Hs 766THomo sapiens (Human)Cancer cell line

Also known as: Hs 766.T, HS-766T, Hs-766T, HS 766T, HS-766-T, Hs-766-T, HS766T, Hs766T, H766T, 766T, Hs 766, Hs-776-T

🤖 AI SummaryBased on 13 publications

Hs766T

Quick Overview

Pancreatic cancer cell line with known genetic alterations and metastatic potential.

Detailed Summary

Hs766T is a pancreatic cancer cell line derived from a primary tumor with metastatic potential. It exhibits significant genomic instability, including multiple copy number variations and mutations in key oncogenes and tumor suppressor genes. This cell line has been extensively used in studies to investigate the molecular mechanisms of pancreatic cancer progression, including the identification of amplification targets and chromosomal abnormalities. Research on Hs766T has contributed to understanding the role of genetic alterations in tumor development and metastasis, making it a valuable tool for preclinical studies and drug development.

Research Applications

Genomic instability analysisGene amplification studiesMetastasis researchDrug sensitivity profiling

Key Characteristics

High genomic complexityMutations in K-ras and p53Amplification of oncogenesMetastatic potential
Generated on 6/15/2025

Basic Information

Database IDCVCL_0334
SpeciesHomo sapiens (Human)
Tissue SourceLymph node[UBERON:UBERON_0000029]

Donor Information

Age64
Age CategoryAdult
SexMale
Racecaucasian

Disease Information

DiseasePancreatic adenocarcinoma
LineagePancreas
SubtypePancreatic Adenocarcinoma
OncoTree CodePAAD

DepMap Information

Source TypeATCC
Source IDACH-000178_source

Known Sequence Variations

TypeGene/ProteinDescriptionZygosityNoteSource
Gene deletionSMAD4-Homozygous-from parent cell line BxPC-3
MutationSimpleKRASp.Gln61His (c.183A>C)Heterozygous1 of 3 allelesUnknown, PubMed=8426738
MutationNone reportedTP53---PubMed=19787792

Haplotype Information (STR Profile)

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

Amelogenin
X
CSF1PO
12
D13S317
8,11
D16S539
9,11,12
D18S51
13
D19S433
15
D21S11
28
D2S1338
18,26
D3S1358
16
D5S818
11
D7S820
10
D8S1179
12,14
FGA
19,20
Penta D
9
Penta E
7,12
TH01
6,9.3
TPOX
8
vWA
18
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

The proteomic profile of pancreatic cancer cell lines corresponding to carcinogenesis and metastasis.

Yamada M., Fujii K., Koyama K., Hirohashi S., Kondo T.

J. Proteomics Bioinformatics 2:1-18(2009).

Epithelial cell cultures from normal and cancerous human tissues.";

Owens R.B., Smith H.S., Nelson-Rees W.A., Springer E.L.

J. Natl. Cancer Inst. 56:843-849(1976).

In vitro properties of epithelial cell lines established from human carcinomas and nonmalignant tissue.

Smith H.S.

J. Natl. Cancer Inst. 62:225-230(1979).

Nuclear ultrastructure of epithelial cell lines derived from human carcinomas and nonmalignant tissues.

Smith H.S., Springer E.L., Hackett A.J.

Cancer Res. 39:332-344(1979).

Human pancreatic carcinomas and cell lines reveal frequent and multiple alterations in the p53 and Rb-1 tumor-suppressor genes.

Klein-Szanto A.J.P.

Oncogene 7:1503-1511(1992).

Relationship between karyotype of tissue culture lines and tumorigenicity in nude mice.

Gershwin M.E., Lentz D., Owens R.B.

Exp. Cell Biol. 52:361-370(1984).

Comparative analysis of mutations in the p53 and K-ras genes in pancreatic cancer.

Berrozpe G., Schaeffer J., Peinado M.A., Real F.X., Perucho M.

Int. J. Cancer 58:185-191(1994).

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).

Higher frequency of DPC4/Smad4 alterations in pancreatic cancer cell lines than in primary pancreatic adenocarcinomas.

Chaloupka B., Deiss Y., Simon B., Schudy A.

Cancer Lett. 139:43-49(1999).

Non-random chromosomal rearrangements in pancreatic cancer cell lines identified by spectral karyotyping.

Sheer D., Moore P.S., Scarpa A., Edwards P.A.W., Lemoine N.R.

Int. J. Cancer 91:350-358(2001).

Highly expressed genes in pancreatic ductal adenocarcinomas: a comprehensive characterization and comparison of the transcription profiles obtained from three major technologies.

Kern S.E., Goggins M.G., Hruban R.H.

Cancer Res. 63:8614-8622(2003).

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).

Orthotopic transplantation models of pancreatic adenocarcinoma derived from cell lines and primary tumors and displaying varying metastatic activity.

Hirohashi S.

Pancreas 29:193-203(2004).

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).

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).

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).

Hybrids of aneuploid human cancer cells permit complementation of simple and complex cancer defects.

Chakravarti A., Kern S.E.

Cancer Biol. Ther. 8:347-355(2009).

Phenotype and genotype of pancreatic cancer cell lines.";

Scaife C.L., Firpo M.A., Mulvihill S.J.

Pancreas 39:425-435(2010).

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).

Essential gene profiles in breast, pancreatic, and ovarian cancer cells.

Rottapel R., Neel B.G., Moffat J.

Cancer Discov. 2:172-189(2012).

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).

A comprehensive transcriptional portrait of human cancer cell lines.

Settleman J., Seshagiri S., Zhang Z.-M.

Nat. Biotechnol. 33:306-312(2015).

A resource for cell line authentication, annotation and quality control.

Neve R.M.

Nature 520:307-311(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).

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).

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).

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).

A landscape of pharmacogenomic interactions in cancer.";

Wessels L.F.A., Saez-Rodriguez J., McDermott U., Garnett M.J.

Cell 166:740-754(2016).

Differential effector engagement by oncogenic KRAS.";

McCormick F.

Cell Rep. 22:1889-1902(2018).

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).

Next-generation characterization of the Cancer Cell Line Encyclopedia.

Sellers W.R.

Nature 569:503-508(2019).

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).