Antiprogestins in breast cancer treatment: are we ready?
- Instituto de Biología y Medicina Experimental (IBYME‐CONICET), Buenos Aires, Argentina
1Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, NIH, Bethesda, Maryland 20892-4340, USA
- (Correspondence should be addressed to A A Molinolo; Email: amolinol{at}mail.nih.gov)
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Figure 1
Different PR-B and PR-A ratios in MIF-resistant and MIF-responsive mammary carcinomas. (A) Schematic representation of the two PR isoforms. DBD, DNA binding domain; H, hinge; LBD, Ligand binding domain – PR-A lacks the first 164 amino acids. (B) Representative growth curves of the patterns of MIF responsiveness of tumors with high levels of PR-B (left) or higher levels of PR-A (right). The insets show representative western blots of each tumor.
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Figure 2
MIF-induced tumor regression. (A) MIF induces an increase in apoptosis and cytostasis, which is associated with a concomitant increase of the stromal compartment (left). In other tumors, MIF induces differentiation (right). (B) C4-PI tumors treated with TAM, Fulvestrant, or with an FGFR inhibitor PD 173074 show an inhibition of tumor growth (P<0.01) MIF induced complete regression (P<0.001).
- © 2012 Society for Endocrinology
