SEM

Cat.No.: CSC-C0554

Species: Homo sapiens (Human)

Source: Blood; Peripheral Blood

Morphology: round to polygonal single rather small cells in suspension

Culture Properties: suspension

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Cat.No.
CSC-C0554
Description
Established from the peripheral blood of a 5-year-old girl at relapse of acute lymphoblastic leukemia (ALL) in 1990; reported to carry the t(4;11) MLL-AFF1 (MLL-AF4)
Species
Homo sapiens (Human)
Source
Blood; Peripheral Blood
Recommended Medium
Culture Properties
suspension
Morphology
round to polygonal single rather small cells in suspension
Karyotype
Human hypodiploid karyotype with 1.5% polyploidy - 45(40-46)<2n>XX, -13, t(4;11)(q21;q23), del(7)(p14) - carries t(4;11) with breakpoints at AFF1 (AF4) and MLL - matches published karyotype
Disease
Childhood B Acute Lymphoblastic Leukemia
Quality Control
Mycoplasma: negative in microbiological culture, PCR assays
Immunology: CD3-, CD4-, CD11b-, CD13+, CD14-, CD15+, CD19+, CD33+, CD34-, cyCD68-, HLA-DR+, sm/cyIgG-, sm/cyIgM-, sm/cykappa-, sm/cylamda-
Viruses: PCR: EBV -, HBV -, HCV -, HIV -, HTLV-I/II -, S
Storage and Shipping
Frozen with 70% medium, 20% FBS, 10% DMSO at about 5 x 10^6 cells/ampoule; ship in dry ice; store in liquid nitrogen
Citation Guidance
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The establishment of the SEM cell line in 1990 provided researchers with a valuable in vitro model system to investigate the unique biology and molecular pathogenesis of this specific subtype of acute lymphoblastic leukemia (ALL). Before the availability of the SEM cell line, researchers had limited access to primary samples from patients with the t(4;11) translocation, which hindered the progress of research in this area.

By utilizing the SEM cell line, researchers have been able to elucidate the underlying mechanisms by which the MLL-AFF1 fusion protein drives leukemogenesis, including its effects on gene expression, epigenetic regulation, and cellular signaling pathways. This knowledge has been crucial for the development of targeted therapies and personalized treatment approaches for patients with MLL-rearranged ALL.

Furthermore, the SEM cell line has been extensively characterized, with its genomic, transcriptomic, and proteomic profiles being well-documented. This comprehensive characterization has allowed researchers to identify potential therapeutic targets and test the efficacy of various drug candidates in a clinically relevant in vitro model system.

The ALL Cell Line SEM With t(4;11) Chromosomal Rearrangement

A cell line, designated SEM, was established from the peripheral blood of a 5-year-old girl in relapse with t(4;11) ALL. During the first 8 months of culture, SK-HEP-1 hepatoma culture supernatant appeared necessary for the growth of SEM cells. During the first 8 months of culture, the doubling time of SEM cells was 7-10 d. After this period, the growth of SEM cells increased and the cell doubling time was approximately 48 h. Then SK-HEP-1 culture supernatant was omitted from the culture medium. The cell line has been propagated for more than 2 years in IMDM containing 10% FCS. SEM cell line was growing as single cell suspension and was found to be free of mycoplasma contamination and Epstein-Barr virus nuclear antigen.

SEM cells showed a lymphoblastic morphology with cell nuclei exhibiting one or more prominent nucleoli. Cells were pleomorphic in size and had cytoplasmic vacuolations (Fig. 1). Cytochemical staining of SEM cells revealed negativity for peroxidase. Sudan black, non-specific esterase activity and PAS reaction following staining results of the lymphoblasts of the patient. SEM cells were positive for TdT activity. Cytogenetic analysis of the SEM cell line was performed 5 and 10 months after the beginning of the culture. A t(4;11)(q21;q23), deletion of the short arm of chromosome 7 del(7)(p15), and deletion of the long arm of chromosome 13 del(13)(q12) were found as clonal karyotypic abnormalities (Fig. 2). Cytogenetic analysis of the leukemic cells from the patient's peripheral blood revealed identical cytogenetic abnormalities.

Morphology of SEM cells with Pappenheim's staining.Fig. 1 Photomicrograph of SEM cells stained with Pappenheim's stain. (Greil J, et al., 1994)

A representative karyotype of SEM cell line after GTG banding showing t (4;11) in combination with a deletion of the short arm of chromosome 7 del(7)(p15) and a deletion of the long arm of chromosome 13 del(13)(q12).Fig. 2 A representative karyotype of SEM cell line after GTG banding. (Greil J, et al., 1994)

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