Inhibition and stimulation of the proliferative activity of tumor cells with different degrees of malignancy in close contact with normal embryonal fibroblasts of Syrian hamster

1993 ◽  
Vol 115 (4) ◽  
pp. 442-445
Author(s):  
E. V. Gurova
Keyword(s):  
Tumor Cells ◽  
Syrian Hamster ◽  
Proliferative Activity ◽  
Close Contact ◽  
Stimulation Of

Antibody Stimulation of Tumor Cells

1977 ◽  
Vol 155 (3) ◽  
pp. 420-423 ◽  
Author(s):  
W. L. Ryan ◽  
M. A. Durick
Keyword(s):  
Tumor Cells ◽  
Stimulation Of

scholarly journals Examination of the proliferative activity of tumor cells in human lymphoid neoplasms using a morphometric approach

Cancer ◽  
2004 ◽  
Vol 102 (3) ◽  
pp. 174-185 ◽  
Author(s):  
Eugene V. Sheval ◽  
Janna V. Churakova ◽  
Oksana A. Dudnik ◽  
Ivan A. Vorobjev
Keyword(s):  
Tumor Cells ◽  
Proliferative Activity ◽  
Lymphoid Neoplasms

Cholera enterotoxin stimulation of cAMP in cultured adrenal tumor cells

1974 ◽  
Vol 87 (2) ◽  
pp. 436-438 ◽  
Author(s):  
Catherine N. Kwan ◽  
R.M. Wishnow
Keyword(s):  
Tumor Cells ◽  
Adrenal Tumor ◽  
Cholera Enterotoxin ◽  
Stimulation Of

scholarly journals Aberrant corticosteroid metabolism in tumor cells enables GR takeover in enzalutamide resistant prostate cancer

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Jianneng Li ◽  
Mohammad Alyamani ◽  
Ao Zhang ◽  
Kai-Hsiung Chang ◽  
Michael Berk ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Glucocorticoid Receptor ◽  
Tumor Cells ◽  
Target Genes ◽  
Hydroxysteroid Dehydrogenase ◽  
Mouse Xenograft ◽  
Ubiquitin E3 Ligase ◽  
Metabolic Mechanism ◽  
Stimulation Of

Prostate cancer is driven by androgen stimulation of the androgen receptor (AR). The next-generation AR antagonist, enzalutamide, prolongs survival, but resistance and lethal disease eventually prevail. Emerging data suggest that the glucocorticoid receptor (GR) is upregulated in this context, stimulating expression of AR-target genes that permit continued growth despite AR blockade. However, countering this mechanism by administration of GR antagonists is problematic because GR is essential for life. We show that enzalutamide treatment in human models of prostate cancer and patient tissues is accompanied by a ubiquitin E3-ligase, AMFR, mediating loss of 11β-hydroxysteroid dehydrogenase-2 (11β-HSD2), which otherwise inactivates cortisol, sustaining tumor cortisol concentrations to stimulate GR and enzalutamide resistance. Remarkably, reinstatement of 11β-HSD2 expression, or AMFR loss, reverses enzalutamide resistance in mouse xenograft tumors. Together, these findings reveal a surprising metabolic mechanism of enzalutamide resistance that may be targeted with a strategy that circumvents a requirement for systemic GR ablation.

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