Constitutive activation of Stat3 signaling abrogates apoptosis in squamous cell carcinogenesis in vivo.

By J. Grandis, S. D. Drenning, Q. Zeng, Simon C Watkins, M. Melhem, S. Endo, D. Johnson, L. Huang, Y. He, J. D. Kim. Proceedings of the National Academy of Sciences of the United States of America, 2000

649 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/47f88f45268db71a6836e43856166b299bb9053f

How researchers see this paper

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In Cancer Research

1. P. Johnston
2. R. Jove
3. Hua Yu
4. L. Ellis
5. D. Longley
6. D. Pardoll

In Molecular Biology

1. N. Hynes
2. R. Jove
3. P. Johnston
4. D. Longley
5. Hua Yu
6. L. Ellis
7. Eric B. Haura
8. C. Heinlein

In Oncology

1. R. Jove
2. Hua Yu
3. D. Pardoll
4. N. Hynes
5. P. Johnston
6. D. Longley
7. R. Buettner
8. L. Ellis

Citations in the corpus

• Molecular mechanisms of drug resistance (2005, background): “STAT3 and STAT5 have been shown to regulate Bcl-XL expression and apoptosis in wide range of tumour cells [231–236].”
• ERBB receptors and cancer: the complexity of targeted inhibitors (2005, background): “8 ), which, in cancer, have often been associated with EGFR activatio”
• Constitutive Stat3 activity up-regulates VEGF expression and tumor angiogenesis (2002, background): “Previous studies have demonstrated that activation of Stat3 by oncogenic tyrosine kinases regulates the expression of genes that are essential for cell growth and survival (Bowman et al., 2001; Bromberg et al., 1999; Catlett-Falcone et al., 1999b; Grandis et al., 2000; Sinibaldi et al., 2000).”
• Activated STAT signaling in human tumors provides novel molecular targets for therapeutic intervention. (2002, background): “Many studies have shown that the antiapoptotic gene encoding Bcl-xL protein is a downstream target of Stat3 and Stat5 (31, 53, 68, 84, 85).”
• STAT proteins: novel molecular targets for cancer drug discovery (2000, background): “Given that EGF-R mediates Stat3 activation in HNSCC (Grandis et al., 1998, 2000a; Song and Grandis, 2000), it would be presumed that clinical responses in HNSCC to therapeutic C225 is a function of inhibition of EGF-R-mediated constitutive activation of downstream signaling components, including Sta”
• Androgen receptor in prostate cancer. (2004, background): “Inhibition of STAT3 in multiple myeloma-derived cells and in a head and neck squamous cell carcinoma xenograft enhanced apoptosis, suggesting that STAT3 may be an important mediator of cell survival in some cancer types (314, 315) and raising the possibility that the AR-STAT3 interaction could promo”