SU.86.86Homo sapiens (Human)Cancer cell line
Also known as: SU.86, SU8686, Su86_86, SU86_86, SU86-86, SU86.86, Su-86-86, SU-86-86, SU 86.86, Su.86.86, Su_86_96, SU-88-86
Quick Overview
SU.86.86 is a human pancreatic cancer cell line used in cancer research.
Detailed Summary
Research Applications
Key Characteristics
Basic Information
| Database ID | CVCL_3881 |
|---|---|
| Species | Homo sapiens (Human) |
| Tissue Source | Liver[UBERON:UBERON_0002107] |
Donor Information
| Age | 57 |
|---|---|
| Age Category | Adult |
| Sex | Female |
| Race | caucasian |
Disease Information
| Disease | Pancreatic adenocarcinoma |
|---|---|
| Lineage | Pancreas |
| Subtype | Pancreatic Adenocarcinoma |
| OncoTree Code | PAAD |
DepMap Information
| Source Type | ATCC |
|---|---|
| Source ID | ACH-000114_source |
Known Sequence Variations
| Type | Gene/Protein | Description | Zygosity | Note | Source |
|---|---|---|---|---|---|
| MutationSimple | TP53 | p.Gly245Ser (c.733G>A) | Unspecified | Somatic mutation acquired during proliferation | PubMed=28445466 |
| MutationSimple | KRAS | p.Gly12Asp (c.35G>A) | Unspecified | - | PubMed=29786757 |
Haplotype Information (STR Profile)
Short Tandem Repeat (STR) profile for cell line authentication.
Loading gene expression data...
Publications
Pan-cancer proteomic map of 949 human cell lines.";
Robinson P.J., Zhong Q., Garnett M.J., Reddel R.R.
Cancer Cell 40:835-849.e8(2022).
Quantitative proteomics of the Cancer Cell Line Encyclopedia.";
Sellers W.R., Gygi S.P.
Cell 180:387-402.e16(2020).
Next-generation characterization of the Cancer Cell Line Encyclopedia.
Sellers W.R.
Nature 569:503-508(2019).
Prioritization of cancer therapeutic targets using CRISPR-Cas9 screens.
Stronach E.A., Saez-Rodriguez J., Yusa K., Garnett M.J.
Nature 568:511-516(2019).
An interactive resource to probe genetic diversity and estimated ancestry in cancer cell lines.
Dutil J., Chen Z.-H., Monteiro A.N.A., Teer J.K., Eschrich S.A.
Cancer Res. 79:1263-1273(2019).
Differential effector engagement by oncogenic KRAS.";
McCormick F.
Cell Rep. 22:1889-1902(2018).
A landscape of pharmacogenomic interactions in cancer.";
Wessels L.F.A., Saez-Rodriguez J., McDermott U., Garnett M.J.
Cell 166:740-754(2016).
Resolution of novel pancreatic ductal adenocarcinoma subtypes by global phosphotyrosine profiling.
Biankin A.V., Wu J.-M., Daly R.J.
Mol. Cell. Proteomics 15:2671-2685(2016).
TCLP: an online cancer cell line catalogue integrating HLA type, predicted neo-epitopes, virus and gene expression.
Loewer M., Sahin U., Castle J.C.
Genome Med. 7:118.1-118.7(2015).
Metabolite profiling stratifies pancreatic ductal adenocarcinomas into subtypes with distinct sensitivities to metabolic inhibitors.
Manning G., Settleman J., Hatzivassiliou G., Evangelista M.
Proc. Natl. Acad. Sci. U.S.A. 112:E4410-E4417(2015).
Parallel genome-scale loss of function screens in 216 cancer cell lines for the identification of context-specific genetic dependencies.
Golub T.R., Root D.E., Hahn W.C.
Sci. Data 1:140035-140035(2014).
A resource for cell line authentication, annotation and quality control.
Neve R.M.
Nature 520:307-311(2015).
A comprehensive transcriptional portrait of human cancer cell lines.
Settleman J., Seshagiri S., Zhang Z.-M.
Nat. Biotechnol. 33:306-312(2015).
KRAS mutational subtype and copy number predict in vitro response of human pancreatic cancer cell lines to MEK inhibition.
Linnartz R., Zubel A., Slamon D.J., Finn R.S.
Br. J. Cancer 111:1788-1801(2014).
Essential gene profiles in breast, pancreatic, and ovarian cancer cells.
Rottapel R., Neel B.G., Moffat J.
Cancer Discov. 2:172-189(2012).
The Cancer Cell Line Encyclopedia enables predictive modelling of anticancer drug sensitivity.
Morrissey M.P., Sellers W.R., Schlegel R., Garraway L.A.
Nature 483:603-607(2012).
Phenotype and genotype of pancreatic cancer cell lines.";
Scaife C.L., Firpo M.A., Mulvihill S.J.
Pancreas 39:425-435(2010).
A resource for analysis of microRNA expression and function in pancreatic ductal adenocarcinoma cells.
Mendell J.T.
Cancer Biol. Ther. 8:2013-2024(2009).
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.
Shiratori K., Hirohashi S., Inazawa J., Imoto I.
Cancer Sci. 99:986-994(2008).
Identifying allelic loss and homozygous deletions in pancreatic cancer without matched normals using high-density single-nucleotide polymorphism arrays.
Kern S.E.
Cancer Res. 66:7920-7928(2006).
Microarray analyses reveal strong influence of DNA copy number alterations on the transcriptional patterns in pancreatic cancer: implications for the interpretation of genomic amplifications.
Gorunova L., van Kessel A.G., Schoenmakers E.F.P.M., Hoglund M.
Oncogene 24:1794-1801(2005).
Genome-wide array-based comparative genomic hybridization reveals multiple amplification targets and novel homozygous deletions in pancreatic carcinoma cell lines.
Veltman J.A., van Kessel A.G., Hoglund M.
Cancer Res. 64:3052-3059(2004).
Characterization of the mutations of the K-ras, p53, p16, and SMAD4 genes in 15 human pancreatic cancer cell lines.
Sun C.-L., Yamato T., Furukawa T., Ohnishi Y., Kijima H., Horii A.
Oncol. Rep. 8:89-92(2001).
Specific chromosomal aberrations and amplification of the AIB1 nuclear receptor coactivator gene in pancreatic carcinomas.
Meltzer P.S., Ried T.
Am. J. Pathol. 154:525-536(1999).