Roberta Buono
YOU?
Author Swipe
View article: Pitavastatin counteracts venetoclax resistance mechanisms in acute myeloid leukemia by depleting geranylgeranyl pyrophosphate
Pitavastatin counteracts venetoclax resistance mechanisms in acute myeloid leukemia by depleting geranylgeranyl pyrophosphate Open
The BCL2 inhibitor venetoclax has therapeutic activity in several hematological malignancies. In acute myeloid leukemia (AML), venetoclax combined with hypomethylating agents is the standard of care for patients unfit for intensive chemoth…
View article: Mevalonate Biosynthesis is a Metabolic Vulnerability of Gemcitabine-resistant Pancreatic Cancer
Mevalonate Biosynthesis is a Metabolic Vulnerability of Gemcitabine-resistant Pancreatic Cancer Open
Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy with a devastating prognosis. Gemcitabine, a pyrimidine anti-metabolite, is a cornerstone in PDAC therapy. However, resistance remains a major hurdle in clinical care. Resistan…
View article: Chemoresistance of TP53 mutant acute myeloid leukemia requires the mevalonate byproduct, geranylgeranyl pyrophosphate, for induction of an adaptive stress response
Chemoresistance of TP53 mutant acute myeloid leukemia requires the mevalonate byproduct, geranylgeranyl pyrophosphate, for induction of an adaptive stress response Open
Acute myeloid leukemia with mutations in TP53 ( TP53 mut AML) is fatal with a median survival of 6 months. RNA sequencing on purified AML patient samples showed that TP53 mut AML had higher expression of mevalonate pathway genes. Using nov…
View article: Sphingosine simultaneously inhibits nuclear import and activates PP2A by binding importins and PPP2R1A
Sphingosine simultaneously inhibits nuclear import and activates PP2A by binding importins and PPP2R1A Open
Sphingosine and constrained analogs like FTY720 and SH-BC-893 restrain tumor growth through incompletely defined mechanisms that include protein phosphatase 2A (PP2A) activation. Here we show that these compounds directly bind not only the…
View article: Data from Targeting Cholesterol Biosynthesis with Statins Synergizes with AKT Inhibitors in Triple-Negative Breast Cancer
Data from Targeting Cholesterol Biosynthesis with Statins Synergizes with AKT Inhibitors in Triple-Negative Breast Cancer Open
Triple-negative breast cancer (TNBC) is responsible for a disproportionate number of breast cancer patient deaths due to extensive molecular heterogeneity, high recurrence rates, and lack of targeted therapies. Dysregulation of the phospho…
View article: Supplementary Data from Targeting Cholesterol Biosynthesis with Statins Synergizes with AKT Inhibitors in Triple-Negative Breast Cancer
Supplementary Data from Targeting Cholesterol Biosynthesis with Statins Synergizes with AKT Inhibitors in Triple-Negative Breast Cancer Open
Supplementary figures and information
View article: Targeting Cholesterol Biosynthesis with Statins Synergizes with AKT Inhibitors in Triple-Negative Breast Cancer
Targeting Cholesterol Biosynthesis with Statins Synergizes with AKT Inhibitors in Triple-Negative Breast Cancer Open
Triple-negative breast cancer (TNBC) is responsible for a disproportionate number of breast cancer patient deaths due to extensive molecular heterogeneity, high recurrence rates, and lack of targeted therapies. Dysregulation of the phospho…
View article: Chemoresistance of<i>TP53</i>mutant AML requires the mevalonate byproduct, GGPP, for regulation of ROS and induction of a mitochondria stress response
Chemoresistance of<i>TP53</i>mutant AML requires the mevalonate byproduct, GGPP, for regulation of ROS and induction of a mitochondria stress response Open
Acute myeloid leukemia (AML) with mutations in the tumor suppressor gene, TP53 ( TP53 mut AML), is fatal with a median survival of only 6 months. RNA sequencing on purified AML patient samples show TP53 mut AML has higher expression of mev…
View article: Cholesterol biosynthesis inhibition synergizes with AKT inhibitors in triple-negative breast cancer
Cholesterol biosynthesis inhibition synergizes with AKT inhibitors in triple-negative breast cancer Open
Triple-negative breast cancer (TNBC) is responsible for a disproportionate number of breast cancer deaths due to its molecular heterogeneity, high recurrence rate and lack of targeted therapies. Dysregulation of the phosphoinositide 3-kina…
View article: Table S5 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors
Table S5 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors Open
Supplementary Table S5 presents multivariate analysis of pooled clinical trial data on R/R MM patients achieving complete response (CR) or better – variables include statin use, t11;14 status, prior lines of therapy, cytogenetic risk.
View article: Table S3 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors
Table S3 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors Open
Supplementary Table S3 presents statistical analysis of pooled clinical trial data on R/R MM patient response to venetoclax treatment, comparing t11;14 patients to non-t11;14.
View article: Figure S4 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors
Figure S4 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors Open
Supplementary Figure 4 contains BH3 profiling data, and viability assays in cells expressing p53 dominant negative
View article: Data from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors
Data from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors Open
The BCL2 inhibitor venetoclax promotes apoptosis in blood cancer cells and is approved for treatment of chronic lymphocytic leukemia and acute myeloid leukemia. However, multiple myeloma cells are frequently more dependent on MCL-1 for sur…
View article: Figure S5 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors
Figure S5 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors Open
Supplementary Figure 5 contains viability data and PUMA expression data from PBMCs
View article: FIGURE 1 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors
FIGURE 1 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors Open
Statins significantly improve responses in a retrospective analysis of venetoclax clinical trials in R/R multiple myeloma. Results of patients with R/R multiple myeloma from venetoclax clinical trials receiving the standard therapy of Dex …
View article: Figure S2 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors
Figure S2 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors Open
Supplementary Figure 2 contains PFS data from venetoclax clinical trials in MM
View article: FIGURE 5 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors
FIGURE 5 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors Open
Activation of stress pathways is induced by pitavastatin and the ISR inhibitor, ISRIB, partially rescues from statin-mediated sensitization of BH3 mimetics. A, ATF4 and stress activated factors were assessed across our panel of cell lines …
View article: Figure S7 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors
Figure S7 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors Open
Supplementary Figure 7 contains data comparing pitavastatin with simavastatin in western blots (panel A) and BH3 profiling data with pitavastatin (panel B).
View article: Figure S10 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors
Figure S10 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors Open
Supplementary Figure 10 contains additional data on ISR-dependent changes in protein synthesis rates and viability.
View article: Figure S2 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors
Figure S2 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors Open
Supplementary Figure 2 contains PFS data from venetoclax clinical trials in MM
View article: Figure S3 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors
Figure S3 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors Open
Supplementary Figure 3 contains additional viability assay data and synergy contour plots
View article: Table S6 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors
Table S6 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors Open
Supplementary Table S6 presents multivariate analysis of pooled clinical trial data on R/R MM patients achieving stringent complete response (sCR) – variables include statin use, t11;14 status, prior lines of therapy, cytogenetic risk.
View article: FIGURE 3 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors
FIGURE 3 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors Open
Simvastatin induces p53-independent PUMA upregulation. A, A BCL2 family model figure depicting protein interactions and how BH3 mimetics can cooperate with apoptotic sensitizers. B, A representative Western blot analysis of statin-insensit…
View article: Figure S8 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors
Figure S8 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors Open
Supplementary Figure 8 contains data on GILZ mRNA expression in MM1S and MM1R cells
View article: Figure S7 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors
Figure S7 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors Open
Supplementary Figure 7 contains data comparing pitavastatin with simavastatin in western blots (panel A) and BH3 profiling data with pitavastatin (panel B).
View article: FIGURE 3 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors
FIGURE 3 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors Open
Simvastatin induces p53-independent PUMA upregulation. A, A BCL2 family model figure depicting protein interactions and how BH3 mimetics can cooperate with apoptotic sensitizers. B, A representative Western blot analysis of statin-insensit…
View article: Table S1 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors
Table S1 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors Open
Supplementary Table S1 presents statistical analysis of pooled clinical trial data on R/R MM patient response to venetoclax treatment, comparing statin users to non-statin users.
View article: Figure S1 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors
Figure S1 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors Open
Figure S1 contains additional data from retrospective analysis of venetoclax clinical trials in MM
View article: Table S5 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors
Table S5 from Statin-induced Mitochondrial Priming Sensitizes Multiple Myeloma Cells to BCL2 and MCL-1 Inhibitors Open
Supplementary Table S5 presents multivariate analysis of pooled clinical trial data on R/R MM patients achieving complete response (CR) or better – variables include statin use, t11;14 status, prior lines of therapy, cytogenetic risk.