SUM149PTHomo sapiens (Human)Cancer cell line

Also known as: BrCL12, 149PT, 149 PT, SUM 149, SUM-149, SUM149, SUM149-PT, SUM 149PT, SUM-149PT

🤖 AI SummaryBased on 15 publications

Quick Overview

Breast cancer cell line with triple-negative characteristics, used in cancer research.

Detailed Summary

SUM149PT is a breast cancer cell line derived from a human tumor, characterized by its triple-negative phenotype, which means it lacks expression of estrogen receptor (ER), progesterone receptor (PR), and HER2. This cell line is widely used in research to study the molecular mechanisms of breast cancer, particularly in the context of triple-negative breast cancer (TNBC), which is known for its aggressive behavior and limited therapeutic options. SUM149PT has been utilized in studies involving gene expression profiling, genomic alterations, and drug sensitivity assays. It is part of a panel of cell lines that have been extensively characterized for their molecular features, making them valuable tools for understanding the heterogeneity of breast cancer and developing targeted therapies. The cell line is also noted for its ability to form mammospheres, indicating the presence of cancer stem cell-like properties, which are important in tumor initiation and progression.

Research Applications

Gene expression profilingGenomic alterations analysisDrug sensitivity assaysCancer stem cell research

Key Characteristics

Triple-negative phenotype (ER-, PR-, HER2-)Mammosphere formationHigh genomic heterogeneityRelevance to triple-negative breast cancer research
Generated on 6/20/2025

Basic Information

Database IDCVCL_3422
SpeciesHomo sapiens (Human)
Tissue SourceBreast[UBERON:UBERON_0000310]

Donor Information

Age40
Age CategoryAdult
SexFemale
Subtype Featuresbasal_B TNBC

Disease Information

DiseaseBreast inflammatory carcinoma
LineageBreast
SubtypeBreast Invasive Ductal Carcinoma
OncoTree CodeIDC

DepMap Information

Source TypeAsterand
Source IDACH-001390_source

Known Sequence Variations

TypeGene/ProteinDescriptionZygosityNoteSource
MutationSimpleTP53p.Met237Ile (c.711G>A)Homozygous-PubMed=22525470, PubMed=11221843, PubMed=7744731
MutationSimpleEP300c.4025+26_4025+30 (c.5224+28del3)Heterozygous-from parent cell line SUM149PT
MutationSimpleBRCA1p.Pro724Leufs*12 (c.2169delT) (p.Asn723fs*13) (2288delT)Hemizygous-from parent cell line SUM149PT
Gene deletionCDKN2A-HomozygousPossiblePubMed=26870271

Haplotype Information (STR Profile)

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

Amelogenin
X
CSF1PO
12
D12S391
15,18
D13S317
12
D16S539
11
D18S51
14,15
D19S433
12,14
D21S11
28,31.2
D2S1338
20
D3S1358
17
D5S818
11
D6S1043
18
D7S820
11
D8S1179
14,16
FGA
29
Penta D
8,9
Penta E
11
TH01
9.3
TPOX
9
vWA
16,18
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

Comparative transcriptional analyses of preclinical models and patient samples reveal MYC and RELA driven expression patterns that define the molecular landscape of IBC.

Viens P., Birnbaum D., Devi G.R., Cristofanilli M., Van Laere S.

NPJ Breast Cancer 8:12.1-12.12(2022).

Development and implementation of the SUM breast cancer cell line functional genomics knowledge base.

Duchinski K., Couch D., Gray J.W., Kappler C.S.

NPJ Breast Cancer 6:30.1-30.14(2020).

Synthetic lethal and resistance interactions with BET bromodomain inhibitors in triple-negative breast cancer.

Polyak K.

Mol. Cell 78:1096-1113.e8(2020).

Glycoproteins in claudin-low breast cancer cell lines have a unique expression profile.

Yen T.-Y., Bowen S., Yen R., Piryatinska A., Macher B.A., Timpe L.C.

J. Proteome Res. 16:1391-1400(2017).

Response and resistance to BET bromodomain inhibitors in triple-negative breast cancer.

Meyer C.A., Bradner J.E., Polyak K.

Nature 529:413-417(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).

Steroid hormone secretion in inflammatory breast cancer cell lines.";

Illera M.J., Woodward W.A., Reuben J.M., Silvan G.

Horm. Mol. Biol. Clin. Investig. 24:137-145(2015).

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).

Modeling precision treatment of breast cancer.";

Collisson E.A., van 't Veer L.J., Spellman P.T., Gray J.W.

Genome Biol. 14:R110.1-R110.14(2013).

Characterization of cell lines derived from breast cancers and normal mammary tissues for the study of the intrinsic molecular subtypes.

Harrell J.C., Roman E., Adamo B., Troester M.A., Perou C.M.

Breast Cancer Res. Treat. 142:237-255(2013).

Inflammatory breast cancer (IBC): clues for targeted therapies.";

Cristofanilli M.

Breast Cancer Res. Treat. 140:23-33(2013).

miRNA expression profiling of 51 human breast cancer cell lines reveals subtype and driver mutation-specific miRNAs.

Martens J.W.M.

Breast Cancer Res. 15:R33.1-R33.17(2013).

Phenotypic and molecular characterization of MCF10DCIS and SUM breast cancer cell lines.

Barnabas N., Cohen D.

Int. J. Breast Cancer 2013:872743.1-872743.16(2013).

Molecular characterisation of cell line models for triple-negative breast cancers.

Reis-Filho J.S., Tutt A.

BMC Genomics 13:619.1-619.14(2012).

Identification of gene fusion transcripts by transcriptome sequencing in BRCA1-mutated breast cancers and cell lines.

Majewski J., Foulkes W.D.

BMC Med. Genomics 4:75.1-75.13(2011).

Distinct gene mutation profiles among luminal-type and basal-type breast cancer cell lines.

den Bakker M.A., Foekens J.A., Martens J.W.M., Schutte M.

Breast Cancer Res. Treat. 121:53-64(2010).

Molecular profiling of breast cancer cell lines defines relevant tumor models and provides a resource for cancer gene discovery.

Pollack J.R.

PLoS ONE 4:E6146-E6146(2009).

A collection of breast cancer cell lines for the study of functionally distinct cancer subtypes.

Johnson M.D., Lippman M.E., Ethier S.P., Gazdar A.F., Gray J.W.

Cancer Cell 10:515-527(2006).

Thirteen new p53 gene mutants identified among 41 human breast cancer cell lines.

Wasielewski M., Elstrodt F., Klijn J.G.M., Berns E.M.J.J., Schutte M.

Breast Cancer Res. Treat. 99:97-101(2006).

BRCA1 mutation analysis of 41 human breast cancer cell lines reveals three new deleterious mutants.

van den Ouweland A.M.W., Merajver S.D., Ethier S.P., Schutte M.

Cancer Res. 66:41-45(2006).

In vitro analysis of the invasive phenotype of SUM 149, an inflammatory breast cancer cell line.

Hoffmeyer M.R., Wall K.M., Dharmawardhane S.F.

Cancer Cell Int. 5:11.1-11.10(2005).

Evidence that both genetic instability and selection contribute to the accumulation of chromosome alterations in cancer.

Edwards P.A.W., Caldas C.

Carcinogenesis 26:923-930(2005).

A recurrent chromosome translocation breakpoint in breast and pancreatic cancer cell lines targets the neuregulin/NRG1 gene.

Edwards P.A.W., Chaffanet M.

Genes Chromosomes Cancer 37:333-345(2003).

Reciprocal translocations in breast tumor cell lines: cloning of a t(3;20) that targets the FHIT gene.

Birnbaum D., Chaffanet M.

Genes Chromosomes Cancer 35:204-218(2002).

Comparative genomic hybridization analysis of 38 breast cancer cell lines: a basis for interpreting complementary DNA microarray data.

Gooden G.C., Ethier S.P., Kallioniemi A.H., Kallioniemi O.-P.

Cancer Res. 60:4519-4525(2000).

Mutations truncating the EP300 acetylase in human cancers.";

Delhanty J.D.A., Ponder B.A.J., Kouzarides T., Caldas C.

Nat. Genet. 24:300-303(2000).

Molecular cytogenetic analysis of 11 new breast cancer cell lines.";

Kallioniemi O.-P., Ethier S.P.

Br. J. Cancer 81:1328-1334(1999).

Constitutive activation of pp125fak in newly isolated human breast cancer cell lines.

Ignatoski K.M.W., Ethier S.P.

Breast Cancer Res. Treat. 54:173-182(1999).

Genomic profiling of pre-clinical models of inflammatory breast cancer identifies a signature of epithelial plasticity and suppression of TGFbeta signaling.

Wu H., Zook M.B., Barsky S.H., Krishnamurthy S., Cristofanilli M.

J. Clin. Exp. Pathol. 2:119.1-119.11(2012).