Inhibition of STAT3 signaling leads to apoptosis of leukemic large granular lymphocytes and decreased Mcl-1 expression.

By P. Epling-Burnette, Jin Hong Liu, Robyn Catlett-Falcone, J. Turkson, M. Oshiro, R. Kothapalli, Yongxiang Li, Ju-Ming Wang, H. Yang-Yen, J. Karras and 2 more. Journal of Clinical Investigation, 2001

661 citations recorded by the source corpus.

Subfields: Genetics, Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/1a36b33142a23ecde19fc1e73d3cd2ef7849acdc

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In Immunology

1. R. Jove
2. Hua Yu

In Oncology

1. R. Jove
2. Hua Yu
3. Jacqueline F. Bromberg
4. R. Buettner
5. T. Hirano
6. D. Gabrilovich
7. M. Karin
8. S. Grivennikov

Citations in the corpus

• Activated STAT signaling in human tumors provides novel molecular targets for therapeutic intervention. (2002, background): “Mcl-1, another antiapoptotic protein, was shown to be regulated by Stat3 in leukemic large granular lymphocytes (41) and by Stat5 in CML cells.”
• The STATs of cancer — new molecular targets come of age (2004, background): “Blocking either of these STAT proteins in human tumour cells has been shown to downregulate MCL1 expression and induce tumour-cell apoptosi”
• Stat proteins and oncogenesis. (2002, background): “Cooperative regulation of Mcl-1 by Janus kinase/stat and phosphatidylinositol 3-kinase contribute to granulocytemacrophage colony-stimulating factor-delayed apoptosis in human neutrophils.”
• STAT proteins: From normal control of cellular events to tumorigenesis (2003, background): “One of these is the use of antisense oligomers against STAT3 in order to inhibit cell growth in head and neck squamous carcinoma cell lines and in prostate cancer cells (Grandis et al., 1998; Epling-Burnette et al., 2001).”