Journal of Cancer Biology and Research

Breast Cancer Agents: Treatment & Prevention

Short Communication | Open Access

  • 1. College of Chemistry & Pharmaceutical Sciences, Qingdao Agricultural University, China
  • 2. Department of Physiology, Michigan State University, USA
  • 3. Department of Microbiology and Molecular Genetics, Michigan State University, USA
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Corresponding Authors
Yong Zhao, College of Chemistry & Pharmaceutical Sciences, Qingdao Agricultural University, China

Zhao Y, Yang C, Haslam SZ, Schwartz RC (2014) Breast Cancer Agents: Treatment & Prevention. J Cancer Biol Res 2(1): 1033.


The heterogeneous disease Breast Cancer (BC) is an ancient disease which was noted 3500 years ago by ancient Egyptians [1] .The heterogeneity, including intratumor heterogeneity and intertumor heterogeneity, is influenced by genetic and nongenetic factors. Furthermore, BC is the most common malignant tumor and the second leading cause of cancer death in women. Because BC is a heterogeneous disease, no single therapy is sufficient to treat all patients. In order to assess prognosis and determine the appropriate therapies for BC patients, many criteria like patient age, axillary lymph node status, tumor size, histological grade and lymphovascular invasion, hormone receptor status, and HER2 status have been used to categorize the disease. Based on recent molecular techniques, particularly gene expression profiling and immuno- histology, BC can be classified into four major types: estrogen and progesterone receptor positive luminal A and luminal B, HER2 and basal-like/ triple negative BC [2]. If BC is diagnosed early, women have better prospects for survival. However, most women diagnosed with this disease will undergo systemic or local therapies to treat the disease. The therapies involve.

Surgeons, radiation oncologists, medical oncologists and others working together to provide treatment. Surgery is the first line treatment. However, a variety of other medical therapies have also been used: radiotherapy, chemotherapy, hormonal therapy, bisphosphonate therapy and targeted biological therapy and others [3-12].

Table 1 summarizes the agents which are approved by the USFDA to treat BC. There are four major common classes of agents for BC treatment: chemotherapy agents, hormonal therapy agents, bisphosphonate therapy agents, and targeted biological agents.


Chemotherapy agents consist of systemic drug treatments intended to stop cancer cells dividing and growing [13-15]. There are 6 types of chemotherapeutic agents: alkylating agents, anthracyclines, platinum agents, taxanes, vinca agents, and other chemotherapeutic agents. Alkylating agents work by inserting an “alkyl group (CnH2n+1)” into the DNA structure to interfere with DNA replication and prevent cancer cells from dividing. The alkyl group is attached to the number 7 nitrogen atom of the purine ring of the guanine base of DNA. In general, cancer cells are proliferating faster with less active DNA error-correcting repair than healthy cells; therefore cancer cells are more sensitive to DNA damage. Anthracyclines, antibiotics derived from the bacterium Streptomyces peucetius var. caesius, attack cancer cells largely by disrupting DNA structure and preventing cell division. The anthracyclines are among the most effective anticancer agents ever developed and are effective against many types of cancer. However, they cause significant cardiotoxicity and neurotoxicity. Platinum agents, anti-cancer drugs that contain the metal platinum, cause crosslinking of DNA as monoadduct, interstrand crosslinks, intrastrand crosslinks, or DNA protein crosslinks, all of which block DNA repair and/or DNA synthesis in cancer cells. These agents sometimes also included among alkylating agents because they have similar mechanisms as anti-cancer agents. Taxanes, mitotic inhibitors, act by interfering and disrupting the cellular microtubules. The microtubules play an important role in many cellular functions, including cell division. Taxanes are often used in combination with other chemotherapy agents. Vinca alkaloid agents, originally derived from the Periwinkle plant Catharanthus roseus, are a set of anti-mitotic and antimicrotubule agents. They are cell- cycle-specific cytotoxic drugs that inhibit the ability of cancer cells to divide by preventing the polymerization of tubulin into microtubules. There are also some chemicals agents that can be used to treat breast cancer, which do not belong to the aforementioned groups: Fluorouracil (5-FU), Irinotecan, Gemcitabine, Eribulin, Ixabepilone, Methotrexate, Temozolomide, Topotecan, Vincristine, Vinblastine, and Capecitabine. Collectively, all of these chemotherapeutic agents are often associated with unpleasant side effects because, in addition to cancer cells, they target all rapidly growing cells, including those in the gastrointestinal tract, bone marrow, testicles and ovaries [16,17].

BC is a hormonally dependent disease in, at least, a proportion of patients [1,18]. Hormonal therapy agents, through manipulation of the endocrine system, inhibit production

or activity of hormones (hormone antagonists), largely 17 β-estradiol, that promote tumor growth. These agents include anti-estrogen agents, aromatase inhibitors, ovarian suppression, and other Endocrine/Hormone agents. For patients with luminal A/B breast cancer, hormone-receptor positive (ER, PR-positive), hormone therapy with anti-estrogen agents (Raloxifene, Toremifine and Fulvestrant) and aromatase inhibitors (anastrozole, letrozole, exemestane) or ovarian suppression (in premenopausal patients) are the common strategies to treat this disease, often combined with other therapies [18]

Bisphosphonate therapy agents, commonly used for osteoporosis, have been approved by FDA to treat Metastatic Breast Cancer (MBC) which has spread to the bones [19,20]. Bisphosphonate therapy agents may also be used in combinations with aromatase inhibitors for early stage breast cancer to lessen the adverse effect of aromatase inhibitors to weaken bone in some patients. This sub-class of agents includes risedronate, pamidronate, ibandronate, alendronate, denosumab and zoledronate..

Targeted biological agents can selectively inhibit various mechanisms, include autocrine growth signals, continuous replicative potential, angiogenesis, and stromal invasion with the development of metastases. mTOR, angiogenesis and HER2 are among the targets for which these agents have been developed. HER2 positive breast cancer accounts for 20– 25% of all breast cancer patients, and HER2 over expression deregulates activation of intracellular mitogenic signaling and leads to aggressive tumor behavior. The first drug to target HER2, Trastuzumab, is a recombinant humanized monoclonal antibody which binds to HER-2/neu protein to interfere with ligand binding and subsequent activation of the HER2 signaling pathway. Other FDA approved agents in this category include T-DM1, Tykerb and Pertuzuma, which work in different ways to block the HER2 pathway [21-23]. The vascular endothelial growth factor (VEGF) receptor family plays an essential role in angiogenesis that supports tumor growth. Therefore, targeting the VEGF pathway is another way to treat BC [24,25]. The FDA approved agent Bevacizumab is a monoclonal anti-body that can block angiogenesis in cancer. The mammalian target of rapamycin, mTOR, a human protein encoded by the MTOR gene, is a serine/threonine protein kinase that regulates cell growth, cell proliferation, cell motility, cell survival, protein synthesis and transcription. mTOR is a member of the phosphatidylinositol 3-kinase-related kinase protein family. The inhibitor everolimus interferes with cancer cell growth by blocking the mTOR pathway [26,27]. Resistance to anti-HER2 agents is a problem for targeted HER2 therapy. The resistance may be because of aberrant activation of signaling pathways downstream of the receptor, such as the presence of activating PI3K mutations or loss of function of the phosphatase PTEN or increase Rac1 activation. In our study we have found that inhibition of both Akt and Rac1 pathways resulted in a significantly more decrease of Trastuzumab resistance than inactivation of Rac1 or Akt alone [28]. Combination therapies are under investigation to overcome the resistance problem. In a recent Phase Ib study, paclitaxel, mTOR inhibitor everolimus and trastuzumab were combined together to treat the patients with HER2-overexpressing metastatic breast cancer pretreated with trastuzumab [29].

Basel like/Triple negative breast cancer, defined as tumors that are negative for Estrogen Receptor (ER), progesterone receptor (PR), and HER2, is a biologically aggressive disease with limited treatment options, in part due to the lack of these receptor targets. Chemotherapy is one treatment option [30].

Chemoprevention has been defined by Sporn as “the use of pharmacologic or natural agents that inhibit the development of invasive breast cancer either by blocking the DNA damage that initiates carcinogenesis, or by arresting or reversing the progression of premalignant cells in which such damage has already occurred” [31]. Selective Estrogen Receptor Modulators (SERMs) and Aromatase Inhibitors (AIs) have been investigated as BC chemoprevention agents. While they are effective in prevention of endocrine responsive lesions, they have no effect in reducing the risk of estrogen receptor-negative BC. Tamoxifen and raloxifene are two effective agents used for the prevention of breast cancer in women at high risk for the development of the disease. Raloxifene has more side effects than tamoxifen. New agents are still under investigation for BC prevention [31-33].

Even though progress has been made in BC diagnosis and treatment, BC is still a major health problem for women. The identification of new potential molecular targets and development of new agents to target these molecules in BC will have a significant impact on future BC therapy and provide a wealth of opportunities for chemoprevention also. There are many new targets currently being investigated, including the programmed death-1 (PD-1) pathway [34], protein phosphatase 2A(PP2A) [35], the BCL-2 pathway [36], cell cycle machinery [37], the quiescin sulfhydryl oxidase 1 (QSOX1) pathway [38],microRNA pathways [39] and some others [40-42].

Also many novel delivery systems are currently being investigated: nano-particles, polymeric micelles, nano-micellar carriers, and others [43-45]. Even though the full mechanisms of action have not yet been elucidated, traditional Chinese herbal medicines have been used in disease prevention and treatment for centuries [46,47]. These agents may present alternative strategies to western cancer therapies. In addition, life styles decisions are likely also important factors for BC development, prevention and treatment. In a recent study in mice, we found that high fat diet initiated in puberty increases the breast cancer risk in adulthood [48].Other factors, including alcohol, tobacco, and cosmetics may also influence BC risk [47,49-52].

Table 1: FDA approved agents for management of BC.

Classes Sub-classes Name of agents Mechanism of Action
Chemotherapy Agents Alkylating Agents Cytoxan® / Cyclophosphamide 
Inserts an alkyl moiety into the DNA 
structure, which blocks cell division
  Anthracyclines Adriamycin® / Doxorubicin
Doxil® / Liposomal Doxorubicin 
Ellence® / Epirubicin
Novantrone® / Mitoxantrone
Disrupts duplex DNA structure, 
which blocks cell division
  Platinum Drugs Paraplatin® / Carboplatin
Platinol® / Cisplatin
DNA crosslinking that inhibits DNA 
repair mechanisms, leading to cell 
  Taxanes Abraxane® / Paclitaxel Proteinbound
Taxol® / Paclitaxel Taxotere® / 
Disrupts cellular microtubules to 
inhibit cell growth and stopcell 
  Vinca Agents Navelbine® / Vinorelbine Disrupts cellular
microtubules to inhibit cell growth 
and stop cell division
  Other Chemotherapy Agents Adrucil® / Fluorouracil (5- FU)
Camptosor® / Irinotecan Gemzar® 
/ Gemcitabine
    Halaven® / Eribulin  
    Ixempra® / Ixabepilone 
    Temodar® / Temozolomide  
    Xeloda® / Capecitabine  
Hormonal Anti-Estrogen Evista® / Raloxifene Binds to estrogen receptors
Therapy Agents Fareston® / Toremifine to block estrogen activity
Agents   Faslodex® / Fulvestrant and its associated growth
    Nolvadex® / Tamoxifen promoting activities
  Aromatase Arimidex / Anastrozole Inhibits aromatase to block
  Inhibitors Aromasin / Exemestane estrogen production
    Femara / Letrozole  
  Ovarian Lupron® / Leuprolide Reduces the ovarian
  Suppression Plenaxis® / Abarelix capacity to produce estrogen
    Suprefact® / Buserlin  
    Zoladex® / Goserelin  
  Other Megace® / Megestrol Acetate  
  mone agents    
Bisphosphon Bisphosphonate    
ate Therapy agents Actonel® / Risedronate Inhibits breast cancer bone
Agent   Aredia® / Pamidronate metastasis
    Boniva® / Ibandronate  
    Fosamex® /Alendronate  
    Xgeva® /Denosumab  
    Zometa® / Zoledronate  
Targeted Targeted Afinitor® / Everolimus Inhibits the mammalian
Biological mTOR   enzyme target of rapamycin
Agent     (mTOR)
  Targeted Avastin® / Bevacizumab Suppresses tumor growth by
  Angiogenesis   blocking angiogenesis to
      reduce the blood supply to
  Targeted Her2 Herceptin® / Trastuzumab Monoclonal antibody; Inhibits cell division by
      blocking growth factors
      binding to Her2 receptor
    Kadcyla® / T-DM1 (Ado A combination of Herceptin
    trastuzumab emtansine) and a chemotherapy drug
      (DM1) to inhibit cell growth
    Lapatinib® / Tykerb Blocks the HER2/neu



The progress in breast cancer management requires multidisciplinary team efforts which involve basic researchers, radiologists, pathologists, surgeons, radiation oncologists, medical oncologists and psychologists. The development of rational, effective, and safe agents for prevention or treatment, involving targets in multiple regulatory pathways and with the ability to modify carcinogenesis in its early phases, will be desirable.


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Received : 30 Jan 2014
Accepted : 03 Mar 2014
Published : 17 Mar 2014
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Launched : 2014
JSM Biotechnology and Biomedical Engineering
ISSN : 2333-7117
Launched : 2013
Journal of Hematology and Transfusion
ISSN : 2333-6684
Launched : 2013
JSM Environmental Science and Ecology
ISSN : 2333-7141
Launched : 2013
Journal of Cardiology and Clinical Research
ISSN : 2333-6676
Launched : 2013
JSM Nanotechnology and Nanomedicine
ISSN : 2334-1815
Launched : 2013
Journal of Ear, Nose and Throat Disorders
ISSN : 2475-9473
Launched : 2016
JSM Ophthalmology
ISSN : 2333-6447
Launched : 2013
Journal of Pharmacology and Clinical Toxicology
ISSN : 2333-7079
Launched : 2013
Annals of Psychiatry and Mental Health
ISSN : 2374-0124
Launched : 2013
Medical Journal of Obstetrics and Gynecology
ISSN : 2333-6439
Launched : 2013
Annals of Pediatrics and Child Health
ISSN : 2373-9312
Launched : 2013
JSM Clinical Pharmaceutics
ISSN : 2379-9498
Launched : 2014
JSM Foot and Ankle
ISSN : 2475-9112
Launched : 2016
JSM Alzheimer's Disease and Related Dementia
ISSN : 2378-9565
Launched : 2014
Journal of Addiction Medicine and Therapy
ISSN : 2333-665X
Launched : 2013
Journal of Veterinary Medicine and Research
ISSN : 2378-931X
Launched : 2013
Annals of Public Health and Research
ISSN : 2378-9328
Launched : 2014
Annals of Orthopedics and Rheumatology
ISSN : 2373-9290
Launched : 2013
Journal of Clinical Nephrology and Research
ISSN : 2379-0652
Launched : 2014
Annals of Community Medicine and Practice
ISSN : 2475-9465
Launched : 2014
Annals of Biometrics and Biostatistics
ISSN : 2374-0116
Launched : 2013
JSM Clinical Case Reports
ISSN : 2373-9819
Launched : 2013
Journal of Surgery and Transplantation Science
ISSN : 2379-0911
Launched : 2013
Journal of Dermatology and Clinical Research
ISSN : 2373-9371
Launched : 2013
JSM Gastroenterology and Hepatology
ISSN : 2373-9487
Launched : 2013
Annals of Nursing and Practice
ISSN : 2379-9501
Launched : 2014
JSM Dentistry
ISSN : 2333-7133
Launched : 2013
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