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Contributor Information

  • Name Dimitar Efremov
  • Institute International Centre For Genetic Engineering And Biotechnology (ICGEB)

Tool Details

  • Tool name: TCL1-002 cell line
  • Tool type: Cell Lines
  • Tool sub-type: Continuous
  • Parental cell line: E-TCL1
  • Organism: Mouse
  • Tissue: Lymphatic Tissue
  • Cancer type: Chronic lymphocytic leukemia, CLL
  • Disease: Cancer
  • Description: The proliferation and survival of chronic lymphocytic leukemia (CLL) B-cells is regulated by intracellular signaling pathways which are activated by various stimuli such as antigenic stimuli propagaged through the B-cell receptor (BCR). For this reason inhibition of antigen-dependent BCR signalling can be considered a promising therapeutic approach in CLL. Some studies have shown that sustained engagement of the BCR induces a powerful antiapoptotic program in CLL cells. Transduction of the prosurvival BCR signal was shown to involve the recruitment and activation of several kinases, including Syk. Increased basal activity of Syk kinase has been described in CLL and several other B-cell malignancies and shown to contribute to the increased apoptosis resistance of the malignant lymphocytes. Interestingly, the antiapoptotic program in CLL cells caused by sustained BCR engagement can be completely abrogated with selective inhibition of Syk kinase, suggesting that the Syk kinase could be a potential target for therapeutic intervention. This E-TCL1-002 cell line (a transgenic mouse model of chronic lymphocytic leukemia) strongly expresses Syk kinase.
  • Research area: Cancer ; Apoptosis and Programmed Cell Death ; Cell Signaling & Signal Transduction

  • For Research Use Only

Target Details

Application Details

Handling

  • Format: Frozen
  • Growth medium: Must be propagated in vivo.
  • Shipping conditions: Dry ice

Documentation

  • Available on request

References

  •   The Syk inhibitor fostamatinib disodium (R788) inhibits tumor growth in the E-TCL1 transgenic mouse model of CLL by blocking antigen-dependent B-cell receptor signalling.