PaTu 8988sHomo sapiens (Human)Cancer cell line

Also known as: PA-TU S, PATU-S, PATU-8988S, PaTu-8988s, PaTu 8988 S, PATU8988S, PaTu8988S, PaTu8988s, PA-TU-8988S

🤖 AI SummaryBased on 12 publications

Quick Overview

Human pancreatic cancer cell line with known genetic alterations and metastatic potential.

Detailed Summary

PaTu 8988s is a human pancreatic cancer cell line derived from a primary tumor. It exhibits distinct genetic alterations, including amplifications and deletions, which are characteristic of pancreatic carcinomas. This cell line is used in research to study the molecular mechanisms of pancreatic cancer, including the role of specific genes in tumor progression and metastasis. The cell line has been characterized for its ability to form tumors in nude mice, showing a solid growth pattern with limited polar organization of the cytoplasm. It is also noted for its potential in studying the effects of genetic mutations on protein expression and drug sensitivity.

Research Applications

Genomic profiling of pancreatic cancerStudy of gene copy number alterationsInvestigation of metabolic subtypes in pancreatic cancerAnalysis of drug sensitivity and resistanceCharacterization of tumor metastasis potential

Key Characteristics

Amplifications and deletions in genomic regionsExpression of specific oncogenes and tumor suppressorsMetastatic potential in nude miceUse in studying pancreatic cancer biology
Generated on 6/17/2025

Basic Information

Database IDCVCL_1846
SpeciesHomo sapiens (Human)
Tissue SourceLiver[UBERON:UBERON_0002107]

Donor Information

Age64
Age CategoryAdult
SexFemale

Disease Information

DiseasePancreatic adenocarcinoma
LineagePancreas
SubtypePancreatic Adenocarcinoma
OncoTree CodePAAD

DepMap Information

Source TypeDSMZ
Source IDACH-000022_source

Known Sequence Variations

TypeGene/ProteinDescriptionZygosityNoteSource
MutationSimpleTP53p.Arg282Trp (c.844C>T)Unspecified-PubMed=21173094, PubMed=1373872
MutationSimpleKRASp.Gly12Val (c.35G>T)HeterozygousAcquiredUnknown, Unknown

Haplotype Information (STR Profile)

Short Tandem Repeat (STR) profile for cell line authentication.

Amelogenin
X
CSF1PO
11,13
D13S317
12,13
D16S539
11,12
D18S51
12
D19S433
14,15
D21S11
26
D2S1338
23
D3S1358
15,17
D5S818
11,13
D7S820
7,8
D8S1179
13,16
FGA
23
Penta D
8
Penta E
13
TH01
6
TPOX
8,11
vWA
16
Gene Expression Profile
Gene expression levels and statistical distribution
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Full DepMap dataset with combined data across cell lines

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Publications

Comprehensive transcriptomic analysis of cell lines as models of primary tumors across 22 tumor types.

van 't Veer L.J., Butte A.J., Goldstein T., Sirota M.

Nat. Commun. 10:3574.1-3574.11(2019).

Next-generation characterization of the Cancer Cell Line Encyclopedia.

Sellers W.R.

Nature 569:503-508(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).

Characterization of human cancer cell lines by reverse-phase protein arrays.

Liang H.

Cancer Cell 31:225-239(2017).

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).

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).

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).

Immunocytochemical analysis of cell lines derived from solid tumors.

Quentmeier H., Osborn M., Reinhardt J., Zaborski M., Drexler H.G.

J. Histochem. Cytochem. 49:1369-1378(2001).

Short tandem repeat profiling provides an international reference standard for human cell lines.

Harrison M., Virmani A.K., Ward T.H., Ayres K.L., Debenham P.G.

Proc. Natl. Acad. Sci. U.S.A. 98:8012-8017(2001).

Frequent alterations of the tumor suppressor genes p53 and DCC in human pancreatic carcinoma.

Arnold R.

Gastroenterology 106:1645-1651(1994).

Establishment and characterisation of two cell lines with different grade of differentiation derived from one primary human pancreatic adenocarcinoma.

Elsasser H.-P., Lehr U., Agricola B., Kern H.F.

Virchows Arch. B. Cell. Pathol. Incl. Mol. Pathol. 61:295-306(1992).

Distribution of characteristic mutations in native ductal adenocarcinoma of the pancreas and pancreatic cancer cell lines.

Saeger H.-D.

Cell Biol. Res. Ther. 2:1000104.1-1000104.5(2013).