Login Register Cart 0
Generic placeholder image

当代肿瘤药物靶点

Editor-in-Chief

ISSN (Print): 1568-0096
ISSN (Online): 1873-5576

Back
Journal Home About Journal Editorial Board Journal Insight Current Issue Volumes/Issues
Subscribe Translate in English
Opinion Article

具有独立耐药机制的癌症药物靶点的实验测定

卷 22, 期 2, 2022

发表于: 08 March, 2022

页: [97 - 107] 页: 11

弟呕挨: 10.2174/1568009622666220107152014

价格: $65

摘要

肿瘤突变动力学的数学模型表明，具有不同耐药机制的癌症药物靶点应该是联合治疗的良好候选者。 这是因为同时导致对所有药物产生耐药性的突变的发展应该相对不常见。 然而，很难确定满足特定癌症这一要求的药物靶点。 在这里，我们提出了四个实验标准，我们认为这些是药物组合应满足的必要（但不是充分）条件，以便考虑用于旨在延迟或克服癌症耐药性的联合药物治疗。 我们展示了我们自己的实验结果——在这些标准的指导下——使用间变性淋巴瘤激酶突变的肺癌细胞。 每组实验都展示了不同药物组合的结果。 我们得出结论，ALK 和 MEK 抑制剂的组合最接近我们的所有标准。

关键词: ALK、耐药性、联合治疗、肺癌、数学模型、药物靶点。

« Previous Next »
图形摘要

[1]
Siegel, R.L.; Miller, K.D.; Jemal, A. Cancer statistics, 2015. CA Cancer J. Clin., 2015, 65(1), 5-29.
[http://dx.doi.org/10.3322/caac.21254] [PMID: 25559415]
[2]
Wilcox, W.S. The last surviving cancer cell: The chances of killing it. Cancer Chemother. Rep., 1966, 50(8), 541-542.
[PMID: 5978726]
[3]
Perelson, A.S.; Neumann, A.U.; Markowitz, M.; Leonard, J.M.; Ho, D.D. HIV-1 dynamics in vivo: Virion clearance rate, infected cell life-span, and viral generation time. Science, 1996, 271(5255), 1582-1586.
[http://dx.doi.org/10.1126/science.271.5255.1582] [PMID: 8599114]
[4]
Altrock, P.M.; Liu, L.L.; Michor, F. The mathematics of cancer: Integrating quantitative models. Nat. Rev. Cancer, 2015, 15(12), 730-745.
[http://dx.doi.org/10.1038/nrc4029] [PMID: 26597528]
[5]
Chisholm, R.H.; Lorenzi, T.; Clairambault, J. Cell population heterogeneity and evolution towards drug resistance in cancer: Biological and mathematical assessment, theoretical treatment optimisation. Biochim. Biophys. Acta, 2016, 1860(11 Pt B), 2627-2645.
[http://dx.doi.org/10.1016/j.bbagen.2016.06.009] [PMID: 27339473]
[6]
Bozic, I.; Nowak, M.A. Resisting resistance. Ann. Rev. Cancer Biol., 2017, 1, 203-221.
[http://dx.doi.org/10.1146/annurev-cancerbio-042716-094839]
[7]
Bozic, I.; Reiter, J.G.; Allen, B.; Antal, T.; Chatterjee, K.; Shah, P.; Moon, Y.S.; Yaqubie, A.; Kelly, N.; Le, D.T.; Lipson, E.J.; Chapman, P.B.; Diaz, L.A., Jr; Vogelstein, B.; Nowak, M.A. Evolutionary dynamics of cancer in response to targeted combination therapy. elife, 2013, 2, e00747.
[8]
Sun, X.; Hu, B. Mathematical modeling and computational prediction of cancer drug resistance. Brief. Bioinform., 2018, 19(6), 1382-1399.
[http://dx.doi.org/10.1093/bib/bbx065] [PMID: 28981626]
[9]
Camidge, D.R.; Kono, S.A.; Lu, X.; Okuyama, S.; Barón, A.E.; Oton, A.B.; Davies, A.M.; Varella-Garcia, M.; Franklin, W.; Doebele, R.C. Anaplastic lymphoma kinase gene rearrangements in non-small cell lung cancer are associated with prolonged progression-free survival on pemetrexed. J. Thorac. Oncol., 2011, 6(4), 774-780.
[http://dx.doi.org/10.1097/JTO.0b013e31820cf053] [PMID: 21336183]
[10]
Shaw, A.T.; Varghese, A.M.; Solomon, B.J.; Costa, D.B.; Novello, S.; Mino-Kenudson, M.; Awad, M.M.; Engelman, J.A.; Riely, G.J.; Monica, V.; Yeap, B.Y.; Scagliotti, G.V. Pemetrexed-based chemotherapy in patients with advanced, ALK-positive non-small cell lung cancer. Ann. Oncol., 2013, 24(1), 59-66.
[http://dx.doi.org/10.1093/annonc/mds242] [PMID: 22887466]
[11]
Berge, E.M.; Lu, X.; Maxson, D.; Barón, A.E.; Gadgeel, S.M.; Solomon, B.J.; Doebele, R.C.; Varella-Garcia, M.; Camidge, D.R. Clinical benefit from pemetrexed before and after crizotinib exposure and from crizotinib before and after pemetrexed exposure in patients with anaplastic lymphoma kinase-positive non-small-cell lung cancer. Clin. Lung Cancer, 2013, 14(6), 636-643.
[http://dx.doi.org/10.1016/j.cllc.2013.06.005] [PMID: 23931899]
[12]
Shaw, A.T.; Friboulet, L.; Leshchiner, I.; Gainor, J.F.; Bergqvist, S.; Brooun, A.; Burke, B.J.; Deng, Y.L.; Liu, W.; Dardaei, L.; Frias, R.L.; Schultz, K.R.; Logan, J.; James, L.P.; Smeal, T.; Timofeevski, S.; Katayama, R.; Iafrate, A.J.; Le, L.; McTigue, M.; Getz, G.; Johnson, T.W.; Engelman, J.A. Resensitization to crizotinib by the lorlatinib ALK resistance mutation L1198F. N. Engl. J. Med., 2016, 374(1), 54-61.
[http://dx.doi.org/10.1056/NEJMoa1508887] [PMID: 26698910]
[13]
Bland, A.R.; Bower, R.L.; Nimick, M.; Hawkins, B.C.; Rosengren, R.J.; Ashton, J.C. Cytotoxicity of curcumin derivatives in ALK positive non-small cell lung cancer. Eur. J. Pharmacol., 2019, 865, 172749.
[http://dx.doi.org/10.1016/j.ejphar.2019.172749] [PMID: 31654622]
[14]
Kashif, M.; Andersson, C.; Mansoori, S.; Larsson, R.; Nygren, P.; Gustafsson, M.G. Bliss and Loewe interaction analyses of clinically relevant drug combinations in human colon cancer cell lines reveal complex patterns of synergy and antagonism. Oncotarget, 2017, 8(61), 103952-103967.
[http://dx.doi.org/10.18632/oncotarget.21895] [PMID: 29262612]
[15]
Goutelle, S.; Maurin, M.; Rougier, F.; Barbaut, X.; Bourguignon, L.; Ducher, M.; Maire, P. The Hill equation: A review of its capabilities in pharmacological modelling. Fundam. Clin. Pharmacol., 2008, 22(6), 633-648.
[http://dx.doi.org/10.1111/j.1472-8206.2008.00633.x] [PMID: 19049668]
[16]
Sosman, J.A.; Kim, K.B.; Schuchter, L.; Gonzalez, R.; Pavlick, A.C.; Weber, J.S.; McArthur, G.A.; Hutson, T.E.; Moschos, S.J.; Flaherty, K.T.; Hersey, P.; Kefford, R.; Lawrence, D.; Puzanov, I.; Lewis, K.D.; Amaravadi, R.K.; Chmielowski, B.; Lawrence, H.J.; Shyr, Y.; Ye, F.; Li, J.; Nolop, K.B.; Lee, R.J.; Joe, A.K.; Ribas, A. Survival in BRAF V600-mutant advanced melanoma treated with vemurafenib. N. Engl. J. Med., 2012, 366(8), 707-714.
[http://dx.doi.org/10.1056/NEJMoa1112302] [PMID: 22356324]
[17]
Vogel, C.L.; Cobleigh, M.A.; Tripathy, D.; Gutheil, J.C.; Harris, L.N.; Fehrenbacher, L.; Slamon, D.J.; Murphy, M.; Novotny, W.F.; Burchmore, M.; Shak, S.; Stewart, S.J.; Press, M. Efficacy and safety of trastuzumab as a single agent in first-line treatment of HER2-overexpressing metastatic breast cancer. J. Clin. Oncol., 2002, 20(3), 719-726.
[http://dx.doi.org/10.1200/JCO.2002.20.3.719] [PMID: 11821453]
[18]
Wilson, C.; Nimick, M.; Nehoff, H.; Ashton, J.C. ALK and IGF-1R as independent targets in crizotinib resistant lung cancer. Sci. Rep., 2017, 7(1), 13955.
[http://dx.doi.org/10.1038/s41598-017-14289-w] [PMID: 29066738]
[19]
Morris, S.W.; Kirstein, M.N.; Valentine, M.B.; Dittmer, K.G.; Shapiro, D.N.; Saltman, D.L.; Look, A.T. Fusion of a kinase gene, ALK, to a nucleolar protein gene, NPM, in non-Hodgkin’s lymphoma. Science, 1994, 263(5151), 1281-1284.
[http://dx.doi.org/10.1126/science.8122112] [PMID: 8122112]
[20]
Soda, M.; Choi, Y.L.; Enomoto, M.; Takada, S.; Yamashita, Y.; Ishikawa, S.; Fujiwara, S.; Watanabe, H.; Kurashina, K.; Hatanaka, H.; Bando, M.; Ohno, S.; Ishikawa, Y.; Aburatani, H.; Niki, T.; Sohara, Y.; Sugiyama, Y.; Mano, H. Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer. Nature, 2007, 448(7153), 561-566.
[http://dx.doi.org/10.1038/nature05945] [PMID: 17625570]
[21]
Pacheco, J.M.; Gao, D.; Smith, D.; Purcell, T.; Hancock, M.; Bunn, P.; Robin, T.; Liu, A.; Karam, S.; Gaspar, L.; Kavanagh, B.; Rusthoven, C.; Aisner, D.; Doebele, R.; Camidge, D.R. Natural history and factors associated with overall survival in stage IV ALK-rearranged non-small cell lung cancer. J. Thorac. Oncol., 2019, 14(4), 691-700.
[http://dx.doi.org/10.1016/j.jtho.2018.12.014] [PMID: 30599201]
[22]
Witek, B.; El Wakil, A.; Nord, C.; Ahlgren, U.; Eriksson, M.; Vernersson-Lindahl, E.; Helland, Å.; Alexeyev, O.A.; Hallberg, B.; Palmer, R.H. Targeted disruption of ALK reveals a potential role in hypogonadotropic hypogonadism. PLoS One, 2015, 10(5), e0123542.
[http://dx.doi.org/10.1371/journal.pone.0123542] [PMID: 25955180]
[23]
Peters, S.; Camidge, D.R.; Shaw, A.T.; Gadgeel, S.; Ahn, J.S.; Kim, D.W.; Ou, S.I.; Pérol, M.; Dziadziuszko, R.; Rosell, R.; Zeaiter, A.; Mitry, E.; Golding, S.; Balas, B.; Noe, J.; Morcos, P.N.; Mok, T. Alectinib versus crizotinib in untreated ALK-positive non small-cell lung cancer. N. Engl. J. Med., 2017, 377(9), 829-838.
[http://dx.doi.org/10.1056/NEJMoa1704795] [PMID: 28586279]
[24]
Chae, Y.K.; Arya, A.; Malecek, M.K.; Shin, D.S.; Carneiro, B.; Chandra, S.; Kaplan, J.; Kalyan, A.; Altman, J.K.; Platanias, L.; Giles, F. Repurposing metformin for cancer treatment: Current clinical studies. Oncotarget, 2016, 7(26), 40767-40780.
[http://dx.doi.org/10.18632/oncotarget.8194] [PMID: 27004404]
[25]
Li, L.; Wang, Y.; Peng, T.; Zhang, K.; Lin, C.; Han, R.; Lu, C.; He, Y. Metformin restores crizotinib sensitivity in crizotinib-resistant human lung cancer cells through inhibition of IGF1-R signaling pathway. Oncotarget, 2016, 7(23), 34442-34452.
[http://dx.doi.org/10.18632/oncotarget.9120] [PMID: 27144340]
[26]
Mohammed, A.; Janakiram, N.B.; Brewer, M.; Ritchie, R.L.; Marya, A.; Lightfoot, S.; Steele, V.E.; Rao, C.V. Antidiabetic drug metformin prevents progression of pancreatic cancer by targeting in part cancer stem cells and mTOR signaling. Transl. Oncol., 2013, 6(6), 649-659.
[http://dx.doi.org/10.1593/tlo.13556] [PMID: 24466367]
[27]
Wheaton, W.W.; Weinberg, S.E.; Hamanaka, R.B.; Soberanes, S.; Sullivan, L.B.; Anso, E.; Glasauer, A.; Dufour, E.; Mutlu, G.M.; Budigner, G.S.; Chandel, N.S. Chandel, Metformin inhibits mitochondrial complex I of cancer cells to reduce tumorigenesis. elife, 2014, 3, e02242.
[28]
Zhuang, Y.; Miskimins, W.K. Cell cycle arrest in Metformin treated breast cancer cells involves activation of AMPK, downregulation of cyclin D1, and requires p27Kip1 or p21Cip1. J. Mol. Signal., 2008, 3(1), 18.
[http://dx.doi.org/10.1186/1750-2187-3-18] [PMID: 19046439]
[29]
Jalving, M.; Gietema, J.A.; Lefrandt, J.D.; de Jong, S.; Reyners, A.K.L.; Gans, R.O.B.; de Vries, E.G.E. Metformin: Taking away the candy for cancer? Eur. J. Cancer, 2010, 46(13), 2369-2380.
[http://dx.doi.org/10.1016/j.ejca.2010.06.012] [PMID: 20656475]
[30]
Kourelis, T.V.; Siegel, R.D. Metformin and cancer: New applications for an old drug. Med. Oncol., 2012, 29(2), 1314-1327.
[http://dx.doi.org/10.1007/s12032-011-9846-7] [PMID: 21301998]
[31]
Bland, A.R.; Shrestha, N.; Bower, R.L.; Rosengren, R.J.; Ashton, J.C. The effect of metformin in EML4-ALK+ lung cancer alone and in combination with crizotinib in cell and rodent models. Biochem. Pharmacol., 2021, 183, 114345.
[http://dx.doi.org/10.1016/j.bcp.2020.114345] [PMID: 33227290]
[32]
DaCosta Byfield, S.; Chastek, B.; Korrer, S.; Horstman, T.; Malin, J.; Newcomer, L. Real-world outcomes and value of first-line therapy for metastatic non-small cell lung cancer†. Cancer Invest., 2020, 38(10), 608-617.
[http://dx.doi.org/10.1080/07357907.2020.1827415] [PMID: 33107767]
[33]
Lovly, C.M.; McDonald, N.T.; Chen, H.; Ortiz-Cuaran, S.; Heukamp, L.C.; Yan, Y.; Florin, A.; Ozretić, L.; Lim, D.; Wang, L.; Chen, Z.; Chen, X.; Lu, P.; Paik, P.K.; Shen, R.; Jin, H.; Buettner, R.; Ansén, S.; Perner, S.; Brockmann, M.; Bos, M.; Wolf, J.; Gardizi, M.; Wright, G.M.; Solomon, B.; Russell, P.A.; Rogers, T.M.; Suehara, Y.; Red-Brewer, M.; Tieu, R.; de Stanchina, E.; Wang, Q.; Zhao, Z.; Johnson, D.H.; Horn, L.; Wong, K.K.; Thomas, R.K.; Ladanyi, M.; Pao, W. Rationale for co-targeting IGF-1R and ALK in ALK fusion-positive lung cancer. Nat. Med., 2014, 20(9), 1027-1034.
[http://dx.doi.org/10.1038/nm.3667] [PMID: 25173427]
[34]
Tanizaki, J.; Okamoto, I.; Takezawa, K.; Sakai, K.; Azuma, K.; Kuwata, K.; Yamaguchi, H.; Hatashita, E.; Nishio, K.; Janne, P.A.; Nakagawa, K. Combined effect of ALK and MEK inhibitors in EML4-ALK-positive non-small-cell lung cancer cells. Br. J. Cancer, 2012, 106(4), 763-767.
[http://dx.doi.org/10.1038/bjc.2011.586] [PMID: 22240786]
[35]
Hrustanovic, G.; Olivas, V.; Pazarentzos, E.; Tulpule, A.; Asthana, S.; Blakely, C.M.; Okimoto, R.A.; Lin, L.; Neel, D.S.; Sabnis, A.; Flanagan, J.; Chan, E.; Varella-Garcia, M.; Aisner, D.L.; Vaishnavi, A.; Ou, S.H.; Collisson, E.A.; Ichihara, E.; Mack, P.C.; Lovly, C.M.; Karachaliou, N.; Rosell, R.; Riess, J.W.; Doebele, R.C.; Bivona, T.G. RAS-MAPK dependence underlies a rational polytherapy strategy in EML4-ALK-positive lung cancer. Nat. Med., 2015, 21(9), 1038-1047.
[http://dx.doi.org/10.1038/nm.3930] [PMID: 26301689]
[36]
Crystal, A.S.; Shaw, A.T.; Sequist, L.V.; Friboulet, L.; Niederst, M.J.; Lockerman, E.L.; Frias, R.L.; Gainor, J.F.; Amzallag, A.; Greninger, P.; Lee, D.; Kalsy, A.; Gomez-Caraballo, M.; Elamine, L.; Howe, E.; Hur, W.; Lifshits, E.; Robinson, H.E.; Katayama, R.; Faber, A.C.; Awad, M.M.; Ramaswamy, S.; Mino-Kenudson, M.; Iafrate, A.J.; Benes, C.H.; Engelman, J.A. Patient-derived models of acquired resistance can identify effective drug combinations for cancer. Science, 2014, 346(6216), 1480-1486.
[http://dx.doi.org/10.1126/science.1254721] [PMID: 25394791]
[37]
Yoshida, R.; Sasaki, T.; Minami, Y.; Hibino, Y.; Okumura, S.; Sado, M.; Miyokawa, N.; Hayashi, S.; Kitada, M.; Ohsaki, Y. Activation of Src signaling mediates acquired resistance to ALK inhibition in lung cancer. Int. J. Oncol., 2017, 51(5), 1533-1540.
[http://dx.doi.org/10.3892/ijo.2017.4140] [PMID: 29048652]
[38]
Dagogo-Jack, I. A, Phase IB/II Study of Alectinib Combined With Cobimetinib in Advanced ALK-Rearranged (ALK+) NSCLC. ClinicalTrials.gov, 2020. Available from: https://clinicaltrials.gov/ct2/show/NCT03202940.
[39]
Potter, L.; Blakely, C. Ceritinib + trametinib in patients with advanced ALK-positive non-small cell lung cancer (NSCLC). ClinicalTrials.gov, 2020. Avaialble from: https://clinicaltrials.gov/ct2/show/NCT03087448.
[40]
Shrestha, N.; Nimick, M.; Dass, P.; Rosengren, R.J.; Ashton, J.C. Mechanisms of suppression of cell growth by dual inhibition of ALK and MEK in ALK-positive non-small cell lung cancer. Sci. Rep., 2019, 9(1), 18842.
[http://dx.doi.org/10.1038/s41598-019-55376-4] [PMID: 31827192]

Rights & Permissions Print Cite
Article Metrics
24
1
© 2024 Bentham Science Publishers | Privacy Policy