Research progress on target therapy of advanced non-small cell lung cancer

JIANG Wenli; HANG Caiguo

doi:10.3969/j.issn.1006-0111.2016.04.004

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Volume 34 Issue 4

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Article Navigation > Journal of Pharmaceutical Practice and Service > 2016 > 34(4): 301-304,333

JIANG Wenli, HANG Caiguo. Research progress on target therapy of advanced non-small cell lung cancer[J]. Journal of Pharmaceutical Practice and Service, 2016, 34(4): 301-304,333. doi: 10.3969/j.issn.1006-0111.2016.04.004

Citation:

JIANG Wenli, HANG Caiguo. Research progress on target therapy of advanced non-small cell lung cancer[J]. Journal of Pharmaceutical Practice and Service, 2016, 34(4): 301-304,333. doi: 10.3969/j.issn.1006-0111.2016.04.004

Research progress on target therapy of advanced non-small cell lung cancer

doi: 10.3969/j.issn.1006-0111.2016.04.004

Department of Biochemistry and Molecular Biology, Faculty of Basic Medicine, Second Military Medical University, Shanghai 200433, China

Received Date: 2016-01-26
Rev Recd Date: 2016-03-25

Abstract

Detection of biomarkers benefited many advanced non-small cell lung cancer (NSCLC) patients. In recent years, epidermal growth factor (EGFR) tyrosine kinase inhibitors (TKIs) represented by Gefitinib, Erlotinib, Afatinib and anaplastic lymphoma kinase (ALK) TKIs represented by Crizotinib have remarkable efficacy. However, the efficacy for most first-generation EGFR-TKI and ALK-TKI is weakened due to secondary resistance. Currently, the third-generation EGFR-TKI which successfully against drug resistance is based on research and development of the second-generation. In addition, there are many other targeted inhibitors of mutation sites for advanced NSCLC. Unfortunately, the largest proportion of Kirsten rat sarcoma viral oncogene homolog (K-RAS) mutation is not targetable with small molecule inhibitors currently. Therefore, based on mechanisms exploration of tumor driven gene mutation, its target drug research and development will be greatly addressed in the future.
- non-small cell lung cancer (NSCLC),
- molecular targeting agents,
- tumour

References

[1]	Chen W, Zheng R, Baade PD, et al. Cancer statistics in China, 2015[J]. CA Cancer J Clin, 2016,66(2):115-132.
[2]	Jorge S, Kobayashi SS, Costa DB. Epidermal growth factor receptor (EGFR) mutations in lung cancer:preclinical and clinical data[J]. Brazil J Med Biolog Res, 2014,47(11):929-939.
[3]	Sequist LV, Yang JC, Yamamoto N, et al. Phase Ⅲ study of Afatinib or cisplatin plus pemetrexed in patients with metastatic lung adenocarcinoma with EGFR mutations[J]. J Clin Oncol, 2013, 31(27):3327-3334.
[4]	Banno E, Togashi Y, Kobayashi Y, et al. Afatinib is especially effective against non-small cell lung cancer carrying an EGFR exon 19 deletion[J]. Anticancer Res, 2015,35(4):2005-2008.
[5]	Karachaliou N, Mayo-de las Casas C, Queralt C, et al. Association of EGFR L858R mutation in circulating free DNA with survival in the EURTAC trial[J]. JAMA Oncol, 2015,1(2):149-157.
[6]	Sadek M, Alexakis A, Fauve S. OPTIMAL length scale for a turbulent dynamo[J]. Phys Rev Lett, 2016, 116(7):074501.
[7]	Choi SH, Mendrola JM, Lemmon MA. EGF-independent activation of cell-surface EGF receptors harboring mutations found in Gefitinib-sensitive lung cancer[J]. Oncogene, 2007, 26(11):1567-1576.
[8]	Steuer CE, Ramalingam SS. Targeting EGFR in lung cancer:Lessons learned and future perspectives[J]. Mol Aspects Med, 2015, 45:67-73.
[9]	Vacondio F, Carmi C, Galvani E, et al. Long-lasting inhibition of EGFR autophosphorylation in A549 tumor cells by intracellular accumulation of non-covalent inhibitors[J]. Bioorg Med Chem Lett, 2013, 23(19):5290-5294.
[10]	Giordano P, Manzo A, Montanino A, et al. Afatinib:An overview of its clinical development in non-small-cell lung cancer and other tumors[J]. Crit Rev Oncol Hematol, 2016, 97:143-151.
[11]	Kato T, Yoshioka H, Okamoto I, et al. Afatinib versus cisplatin plus pemetrexed in Japanese patients with advanced non-small cell lung cancer harboring activating EGFR mutations:Subgroup analysis of LUX-Lung 3[J]. Cancer Sci, 2015, 106(9):1202-1211.
[12]	Soria JC, Felip E, Cobo M, et al. Afatinib versus Erlotinib as second-line treatment of patients with advanced squamous cell carcinoma of the lung (LUX-Lung 8):an open-label randomised controlled phase 3 trial[J]. Lancet Oncol, 2015, 16(8):897-907.
[13]	Janne PA, Yang JC, Kim DW, et al. AZD9291 in EGFR inhibitor-resistant non-small-cell lung cancer[J]. N Engl J Med, 2015, 372(18):1689-1699.
[14]	Greig SL. Osimertinib:First global approval[J]. Drugs, 2016, 76(2):263-273.
[15]	Shea M, Costa DB, Rangachari D. Management of advanced non-small cell lung cancers with known mutations or rearrangements:Latest evidence and treatment approaches[J]. Ther Adv Respir Dis, 2016, 10(2):113-129.
[16]	Yu HA, Arcila ME, Rekhtman N, et al. Analysis of tumor specimens at the time of acquired resistance to EGFR-TKI therapy in 155 patients with EGFR-mutant lung cancers[J]. Clin Cancer Res, 2013, 19(8):2240-2247.
[17]	Chong CR, Janne PA. The quest to overcome resistance to EGFR-targeted therapies in cancer[J]. Nat Med, 2013,19(11):1389-1400.
[18]	Li D, Ambrogio L, Shimamura T, et al. BIBW2992, an irreversible EGFR/HER2 inhibitor highly effective in preclinical lung cancer models[J]. Oncogene, 2008, 27(34):4702-4711.
[19]	Soda M, Choi YL, Enomoto M, et al. Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer[J]. Nature, 2007, 448(7153):561-566.
[20]	Cameron L, Solomon B. New treatment options for ALK-rearranged non-small cell lung cancer[J]. Curr Treat Options Oncol, 2015, 16(10):49.
[21]	Costa DB, Shaw AT, Ou SH, et al. Clinical experience with crizotinib in patients with advanced ALK-rearranged non-small-cell lung cancer and brain metastases[J]. J Clin Oncol, 2015,33(17):1881-1888.
[22]	Lukas RV, Hasan Y, Nicholas MK, et al. ROS1 rearranged non-small cell lung cancer brain metastases respond to low dose radiotherapy[J]. J Clin Neurosci, 2015,22(12):1978-1979.
[23]	Marchetti A, Felicioni L, Malatesta S, et al. Clinical features and outcome of patients with non-small-cell lung cancer harboring BRAF mutations[J]. J Clin Oncol,2011,29(26):3574-3579.
[24]	石远凯,孙燕,于金明,等.中国晚期原发性肺癌诊治专家共识(2016年版)[J].中国肺癌杂志,2016,19(1):1-15.
[25]	Lipson D, Capelletti M, Yelensky R, et al. Identification of new ALK and RET gene fusions from colorectal and lung cancer biopsies[J]. Nat Med, 2012, 18(3):382-384.
[26]	Li BT, Ross DS, Aisner DL, et al. HER2 amplification and HER2 mutation are distinct molecular targets in lung cancers[J]. J Thorac Oncol, 2016, 11(3):414-419.
[27]	Mar N, Vredenburgh JJ, Wasser JS. Targeting HER2 in the treatment of non-small cell lung cancer[J]. Lung Cancer, 2015, 87(3):220-225.

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通讯作者: 陈斌, bchen63@163.com

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沈阳化工大学材料科学与工程学院沈阳 110142

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Research progress on target therapy of advanced non-small cell lung cancer

Department of Biochemistry and Molecular Biology, Faculty of Basic Medicine, Second Military Medical University, Shanghai 200433, China

Received Date: 2016-01-26

Rev Recd Date: 2016-03-25

Key words:

Abstract: Detection of biomarkers benefited many advanced non-small cell lung cancer (NSCLC) patients. In recent years, epidermal growth factor (EGFR) tyrosine kinase inhibitors (TKIs) represented by Gefitinib, Erlotinib, Afatinib and anaplastic lymphoma kinase (ALK) TKIs represented by Crizotinib have remarkable efficacy. However, the efficacy for most first-generation EGFR-TKI and ALK-TKI is weakened due to secondary resistance. Currently, the third-generation EGFR-TKI which successfully against drug resistance is based on research and development of the second-generation. In addition, there are many other targeted inhibitors of mutation sites for advanced NSCLC. Unfortunately, the largest proportion of Kirsten rat sarcoma viral oncogene homolog (K-RAS) mutation is not targetable with small molecule inhibitors currently. Therefore, based on mechanisms exploration of tumor driven gene mutation, its target drug research and development will be greatly addressed in the future.

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Reference (27)

[1]	Chen W, Zheng R, Baade PD, et al. Cancer statistics in China, 2015[J]. CA Cancer J Clin, 2016,66(2):115-132.
[2]	Jorge S, Kobayashi SS, Costa DB. Epidermal growth factor receptor (EGFR) mutations in lung cancer:preclinical and clinical data[J]. Brazil J Med Biolog Res, 2014,47(11):929-939.
[3]	Sequist LV, Yang JC, Yamamoto N, et al. Phase Ⅲ study of Afatinib or cisplatin plus pemetrexed in patients with metastatic lung adenocarcinoma with EGFR mutations[J]. J Clin Oncol, 2013, 31(27):3327-3334.
[4]	Banno E, Togashi Y, Kobayashi Y, et al. Afatinib is especially effective against non-small cell lung cancer carrying an EGFR exon 19 deletion[J]. Anticancer Res, 2015,35(4):2005-2008.
[5]	Karachaliou N, Mayo-de las Casas C, Queralt C, et al. Association of EGFR L858R mutation in circulating free DNA with survival in the EURTAC trial[J]. JAMA Oncol, 2015,1(2):149-157.
[6]	Sadek M, Alexakis A, Fauve S. OPTIMAL length scale for a turbulent dynamo[J]. Phys Rev Lett, 2016, 116(7):074501.
[7]	Choi SH, Mendrola JM, Lemmon MA. EGF-independent activation of cell-surface EGF receptors harboring mutations found in Gefitinib-sensitive lung cancer[J]. Oncogene, 2007, 26(11):1567-1576.
[8]	Steuer CE, Ramalingam SS. Targeting EGFR in lung cancer:Lessons learned and future perspectives[J]. Mol Aspects Med, 2015, 45:67-73.
[9]	Vacondio F, Carmi C, Galvani E, et al. Long-lasting inhibition of EGFR autophosphorylation in A549 tumor cells by intracellular accumulation of non-covalent inhibitors[J]. Bioorg Med Chem Lett, 2013, 23(19):5290-5294.
[10]	Giordano P, Manzo A, Montanino A, et al. Afatinib:An overview of its clinical development in non-small-cell lung cancer and other tumors[J]. Crit Rev Oncol Hematol, 2016, 97:143-151.
[11]	Kato T, Yoshioka H, Okamoto I, et al. Afatinib versus cisplatin plus pemetrexed in Japanese patients with advanced non-small cell lung cancer harboring activating EGFR mutations:Subgroup analysis of LUX-Lung 3[J]. Cancer Sci, 2015, 106(9):1202-1211.
[12]	Soria JC, Felip E, Cobo M, et al. Afatinib versus Erlotinib as second-line treatment of patients with advanced squamous cell carcinoma of the lung (LUX-Lung 8):an open-label randomised controlled phase 3 trial[J]. Lancet Oncol, 2015, 16(8):897-907.
[13]	Janne PA, Yang JC, Kim DW, et al. AZD9291 in EGFR inhibitor-resistant non-small-cell lung cancer[J]. N Engl J Med, 2015, 372(18):1689-1699.
[14]	Greig SL. Osimertinib:First global approval[J]. Drugs, 2016, 76(2):263-273.
[15]	Shea M, Costa DB, Rangachari D. Management of advanced non-small cell lung cancers with known mutations or rearrangements:Latest evidence and treatment approaches[J]. Ther Adv Respir Dis, 2016, 10(2):113-129.
[16]	Yu HA, Arcila ME, Rekhtman N, et al. Analysis of tumor specimens at the time of acquired resistance to EGFR-TKI therapy in 155 patients with EGFR-mutant lung cancers[J]. Clin Cancer Res, 2013, 19(8):2240-2247.
[17]	Chong CR, Janne PA. The quest to overcome resistance to EGFR-targeted therapies in cancer[J]. Nat Med, 2013,19(11):1389-1400.
[18]	Li D, Ambrogio L, Shimamura T, et al. BIBW2992, an irreversible EGFR/HER2 inhibitor highly effective in preclinical lung cancer models[J]. Oncogene, 2008, 27(34):4702-4711.
[19]	Soda M, Choi YL, Enomoto M, et al. Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer[J]. Nature, 2007, 448(7153):561-566.
[20]	Cameron L, Solomon B. New treatment options for ALK-rearranged non-small cell lung cancer[J]. Curr Treat Options Oncol, 2015, 16(10):49.
[21]	Costa DB, Shaw AT, Ou SH, et al. Clinical experience with crizotinib in patients with advanced ALK-rearranged non-small-cell lung cancer and brain metastases[J]. J Clin Oncol, 2015,33(17):1881-1888.
[22]	Lukas RV, Hasan Y, Nicholas MK, et al. ROS1 rearranged non-small cell lung cancer brain metastases respond to low dose radiotherapy[J]. J Clin Neurosci, 2015,22(12):1978-1979.
[23]	Marchetti A, Felicioni L, Malatesta S, et al. Clinical features and outcome of patients with non-small-cell lung cancer harboring BRAF mutations[J]. J Clin Oncol,2011,29(26):3574-3579.
[24]	石远凯,孙燕,于金明,等.中国晚期原发性肺癌诊治专家共识(2016年版)[J].中国肺癌杂志,2016,19(1):1-15.
[25]	Lipson D, Capelletti M, Yelensky R, et al. Identification of new ALK and RET gene fusions from colorectal and lung cancer biopsies[J]. Nat Med, 2012, 18(3):382-384.
[26]	Li BT, Ross DS, Aisner DL, et al. HER2 amplification and HER2 mutation are distinct molecular targets in lung cancers[J]. J Thorac Oncol, 2016, 11(3):414-419.
[27]	Mar N, Vredenburgh JJ, Wasser JS. Targeting HER2 in the treatment of non-small cell lung cancer[J]. Lung Cancer, 2015, 87(3):220-225.

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Research progress on target therapy of advanced non-small cell lung cancer

doi: 10.3969/j.issn.1006-0111.2016.04.004

Abstract

References

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通讯作者: 陈斌, bchen63@163.com

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