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T25
SK-MES-1/SK-MES-1细胞系/SK-MES-1细胞株/SK-MES-1人肺鳞癌细胞
Cell line name SK-MES-1
Synonyms SK MES 1; SKMES-1; SK-Mes-1; SK-MES1; SKMES1; SK-MES; SKMES
Accession CVCL_0630
Secondary accession CVCL_8913
Resource Identification Initiative To cite this cell line use: SK-MES-1 (RRID:CVCL_0630)
Comments Part of: Cancer Dependency Map project (DepMap) (includes Cancer Cell Line Encyclopedia - CCLE).
Part of: COSMIC cell lines project.
Part of: MD Anderson Cell Lines Project.
From: Memorial Sloan Kettering Cancer Center; New York; USA.
Registration: Memorial Sloan Kettering Cancer Center Office of Technology Development; SK2009-091.
Population: Caucasian.
Doubling time: ~50 hours (DSMZ=ACC-353).
Microsatellite instability: Stable (MSS) (Sanger).
Omics: Array-based CGH.
Omics: CRISPR phenotypic screen.
Omics: Deep exome analysis.
Omics: Deep quantitative proteome analysis.
Omics: DNA methylation analysis.
Omics: Protein expression by reverse-phase protein arrays.
Omics: SNP array analysis.
Omics: Transcriptome analysis by microarray.
Omics: Transcriptome analysis by RNAseq.
Derived from site: Metastatic; Pleural effusion; UBERON=UBERON_0000175.
PubMed=4005855
Kyoizumi S., Akiyama M., Kouno N., Kobuke K., Hakoda M., Jones S.L., Yamakido M.
Monoclonal antibodies to human squamous cell carcinoma of the lung and their application to tumor diagnosis.
Cancer Res. 45:3274-3281(1985)
PubMed=3518877; DOI=10.3109/07357908609038260
Fogh J.
Human tumor lines for cancer research.
Cancer Invest. 4:157-184(1986)
PubMed=3335022
Alley M.C., Scudiero D.A., Monks A., Hursey M.L., Czerwinski M.J., Fine D.L., Abbott B.J., Mayo J.G., Shoemaker R.H., Boyd M.R.
Feasibility of drug screening with panels of human tumor cell lines using a microculture tetrazolium assay.
Cancer Res. 48:589-601(1988)
PubMed=8385084; DOI=10.1111/j.1349-7006.1993.tb02851.x; PMCID=PMC5919128
Suzuki S., Takahashi T., Nakamura S., Koike K., Ariyoshi Y., Takahashi T., Ueda R.
Alterations of integrin expression in human lung cancer.
Jpn. J. Cancer Res. 84:168-174(1993)
PubMed=7736387; DOI=10.1002/1097-0142(19950515)75:10<2442::AID-CNCR2820751009>3.0.CO;2-Q
Campling B.G., Sarda I.R., Baer K.A., Pang S.C., Baker H.M., Lofters W.S., Flynn T.G.
Secretion of atrial natriuretic peptide and vasopressin by small cell lung cancer.
Cancer 75:2442-2451(1995)
PubMed=11583962; DOI=10.1016/S0002-9440(10)62521-7; PMCID=PMC1850523
Haruki N., Harano T., Masuda A., Kiyono T., Takahashi T., Tatematsu Y., Shimizu S., Mitsudomi T., Konishi H., Osada H., Fujii Y., Takahashi T.
Persistent increase in chromosome instability in lung cancer: possible indirect involvement of p53 inactivation.
Am. J. Pathol. 159:1345-1352(2001)
PubMed=12794755; DOI=10.1002/ijc.11184
Endoh H., Yatabe Y., Shimizu S., Tajima K., Kuwano H., Takahashi T., Mitsudomi T.
RASSF1A gene inactivation in non-small cell lung cancer and its clinical implication.
Int. J. Cancer 106:45-51(2003)
PubMed=14581340
Yokoi S., Yasui K., Iizasa T., Imoto I., Fujisawa T., Inazawa J.
TERC identified as a probable target within the 3q26 amplicon that is detected frequently in non-small cell lung cancers.
Clin. Cancer Res. 9:4705-4713(2003)
PubMed=15746151; DOI=10.1093/hmg/ddi092
Izumi H., Inoue J., Yokoi S., Hosoda H., Shibata T., Sunamori M., Hirohashi S., Inazawa J., Imoto I.
Frequent silencing of DBC1 is by genetic or epigenetic mechanisms in non-small cell lung cancers.
Hum. Mol. Genet. 14:997-1007(2005)
PubMed=16187286; DOI=10.1002/ijc.21491
Garnis C., Lockwood W.W., Vucic E., Ge Y., Girard L., Minna J.D., Gazdar A.F., Lam S., MacAulay C., Lam W.L.
High resolution analysis of non-small cell lung cancer cell lines by whole genome tiling path array CGH.
Int. J. Cancer 118:1556-1564(2006)
PubMed=18083107; DOI=10.1016/j.cell.2007.11.025
Rikova K., Guo A.-L., Zeng Q.-F., Possemato A., Yu J., Haack H., Nardone J., Lee K., Reeves C., Li Y., Hu Y.-R., Tan Z.-P., Stokes M.P., Sullivan L., Mitchell J., Wetzel R., MacNeill J., Ren J.-M., Yuan J., Bakalarski C.E., Villen J., Kornhauser J.M., Smith B., Li D.-Q., Zhou X.-M., Gygi S.P., Gu T.-L., Polakiewicz R.D., Rush J., Comb M.J.
Global survey of phosphotyrosine signaling identifies oncogenic kinases in lung cancer.
Cell 131:1190-1203(2007)
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文献和实验*发表【中文论文】请标注:由上海酶研生物科技有限公司提供;
*发表【英文论文】请标注:From Shanghai EK-Bioscience Biotechnology Co., Ltd.
细胞治疗是细胞和基因治疗的重要组成部分,它通过使用特定类型的细胞来修复、替换或调节受损的组织和器官。在细胞治疗中,不同类型的细胞因其独特的生物学特性而被广泛应用于多种疾病的治疗。以下是一些常用的细胞类型及其在细胞治疗中的应用。 (1)免疫细胞 免疫细胞是细胞治疗中最重要且研究最多的细胞类型之一,主要包括 T 细胞、自然杀伤细胞(NK 细胞)和树突状细胞(DC 细胞)。 T 细胞:T 细胞是人体免疫系统的核心细胞,具有强大的抗肿瘤能力。CAR-T 细胞疗法是目前最成功的免疫细胞治疗技术
简介 细胞增殖/细胞毒性测定是涉及培养细胞的研究中最常用的测试之一。 其是检查用于治疗的药物浓度的基本初步测试,也是确定各种研究领域(如肿瘤学和细胞死亡)药物疗效和安全性的非常重要的测试。 传统上,WST-8 或 ATP 检测(使用代谢活性作为指标)和 BrdU 或胸腺嘧啶核苷检测(使用 DNA 合成水平作为指标)已用于细胞生长特性的定量评估。 尽管这些检测由于其简易性和吞吐量而对我们有益,但这些检测都是间接评估方法,因此结果可能与实际细胞数无关。 在许多情况下,这些检测是终点评估,有时会
对于贴壁生长的细胞,相对来说比较简单但也很麻烦。以下我主要讨论贴壁生长的细胞。 在讨论之前,大家首先要有一个概念,即洁净区,并不是没有细菌,而是细菌的数量非常少,国家标准100级的洁净标准是浮游菌数不得超过5个每立方米,沉降菌数不得超过1个每培养皿.而国外的标准比我国的还要高一点,要求的数量更少。 所以在我们的洁净操作台里,并不是真正一个细菌都没有的,所以在操作的时候还是要尽量利索迅速地完成操作。尽量减少进入培养体系细菌的数量。 所以处理细菌污染的重要原则就是:无限地稀释细菌的浓度,无限地减少
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