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T25
【BxPC-3】BxPC-3细胞/BxPC-3细胞/BxPC-3人原位胰腺腺癌细胞Cell line name BxPC-3
Synonyms BxPc-3; BXPC-3; Bx-PC3; BXPC3; BxPC3; BxPc3; Biopsy xenograft of Pancreatic Carcinoma line-3
Accession CVCL_0186
Resource Identification Initiative To cite this cell line use: BxPC-3 (RRID:CVCL_0186)
Comments Part of: Cancer Dependency Map project (DepMap) (includes Cancer Cell Line Encyclopedia - CCLE).
Part of: COSMIC cell lines project.
Part of: KuDOS 95 cell line panel.
Part of: MD Anderson Cell Lines Project.
Population: Caucasian.
Doubling time: 48-60 hours (PubMed=3754176); 48 hours (PubMed=25984343); ~48 hours (DSMZ=ACC-760).
Microsatellite instability: Stable (MSS) (Sanger).
Omics: Array-based CGH.
Omics: CRISPR phenotypic screen.
Omics: Deep exome analysis.
Omics: Deep proteome analysis.
Omics: Deep quantitative proteome analysis.
Omics: DNA methylation analysis.
Omics: Metabolome analysis.
Omics: miRNA expression profiling.
Omics: Protein expression by reverse-phase protein arrays.
Omics: shRNA library screening.
Omics: SNP array analysis.
Omics: Transcriptome analysis by microarray.
Omics: Transcriptome analysis by RNAseq.
Caution: Additional TP53 mutation in c.793C>T indicated incorrectly in PubMed=1630814.
Derived from site: In situ; Pancreas; UBERON=UBERON_0001264.
PubMed=8026879; DOI=10.1002/ijc.2910580207
Berrozpe G., Schaeffer J., Peinado M.A., Real F.X., Perucho M.
Comparative analysis of mutations in the p53 and K-ras genes in pancreatic cancer.
Int. J. Cancer 58:185-191(1994)
PubMed=8194712; DOI=10.1016/0016-5085(94)90422-7
Simon B., Weinel R., Hohne M., Watz J., Schmidt J., Kortner G., Arnold R.
Frequent alterations of the tumor suppressor genes p53 and DCC in human pancreatic carcinoma.
Gastroenterology 106:1645-1651(1994)
PubMed=8286197; DOI=10.1038/bjc.1994.24; PMCID=PMC1968784
Lohr J.-M., Trautmann B., Gottler M., Peters S., Zauner I., Maillet B., Kloppel G.
Human ductal adenocarcinomas of the pancreas express extracellular matrix proteins.
Br. J. Cancer 69:144-151(1994)
PubMed=21607521; DOI=10.3892/or.1.6.1223
Iguchi H., Morita R., Yasuda D., Takayanagi R., Ikeda Y., Takada Y., Shimazoe T., Nawata H., Kono A.
Alterations of the p53 tumor-suppressor gene and ki-ras oncogene in human pancreatic cancer-derived cell-lines with different metastatic potential.
Oncol. Rep. 1:1223-1227(1994)
PubMed=9788440; DOI=10.1038/sj.onc.1202118
Villanueva A., Garcia C., Paules Blazquez A.B., Vicente M., Megias M., Reyes G., de Villalonga P., Agell N., Lluis F., Bachs O., Capella G.
Disruption of the antiproliferative TGF-beta signaling pathways in human pancreatic cancer cells.
Oncogene 17:1969-1978(1998)
PubMed=10027410; DOI=10.1016/S0002-9440(10)65298-4; PMCID=PMC1850008
Ghadimi B.M., Schrock E., Walker R.L., Wangsa D., Jauho A., Meltzer P.S., Ried T.
Specific chromosomal aberrations and amplification of the AIB1 nuclear receptor coactivator gene in pancreatic carcinomas.
Am. J. Pathol. 154:525-536(1999)
PubMed=10408907; DOI=10.1016/S0304-3835(98)00380-2
Bartsch D.K., Barth P., Bastian D., Ramaswamy A., Gerdes B., Chaloupka B., Deiss Y., Simon B., Schudy A.
Higher frequency of DPC4/Smad4 alterations in pancreatic cancer cell lines than in primary pancreatic adenocarcinomas.
Cancer Lett. 139:43-49(1999)
PubMed=11115575; DOI=10.3892/or.8.1.89
Sun C.-L., Yamato T., Furukawa T., Ohnishi Y., Kijima H., Horii A.
Characterization of the mutations of the K-ras, p53, p16, and SMAD4 genes in 15 human pancreatic cancer cell lines.
Oncol. Rep. 8:89-92(2001)
PubMed=11169959; DOI=10.1002/1097-0215(200002)9999:9999<::AID-IJC1049>3.0.CO;2-C
Sirivatanauksorn V., Sirivatanauksorn Y., Gorman P.A., Davidson J.M., Sheer D., Moore P.S., Scarpa A., Edwards P.A.W., Lemoine N.R.
Non-random chromosomal rearrangements in pancreatic cancer cell lines identified by spectral karyotyping.
Int. J. Cancer 91:350-358(2001)
PubMed=12692724; DOI=10.1007/s00428-003-0784-4
Sipos B., Moser S., Kalthoff H., Torok V., Lohr J.-M., Kloppel G.
A comprehensive characterization of pancreatic ductal carcinoma cell lines: towards the establishment of an in vitro research platform.
Virchows Arch. 442:444-452(2003)
PubMed=15126341; DOI=10.1158/0008-5472.CAN-03-3159
Heidenblad M., Schoenmakers E.F.P.M., Jonson T., Gorunova L., Veltman J.A., van Kessel A.G., Hoglund M.
Genome-wide array-based comparative genomic hybridization reveals multiple amplification targets and novel homozygous deletions in pancreatic carcinoma cell lines.
Cancer Res. 64:3052-3059(2004)
PubMed=15367885; DOI=10.1097/00006676-200410000-00004
Loukopoulos P., Kanetaka K., Takamura M., Shibata T., Sakamoto M., Hirohashi S.
Orthotopic transplantation models of pancreatic adenocarcinoma derived from cell lines and primary tumors and displaying varying metastatic activity.
Pancreas 29:193-203(2004)
PubMed=15688027; DOI=10.1038/sj.onc.1208383
Heidenblad M., Lindgren D., Veltman J.A., Jonson T., Mahlamaki E.H., Gorunova L., van Kessel A.G., Schoenmakers E.F.P.M., Hoglund M.
Microarray analyses reveal strong influence of DNA copy number alterations on the transcriptional patterns in pancreatic cancer: implications for the interpretation of genomic amplifications.
Oncogene 24:1794-1801(2005)
PubMed=16912165; DOI=10.1158/0008-5472.CAN-06-0721
Calhoun E.S., Hucl T., Gallmeier E., West K.M., Arking D.E., Maitra A., Iacobuzio-Donahue C.A., Chakravarti A., Hruban R.H., Kern S.E.
Identifying allelic loss and homozygous deletions in pancreatic cancer without matched normals using high-density single-nucleotide polymorphism arrays.
Cancer Res. 66:7920-7928(2006)
PubMed=18298655; DOI=10.1111/j.1582-4934.2008.00289.x; PMCID=PMC3828895
Pilarsky C., Ammerpohl O., Sipos B., Dahl E., Hartmann A., Wellmann A., Braunschweig T., Lohr J.-M., Jesenofsky R., Friess H., Wente M.N., Kristiansen G., Jahnke B., Denz A., Ruckert F., Schackert H.K., Kloppel G., Kalthoff H., Saeger H.-D., Grutzmann R.
Activation of Wnt signalling in stroma from pancreatic cancer identified by gene expression profiling.
J. Cell. Mol. Med. 12:2823-2835(2008)
PubMed=18380791; DOI=10.1111/j.1349-7006.2008.00779.x; PMCID=PMC11158928
Suzuki A., Shibata T., Shimada Y., Murakami Y., Horii A., Shiratori K., Hirohashi S., Inazawa J., Imoto I.
Identification of SMURF1 as a possible target for 7q21.3-22.1 amplification detected in a pancreatic cancer cell line by in-house array-based comparative genomic hybridization.
Cancer Sci. 99:986-994(2008)
CLPUB00416
Oberlin L.
Treatment of pancreatic carcinoma cell lines in vitro and vivo with a monoclonal antibody against the transferrin receptor.
Thesis VMD (2009); Justus-Liebig-Universitat Giessen; Giessen; Germany
PubMed=20037478; DOI=10.4161/cbt.8.21.9685; PMCID=PMC2824894
Kent O.A., Mullendore M.E., Wentzel E.A., Lopez-Romero P., Tan A.-C., Alvarez H., West K.M., Ochs M.F., Hidalgo M., Arking D.E., Maitra A., Mendell J.T.
A resource for analysis of microRNA expression and function in pancreatic ductal adenocarcinoma cells.
Cancer Biol. Ther. 8:2013-2024(2009)
PubMed=20164919; DOI=10.1038/nature08768; PMCID=PMC3145113
Bignell G.R., Greenman C.D., Davies H.R., Butler A.P., Edkins S., Andrews J.M., Buck G., Chen L., Beare D., Latimer C., Widaa S., Hinton J., Fahey C., Fu B.-Y., Swamy S., Dalgliesh G.L., Teh B.T., Deloukas P., Yang F.-T., Campbell P.J., Futreal P.A., Stratton M.R.
Signatures of mutation and selection in the cancer genome.
Nature 463:893-898(2010)
PubMed=20418756; DOI=10.1097/MPA.0b013e3181c15963; PMCID=PMC2860631
Deer E.L., Gonzalez-Hernandez J., Coursen J.D., Shea J.E., Ngatia J., Scaife C.L., Firpo M.A., Mulvihill S.J.
Phenotype and genotype of pancreatic cancer cell lines.
Pancreas 39:425-435(2010)
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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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