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The Leukemia Cell Line: 697 Pre-B Cell Line

There are two new acute lymphoblastic leukemia cell lines with early B-cell phenotypes: leukemic cell lines 697 and 207. These cell lines are established from bone marrow cells obtained from human with ALL in relapse.

These cell lines are positive for the common-ALL antigen , the HLA-DR antigen, and for cytoplasmic and surface IgM heavy chains,while negative for other immunoglobulin heavy chains and light chains. The lines have elevated levels of terminal deoxynucleotidyl transferase enzyme and can express surface antigens on normal myeloid- macrophage cells (MMA) and natural killer cells (HNK-1). Line 697 is positive for Epstein- Barr virus (EBV) and will carry a marker chromosome, patient's fresh leukemic cells. The leukemic origin of the cell lines is indicated by their morphological, cytochemical, and immunologic similarity to the patients' leukemic cells. Phenotypically, the cell lines appear to be arrested in a transitional stage of development between pre-B and B cells and express surface antigens usually found on normal and fresh leukemic cells of non-B-cell lineages.

Applications of 697 pre-B cell line in Researches

  • lInhibition of Glucocorticoid-induced Apoptosis in 697 Pre-B Lymphocytes by the Mineralocorticoid Receptor N-terminal Domain

The scientists examined the effect of NTD-MR on GC-induced apoptosis in the GC-sensitive pre-B lymphoma cell line, 697. In GC-treated 697 cells, they demonstrated that stable expression of NTD-MR blocked apoptosis and inhibited proteolytic processing of pro-caspases-3, -8, and -9 and poly(ADP-ribose) polymerase. The results demonstrated that in GC-induced apoptosis of 697 cells, the NTD of MR inhibited apoptosis prior to commitment to cell death. This research concluded that in normal physiology, in cells where MR and GR are coexpressed, the MR may function to counteract the role of activated GR by increasing the ratio of anti-apoptotic molecules relative to pro-apoptotic molecules.

  • lDexamethasone-resistant human Pre-B leukemia 697 cell line evolving elevation of intracellular glutathione level: an additional resistance mechanism.

The mechanisms of glucocorticoid resistance have been studied in some T-cell leukemic cell lines, but less work has been done with B-cell lines. And so, a group of scientists has initiated in establishing a dexamethasone (DEX)-resistant human pre-B lineage leukemia cell line (697/DEX) to investigate the mechanism of the resistance of the disease. In this research, the scientists concluded that, DEX-resistance in 697/DEX was related not only to a GR decrease, but also to an increase in intracellular GSH level in the DEX-resistant B-cell leukemia cell line. And circumvention of DEX-resistance with BSO might offer an approach to overcoming resistance to chemotherapy in B-cell lineage ALL.

  • lInterleukin-7 induces apoptosis of 697 pre-B cells expressing dominant-negative forms of STAT5: evidence for caspase-dependent and -independent mechanisms

The transcription factors STAT5 A and STAT5 B play a major role in the signaling events. And this study was aimed to investigate the role of STAT5 in human precursor B cell survival by introducing dominant-negative (DN) forms of STAT5A or STAT5B in the 697 pre-B cell line. The study found out that all clones expressing DN forms of either transcription factor exhibited a higher spontaneous apoptotic rate that was massively enhanced upon interleukin-7 (IL-7) stimulation and the DN forms of STAT5 did not alter the expression of Bcl-2, Bax, Bcl-x, Bim, A1 and Mcl1 proteins in IL-7-stimulated cells. And other results altogether suggested that IL-7 induced the death of DN STAT5 expressing 697 cells through caspase-dependent and -independent mechanisms that both require mitochondrial activation.

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