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Breast Cancer Medication

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Breast Cancer Medication

Author: Alison T Stopeck, MD; Chief Editor: Jules E Harris, MD more... Updated: Nov 30, 2012

Medication Summary
Adjuvant treatment for breast cancer involves radiation therapy and a variety of chemotherapeutic and biologic agents. Adjuvant treatment of breast cancer is designed to treat micrometastatic disease, or breast cancer cells that have escaped the breast and regional lymph nodes but which have not yet had an established identifiable metastasis. Treatment is aimed at reducing the risk of future recurrence, thereby reducing breast cancer-related morbidity and mortality. The 2011 NCCN guidelines include recommendations for the use of two new drugs, denosumab and eribulin, both of which received FDA approval in 2010. The 2011 guidelines support the use of biologic denosumab for the prevention of skeletal events. When compared with zoledronic acid, denosumab, which is administered subcutaneously, delayed the onset of skeletal events by 8% and the time to multiple skeletal events by 23%. In addition, toxicities, such as hypercalcemia and renal failure, were less frequent. The guidelines recommend eribulin, an antimicrotubular drug, as the "preferred single agent" in chemotherapy treatment for women with advanced disease. Trials have shown significant improvement in survival when compared with patients receiving "treatment by physician's choice."[6] In June 2011, an FDA panel recommended that bevacizumab (Avastin) no longer be used to treat breast cancer, and in November officially rescinded its approval.

Antineoplastic Agents
Class Summary
Various chemotherapy regimens are recommended for the treatment of breast cancer. Common regimens include docetaxel, cyclophosphamide, doxorubicin, carboplatin, methotrexate, and trastuzumab, among others. View full drug information

Docetaxel (Taxotere)
Docetaxel is indicated for use in combination with doxorubicin and cyclophosphamide for adjuvant treatment of operable node-positive breast cancer. It is also indicated for locally advanced or metastatic breast cancer after failure of prior chemotherapy. It is a semisynthetic taxane, a class of drugs that inhibits cancer cell growth by
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promoting assembly and blocking the disassembly of microtubules, thereby preventing cancer cell division, leading to cell death. View full drug information

Carboplatin
Carboplatin is an analog of cisplatin. This is a heavy metal coordination complex that exerts its cytotoxic effect by platination of DNA, a mechanism analogous to alkylation, leading to interstrand and intrastrand DNA cross-links and inhibition of DNA replication. It binds to protein and other compounds containing the SH group. Cytotoxicity can occur at any stage of the cell cycle, but the cell is most vulnerable to the action of these drugs in the G1 and S phases. It has the same efficacy as cisplatin, but with a better toxicity profile. The main advantages over cisplatin include less nephrotoxicity and ototoxicity, not requiring extensive prehydration, and less likelihood of inducing nausea and vomiting; however, it is more likely to induce myelotoxicity. View full drug information

Doxorubicin (Liposomal)
Doxorubicin is a cytotoxic anthracycline that inhibits topoisomerase II and produces free radicals, which may cause destruction of DNA. It blocks DNA and RNA synthesis by inserting between adjacent base pairs and binding to the sugar-phosphate backbone of DNA, which causes DNA polymerase inhibition. It binds to nucleic acids, presumably by specific intercalation of the anthracycline nucleus with the DNA double helix. It is also a powerful iron chelator. The iron-doxorubicin complex induces production of free radicals that can destroy DNA and cancer cells. Maximum toxicity occurs during the S phase of the cell cycle. View full drug information

Capecitabine (Xeloda)
Capecitabine is a pyrimidine analog, which, in combination with docetaxel, is indicated for metastatic breast cancer after the failure of prior anthracycline-containing chemotherapy. Monotherapy with capecitabine is indicated for the treatment of patients with metastatic breast cancer resistant to both paclitaxel and an anthracycline containing chemotherapy regimen or resistant to paclitaxel and for whom further anthracycline therapy is not indicated.[16] View full drug information

Paclitaxel
Paclitaxel is indicated for adjuvant treatment of node-positive breast cancer (ie, administered sequentially to doxorubicin-containing combination chemotherapy). Dose-dense regimens (ie, more frequent administration) are currently being studied and resulting disease-free interval examined. Mechanisms of action are tubulin polymerization and microtubule stabilization, which, in turn, inhibit mitosis and may result in the breakage of chromosomes. View full drug information

Gemcitabine (Gemzar)
Gemcitabine is a pyrimidine analog that is metabolized intracellularly to an active nucleotide. It inhibits ribonucleotide reductase and competes with deoxycytidine triphosphate for incorporation into DNA. It is cell-cycle specific for the S phase. Gemcitabine, in combination with paclitaxel, is indicated as a first-line treatment for metastatic breast cancer after the failure of prior anthracycline-containing adjuvant chemotherapy (unless anthracyclines were clinically contraindicated). View full drug information

Cyclophosphamide
Cyclophosphamide is chemically related to nitrogen mustards. It is indicated for use in patients with carcinoma of the breast. It is activated in the liver to its active metabolite, 4-hydroxycyclophosphamide, which alkylates the target sites in susceptible cells in emedicine.medscape.com/article/1947145-medication an all-or-none type of reaction. As an alkylating agent, the mechanism of action 2/9

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target sites in susceptible cells in an all-or-none type of reaction. As an alkylating agent, the mechanism of action of the active metabolites may involve cross-linking of DNA, which may interfere with the growth of normal and neoplastic cells. View full drug information

Methotrexate (Trexall)
Methotrexate is an antimetabolite that inhibits dihydrofolate reductase, thereby hindering DNA synthesis and cell reproduction in malignant cells. Methotrexate is indicated alone or in combination with other anticancer agents for the treatment of breast cancer. View full drug information

Epirubicin (Ellence)
Epirubicin is indicated as a part of adjuvant therapy in patients with evidence of axillary-node tumor involvement following resection of primary breast cancer.[17] It is a cell cycle phase inhibitornonspecific anthracycline derivative of doxorubicin with maximum cytotoxic effects on the S and G2 phases of the cell cycle. View full drug information

Vinorelbine (Navelbine)
Vinorelbine is a semisynthetic vinca alkaloid that inhibits tubulin polymerization during the G2 phase of cell division, thereby inhibiting mitosis.

Antineoplastics, Monoclonal Antibodies

Class Summary
Monoclonal antibodies have been engineered to react against specific antigens on cancer cells, which can help to enhance the patients immune response and prevent cancer cell growth. The combination of both HER2 receptor antibodies (pertuzumab plus trastuzumab) is superior to either agent alone.[18] The indication for metastatic breast cancer (HER2-negative) was revoked by the FDA in November 2011 due to failure to delay tumor growth or provide survival benefit. The NCCN 2011 guidelines still recommend bevacizumab for targeted therapy [6] despite concerns expressed by the FDA.[19, 20] View full drug information

Trastuzumab (Herceptin)
Trastuzumab is a monoclonal antibody that binds to the extracellular human epidermal growth receptor 2 (HER2). It mediates antibody-dependent cellular cytotoxicity against cells that overproduce HER2. It is indicated for adjuvant treatment of HER2-overexpressing, node-positive or node-negative (ER/PR negative or with one high-risk feature) breast cancer, as part of a treatment regimen consisting of doxorubicin, cyclophosphamide, and either paclitaxel or docetaxel; with docetaxel and carboplatin; or as a single agent following multimodality anthracyclinebased therapy. It is also used in combination with paclitaxel for first-line treatment of HER2-overexpressing metastatic breast cancer and as a single agent for treatment of HER2-overexpressing breast cancer in patients who have received one or more chemotherapy regimens for metastatic disease.[21] View full drug information

Pertuzumab (Perjeta)
Pertuzumab is an HER2/neu receptor antagonist that elicits action at a different ligand binding site from trastuzumab to prevent HER2 dimerization. It is indicated in combination with trastuzumab and docetaxel for treatment of HER2-positive metastatic breast cancer in patients who have not previously received anti-HER2 therapy or chemotherapy.
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View full drug information

Denosumab (Xgeva)
Monoclonal antibody that specifically targets RANK ligand, an essential regulator of osteoclasts. Indicated to prevent SREs (ie, bone fractures and pain) in patients with bone metastases from solid tumors. View full drug information

Bevacizumab (Avastin)
The indication for metastatic breast cancer (HER2-negative) was revoked by the FDA in November 2011 due to failure to delay tumor growth or provide survival benefit. bevacizumab is a murine derived monoclonal antibody that inhibits angiogenesis by targeting and inhibiting vascular endothelial growth factor (VEGF). Inhibiting new blood vessel formation denies blood, oxygen, and other nutrients needed for tumor growth. This agent is used in combination with standard chemotherapy.

Tyrosine Kinase Inhibitors

Class Summary
Tyrosine kinase inhibitors play an important role in the modulation of growth factor signaling. They are commonly combined with other forms of chemotherapy or radiation therapy. View full drug information

Lapatinib (Tykerb)
Lapatinib is a 4-anilinoquinazoline kinase that inhibits intracellular tyrosine kinase domains of epidermal growth factor receptors (EGFR [ErbB1]) and HER2 (ErbB2). It is indicated in combination with capecitabine for advanced or metastatic breast cancer with tumors that over-express HER2 for which previous therapy (ie, anthracycline, taxane, and trastuzumab) was not effective. It is also used in combination with letrozole for the treatment of postmenopausal women with hormone receptorpositive metastatic breast cancer tumors that over expresses the HER2 receptor for whom hormonal therapy is indicated.[22] View full drug information

Everolimus (Afinitor)
An mTOR kinase inhibitor; binds to intracellular protein, FKBP-12, resulting in an inhibitory complex formation with mTOR complex 1. Indicated in postmenopausal women with advanced hormone receptor-positive, HER2-negative breast cancer in combination with exemestane after failure of treatment with letrozole or anastrozole.

Aromatase Inhibitors
Class Summary
Aromatase inhibitors play a role in adjuvant therapy in breast cancer. These agents work by inhibiting aromatase, the enzyme responsible for converting other steroid hormones into estrogen. View full drug information

Anastrozole (Arimidex)
Anastrozole significantly lowers serum estradiol concentrations by inhibiting the conversion of adrenally generated androstenedione to estrone. It is used as first-line treatment of breast cancer in postmenopausal women with hormone receptorpositive or hormone receptorunknown locally advanced or metastatic disease. It is also used to treat advanced breast cancer in postmenopausal women with disease progression following tamoxifen therapy. View full drug information
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Letrozole (Femara)
Letrozole is a nonsteroidal competitive inhibitor of the aromatase enzyme system. It inhibits the conversion of androgens to estrogens. Letrozole is indicated for the adjuvant treatment of postmenopausal women with hormone receptorpositive early breast cancer. It is also used for first-line treatment of postmenopausal women with hormone receptorpositive or hormone receptorunknown locally advanced or metastatic breast cancer. It is also indicated for the treatment of advanced breast cancer in postmenopausal women with disease progression following antiestrogen therapy and for the extended adjuvant treatment of early breast cancer in postmenopausal women who have received 5 years of adjuvant tamoxifen therapy.[23] View full drug information

Exemestane (Aromasin)
Exemestane elicits irreversible steroidal aromatase inactivation by acting as a false substrate for the aromatase enzyme. It binds irreversibly to the aromatase enzyme active site, causing inactivation (ie, suicide inhibition). It significantly lowers circulating estrogen concentrations in postmenopausal women. It differs from tamoxifen in that it inhibits estrogen production, whereas tamoxifen inhibits estrogen at the receptor site. It is indicated for advanced breast cancer in postmenopausal women whose disease has progressed following tamoxifen therapy.

Bisphosphonate Agents
Class Summary
Bisphosphonates are complementary to chemotherapy and hormone therapy because they may lessen the damage to bone from metastatic disease. Bisphosphonates inhibit osteoclast function and reduce the resorption of bone. View full drug information

Zoledronic Acid (Zometa, Reclast)

Zoledronic acid inhibits bone resorption, possibly by acting on osteoclasts or osteoclast precursors.

Selective Estrogen Receptor Modulators (SERMs)

Class Summary
SERMs stimulate or inhibit the estrogen receptors of various target tissues. Examples of SERMs include tamoxifen, raloxifene, and toremifene. View full drug information

Tamoxifen
SERMs stimulate or inhibit the estrogen receptors of various target tissues. Examples of SERMs include tamoxifen, raloxifene, and toremifene. View full drug information

Raloxifene (Evista)
Raloxifene is a selective nonsteroidal benzothiophene, estrogen receptor modulator. It is indicated for risk reduction for invasive breast cancer in postmenopausal women with osteoporosis. In addition, it is indicated for risk reduction in invasive breast cancer in postmenopausal women at high risk of invasive breast cancer. View full drug information

Toremifene (Fareston)
Toremifene is a nonsteroidal triphenylethylene derivative that binds to estrogen receptors. It may exert estrogenic
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activities, antiestrogenic activities, or both activities. It is indicated for metastatic breast cancer in postmenopausal women with estrogen-receptorpositive or unknown tumors.[24]

Antimicrotubular agent
Class Summary
May consider use in patients who have received at least 2 chemotherapeutic regimens for metastatic disease. View full drug information

Eribulin (Halaven)
Microtubule inhibitor. Inhibits growth phase of microtubules, leading to G2/M cell-cycle block, disruption of mitotic spindles, and, ultimately, apoptotic cell death. Indicated for metastatic breast cancer in patients who have previously received at least 2 chemotherapeutic regimens for the treatment of metastatic disease. Prior therapy should have included an anthracycline and a taxane in either the adjuvant or metastatic setting.

Contributor Information and Disclosures

Author Alison T Stopeck, MD Associate Professor of Medicine, Arizona Cancer Center, University of Arizona Health Sciences Center; Director of Clinical Breast Cancer Program, Arizona Cancer Center; Medical Director of Coagulation Laboratory, University Medical Center; Director of Arizona Hemophilia and Thrombosis Center Alison T Stopeck, MD is a member of the following medical societies: American Association for Cancer Research, American College of Physicians, American Society of Clinical Oncology, American Society of Hematology, Hemophilia and Thrombosis Research Society, and Southwest Oncology Group Disclosure: Genentech Honoraria Speaking and teaching; AstraZeneca Honoraria Speaking and teaching; AstraZeneca Grant/research funds Other Coauthor(s) Patricia A Thompson, PhD Assistant Professor, Department of Pathology, University of Arizona, Tucson Disclosure: Nothing to disclose. Chief Editor Jules E Harris, MD Clinical Professor of Medicine, Section of Hematology/Oncology, University of Arizona College of Medicine, Arizona Cancer Center Jules E Harris, MD is a member of the following medical societies: American Association for Cancer Research, American Association for the Advancement of Science, American Association of Immunologists, American Society of Hematology, and Central Society for Clinical Research Disclosure: Nothing to disclose. Additional Contributors Leona Downey, MD Assistant Professor of Internal Medicine, Section of Oncology and Hematology, University of Arizona, Arizona Cancer Center Leona Downey, MD is a member of the following medical societies: American Geriatrics Society, American Society of Clinical Oncology, and Southwest Oncology Group Disclosure: Nothing to disclose.
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Manjit Singh Gohel, MD, MRCS, MB, ChB Specialist Registrar, Division of Breast and Endocrine Surgery, Northwick Park Hospital Disclosure: Nothing to disclose. Harold Harvey, MD Professor, Department of Medicine, Pennsylvania State University Disclosure: Nothing to disclose. Kanchan Kaur, MBBS, MS (General Surgery), MRCS (Ed) Consulting Breast and Oncoplastic Surgeon, Medanta, The Medicity, India Disclosure: Nothing to disclose. Julie Lang, MD Assistant Professor of Surgery and the BIO5 Institute, Director of Breast Surgical Oncology, University of Arizona College of Medicine Julie Lang, MD is a member of the following medical societies: American College of Surgeons, American Society of Breast Surgeons, American Society of Clinical Oncology, Association for Academic Surgery, and Society of Surgical Oncology Disclosure: Genomic Health Grant/research funds Speaking and teaching; Agendia Grant/research funds Speaking and teaching; Surgical Tools Grant/research funds Research; Sysmex Grant/research funds Research Robert B Livingston, MD Professor of Clinical Medicine and Director, Clinical Research Shared Services, Arizona Cancer Center Robert B Livingston, MD is a member of the following medical societies: American Association for Cancer Research, American Federation for Clinical Research, and American Society of Clinical Oncology Disclosure: Nothing to disclose. Hanan Makhoul, MD Staff Physician, Department of Internal Medicine, University of Arkansas School of Medicine Disclosure: Nothing to disclose. Issam Makhoul, MD Associate Professor, Department of Medicine, Division of Hematology/Oncology, University of Arkansas for Medical Sciences Issam Makhoul, MD is a member of the following medical societies: American Society of Clinical Oncology and American Society of Hematology Disclosure: Nothing to disclose. Robert C Shepard, MD, FACP Associate Professor of Medicine in Hematology and Oncology at University of North Carolina at Chapel Hill; Vice President of Scientific Affairs, Therapeutic Expertise, Oncology, at PRA International Robert C Shepard, MD, FACP is a member of the following medical societies: American Association for Cancer Research, American College of Physician Executives, American College of Physicians, American Federation for Clinical Research, American Federation for Medical Research, American Medical Association, American Medical Informatics Association, American Society of Hematology, Association of Clinical Research Professionals, Eastern Cooperative Oncology Group, European Society for Medical Oncology, Massachusetts Medical Society, and Society for Biological Therapy Disclosure: Nothing to disclose. Hemant Singhal, MD, MBBS, FRCSE, FRCS(C) Senior Lecturer, Director of Breast Service, Department of Surgery, Imperial College School of Medicine; Consultant Surgeon, Northwick Park and St Marks Hospitals, UK Hemant Singhal, MD, MBBS, FRCSE, FRCS(C) is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada and Royal College of Surgeons of Edinburgh Disclosure: Nothing to disclose.
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Carl V Smith, MD The Distinguished Chris J and Marie A Olson Chair of Obstetrics and Gynecology, Professor, Department of Obstetrics and Gynecology, Senior Associate Dean for Clinical Affairs, University of Nebraska Medical Center Carl V Smith, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Institute of Ultrasound in Medicine, Association of Professors of Gynecology and Obstetrics, Central Association of Obstetricians and Gynecologists, Council of University Chairs of Obstetrics and Gynecology, Nebraska Medical Association, and Society for Maternal-Fetal Medicine Disclosure: Nothing to disclose. Wiley Souba, MD Chairman, Professor, Department of General Surgery, Pennsylvania State College of Medicine; Chief Surgeon, The Milton S Hershey Medical Center Disclosure: Nothing to disclose. Rachel Swart, MD, PhD Assistant Professor of Medicine, Department of Hematology and Oncology, Arizona Cancer Center, University of Arizona Rachel Swart, MD, PhD is a member of the following medical societies: American Association for Cancer Research, American Society of Clinical Oncology, Arizona Medical Association, and Southwest Oncology Group Disclosure: Roche Grant/research funds Other Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Medscape Salary Employment Simon Thomson, MB, BCh, MD, FRCS Specialist Registrar, Department of Breast and Endocrine Surgery, Northwick Park Hospital, UK Simon Thomson, MB, BCh, MD, FRCS is a member of the following medical societies: British Medical Association Disclosure: Nothing to disclose.

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dense breast tissue. Available at http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm319867.htm. Accessed September 18, 2012. 8. Taillefer R. The role of 99mTc-sestamibi and other conventional radiopharmaceuticals in breast cancer diagnosis. Semin Nucl Med. Jan 1999;29(1):16-40. 9. Weir L, Worsley D, Bernstein V. The value of FDG positron emission tomography in the management of patients with breast cancer. Breast J. May-Jun 2005;11(3):204-9. 10. [Guideline] National Comprehensive Cancer Network Practice Guidelines. Invasive Breast Cancer. 2009. (Registered Users Only). [Full Text]. 11. [Guideline] Wolff AC, Hammond ME, Schwartz JN, et al. American Society of Clinical Oncology/College of American Pathologists guideline recommendations for human epidermal growth factor receptor 2 testing in breast cancer. J Clin Oncol. Jan 1 2007;25(1):118-45. 12. Fisher B, Costantino JP, Wickerham DL, et al. Tamoxifen for prevention of breast cancer: report of the National Surgical Adjuvant Breast and Bowel Project P-1 Study. J Natl Cancer Inst. Sep 16 1998;90(18):1371-88. 13. Bear HD, Anderson S, Smith RE, et al. Sequential preoperative or postoperative docetaxel added to preoperative doxorubicin plus cyclophosphamide for operable breast cancer:National Surgical Adjuvant Breast and Bowel Project Protocol B-27. J Clin Oncol. May 1 2006;24(13):2019-27. [Medline]. 14. [Best Evidence] [Guideline] Visvanathan K, Chlebowski RT, Hurley P, Col NF, Ropka M, Collyar D, 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. Jul 1 2009;27(19):3235-58. 15. Cristofanilli M. Circulating tumor cells, disease progression, and survival in metastatic breast cancer. Semin Oncol. Jun 2006;33(3 Suppl 9):S9-14. 16. Xeloda [package insert]. South San Francisco, Calif: Genentech; November 2009. 17. Ellence [package insert]. New York, NY: Pfizer; February 2007. 18. Baselga J, Corts J, Kim SB, Im SA, Hegg R, Im YH, et al. Pertuzumab plus trastuzumab plus docetaxel for metastatic breast cancer. N Engl J Med. Jan 12 2012;366(2):109-19. [Medline]. 19. The U.S. Food and Drug Administration. FDA begins process to remove breast cancer indication from Avastin label. FDA NEWS RELEASE: Dec. 16, 2010. Available at http://www.fda.gov/newsevents/newsroom/pressannouncements/ucm237172.htm. Accessed July 15, 2011. 20. The U.S. Food and Drug Administration. Postmarket Drug Safety Information: Avastin (bevacizumab) Information, Update, 6/29/2011. Accessed July 15, 2011. [Full Text]. 21. Herceptin [package insert]. South San Francisco, Calif: Genentech; October 2010. 22. Tykerb [package insert]. Research Triangle Park, NC: GlaxoSmithKline; January 2010. 23. Femara [package insert]. East Hanover, NJ: Novartis; April 2010. 24. Fareston [package insert]. Memphis, Tenn: GTX; December 2004. Medscape Reference 2011 WebMD, LLC 25. James TA, Mace JL, Virnig BA, et al. Preoperative needle biopsy improves the quality of breast cancer surgery. J Am Coll Surg. Oct 2012;215(4):562-8. [Medline]. 26. Mulcahy N. Breast cancer needle biopsy in 'granular' detail. Medscape Medical News. Available at http://www.medscape.com/viewarticle/772152. Accessed Oct 15 2012.

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