PSN1Homo sapiens (Human)Cancer cell line
Also known as: PSN-1
Quick Overview
Human pancreatic adenocarcinoma cell line with c-Ki-ras and c-myc amplifications.
Detailed Summary
Research Applications
Key Characteristics
Basic Information
Database ID | CVCL_1644 |
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Species | Homo sapiens (Human) |
Tissue Source | Pancreas[UBERON:UBERON_0001264] |
Donor Information
Age | 36 |
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Age Category | Adult |
Sex | Male |
Race | caucasian |
Disease Information
Disease | Pancreatic adenocarcinoma |
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Lineage | Pancreas |
Subtype | Pancreatic Adenocarcinoma |
OncoTree Code | PAAD |
DepMap Information
Source Type | ECACC |
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Source ID | ACH-000320_source |
Known Sequence Variations
Type | Gene/Protein | Description | Zygosity | Note | Source |
---|---|---|---|---|---|
MutationSimple | TP53 | p.Lys132Gln (c.394A>C) | Unspecified | - | from parent cell line Jiyoye |
MutationSimple | KRAS | p.Gly12Arg (c.34G>C) | Unspecified | - | PubMed=26124327 |
Gene deletion | SMAD4 | - | Homozygous | - | from parent cell line BxPC-3 |
Gene deletion | CDKN2A | - | Homozygous | Possible | PubMed=26870271 |
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).
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).
Characterization of human cancer cell lines by reverse-phase protein arrays.
Liang H.
Cancer Cell 31:225-239(2017).
A landscape of pharmacogenomic interactions in cancer.";
Wessels L.F.A., Saez-Rodriguez J., McDermott U., Garnett M.J.
Cell 166:740-754(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).
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).
Signatures of mutation and selection in the cancer genome.";
Deloukas P., Yang F.-T., Campbell P.J., Futreal P.A., Stratton M.R.
Nature 463:893-898(2010).
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).
Genetic profile of 22 pancreatic carcinoma cell lines. Analysis of K-ras, p53, p16 and DPC4/Smad4.
Lohr J.-M., Scarpa A.
Virchows Arch. 439:798-802(2001).
Establishment of a human pancreatic adenocarcinoma cell line (PSN-1) with amplifications of both c-myc and activated c-Ki-ras by a point mutation.
Yamada H., Yoshida T., Sakamoto H., Terada M., Sugimura T.
Biochem. Biophys. Res. Commun. 140:167-173(1986).
Amplifications of both c-Ki-ras with a point mutation and c-myc in a primary pancreatic cancer and its metastatic tumors in lymph nodes.
Terada M., Sugimura T.
Jpn. J. Cancer Res. 77:370-375(1986).