Alternative drug therapies are superior to epidermal growth factor receptor -targeted chemotherapeutic drug responses in non-small cell lung cancer
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초록
Cancer is one of the major dreaded diseases causing high mortality. Lung cancer is second in position of all cancer related deaths and mainly divided into two morphologic sub-types: small-cell lung cancer and non-small cell lung cancer (NSCLC). NSCLC is an aggressive neoplasm which hardly responds to any conventional chemotherapy. Epidermal growth factor receptor (EGFR) belongs to the ErbB family of receptor tyrosine kinase that is mainly over-expressed in NSCLC. EGFR is mainly involved in the pathogenesis and progression of different carcinoma. In vivo and in vitro studies suggest that EGFR and EGF like peptides are often over-expressed in human NSCLC and these proteins are able to induce cell transformation. The conventional therapies mostly inhibit the EGFR activity and expression level in human NSCLC with the use of some EGFR-inhibitors like HKI-272, EKB569, CL-387785 etc. and some synthetic chemotherapeutic drugs like erlotinib, gefitinib, plumbagin, docetaxel, cisplatin etc., alone or in combination of two or more drugs. These therapies selectively act by competitive inhibition of the binding of adenosine triphosphate to the tyrosine kinase domain of the EGFR, resulting in inhibition of the EGFR signaling pathway. But these chemotherapeutic drugs have some cytotoxic activities to the normal cells and have some adverse side-effects. Recent studies on some traditional alternative therapies including some herbal and plant extracts, active ingredients like curcumin, different homeopathic drugs, etc. can target EGFR-signalling in NSCLC with less toxic side-effects are being currently developed.
Abstract
Cancer is one of the major dreaded diseases causing high mortality. Lung cancer is second in position of all cancer related deaths and mainly divided into two morphologic sub-types: small-cell lung cancer and non-small cell lung cancer (NSCLC). NSCLC is an aggressive neoplasm which hardly responds to any conventional chemotherapy. Epidermal growth factor receptor (EGFR) belongs to the ErbB family of receptor tyrosine kinase that is mainly over-expressed in NSCLC. EGFR is mainly involved in the pathogenesis and progression of different carcinoma. In vivo and in vitro studies suggest that EGFR and EGF like peptides are often over-expressed in human NSCLC and these proteins are able to induce cell transformation. The conventional therapies mostly inhibit the EGFR activity and expression level in human NSCLC with the use of some EGFR-inhibitors like HKI-272, EKB569, CL-387785 etc. and some synthetic chemotherapeutic drugs like erlotinib, gefitinib, plumbagin, docetaxel, cisplatin etc., alone or in combination of two or more drugs. These therapies selectively act by competitive inhibition of the binding of adenosine triphosphate to the tyrosine kinase domain of the EGFR, resulting in inhibition of the EGFR signaling pathway. But these chemotherapeutic drugs have some cytotoxic activities to the normal cells and have some adverse side-effects. Recent studies on some traditional alternative therapies including some herbal and plant extracts, active ingredients like curcumin, different homeopathic drugs, etc. can target EGFR-signalling in NSCLC with less toxic side-effects are being currently developed.
참고문헌 (47)
- Aaujo A, "Genetic polymorphisms of the epidermal growth factor and related receptor in non-small cell lung cancer—a review of the literature", Oncologist, 12, pp.201~210 (2007)
- Ceppi P, "ERCC1 and RRM1 gene expressions but not EGFR are predictive of shorter survival in advanced non-small-cell lung cancer treated with cisplatin and gemcitabine", Ann Oncol, 17, pp.1818~1825 (2006)
- Cappuzzo F, "Epidermal growth factor receptor gene and protein and gefitinib sensitivity in non-small-cell lung cancer", J Natl Cancer Inst, 97, pp.643~655 (2005)
- Chang TH, "Slug confers resistance to the epidermal growth factor receptor tyrosine kinase inhibitor", Am J Respir Crit Care Med, 183, pp.1071~1079 (2011)
- Dougherty U, "Epidermal growth factor receptor controls flat dysplastic aberrant crypt foci development and colon cancer progression in the rat azoxymethane model", Clin Cancer Res, 14, pp.2253~2262 (2008)
- Dziadziuszko R, "Epidermal growth factor receptor messenger RNA expression, gene dosage, and gefitinib sensitivity in non small cell lung cancer", Clin Cancer Res, 12, pp.3078~3084 (2006)
- Eberhard DA, "Mutations in the epidermal growth factor receptor and in KRAS are predictive and prognostic indicators in patients with non-small-cell lung cancer treated with chemotherapy alone and in combination with erlotinib", J Clin Oncol, 23, pp.5900~5909 (2005)
- Efferth T, "From traditional Chinese medicine to rational cancer therapy", Trends Mol Med, 13, pp.353~361 (2007)
- Fukuoka M, "Multi-institutional randomized phase II trial of gefitinib for previously treated patients with advanced non-small-cell lung cancer", J Clin Oncol, 21, pp.2237~2246 (2003)
- Gomathinayagam R, "Anticancer mechanism of plumbagin, a natural compound, on non-small cell lung cancer cells", Anticancer Res, 28, pp.785~792 (2008)
- Guo H, "Traditional Chinese medicine herbal treatment may have a relevant impact on the prognosis of patients with stage IV adenocarcinoma of the lung treated with platinum-based chemotherapy or combined targeted therapy and chemotherapy", Integr Cancer Ther, 10, pp.127~137 (2011)
- Herbst RS, "Selective oral epidermal growth factor receptor tyrosine kinase inhibitor ZD1839 is generally well-tolerated and has activity in non-small-cell lung cancer and other solid tumors: results of a phase I trial", J Clin Oncol, 20, pp.3815~3825 (2002)
- Herbst RS, "TRIBUTE: a phase III trial of erlotinib hydrochloride (OSI-774) combined with carboplatin and paclitaxel chemotherapy in advanced non-small-cell lung cancer", J Clin Oncol, 23, pp.5892~5899 (2005)
- Hirsch FR, "Combination of EGFR gene copy number and protein expression predicts outcome for advanced non-small-cell lung cancer patients treated with gefitinib", Ann Oncol, 18, pp.752~760 (2007)
- Hirsch FR, "Increased EGFR gene copy number detected by fluorescent in situ hybridization predicts outcome in non-small-cell lung cancer patients treated with cetuximab and chemotherapy", J Clin Oncol, 26, pp.3351~3357 (2008)
- Huang S, "Dual-agent molecular targeting of the epidermal growth factor receptor (EGFR): combining anti-EGFR antibody with tyrosine kinase inhibitor", Cancer Res, 64, pp.5355~5362 (2004)
- Hynes NE, "ERBB receptors and cancer: the complexity of targeted inhibitors", Nat Rev Cancer, 5, pp.341~354 (2005)
- Janmaat ML, "Response to epidermal growth factor receptor inhibitors in non-small cell lung cancer cells: limited antiproliferative effects and absence of apoptosis associated with persistent activity of extracellular signal-regulated kinase or Akt kinase pathways", Clin Cancer Res, 9, pp.2316~2326 (2003)
- Kelly K, "Biological agents in non-small cell lung cancer: a review of recent advances and clinical results with a focus on epidermal growth factor receptor and vascular endothelial growth factor", J Thorac Oncol, 3, pp.664~673 (2008)
- Kobayashi S, "EGFR mutation and resistance of non-small-cell lung cancer to gefitinib", N Engl J Med, 352, pp.786~792 (2005)
- Kosaka T, "Mutations of the epidermal growth factor receptor gene in lung cancer: biological and clinical implications", Cancer Res, 64, pp.8919~8923 (2004)
- Kwak EL, "Irreversible inhibitors of the EGF receptor may circumvent acquired resistance to gefitinib", Proc Natl Acad Sci USA, 102, pp.7665~7670 (2005)
- Larco JEde, "Growth factors from murine sarcoma virus-transformed cells", Proc Natl Acad Sci USA, 75, pp.4001~4005 (1978)
- Lee JY, "Curcumin induces EGFR degradation in lung adenocarcinoma and modulates p38 activation in intestine: the versatile adjuvant for gefitinib therapy", PLoS One, 6, pp.e23756~ (2011)
- Lentini A, "Phytochemicals and proteinepolyamine conjugates by transglutaminase as chemopreventive and chemotherapeutic tools in cancer", Plant Physiol Biochem, 48, pp.627~633 (2010)
- Lev-Ari S, "Inhibition of pancreatic and lung adenocarcinoma cell survival by curcumin is associated with increased apoptosis, down-regulation of COX-2 and EGFR and inhibition of Erk1", 2 activity, 2006, pp.26, 4423~4430
- Maemondo M, "Gefitinib or chemotherapy for non-small cell lung cancer with mutated EGFR", N Engl J Med, 362, pp.2380~2388 (2010)
- Marchetti A, "EGFR mutations in non-small-cell lung cancer: analysis of a large series of cases and development of a rapid and sensitive method for diagnostic screening with potential implications on pharmacologic treatment", J Clin Oncol, 23, pp.857~865 (2005)
- Misra R, "Cancer nanotechnology: application of nanotechnology in cancer therapy", Drug Discov Today, 15, pp.842~850 (2010)
- Mitsudomi T, "Mutations of the epidermal growth factor receptor gene predict prolonged survival after gefitinib treatment in patients with non-small-cell lung cancer with postoperative recurrence", J Clin Oncol, 23, pp.2513~2520 (2005)
- Mukherjee A, "Ethanolic extract of Thuja occidentalis blocks proliferation of A549 cells and induces apoptosis in vitro", Zhong Xi Yi Jie He Xue Bao, 10, pp.1451~1459 (2012)
- Normanno N, "Epidermal growth factor receptor (EGFR) signaling in cancer", Gene, 366, pp.2~16 (2006)
- Pao W, "Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain", PLoS One, 2, pp.e73~ (2005)
- Pollack VA, "Inhibition of epidermal growth factor receptor-associated tyrosine phosphorylation in human carcinomas with CP-358,774: dynamics of receptor inhibition in situ and antitumor effects in athymic mice", J Pharmacol Exp Ther, 291, pp.739~748 (1999)
- Ramalingam S, "Systemic chemotherapy for advanced non-small cell lung cancer: recent advances and future directions", Oncologist, 13, pp.5~13 (2008)
- Rusnak DW, "The effects of the novel, reversible epidermal growth factor receptor", ErbB-2 tyrosine kinase inhibitor, GW2016, on the growth of human normal and tumor-derived cell lines in vitro and in vivo, 2001, pp.1, 85~94
- Schlessinger J, "Common and distinct elements in cellular signaling via EGF and FGF receptors", Science, 306, pp.1506~1507 (2004)
- Shan JZ, "Ursolic acid inhibits proliferation and induces apoptosis of HT-29 colon cancer cells by inhibiting the EGFR", MAPK pathway, 2009, pp.10, 668~674
- Sharma SV, "Epidermal growth factor receptor mutations in lung cancer", Nat Rev Cancer, 7, pp.169~181 (2007)
- "2013", 3(1), 후마니타스의학회
- Tracy S, "Gefitinib induces apoptosis in the EGFRL858R non-small-cell lung cancer cell line H3255", Cancer Res, 64, pp.7241~7244 (2004)
- Traxler P, "AEE788: a dual family epidermal growth factor receptor", ErbB2 and vascular endothelial growth factor receptor tyrosine kinase inhibitor with antitumor and anti-angiogenic activity, 2004, pp.64, 4931~4941
- Tsou HR, "Optimization of 6,7-disubstituted -4- (arylamino) quinoline-3-carbonitriles as orally active, irreversible inhibitors of human epidermal growth factor receptor-2 kinase activity", J Med Chem, 48, pp.1107~1131 (2005)
- Wakeling AE, "ZD1839 (Iressa): an orally active inhibitor of epidermal growth factor signaling with potential for cancer therapy", Cancer Res, 62, pp.5749~5754 (2002)
- Weiss GJ, "EGFR regulation by microRNA in lung cancer: correlation with clinical response and survival to gefitinib and EGFR expression in cell lines", Ann Oncol, 19, pp.1053~1059 (2008)
- Yarden Y, "Untangling the ErbB signalling network", Nat Rev Mol Cell Biol, 2, pp.127~137 (2001)
- Yun CH, "Structures of lung cancer-derived EGFR mutants and inhibitor complexes: mechanism of activation and insights into differential inhibitor sensitivity", Cancer Cell, 11, pp.217~227 (2007)