title: Cell-cycle dysregulation in breast cancer: breast cancer therapies targeting the cell cycle.
abstract: Breast cancer is the most commonly diagnosed cancer in American women. The underlying mechanisms that cause aberrant cell proliferation and tumor growth involve conserved pathways, which include components of the cell cycle machinery. Proto-oncogenes, growth factors, and steroids have been implicated in the pathogenesis of breast cancer. Surgery, local irradiation, and chemotherapy have been the mainstay of treatment for early and advanced stage disease. Potential targets for selective breast cancer therapy are herein reviewed. Improved understanding of the biology of breast cancer has led to more specific "targeted therapies" directed at biological processes that are selectively deregulated in the cancerous cells. Examples include tamoxifen for estrogen receptor positive tumors and imunoneutralizing antibodies such as trastuzumab for Her2/neu overexpressing tumors. Other novel anticancer agents such as paclitaxel, a microtubule binding molecule, and flavopiridol, a cyclin dependent kinase inhibitor, exert their anticancer effects by inhibiting cell cycle progression.
authors: Division of Hormone-Dependent Tumor Biology, The Albert Einstein Comprehensive Cancer Center, Department of Development and Molecular Biology, Bronx, New York 10461, USA.
authors: B T
authors: BT
authors: Zafonte
authors: J
authors: J
authors: Hulit
authors: D F
authors: DF
authors: Amanatullah
authors: C
authors: C
authors: Albanese
authors: C
authors: C
authors: Wang
authors: E
authors: E
authors: Rosen
authors: A
authors: A
authors: Reutens
authors: J A
authors: JA
authors: Sparano
authors: M P
authors: MP
authors: Lisanti
authors: R G
authors: RG
authors: Pestell
mesh_terms: D000230:Adenocarcinoma / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D000818:Animals; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D000970:Antineoplastic Agents / Q000627:therapeutic use; D001943:Breast Neoplasms / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D002453:Cell Cycle / Q000187:drug effects; D018797:Cell Cycle Proteins; D050760:Cyclin-Dependent Kinase Inhibitor p27; D016213:Cyclins / Q000378:metabolism; D016208:Databases, Factual; D004791:Enzyme Inhibitors / Q000627:therapeutic use; D005419:Flavonoids / Q000627:therapeutic use; D006801:Humans; D008869:Microtubule-Associated Proteins / Q000235:genetics / Q000378:metabolism; D009389:Neovascularization, Pathologic; D009857:Oncogenes; D017239:Paclitaxel / Q000627:therapeutic use; D010880:Piperidines / Q000627:therapeutic use; D011960:Receptors, Estrogen / Q000378:metabolism; D013629:Tamoxifen / Q000627:therapeutic use; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000378:metabolism; D000068878:Trastuzumab; D025521:Tumor Suppressor Proteins
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D000970:Antineoplastic Agents; D018797:Cell Cycle Proteins; D016213:Cyclins; D004791:Enzyme Inhibitors; D005419:Flavonoids; D008869:Microtubule-Associated Proteins; D010880:Piperidines; D011960:Receptors, Estrogen; D016212:Transforming Growth Factor beta; D025521:Tumor Suppressor Proteins; D013629:Tamoxifen; D050760:Cyclin-Dependent Kinase Inhibitor p27; C077990:alvocidib; D000068878:Trastuzumab; D017239:Paclitaxel