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Breast Cancer Medication

  • Author: Pavani Chalasani, MD, MPH; Chief Editor: Jules E Harris, MD, FACP, FRCPC  more...
 
Updated: Feb 23, 2016
 

Medication Summary

Adjuvant treatment for breast cancer involves radiation therapy and a variety of chemotherapeutic and biologic agents. It 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.

In patients receiving adjuvant aromatase inhibitor therapy for breast cancer who are at high risk for fracture, the monoclonal antibody denosumab or either of the bisphosphonates zoledronic acid and pamidronate may be added to the treatment regimen to increase bone mass. These agents are given along with calcium and vitamin D supplementation.

Bevacizumab, a humanized monoclonal antibody that inhibits angiogenesis, had been approved for use in combination therapy for metastatic breast cancer. In November 2011, however, the US Food and Drug Administration (FDA) revoked its approval for this indication, after concluding that bevacizumab had not been shown to be safe and effective for that use.[147]

In December 2013, Hoffmann-La Roche, manufacturer of capecitabine (Xeloda), an oral agent for the treatment of breast and colorectal cancers, reported that in rare cases, patients using the drug may develop potentially fatal cutaneous disease, such as Stevens-Johnson syndrome or toxic epidermal necrolysis. Signs and symptoms of severe skin reactions may include flu-like symptoms, fever, itching, mouth sores, and burning eyes, as well as a painful, red or purplish rash that causes the skin to shed.[148]

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Antineoplastics, Antimicrotubular

Class Summary

Use of antimicrotubular therapy may be considered in patients who have received at least 2 chemotherapeutic regimens for metastatic disease.

Eribulin (Halaven)

 

Eribulin inhibits the growth phase of microtubules, leading to G2/M cell-cycle block, disruption of mitotic spindles, and, ultimately, apoptotic cell death. It is 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 the metastatic setting.

Docetaxel (Taxotere, Docefrez)

 

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 promoting assembly and blocking the disassembly of microtubules, thereby preventing cancer cell division and leading to cell death.

Paclitaxel (Abraxane)

 

Paclitaxel is indicated for adjuvant treatment of node-positive breast cancer; it is administered sequentially after 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.

Ixabepilone (Ixempra)

 

Ixabepilone is a semisynthetic analogue of epothilone B that inhibits microtubules, halting cell division in the mitotic phase and resulting in cell death. It is used mostly in combination with capecitabine in patients with recurrent or metastatic breast cancer in whom therapy with other first-line agents (eg, an anthracycline and a taxane) has failed.

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Antineoplastics, Alkylating

Class Summary

Alkylating agents constitute one of the earliest classes of antineoplastic agents used to treat cancer. They work by cross-linking DNA, which impedes cellular growth. They can be used alone or in combination with other chemotherapeutic agents.

Carboplatin (Paraplatin)

 

Carboplatin is an analogue of cisplatin. It 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.

Carboplatin has the same efficacy as cisplatin but a better toxicity profile. Its main advantages over cisplatin include less nephrotoxicity and ototoxicity, absence of a need for extensive prehydration, and reduced likelihood of inducing nausea and vomiting; however, it is more likely to induce myelotoxicity.

Cyclophosphamide (Cytoxan)

 

Cyclophosphamide is chemically related to nitrogen mustards. It can be used as a single agent or in various combination chemotherapy regimens for recurrent or metastatic breast cancer.

Cyclophosphamide is activated in the liver to its active metabolite, 4-hydroxycyclophosphamide, which alkylates the target sites in susceptible cells in an all-or-none type of reaction. 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.

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Antineoplastics, Anthracycline

Class Summary

Anthracyclines work in multiple ways, including intercalation between DNA base pairs and inhibition of type II topoisomerase function, resulting in inhibition of cell replication and transcription. They also work by inhibition of DNA helicase, resulting in DNA cleavage.

Doxorubicin (Liposomal) (Adriamycin, Doxil)

 

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.

This agent 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.

Epirubicin (Ellence)

 

Epirubicin is indicated as a part of adjuvant therapy in patients with evidence of axillary-node tumor involvement after resection of primary breast cancer.[142] It can be used as a single agent, but such use is much less common in the setting of recurrent or metastatic disease. Epirubicin is a cell cycle phase inhibitor–nonspecific anthracycline derivative of doxorubicin with maximum cytotoxic effects on the S and G2 phases of the cell cycle.

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Antineoplastics, Antimetabolite

Class Summary

Antimetabolite therapy can stop cancer cell growth and cell division by interfering with DNA replication of these cells. These drugs are often first-line agents for breast cancer.

Capecitabine (Xeloda)

 

Capecitabine is a pyrimidine analogue that, 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 that either is resistant to both paclitaxel and an anthracycline-containing chemotherapy regimen or is resistant to paclitaxel in a situation where further anthracycline therapy is not indicated.[143] It is the preferred first-line agent for human epidermal growth receptor 2 (HER2)-positive disease, along with trastuzumab.

Gemcitabine (Gemzar)

 

Gemcitabine is a pyrimidine analogue 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).

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.

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Antineoplastics, Vinca Alkaloid

Class Summary

Monoclonal antibodies have been engineered to react against specific antigens on cancer cells, thereby potentially helping to enhance the patient’s immune response and prevent cancer cell growth.

Vinorelbine (Navelbine)

 

Vinorelbine is a semisynthetic vinca alkaloid that inhibits tubulin polymerization during the G2 phase of cell division, thereby inhibiting mitosis. This agent is a preferred first-line agent, with trastuzumab, for HER2-positive breast cancer. It is also used alone to treat recurrent or metastatic disease.

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Monoclonal Antibodies

Class Summary

Monoclonal antibodies have been engineered to react against specific antigens on cancer cells, which can help to enhance the patient’s immune response and prevent cancer cell growth. The combination of both HER2 receptor antibodies (pertuzumab plus trastuzumab) is superior to either agent alone.

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 despite concerns expressed by the FDA.

ado-trastuzumab emtansine (Kadcyla, TDMI-1)

 

Ado-trastuzumab emtansine is an HER2-targeted antibody (trastuzumab) covalently linked to a microtubule inhibitor (DM1, a maytansine derivative). It is indicated for the treatment of HER2-positive metastatic breast cancer after prior trastuzumab and taxane therapy.

Upon binding to sub-domain IV of the HER2 receptor, ado-trastuzumab emtansine undergoes receptor-mediated internalization and subsequent lysosomal degradation, resulting in intracellular release of DM1-containing cytotoxic catabolites. Binding of DM1 to tubulin disrupts microtubule networks in the cell, which results in cell cycle arrest and apoptotic cell death

Denosumab (Prolia, Xgeva)

 

Denosumab is a monoclonal antibody that specifically targets RANK ligand, an essential regulator of osteoclasts. This agent is indicated to prevent skeletal-related events (ie, bone fractures, spinal cord compression, or hypercalcemia) in patients with bone metastases from solid tumors whose expected survival exceeds 3 months.

Osteonecrosis of the jaw in patients receiving denosumab has often been associated with dental procedures. Consequently, patients should undergo a dental examination before the initiation of denosumab therapy to determine whether they might benefit from preventive dentistry procedures.

Trastuzumab (Herceptin)

 

Trastuzumab is a monoclonal antibody that binds to extracellular HER2. It mediates antibody-dependent cellular cytotoxicity against cells that overproduce HER2.

Trastuzumab is indicated for adjuvant treatment of HER2-overexpressing, node-positive or node-negative (estrogen receptor [ER]/progesterone receptor [PR]-negative or with 1 high-risk feature) breast cancer, either as part of a treatment regimen consisting of doxorubicin, cyclophosphamide, and either paclitaxel or docetaxel or as part of a regimen that also includes docetaxel and carboplatin.

Trastuzumab is also indicated for use as a single agent after multimodality anthracycline-based therapy. The combination of trastuzumab and an anthracycline is associated with significant cardiac toxicity.

This agent 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 1 or more chemotherapy regimens for metastatic disease.[144]

Pertuzumab (Perjeta)

 

Pertuzumab is a monoclonal antibody that binds to the extracellular domain of the HER2 receptor. It is indicated for the treatment of metastatic HER2-positive breast cancer in combination with trastuzumab and docetaxel. It is also the first drug approved for neoadjuvant treatment of breast cancer for patients with HER2-positive, locally advanced, inflammatory, or early stage breast cancer. It is also used in combination with trastuzumab and docetaxel for neoadjuvant treatment.

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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.

Lapatinib (Tykerb)

 

Lapatinib is a 4-anilinoquinazoline kinase that inhibits the intracellular tyrosine kinase domains of epidermal growth factor receptor (EGFR [ErbB1]) and HER2 (ErbB2). This agent is indicated in combination with capecitabine for advanced or metastatic breast cancer in patients with tumors that overexpress HER2 and for which previous therapy (ie, anthracycline, taxane, and trastuzumab) was not effective.

This agent is also used in combination with letrozole for the treatment of postmenopausal women with hormone receptor–positive metastatic breast cancer tumors that overexpress the HER2 receptor, for whom hormonal therapy is indicated.[145]

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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. All 3 selective aromatase inhibitors (anastrozole, letrozole, and exemestane) have similar antitumor efficacy and similar toxicity profiles.

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 receptor–positive or hormone receptor–unknown locally advanced or metastatic disease. It is also used to treat advanced breast cancer in postmenopausal women with disease progression after tamoxifen therapy.

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 adjuvant treatment of postmenopausal women with hormone receptor–positive early breast cancer. It is also used for first-line treatment of postmenopausal women with hormone receptor–positive or hormone receptor–unknown locally advanced or metastatic breast cancer.

Letrozole is also indicated for treatment of advanced breast cancer in postmenopausal women with disease progression after antiestrogen therapy and for extended adjuvant treatment of early breast cancer in postmenopausal women who have received 5 years of adjuvant tamoxifen therapy.[146]

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.

Exemestane differs from tamoxifen in that it inhibits estrogen production, whereas tamoxifen inhibits estrogen at the receptor site. It may be superior to tamoxifen for breast cancer chemoprevention, with a better safety profile. However, exemestane is not yet indicated for this application by the American Society of Clinical Oncology (ASCO). It is indicated for advanced breast cancer in postmenopausal women whose disease has progressed after tamoxifen therapy. Off-label use of exemestane is suggested as an alternative to tamoxifen or raloxifene in the 2013 ASCO guidelines to reduce the risk of ER-positive breast cancer in high-risk postmenopausal women.[135]

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CDK Inhibitor

Class Summary

Approval of palbociclib for initial endocrine-based therapy in postmenopausal women was based on the phase II trial (PALOMA-1) which measured median progression-free survival (PFS) duration. The mean PFS was 10.2 months (95% CI; 5.7-12.6) in the letrozole group and 20.2 months (95% CI 13.8- 27.5) for palbociclib plus letrozole group.[131]

The approval for ER+/HER2- advanced breast cancer in combination with fulvestrant in women (regardless of menopausal status) with disease progression following endocrine therapy was based on the PALOMA-3 trial (n=521). PFS was prolonged with palbociclib plus fulvestrant compared with fulvestrant alone (9.2 mo vs 3.8 mo; p <0.001).[166]

Palbociclib (Ibrance)

 

Palbociclib is a cyclin dependent kinases (CDK) 4,6 inhibitor. It reduces cellular proliferation of ER-positive breast cancer cell lines by blocking progression of the cell from G1 into S phase of the cell cycle. It is indicated in combination with letrozole for treatment of postmenopausal women with estrogen receptor (ER)-positive, human epidermal growth factor receptor 2 (HER2)-negative advanced breast cancer as initial endocrine-based therapy for their metastatic disease. It is also approved for ER+/HER2- advanced breast cancer in combination with fulvestrant in women (regardless of menopausal status) with disease progression following endocrine therapy.

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Calcium Metabolism Modifiers

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. An intravenous bisphosphonate should be used in combination with oral calcium citrate and vitamin D supplementation in bone metastasis, according to the National Comprehensive Cancer Network (NCCN) 2012 guidelines.[67]

Pamidronate (Aredia)

 

Pamidronate disodium is a bone resorption inhibitor that absorbs calcium phosphate crystals and prevents the dissolution of this mineral. It also inhibits osteoclast activity in the bone.

Zoledronic Acid (Zometa, Reclast)

 

Zoledronic acid inhibits bone resorption by acting on osteoclasts or osteoclast precursors. It may be superior to pamidronate in patients with lytic bone metastases.

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Antineoplastics, Estrogen Receptor Antagonist

Class Summary

Selective estrogen receptor modulators (SERMs) stimulate or inhibit the estrogen receptors of various target tissues. Examples of SERMs include tamoxifen, raloxifene, and toremifene.

Tamoxifen (Nolvadex, Soltamox)

 

Tamoxifen is a nonsteroid with potent antiestrogenic effects in the breast; however, it may be an estrogen agonist in the uterus. CYP2C19 heterozygous*2 carriership may be a predictive factor for longer survival in patients with breast cancer who are taking tamoxifen.[147] Tamoxifen is considered the gold standard for prevention of breast cancer in high-risk women, as adjuvant treatment for breast cancer, and in metastatic breast cancer.

Raloxifene (Evista)

 

Raloxifene is a selective nonsteroidal benzothiophene ER modulator. It is indicated for reducing the risk of invasive breast cancer in postmenopausal women with osteoporosis. In addition, it is indicated for risk reduction in postmenopausal women at high risk for invasive breast cancer.

Toremifene (Fareston)

 

Toremifene is a nonsteroidal triphenylethylene derivative that binds to estrogen receptors. It may exert estrogenic activities, antiestrogenic activities, or both. It is indicated for metastatic breast cancer in postmenopausal women with ER-positive or ER-unknown tumors.[148]

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Contributor Information and Disclosures
Author

Pavani Chalasani, MD, MPH Assistant Professor of Medicine, Section of Hematology/Oncology, Department of Medicine, Arizona Health Sciences Center, University of Arizona College of Medicine

Pavani Chalasani, MD, MPH is a member of the following medical societies: American Association for Cancer Research, American College of Physicians, American Society of Hematology, SWOG, American Society of Clinical Oncology, Hemostasis and Thrombosis Research Society

Disclosure: Nothing to disclose.

Chief Editor

Jules E Harris, MD, FACP, FRCPC Clinical Professor of Medicine, Section of Hematology/Oncology, University of Arizona College of Medicine, Arizona Cancer Center

Jules E Harris, MD, FACP, FRCPC is a member of the following medical societies: American Association for the Advancement of Science, American Society of Hematology, Central Society for Clinical and Translational Research, American Society of Clinical Oncology

Disclosure: Nothing to disclose.

Additional Contributors

Alison T Stopeck, MD 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 Hematology, SWOG, American Society of Clinical Oncology, Hemophilia and Thrombosis Research Society

Disclosure: Received honoraria from Genentech for speaking and teaching; Received honoraria from AstraZeneca for speaking and teaching; Received grant/research funds from AstraZeneca for other.

Patricia A Thompson, PhD Assistant Professor, Department of Pathology, University of Arizona College of Medicine

Disclosure: Nothing to disclose.

Acknowledgements

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.

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.

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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Anatomy of the breast.
Intrinsic subtypes of breast cancer.
Breast cancer. Intraductal carcinoma, comedo type. Distended duct with intact basement membrane and central tumor necrosis.
Breast cancer. Intraductal carcinoma, noncomedo type. Distended duct with intact basement membrane, micropapillary, and early cribriform growth pattern.
Breast cancer. Lobular carcinoma in situ. Enlargement and expansion of lobule with monotonous population of neoplastic cells.
Breast cancer. Lobular carcinoma in situ. Enlargement and expansion of lobule with monotonous population of neoplastic cells.
Breast cancer. Infiltrating ductal carcinoma. Low-grade carcinoma with well-developed glands invading fibrous stroma.
Breast cancer. Colloid (mucinous) carcinoma. Nests of tumor cells in pool of extracellular mucin.
Breast cancer. Papillary carcinoma. Solid papillary growth pattern with early cribriform and well-developed thin papillary fronds.
Anatomy of the breast. Courtesy of Wikimedia Commons (Patrick J Lynch, medical illustrator).
Table 1. Accuracy of Breast Imaging Modalities
Modality Sensitivity Specificity PPV Indications
Mammography 63-95% (>95% palpable, 50% impalpable, 83-92% in women older than 50 y; decreases to 35% in dense breasts) 14-90% (90% palpable) 10-50%



(94% palpable)



Initial investigation for symptomatic breast in women older than 35 y and for screening; investigation of choice for microcalcification
Ultrasonography 68-97% palpable 74-94% palpable 92% (palpable) Initial investigation for palpable lesions in women younger than 35 y
MRI 86-100% 21-97% (< 40% primary cancer) 52% Scarred breast, implants, multifocal lesions, and borderline lesions for breast conservation; may be useful in screening high-risk women
Scintigraphy 76-95% palpable, 52-91% impalpable 62-94% (94% impalpable) 70-83% (83% palpable, 79% impalpable) Lesions >1 cm and axilla assessment; may help predict drug resistance
PET 96% (90% axillary metastases) 100%   Axilla assessment, scarred breast, and multifocal lesions
MRI = magnetic resonance imaging; PET = positron emission tomography; PPV = positive predictive value.
Table 2. Grading System in Invasive Breast Cancer (Modified Bloom and Richardson)
  Score
  1 > 2 > 3
A. Tubule formation >75% 10-75% < 10%
B. Mitotic count/HPF (microscope- and field-dependent) < 7 7-12 >12
C. Nuclear size and pleomorphism Near normal; little variation Slightly enlarged; moderate variation Markedly enlarged; marked variation
Grade I cancer if total score (A + B + C) is 3-5
Grade II cancer if total score (A + B + C) is 6 or 7
Grade III cancer if total score (A + B + C) is 8 or 9
HPF = high-power field.
Table 3. Ductal Carcinoma in Situ Subtypes
DCIS Characteristic Comedo Noncomedo
Nuclear grade High Low
Estrogen receptor Often negative Positive
Distribution Continuous Multifocal
Necrosis Present Absent
Local recurrence High Low
Prognosis Worse Better
DCIS = ductal carcinoma in situ.
Table 4. TNM Staging System for Breast Cancer
Stage Tumor Node Metastases
Stage 0 Tis N0 M0
Stage I T1 N0 M0
Stage IIA T0



T1



T2



N1



N1



N0



M0



M0



M0



Stage IIB T2



T3



N1



N0



M0



M0



Stage IIIA T0



T1



T2



T3



N2



N2



N2



N1-2



M0



M0



M0



M0



Stage IIIB T4



T4



T4



N0



N1



N2



M0



M0



M0



Stage IIIC Any T N3 M0
Stage IV Any T Any N M1
Table 5. Hormone Agents Used in Breast Cancer
Agent Dose and Schedule
Postmenopausal
Tamoxifen 20 mg PO every day
Or
Aromatase inhibitor
Anastrozole 1 mg PO every day
Letrozole 2.5 mg PO every day
Exemestane 25 mg PO every day
Or
Fulvestrant 500 mg IM loading dose followed



by 250 mg IM every month



Or
Megestrol 40 mg PO 4 times a day
Premenopausal
Tamoxifen 20 mg PO every day
Or
Aromatase inhibitor + LHRH*
Leuprolide 7.5 mg IM depot q28d



22.5 mg IM q3mo



30 mg IM q4mo



Goserelin 3.6 mg SC depot q28d



10.8 mg SC q3mo



Megestrol 40 mg PO 4 times a day
*LHRH = luteinizing hormone–releasing hormone.
Table 6. Targeted Chemotherapy for Metastatic Breast Cancer
Drug Class Dose/Schedule Overall Response Rate (ORR) Toxicity
Capecitabine Oral fluoro-pyrimidine 1250 mg/m²/d PO for 2 weeks with 1 wk off 30% Rash, hand-foot syndrome,



diarrhea, mucositis



Docetaxel Antimicrotubule 75-100 mg/m² IV q3wk



or



40 mg/m²/wk X IV for 6 wk with 2 wk off



30-68% Myelosuppression, alopecia,



skin reaction, mucositis,



and fluid retention



Doxorubicin Anthracycline



(antitumor antibiotic)



45-60 mg/m² IV q3wk



or



20 mg/m² IV qwk (not to



exceed a cumulative dose



of 450-500 mg/m²)



35-50% Myelosuppression, nausea/



vomiting, mucositis, diarrhea



cardiotoxicity, alopecia



Doxil (liposomal



encapsulated



doxorubicin)



Anthracycline 20 mg/m² IV q2wk



or



35-40 mg/m² IV q4wk



  Less cardiotoxicity, neutropenia, alopecia, stomatitis, hand-foot



syndrome



Epirubicin Anthracycline 90 mg/m² IV q3wk (not



to exceed cumulative dose



of 900 mg/m²)



35-50% Myelosuppression, mucositis, nausea, vomiting, cardiotoxicity
Gemcitabine Antimetabolite 725 mg/m²/wk IV for 3 wk



then 1 wk off



or



1 g/m²/wk



IV X 2 then 1 wk off



  Myelosuppression, nausea/



vomiting, flulike syndrome,



elevated LFTs



Nab-paclitaxel Antimicrotubule 80-100 mg/m²/wk IV X 3 then 1 wk off



or



260 mg/m² IV q3wk



58-62%



33%



Less neuropathy, and allergic reaction
Paclitaxel Antimicrotubule 80 mg/m²/wk IV



or



175 mg/m² IV over 3 hours q3wk



25-50% Myelosuppression, alopecia,



neuropathy, allergic reaction



Trastuzumab Monoclonal antibody 4 mg/kg loading dose, then 2



mg/kg weekly or



8 mg/kg



loading dose, then 6 mg/kg



q3wk



10-15% Fever, allergic reaction,



cardiotoxicity/congestive heart failure



Pertuzumab Monoclonal antibody 840 mg IV loading dose,



then 420 mg q3wk



Give with trastuzumab and docetaxel



80.2% (objective response rate) Fever, allergic reaction,



cardiotoxicity/congestive heart failure



Palbociclib CDK inhibitor 125 mg/day PO for 3 weeks with 1 wk off



Give with letrozole



Data are not available for ORR



Mean PFS was 10.2 months in the letrozole group and 20.2 months for palbociclib plus letrozole group



Neutropenia, leukopenia, thrombocytopenia, anemia, stomatitis
Vinorelbine Vinca alkaloid 20 mg/m²/wk IV 35-45% Myelosuppression, nausea/



vomiting, constipation, fatigue,



stomatitis, anorexia



Table 7. Combination Regimens for Metastatic Breast Cancer
Chemotherapy Dose and Schedule Cycle
XT
Capecitabine



Docetaxel



1250 mg/m² bid days 1-14



75 mg/m² day 1



Repeat cycle every 21 days



May decrease capecitabine dose



to 850-1000 mg/m² to reduce



toxicity risk



XP
Capecitabine



Paclitaxel



825 mg/m² bid days 1-14



175 mg/m² day 1



Repeat cycle every 21 days
XN
Capecitabine



Navelbine



1000 mg/m² bid days 1-14



25 mg/m² days 1 and 8



Repeat cycle every 21 days
Gemcitabine[128]



Paclitaxel



1250 mg/m² days 1 and 8



175 mg/m² day 1



Repeat cycle every 21 days
Carboplatin[129]



Paclitaxel



AUC of 6 day 1



200 mg/m² day 1



Repeat cycle every 21 days
Carboplatin[130]



Docetaxel



AUC of 6 day 1



75 mg/m² day 1



Repeat cycle every 21 days
Palbociclib[131]



Letrozole



125 mg PO once daily days 1-21



2.5 mg PO once daily days 1-28



Repeat cycle every 28 days
Paclitaxel[132] 90 mg/m² day 1, 8, and 15 Repeat cycle every 28 days
HER2-positive metastatic breast cancer regimens
Trastuzumab



Paclitaxel



4 mg/kg loading dose then



2 mg/kg weekly



80 mg/m² IV weekly



 
Trastuzumab



Docetaxel



8 mg/kg loading dose then



6 mg/kg day 1



100 mg/m² IV day 1



Repeat cycle every 21 days
Trastuzumab



Vinorelbine



4 mg/kg loading dose then



2 mg/kg weekly



25 mg/m² day 1 weekly



 
Lapatinib



Capecitabine



1250 mg PO daily



2000 mg/m² daily days 1-14



Repeat cycle every 21 days
Paclitaxel



Lapatinib



175 mg/m2



1500 mg/d



Repeat cycle every 3 weeks
AUC = systemic exposure.



References for chemotherapy regimens: XT,[133] XP,[134] XN,[134] HER2-positive metastatic breast cancer regimens[135, 136, 137, 138]



Table 5. Follow-up Recommendations for Breast Cancer Survivors
  NCCN ASCO
History and physical examination Year 1, every 3-4 mo



Year 2, every 4 mo



Year 3-5, every 6 mo



Year 6+, annually



Year 1-3, every 3-6 mo



Year 4-5, every 6-12 mo



Year 6+, annually



Breast self-examination No recommendation Counseled to perform monthly breast self-examination
Mammography 6 mo after post-BCS radiation therapy



Annually thereafter



6 mo after definitive radiation therapy



Every 6-12 mo for surveillance of abnormalities



Annually if stability of abnormalities is achieved



Pelvic examination Annually, for women on tamoxifen



Annual exam if uterus present



Regular gynecologic follow-up



Patients on tamoxifen should be advised to report any vaginal bleeding



Routine blood tests Not recommended Not recommended
Imaging studies Not recommended Not recommended
Tumor marker testing Not recommended Not recommended
Table.
Women aged ≥65 years
Woman aged 60-64 years with ≥1 of the following:



1. Family history of osteoporosis



2. Low body weight



3. Prior nontraumatic fracture



4. Other risk factors (eg, smoking, sedentary lifestyle)



Postmenopausal women on aromatase inhibitors
Premenopausal women who develop treatment related premature menopause
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