substrates. Risk C: Monitor therapy
Peginterferon Alfa-2b: May decrease the serum concentration of CYP2D6 Substrates. Risk C: Monitor therapy
P-glycoprotein/ABCB1 Substrates: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of P-glycoprotein/ABCB1 Substrates. P-glycoprotein inhibitors may also enhance the distribution of p-glycoprotein substrates to specific cells/tissues/organs where p-glycoprotein is present in large amounts (e.g., brain, T-lymphocytes, testes, etc.). Risk C: Monitor therapy
Pimozide: CYP3A4 Inhibitors (Weak) may increase the serum concentration of Pimozide. Risk X: Avoid combination
Prucalopride: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Prucalopride. Risk C: Monitor therapy
Rifamycin Derivatives: May increase the metabolism of Tamoxifen. Risk D: Consider therapy modification
Rivaroxaban: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Rivaroxaban. Risk C: Monitor therapy
Silodosin: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Silodosin. Risk X: Avoid combination
Tocilizumab: May decrease the serum concentration of CYP3A4 Substrates. Risk C: Monitor therapy
Topotecan: P-glycoprotein/ABCB1 Inhibitors may increase the serum concentration of Topotecan. Risk X: Avoid combination
Vitamin K Antagonists (eg, warfarin): Tamoxifen may increase the serum concentration of Vitamin K Antagonists. Risk X: Avoid combination
Ethanol/Nutrition/Herb Interactions
Food: Grapefruit juice may decrease the metabolism of tamoxifen. Management: Avoid grapefruit juice.
Herb/Nutraceutical: Black cohosh and dong quai have estrogenic properties. St John's wort may decrease levels/effects of tamoxifen. Management: Avoid black cohosh and dong quai in estrogen-dependent tumors. Avoid St John's wort.
Storage
Store at room temperature of 20°C to 25°C (68°F to 77°F). Protect from light.
Mechanism of Action
Competitively binds to estrogen receptors on tumors and other tissue targets, producing a nuclear complex that decreases DNA synthesis and inhibits estrogen effects; nonsteroidal agent with potent antiestrogenic properties which compete with estrogen for binding sites in breast and other tissues; cells accumulate in the G0 and G1 phases; therefore, tamoxifen is cytostatic rather than cytocidal.
Pharmacodynamics/Kinetics
Absorption: Well absorbed
Distribution: High concentrations found in uterus, endometrial and breast tissue
Protein binding: 99%
Metabolism: Hepatic; via CYP2D6 to 4-hydroxytamoxifen and via CYP3A4/5 to N-desmethyl-tamoxifen. Each is then further metabolized into endoxifen (4-hydroxy-tamoxifen via CYP3A4/5 and N-desmethyl-tamoxifen via CYP2D6); both 4-hydroxy-tamoxifen and endoxifen are 30- to 100-fold more potent than tamoxifen
Half-life elimination: Tamoxifen: ~5-7 days; N-desmethyl tamoxifen: ~14 days
Time to peak, serum: ~5 hours
Excretion: Feces (26% to 51%); urine (9% to 13%)
Dosage
Oral: Note: For the treatment of breast cancer, patients receiving both tamoxifen and chemotherapy, should receive treatment sequentially, with tamoxifen following completion of chemotherapy.
Children: Females: Precocious puberty and McCune-Albright syndrome (unlabeled use): A dose of 20 mg/day has been reported in patients 2-10 years of age; safety and efficacy have not been established for treatment of longer than 1 year duration (Eugster, 2003)
Adults:
Breast cancer treatment:
Adjuvant therapy (females): 20 mg once daily for 5 years
Metastatic (males and females): 20-40 mg/day (doses >20 mg should be given in 2 divided doses). Note: Although the FDA-approved labeling recommends dosing up to 40 mg/day, clinical benefit has not been demonstrated with doses above 20 mg/day (Bratherton, 1984).
Premenopausal women: Duration of treatment is 5 years (NCCN Breast Cancer guidelines v.1.2011)
Postmenopausal women: Duration of tamoxifen treatment is 2-3 years followed by an aromatase inhibitor (AI) to complete 5 years; if contraindications or intolerant to AI, may take tamoxifen for the full 5 years or extended therapy: 4.5-6 years of tamoxifen followed by 5 years of an AI (NCCN Breast Cancer guidelines v.1.2011)
DCIS (females), to reduce the risk for invasive breast cancer: 20 mg once daily for 5 years
Breast cancer risk reduction (pre- and postmenopausal high-risk females): 20 mg once daily for 5 years
Induction of ovulation (unlabeled use): 20 mg once daily (range: 20-80 mg once daily) for 5 days (Steiner, 2005)
Paget's disease of the breast (risk reduction; with DCIS or without associated cancer): 20 mg once daily for 5 years (NCCN Breast Cancer Guidelines, v.1.2011)
Dosage adjustment for DVT, pulmonary embolism, cerebrovascular accident, or prolonged immobilization: Discontinue tamoxifen (NCCN Breast Cancer Risk Reduction Guidelines, v.2.2010)
Dosage: Combination Regimens
Melanoma:
CCDT (Melanoma)
Dartmouth Regimen
Administration: Oral
Administer with or without food.
Monitoring Parameters
CBC with platelets, serum calcium, LFTs; triglycerides and cholesterol (in patients with pre-existing hyperlipidemias); INR and PT (in patients on vitamin K antagonists); abnormal vaginal bleeding; breast and gynecologic exams (baseline and routine), mammogram (baseline and routine); signs/symptoms of DVT (leg swelling, tenderness) or PE (shortness of breath); ophthalmic exam (if vision problem or cataracts); bone mineral density (premenopausal women)
Test Interactions
T4 elevations (which may be explained by increases in thyroid-binding globulin) have been reported; not accompanied by clinical hyperthyroidism
Dietary Considerations
May be taken with or without food. Avoid grapefruit and grapefruit juice.
Patient Education
You should schedule an annual ophthalmic examination, gynecological exam, and mammogram if this medication is used long-term. You may experience hot flashes, hair loss, or loss of libido (these will subside when treatment is completed). May cause nausea, vomiting, and increased blood pressure. Notify prescriber if menstrual irregularities, vaginal bleeding, or intolerable hot flashes occur. Report unusual bleeding or bruising, severe weakness or unusual fatigue, CNS changes (depression, mood changes), persistent bone changes, changes in strength on one side of the body, chest pain or pressure, swelling or pain in calves, respiratory difficulty, or vision changes.
Geriatric Considerations
Studies have shown tamoxifen to be effective in the treatment of primary breast cancer in elderly women. Comparative studies with other antineoplastic agents in elderly women with breast cancer had more favorable survival rates with tamoxifen. Initiation of hormone therapy rather than chemotherapy is justified for elderly patients with metastatic breast cancer who are responsive. Reduction of mortality and recurrence was greater in those studies that used tamoxifen for ≥2 years than those that use it for <2 years.
Additional Information
Estrogen receptor status may predict if adjuvant treatment with tamoxifen is of benefit. In metastatic breast cancer, patients with estrogen receptor positive tumors are more likely to benefit from tamoxifen treatment. With tamoxifen use to reduce the incidence of breast cancer in high risk-women, high risk is defined as women ≥35 years of age with a 5 year NCI Gail model predicted risk of breast cancer ≥1.67%.
Oncology Comment: The American Society of Clinical Oncology (ASCO) guidelines for adjuvant endocrine therapy in postmenopausal women with HR-positive breast cancer (Burstein, 2010) recommend considering aromatase inhibitor (AI) therapy at some point in the treatment course (primary, sequentially, or extended). Optimal duration at this time is not known; however, treatment with an AI should not exceed 5 years in primary and extended therapies, and 2-3 years if followed by tamoxifen in sequential therapy (total of 5 years). If initial therapy with AI has been discontinued before the 5 years, consideration should be taken to receive tamoxifen for a total of 5 years. The optimal time to switch to an AI is also not known; but data supports switching after 2-3 years of tamoxifen (sequential) or after 5 years of tamoxifen (extended). If patient becomes intolerant or has poor adherence, consideration should be made to switch to another AI or initiate tamoxifen.
The adjuvant endocrine therapy of choice is tamoxifen for men with breast cancer and for pre- or perimenopausal women at diagnosis. CYP2D6 genotyping is not recommended, however, due to the potential for drug-drug interactions use caution and consider avoiding concomitant therapy with tamoxifen and known CYP2D6 inhibitors.
Dental Health: Effects on Dental Treatment
No significant effects or complications reported
Dental Health: Vasoconstrictor/Local Anesthetic Precautions
No information available to require special precautions
Mental Health: Effects on Mental Status
May cause dizziness, drowsiness, or confusion
Mental Health: Effects on Psychiatric Treatment
May cause leukopenia; use caution with clozapine and carbamazepine
Nursing: Physical Assessment/Monitoring
Evaluate for use-related precautions prior to beginning therapy. Monitor for thromboembolism, flushing, fluid retention, hot flashes, vaginal bleeding or discharge, constipation, rash, or mood changes. Teach patient importance of periodic ophthalmic evaluations and annual gynecological exams and mammograms with long-term use.
Dosage Forms
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Tablet, oral: 10 mg, 20 mg
Pricing: U.S. (www.drugstore.com)
Tablets (Tamoxifen Citrate)
20 mg (30): $21.99
Extemporaneously Prepared
Hazardous agent: Use appropriate precautions for handling and disposal.
A 0.5 mg/mL oral suspension may be prepared with tablets. Place two 10 mg tablets into 40 mL purified water and let stand ~2-5 minutes. Stir until tablets are completely disintegrated (dispersion time for each 10 mg tablet is ~2-5 minutes). Administer immediately after preparation. To ensure the full dose is administered, rinse glass several times with water and administer residue.
Lam MS, "Extemporaneous Compounding of Oral Liquid Dosage Formulations and Alternative Drug Delivery Methods for Anticancer Drugs," Pharmacotherapy, 2011, 31(2):164-92.
References
Aubert RE, Stanek EJ, Yao J, et al, “Risk of Breast Cancer Recurrence in Women Initiating Tamoxifen With CYP2D6 Inhibitors,” J Clin Oncol, 2009, 27(18S):CRA508 [abstract CRA508 from 2009 ASCO Annual Meeting].
Boostanfar R, Jain JK, Mishell DR Jr, et al, “A Prospective Randomized Trial Comparing Clomiphene Citrate With Tamoxifen Citrate for Ovulation Induction,” Fertil Steril, 2001, 75(5):1024-6.
Bratherton DG, Brown CH, Bucha a R, et al, “A Comparison of Two Doses of Tamoxifen (Nolvadex) in Postmenopausal Women With Advanced Breast Cancer: 10 mg bd Versus 20 mg bd,” Br J Cancer, 1984, 50(2):199-205.
Burstein HJ, Prestrud AA, Seidenfeld J, et al, “American Society of Clinical Oncology Clinical Practice Guideline: Update on Adjuvant Endocrine Therapy for Women with Hormone Receptor-Positive Breast Cancer,” J Clin Oncol, 2010, 28(23):3784-96.
Cohen I, Altaras MM, Lew S, et al, “Ovarian Endometrioid Carcinoma and Endometriosis Developing in a Postmenopausal Breast Cancer Patient During Tamoxifen Therapy: A Case Report and Review of the Literature,” Gynecol Oncol, 1994, 55(3 Pt 1):443-7.
Dezentje V, Van Blijderveen NJ, Gelderblom H, et al, “Concomitant CYP2D6 Inhibitor Use and Tamoxifen Adherence in Early-Stage Breast Cancer: A Pharmacoepidemiologic Study,” J Clin Oncol, 2009, 27(18S):CRA509 [abstract CRA509 from 2009 ASCO Annual Meeting].
Early Breast Cancer Trialists' Collaborative Group (EBCTCG), “Effects of Chemotherapy and Hormonal Therapy for Early Breast Cancer on Recurrence and 15-Year Survival: An Overview of the Randomised Trials,” Lancet, 2005, 365(9472):1687-717.
Eastell R, Adams JE, Coleman RE, et al, “Effect of Anastrozole on Bone Mineral Density: 5-Year Results From the Anastrozole, Tamoxifen, Alone or in Combination Trial 18233230,” J Clin Oncol, 2008, 26(7):1051-7.
Eugster EA, Rubin SD, Reiter EO, et al, “Tamoxifen Treatment for Precocious Puberty in McCune-Albright Syndrome: A Multicenter Trial,” J Pediatr, 2003, 143(1):60-6.
Goetz MP, Kamal A, and Ames MM, “Tamoxifen Pharmacogenomics: The Role of CYP2D6 as a Predictor of Drug Response,” Clin Pharmacol Ther, 2008, 83(1):160-6.
Hochner-Celnikier D, Anteby E, and Yagel S, “Ovarian Cysts in Tamoxifen-Treated Premenopausal Women With Breast Cancer - A Management Dilemma,” Am J Obstet Gynecol, 1995, 172(4 Pt 1):1323-4.
Jin Y, Desta Z, Stearns V, et al, “CYP2D6 Genotype, Antidepressant Use, and Tamoxifen Metabolism During Adjuvant Breast Cancer Treatment,” J Natl Cancer Inst, 2005, 97(1):30-9.
Jordan VC, "Tamoxifen: A Most Unlikely Pioneering Medicine," Nat Rev Drug Discov, 2003, 2(3):205-13.
Jubelirer SJ, “The Management of Menopausal Symptoms in Women With Breast Cancer,” W V Med J, 1995, 91(2):54-6.
Kelly CM, Juurlink DN, Gomes T, et al, “Selective Serotonin Reuptake Inhibitors and Breast Cancer Mortality in Women Receiving Tamoxifen: A Population Based Cohort Study,” BMJ, 2010, 340:c693.
Khatcheressian JL, Wolff AC, Smith TJ, et al, “American Society of Clinical Oncology 2006 Update of the Breast Cancer Follow-Up and Management Guidelines in the Adjuvant Setting,” J Clin Oncol, 2006, 24(31):5091-7.
LiVolsi VA, Salhany KE, and Dowdy YG, “Endocervical Adenocarcinoma in Tamoxifen-Treated Patient,” Am J Obstet Gynecol, 1995, 172(3):1065.
National Comprehensive Cancer Network® (NCCN), “Clinical Practice Guidelines in Oncology™: Breast Cancer,” Version 1.2011. Available at http://www.nccn.org/professionals/physician_gls/PDF/breast.pdf
National Comprehensive Cancer Network® (NCCN), “Clinical Practice Guidelines in Oncology™: Breast Cancer Risk Reduction, Version 2.2010.” Available at http://www.nccn.org/professionals/physician_gls/PDF/breast_risk.pdf
National Comprehensive Cancer Network® (NCCN), “Clinical Practice Guidelines in Oncology™: Ovarian Cancer,” Version 2.2011. Available at http://www.nccn.org/professionals/physician_gls/PDF/ovarian.pdf
National Comprehensive Cancer Network® (NCCN), “Clinical Practice Guidelines in Oncology™: Uterine Neoplasms,” Version 1.2011. Available at http://www.nccn.org/professionals/physician_gls/PDF/uterine.pdf
Pandya KJ, Raubertas RF, Flynn PJ, et al, “Oral Clonidine in Postmenopausal Patients With Breast Cancer Experiencing Tamoxifen-Induced Hot Flashes: A University of Rochester Cancer Center Community Clinical Oncology Program Study,” Ann Intern Med, 2000, 132:788-93.
Rutqvist LE, Johansson H, Signomklao T, et al, “Adjuvant Tamoxifen Therapy for Early Stage Breast Cancer and Second Primary Malignancies. Stockholm Breast Cancer Study Group,” J Natl Cancer Inst, 1995, 87(9):645-51.
Sideras K, Ingle JN, Ames MM, et al, “Coprescription of Tamoxifen and Medications That Inhibit CYP2D6,” J Clin Oncol, 2010, 28(16):2768-76.
Steiner AZ, Terplan M, and Paulson RJ, “Comparison of Tamoxifen and Clomifene Citrate for Ovulation Induction: A Meta-Analysis,” Hum Reprod, 2005, 20(6):1511-5.
Thessaloniki ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group, “Consensus on Infertility Treatment Related to Polycystic Ovary Syndrome,” Fertil Steril, 2008, 89(3):505-22.
Vehmanen L, Elomaa I, Blomqvist C, et al, “Tamoxifen Treatment After Adjuvant Chemotherapy Has Opposite Effects on Bone Mineral Density in Premenopausal Patients Depending on Menstrual Status,” J Clin Oncol, 2006, 24(4):675-80.
Visvanathan K, Chlebowski RT, Hurley P, et al, “American Society of Clinical Oncology Clinical Practice Guideline Update on the Use of Pharmacologic Interventions Including Tamoxifen, Raloxifene, and Aromatase Inhibition for Breast Cancer Risk Reduction,” J Clin Oncol, 2009, 27(19):3235-58.
Winer EP, Hudis C, Burstein HJ, et al, “American Society of Clinical Oncology Technology Assessment on the Use of Aromatase Inhibitors as Adjuvant Therapy for Postmenopausal Women With Hormone Receptor-Positive Breast Cancer: Status Report 2004,” J Clin Oncol, 2005, 23(3):619-29.
International Brand Names
Lexi-Comp.com
Last full review/revision March 2012
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