DMS 114

DMS 114是人類非小細胞肺癌（英语：Non-small-cell lung carcinoma）細胞系，最初是分離自一名尚未接受治療的68歲白人男性非小細胞肺癌患者。DMS 114細胞的早期傳代曾被萊氏無膽甾原體（英语：Acholeplasma laidlawii）污染，而該萊氏無膽甾原體則在冷凍保存之前已被卡納黴素等治愈。

科研用途

2008年，有研究指出在治療中使用β-羥基異戊基紫草苷（一種蛋白酪氨酸激酶的三磷酸腺苷非競爭性抑製劑（英语：Non-competitive inhibition）），可以誘導DMS114細胞凋亡，並且其磷蛋白部分中的dUTPase（英语：dUTP diphosphatase）會減少。同時又發現經5-氟尿嘧啶（一種用作化療藥物的胸苷酸合酶（英语：Thymidylate synthase）的特異性抑製劑）處理的DMS114細胞會被其抑製。這些實驗結果表明，dUTPase的活性是導致肺癌細胞死亡的其中一個關鍵因素^[1]。2011年，有科研人員指出DMS-114細胞最初來自未曾接受過治療的非小細胞肺癌患者，從而能夠確定新化合物的特異性作用^[2]。他們使用發光法 (luminometry) 和生物冷光測定法（英语：Bioluminescence imaging），觀察到此細胞系的發光信號 (luminescence signals) 與細胞數量之間的直接關係，並且發現與基於MTT的傳統細胞存活率分析相比，生物冷光測定法的靈敏度更高^[3]。2017年，有學者為了研究抗成纖維細胞生長因子 (FGFR) 抑制的潛在機制，以DMS114細胞進行實驗，發現其對三種不同的FGFR抑製劑高度敏感，但在治療中仍表現出持續的殘餘細胞活性，表明DMS114細胞有着耐藥細胞的亞群^[4]。

參考資料

^ Kajimoto, S; Horie, M; Manabe, H; Masuda, Y; Shibayama-Imazu, T; Nakajo, S; Gong, XF; Obama, T; Itabe, H; Nakaya, K. A tyrosine kinase inhibitor, beta-hydroxyisovalerylshikonin, induced apoptosis in human lung cancer DMS114 cells through reduction of dUTP nucleotidohydrolase activity.. Biochimica et biophysica acta. 2008-01, 1782 (1): 41–50 [2019-12-21]. PMID 18078828. doi:10.1016/j.bbadis.2007.11.004. （原始内容存档于2019-12-21）.
^ Pettengill, OS; Sorenson, GD; Wurster-Hill, DH; Curphey, TJ; Noll, WW; Cate, CC; Maurer, LH. Isolation and growth characteristics of continuous cell lines from small-cell carcinoma of the lung.. Cancer. 1980-03-01, 45 (5): 906–18 [2019-12-21]. PMID 6266631. doi:10.1002/1097-0142(19800301)45:5<906::aid-cncr2820450513>3.0.co;2-h. （原始内容存档于2019-12-21）.
^ Improgo, MR; Johnson, CW; Tapper, AR; Gardner, PD. Bioluminescence-based high-throughput screen identifies pharmacological agents that target neurotransmitter signaling in small cell lung carcinoma.. PloS one. 2011, 6 (9): e24132 [2019-12-21]. PMID 21931655. doi:10.1371/journal.pone.0024132.
^ Malchers, F; Ercanoglu, M; Schütte, D; Castiglione, R; Tischler, V; Michels, S; Dahmen, I; Brägelmann, J; Menon, R; Heuckmann, JM; George, J; Ansén, S; Sos, ML; Soltermann, A; Peifer, M; Wolf, J; Büttner, R; Thomas, RK. Mechanisms of Primary Drug Resistance in FGFR1-Amplified Lung Cancer.. Clinical cancer research : an official journal of the American Association for Cancer Research. 2017-09-15, 23 (18): 5527–5536 [2019-12-21]. PMID 28630215. doi:10.1158/1078-0432.CCR-17-0478. （原始内容存档于2019-12-21）.

外部連結

Cellosaurus entry for DMS 114（页面存档备份，存于互联网档案馆）

[1] Kajimoto, S; Horie, M; Manabe, H; Masuda, Y; Shibayama-Imazu, T; Nakajo, S; Gong, XF; Obama, T; Itabe, H; Nakaya, K. A tyrosine kinase inhibitor, beta-hydroxyisovalerylshikonin, induced apoptosis in human lung cancer DMS114 cells through reduction of dUTP nucleotidohydrolase activity.. Biochimica et biophysica acta. 2008-01, 1782 (1): 41–50 [2019-12-21]. PMID 18078828. doi:10.1016/j.bbadis.2007.11.004. （原始内容存档于2019-12-21）.

[2] Pettengill, OS; Sorenson, GD; Wurster-Hill, DH; Curphey, TJ; Noll, WW; Cate, CC; Maurer, LH. Isolation and growth characteristics of continuous cell lines from small-cell carcinoma of the lung.. Cancer. 1980-03-01, 45 (5): 906–18 [2019-12-21]. PMID 6266631. doi:10.1002/1097-0142(19800301)45:5<906::aid-cncr2820450513>3.0.co;2-h. （原始内容存档于2019-12-21）.

[3] Improgo, MR; Johnson, CW; Tapper, AR; Gardner, PD. Bioluminescence-based high-throughput screen identifies pharmacological agents that target neurotransmitter signaling in small cell lung carcinoma.. PloS one. 2011, 6 (9): e24132 [2019-12-21]. PMID 21931655. doi:10.1371/journal.pone.0024132.

[4] Malchers, F; Ercanoglu, M; Schütte, D; Castiglione, R; Tischler, V; Michels, S; Dahmen, I; Brägelmann, J; Menon, R; Heuckmann, JM; George, J; Ansén, S; Sos, ML; Soltermann, A; Peifer, M; Wolf, J; Büttner, R; Thomas, RK. Mechanisms of Primary Drug Resistance in FGFR1-Amplified Lung Cancer.. Clinical cancer research : an official journal of the American Association for Cancer Research. 2017-09-15, 23 (18): 5527–5536 [2019-12-21]. PMID 28630215. doi:10.1158/1078-0432.CCR-17-0478. （原始内容存档于2019-12-21）.

[1]

[2]

[3]

[4]