Supplementary data from Strategically Timing Inhibition of Phosphatidylinositol 3-Kinase to Maximize Therapeutic Index in Estrogen Receptor Alpha–Positive, PIK3CA-Mutant Breast Cancer
Year: 2023
Type: supplementary-materials
Abstract: Supplementary Methods; Table. S1- Pairwise comparisons of tumor growth patterns between treatment groups; Fig. S1- PI3K inhibition induces ER activation; Fig. S2- Transient, complete inhibition of PI3K more effectively suppresses cell growth than chronic, partial inhibition; Fig. S3- Short-term and long-term inhibition of PI3K and ER induce similar degrees of apoptosis in ER+ breast cancer cells; Fig. S4- Fulv inhibits ER in MCF-7 tumors; Fig. S5- Tumor GDC-0941 concentrations are inversely correlated with PI3K pathway activation; Fig. S6- Pharmacodynamic effects of GDC-0941 and fulv on MCF-7 tumors; Fig. S7- High-dose GDC-0941 in combination with fulv induces tumor cell apoptosis; Fig. S8- High-dose GDC-0941 in combination with fulv suppresses tumor cell proliferation as indicated by geminin IHC; Fig. S9- High-dose GDC-0941 in combination with fulv suppresses tumor cell proliferation as indicated by Ki67 IHC; Fig. S10- Individual MCF-7 tumor volumes; Fig. S11- Individual T47D/FR tumor volumes; Fig. S12- GDC-0941 inhibits PI3K in T47D/FR and HCI-003 tumors; Fig. S13- Individual HCI-003 tumor volumes; Fig. S14- Intermittent, longer-term inhibition of PI3K and ER induces a bolus of suppression of tumor cell proliferation indicated by Geminin and Ki67 staining, with proliferative rebound after recovery of PI3K activity; Fig. S15- Comparison of BCL-2 family members among HCI-003, MCF-7 and T47D FR tumors
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: gold
OpenAlex ID: W4362396495