ALL-SILHomo sapiens (Human)Cancer cell line

Also known as: Sil-ALL, SIL-ALL, ALLSIL, AL:L-SIL

🤖 AI SummaryBased on 10 publications

Quick Overview

T-cell acute lymphoblastic leukemia cell line with p16INK4A and p15INK4B deletions.

Detailed Summary

ALL-SIL is a T-cell acute lymphoblastic leukemia (T-ALL) cell line derived from a patient with relapsed disease. It is characterized by frequent deletions in the p16INK4A and p15INK4B genes, which are critical tumor suppressor genes involved in cell cycle regulation. These deletions are associated with the inactivation of the CDK4/6 pathway, contributing to uncontrolled cell proliferation. The cell line has been used in studies investigating the role of tyrosine kinase activation in leukemia, including the identification of NUP214-ABL1 fusion transcripts. Additionally, ALL-SIL has been utilized in drug resistance studies, showing sensitivity to imatinib, a tyrosine kinase inhibitor. The cell line is also part of panels used to study genetic diversity and ancestry in cancer research, highlighting its utility in understanding the molecular mechanisms of T-ALL and developing targeted therapies.

Research Applications

Genetic diversity and ancestry studiesDrug resistance profilingTyrosine kinase activation studiesTumor suppressor gene inactivation analysis

Key Characteristics

p16INK4A and p15INK4B deletionsSensitivity to imatinibNUP214-ABL1 fusion transcriptsRelapsed disease origin
Generated on 6/17/2025

Basic Information

Database IDCVCL_1805
SpeciesHomo sapiens (Human)
Tissue SourcePeripheral blood[UBERON:UBERON_0000178]

Donor Information

Age17
Age CategoryPediatric
SexMale
Subtype FeaturesTLX1

Disease Information

DiseasePrecursor T-cell acute lymphoblastic leukemia
LineageLymphoid
SubtypeAdult T-Cell Leukemia/Lymphoma
OncoTree CodeATLL

DepMap Information

Source TypeDSMZ
Source IDACH-000105_source

Known Sequence Variations

TypeGene/ProteinDescriptionZygosityNoteSource
MutationSimpleNOTCH1p.Pro2474fs*4 (c.7418_7419insGG)Heterozygous-PubMed=15472075
MutationSimpleNOTCH1p.Leu1574Pro (c.4721T>C)Heterozygous-from parent cell line PF-382
Gene fusionABL1NUP214-ABL1-NUP214 exon 32 fused to ABL1 exon 2PubMed=35354797, PubMed=15361874

Haplotype Information (STR Profile)

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

Amelogenin
X,Y
CSF1PO
10,12
D13S317
9,12
D16S539
10,12
D18S51
13,16
D19S433
12,17
D21S11
29,31
D2S1338
17,23
D3S1358
14,16
D5S818
11,13
D7S820
11,12
D8S1179
10
FGA
21
Penta D
10,15
Penta E
7,17
TH01
7,9.3
TPOX
10,11
vWA
17
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

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).

Integrative multi-omics and drug response profiling of childhood acute lymphoblastic leukemia cell lines.

Lehtio J., Vesterlund M., Jafari R.

Nat. Commun. 13:1691.1-1691.19(2022).

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).

Screening human cell lines for viral infections applying RNA-Seq data analysis.

Uphoff C.C., Pommerenke C., Denkmann S.A., Drexler H.G.

PLoS ONE 14:E0210404-E0210404(2019).

Profiling the B/T cell receptor repertoire of lymphocyte derived cell lines.

Yang H.H., Koeffler H.P.

BMC Cancer 18:940.1-940.13(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).

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).

High accuracy mutation detection in leukemia on a selected panel of cancer genes.

Cools J., Aerts S.

PLoS ONE 7:E38463-E38463(2012).

Authenticity and drug resistance in a panel of acute lymphoblastic leukaemia cell lines.

Freitas J.R., Firth M.J., Perera K.U., de Klerk N.H., Kees U.R.

Br. J. Cancer 95:1537-1544(2006).

Activating mutations of NOTCH1 in human T cell acute lymphoblastic leukemia.

Sanchez-Irizarry C., Blacklow S.C., Look A.T., Aster J.C.

Science 306:269-271(2004).

Fusion of NUP214 to ABL1 on amplified episomes in T-cell acute lymphoblastic leukemia.

Marynen P., Hagemeijer A.

Nat. Genet. 36:1084-1089(2004).

FLT3 mutations in the activation loop of tyrosine kinase domain are frequently found in infant ALL with MLL rearrangements and pediatric ALL with hyperdiploidy.

Tsuchida M., Sugita K., Ida K., Hayashi Y.

Blood 103:1085-1088(2004).

Corrigendum to: Frequent microsatellite instability and BAX mutations in T cell acute lymphoblastic leukemia cell lines Leukemia Research 24 (2000), 255-262.

Inoue K., Kohno T., Takakura S., Hayashi Y., Mizoguchi H., Yokota J.

Leuk. Res. 25:275-278(2001).

Frequent microsatellite instability and BAX mutations in T cell acute lymphoblastic leukemia cell lines.

Inoue K., Kohno T., Takakura S., Hayashi Y., Mizoguchi H., Yokota J.

Leuk. Res. 24:255-262(2000).

Alterations of the p53, p21, p16, p15 and RAS genes in childhood T-cell acute lymphoblastic leukemia.

Sekiya T., Hayashi Y.

Leuk. Res. 23:115-126(1999).

p16INK4/p15INK4B gene inactivation is a frequent event in malignant T-cell lines.

Einhorn S.

Eur. J. Haematol. 56:313-318(1996).

Interferon system defects in malignant T-cells.";

Xu B., Einhorn S.

Leukemia 8:425-434(1994).

The leukemia-lymphoma cell line factsbook.";

Drexler H.G.

(In book) ISBN 9780122219702; pp.1-733; Academic Press; London; United Kingdom (2001).