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1. Venetoclax combines synergistically with FLT3 inhibition to effectively target leukemic cells in FLT3-ITD+ acute myeloid leukemia models

Author

Singh Mali, Raghuveer, Zhang, Qi, DeFilippis, Rosa Anna, Cavazos, Antonio, Kuruvilla, Vinitha Mary, Raman, Jayant, Mody, Vidhi, Choo, Edna F, Dail, Monique, Shah, Neil P, Konopleva, Marina, Sampath, Deepak, and Lasater, Elisabeth A

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, Orphan Drug, Rare Diseases, Hematology, Childhood Leukemia, Pediatric Cancer, Pediatric, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Adult, Bridged Bicyclo Compounds, Heterocyclic, Cell Line, Tumor, Humans, Leukemia, Myeloid, Acute, Protein Kinase Inhibitors, Sulfonamides, Tumor Microenvironment, fms-Like Tyrosine Kinase 3, Cardiorespiratory Medicine and Haematology, Immunology, Cardiovascular medicine and haematology
Abstract

FLT3 internal tandem duplication (FLT3-ITD) mutations account for ~25% of adult acute myeloid leukemia cases and are associated with poor prognosis. Venetoclax, a selective BCL-2 inhibitor, has limited monotherapy activity in relapsed/refractory acute myeloid leukemia with no responses observed in a small subset of FLT3-ITD+ patients. Further, FLT3-ITD mutations emerged at relapse following venetoclax monotherapy and combination therapy suggesting a potential mechanism of resistance. Therefore, we investigated the convergence of FLT3-ITD signaling on the BCL-2 family proteins and determined combination activity of venetoclax and FLT3-ITD inhibition in preclinical models. In vivo, venetoclax combined with quizartinib, a potent FLT3 inhibitor, showed greater anti-tumor efficacy and prolonged survival compared to monotherapies. In a patient-derived FLT3-ITD+ xenograft model, cotreatment with venetoclax and quizartinib at clinically relevant doses had greater anti-tumor activity in the tumor microenvironment compared to quizartinib or venetoclax alone. Use of selective BCL-2 family inhibitors further identified a role for BCL-2, BCL-XL and MCL-1 in mediating survival in FLT3-ITD+ cells in vivo and highlighted the need to target all three proteins for greatest anti-tumor activity. Assessment of these combinations in vitro revealed synergistic combination activity for quizartinib and venetoclax but not for quizartinib combined with BCL-XL or MCL-1 inhibition. FLT3-ITD inhibition was shown to indirectly target both BCL-XL and MCL-1 through modulation of protein expression, thereby priming cells toward BCL-2 dependence for survival. These data demonstrate that FLT3-ITD inhibition combined with venetoclax has impressive anti-tumor activity in FLT3-ITD+ acute myeloid leukemia preclinical models and provides strong mechanistic rational for clinical studies.

Published
2021

2. Loss of glucocorticoid receptor expression mediates in vivo dexamethasone resistance in T-cell acute lymphoblastic leukemia

Author

Wandler, Anica M, Huang, Benjamin J, Craig, Jeffrey W, Hayes, Kathryn, Yan, Hannah, Meyer, Lauren K, Scacchetti, Alessandro, Monsalve, Gabriela, Dail, Monique, Li, Qing, Wong, Jasmine C, Weinberg, Olga, Hasserjian, Robert P, Kogan, Scott C, Jonsson, Philip, Yamamoto, Keith, Sampath, Deepak, Nakitandwe, Joy, Downing, James R, Zhang, Jinghui, Aster, Jon C, Taylor, Barry S, and Shannon, Kevin

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Cancer, Hematology, Pediatric Cancer, Rare Diseases, Genetics, Childhood Leukemia, Pediatric, Orphan Drug, Animals, Dexamethasone, Drug Resistance, Neoplasm, Humans, Indazoles, Male, Mice, Mice, Inbred C57BL, Mutation, Precursor T-Cell Lymphoblastic Leukemia-Lymphoma, Receptors, Glucocorticoid, Recurrence, Sulfonamides, Clinical Sciences, Oncology and Carcinogenesis, Immunology, Cardiovascular medicine and haematology, Clinical sciences, Oncology and carcinogenesis
Abstract

Despite decades of clinical use, mechanisms of glucocorticoid resistance are poorly understood. We treated primary murine T lineage acute lymphoblastic leukemias (T-ALLs) with the glucocorticoid dexamethasone (DEX) alone and in combination with the pan-PI3 kinase inhibitor GDC-0941 and observed a robust response to DEX that was modestly enhanced by GDC-0941. Continuous in vivo treatment invariably resulted in outgrowth of drug-resistant clones, ~30% of which showed markedly reduced glucocorticoid receptor (GR) protein expression. A similar proportion of relapsed human T-ALLs also exhibited low GR protein levels. De novo or preexisting mutations in the gene encoding GR (Nr3c1) occurred in relapsed clones derived from multiple independent parental leukemias. CRISPR/Cas9 gene editing confirmed that loss of GR expression confers DEX resistance. Exposing drug-sensitive T-ALLs to DEX in vivo altered transcript levels of multiple genes, and this response was attenuated in relapsed T-ALLs. These data implicate reduced GR protein expression as a frequent cause of glucocorticoid resistance in T-ALL.

Published
2020

3. Neutralization of BCL-2/XL Enhances the Cytotoxicity of T-DM1 In Vivo

Author

Zoeller, Jason J, Vagodny, Aleksandr, Taneja, Krishan, Tan, Benjamin Y, O'Brien, Neil, Slamon, Dennis J, Sampath, Deepak, Leverson, Joel D, Bronson, Roderick T, Dillon, Deborah A, and Brugge, Joan S

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Breast Cancer, Cancer, Ado-Trastuzumab Emtansine, Aniline Compounds, Animals, Antineoplastic Agents, Immunological, Apoptosis, Breast Neoplasms, Cytotoxicity, Immunologic, Drug Resistance, Neoplasm, Drug Therapy, Combination, Female, Humans, Immunoconjugates, Mice, Mice, Inbred NOD, Mice, SCID, Proto-Oncogene Proteins c-bcl-2, Receptor, ErbB-2, Sulfonamides, Xenograft Model Antitumor Assays, bcl-X Protein, Receptor, erbB-2, Pharmacology and Pharmaceutical Sciences, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

One of the most recent advances in the treatment of HER2+ breast cancer is the development of the antibody-drug conjugate, T-DM1. T-DM1 has proven clinical benefits for patients with advanced and/or metastatic breast cancer who have progressed on prior HER2-targeted therapies. However, T-DM1 resistance ultimately occurs and represents a major obstacle in the effective treatment of this disease. Because anti-apoptotic BCL-2 family proteins can affect the threshold for induction of apoptosis and thus limit the effectiveness of the chemotherapeutic payload, we examined whether inhibition of BCL-2/XL would enhance the efficacy of T-DM1 in five HER2-expressing patient-derived breast cancer xenograft models. Inhibition of BCL-2/XL via navitoclax/ABT-263 significantly enhanced the cytotoxicity of T-DM1 in two of three models derived from advanced and treatment-exposed metastatic breast tumors. No additive effects of combined treatment were observed in the third metastatic tumor model, which was highly sensitive to T-DM1, as well as a primary treatment-exposed tumor, which was refractory to T-DM1. A fifth model, derived from a treatment naïve primary breast tumor, was sensitive to T-DM1 but markedly benefited from combination treatment. Notably, both PDXs that were highly responsive to the combination therapy expressed low HER2 protein levels and lacked ERBB2 amplification, suggesting that BCL-2/XL inhibition can enhance sensitivity of tumors with low HER2 expression. Toxicities associated with combined treatments were significantly ameliorated with intermittent ABT-263 dosing. Taken together, these studies provide evidence that T-DM1 cytotoxicity could be significantly enhanced via BCL-2/XL blockade and support clinical investigation of this combination beyond ERBB2-amplified and/or HER2-overexpressed tumors.

Published
2019

4. Convergent genetic aberrations in murine and human T lineage acute lymphoblastic leukemias

Author

Huang, Benjamin J, Wandler, Anica M, Meyer, Lauren K, Dail, Monique, Daemen, Anneleen, Sampath, Deepak, Li, Qing, Wang, Xinyue, Wong, Jasmine C, Nakitandwe, Joy, Downing, James R, Zhang, Jinghui, Taylor, Barry S, and Shannon, Kevin

Subjects
Biological Sciences, Genetics, Human Genome, Orphan Drug, Pediatric Cancer, Rare Diseases, Pediatric, Hematology, Biotechnology, Cancer, Childhood Leukemia, 5.1 Pharmaceuticals, Aetiology, 2.1 Biological and endogenous factors, Development of treatments and therapeutic interventions, Animals, Cell Line, Tumor, Chromosome Aberrations, Clonal Evolution, Disease Models, Animal, Drug Resistance, Neoplasm, Genomics, Humans, Mice, Mutagenesis, Insertional, Mutation, Precursor T-Cell Lymphoblastic Leukemia-Lymphoma, Proto-Oncogene Proteins p21(ras), Developmental Biology
Abstract

The lack of predictive preclinical models is a fundamental barrier to translating knowledge about the molecular pathogenesis of cancer into improved therapies. Insertional mutagenesis (IM) in mice is a robust strategy for generating malignancies that recapitulate the extensive inter- and intra-tumoral genetic heterogeneity found in advanced human cancers. While the central role of "driver" viral insertions in IM models that aberrantly increase the expression of proto-oncogenes or disrupt tumor suppressors has been appreciated for many years, the contributions of cooperating somatic mutations and large chromosomal alterations to tumorigenesis are largely unknown. Integrated genomic studies of T lineage acute lymphoblastic leukemias (T-ALLs) generated by IM in wild-type (WT) and Kras mutant mice reveal frequent point mutations and other recurrent non-insertional genetic alterations that also occur in human T-ALL. These somatic mutations are sensitive and specific markers for defining clonal dynamics and identifying candidate resistance mechanisms in leukemias that relapse after an initial therapeutic response. Primary cancers initiated by IM and resistant clones that emerge during in vivo treatment close key gaps in existing preclinical models, and are robust platforms for investigating the efficacy of new therapies and for elucidating how drug exposure shapes tumor evolution and patterns of resistance.

Published
2019

6. KRAS Allelic Imbalance Enhances Fitness and Modulates MAP Kinase Dependence in Cancer

Author

Burgess, Michael R, Hwang, Eugene, Mroue, Rana, Bielski, Craig M, Wandler, Anica M, Huang, Benjamin J, Firestone, Ari J, Young, Amy, Lacap, Jennifer A, Crocker, Lisa, Asthana, Saurabh, Davis, Elizabeth M, Xu, Jin, Akagi, Keiko, Le Beau, Michelle M, Li, Qing, Haley, Benjamin, Stokoe, David, Sampath, Deepak, Taylor, Barry S, Evangelista, Marie, and Shannon, Kevin

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Digestive Diseases, Genetics, Pediatric, Colo-Rectal Cancer, Cancer, Pediatric Cancer, Orphan Drug, Rare Diseases, Biotechnology, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, Animals, Antineoplastic Agents, Benzamides, Cell Line, Tumor, Clonal Evolution, Colorectal Neoplasms, Diphenylamine, Drug Resistance, Neoplasm, Humans, Leukemia, Myeloid, Acute, MAP Kinase Signaling System, Mice, Mutation, Proto-Oncogene Proteins p21(ras), Retroviridae, AML, KRAS, MEK inhibition, allelic imbalance, colorectal cancer, drug resistance, Biological Sciences, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences
Abstract

Investigating therapeutic "outliers" that show exceptional responses to anti-cancer treatment can uncover biomarkers of drug sensitivity. We performed preclinical trials investigating primary murine acute myeloid leukemias (AMLs) generated by retroviral insertional mutagenesis in KrasG12D "knockin" mice with the MEK inhibitor PD0325901 (PD901). One outlier AML responded and exhibited intrinsic drug resistance at relapse. Loss of wild-type (WT) Kras enhanced the fitness of the dominant clone and rendered it sensitive to MEK inhibition. Similarly, human colorectal cancer cell lines with increased KRAS mutant allele frequency were more sensitive to MAP kinase inhibition, and CRISPR-Cas9-mediated replacement of WT KRAS with a mutant allele sensitized heterozygous mutant HCT116 cells to treatment. In a prospectively characterized cohort of patients with advanced cancer, 642 of 1,168 (55%) with KRAS mutations exhibited allelic imbalance. These studies demonstrate that serial genetic changes at the Kras/KRAS locus are frequent in cancer and modulate competitive fitness and MEK dependency.

Published
2017

7. Preclinical Characterization of the Absorption and Disposition of the Brain Penetrant PI3K/mTOR Inhibitor Paxalisib and Prediction of Its Pharmacokinetics and Efficacy in Human

Author

Salphati, Laurent, primary, Pang, Jodie, additional, Alicke, Bruno, additional, Plise, Emile G., additional, Cheong, Jonathan, additional, Jaochico, Allan, additional, Olivero, Alan G., additional, Sampath, Deepak, additional, Wong, Susan, additional, and Zhang, Xiaolin, additional

Published
2024
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8. Metabolic response of prostate cancer to nicotinamide phophoribosyltransferase inhibition in a hyperpolarized MR/PET compatible bioreactor

Author

Keshari, Kayvan R, Wilson, David M, Van Criekinge, Mark, Sriram, Renuka, Koelsch, Bertram L, Wang, Zhen J, VanBrocklin, Henry F, Peehl, Donna M, O'Brien, Tom, Sampath, Deepak, Carano, Richard AD, and Kurhanewicz, John

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Aging, Cancer, Prostate Cancer, Biomedical Imaging, Biotechnology, Urologic Diseases, Bioreactors, Cytokines, Humans, Magnetic Resonance Spectroscopy, Male, Nicotinamide Phosphoribosyltransferase, Positron-Emission Tomography, Prostatic Neoplasms, Tumor Cells, Cultured, translational biomarkers, metabolism, metabolic flux, NAMPT, MRS, Paediatrics and Reproductive Medicine, Oncology & Carcinogenesis, Clinical sciences, Oncology and carcinogenesis
Abstract

BackgroundMetabolic shifts in disease are of great interest for the development of novel therapeutics. In cancer treatment, these therapies exploit the metabolic phenotype associated with oncogenesis and cancer progression. One recent strategy involves the depletion of the cofactors needed to maintain the high rate of glycolysis seen with the Warburg effect. Specifically, blocking nicotinamide adenine dinucleotide (NAD) biosynthesis via nicotinamide phosphoribosyltransferase (NAMPT) inhibition depletes cancer cells of the NAD needed for glycolysis. To characterize this metabolic phenotype in vivo and describe changes in flux with treatment, non-invasive biomarkers are necessary. One such biomarker is hyperpolarized (HP) [1-(13) C] pyruvate, a clinically translatable probe that allows real-time assessment of metabolism.MethodsWe therefore developed a cell perfusion system compatible with HP magnetic resonance (MR) and positron emission tomography (PET) to develop translatable biomarkers of response to NAMPT inhibition in reduced volume cell cultures.ResultsUsing this platform, we observed a reduction in pyruvate flux through lactate dehydrogenase with NAMPT inhibition in prostate cancer cells, and showed that both HP lactate and 2-[(18) F] fluoro-2-deoxy-D-glucose (FDG) can be used as biomarkers for treatment response of such targeted agents. Moreover, we observed dynamic flux changes whereby HP pyruvate was re-routed to alanine, providing both positive and negative indicators of treatment response.ConclusionsThis study demonstrated the feasibility of a MR/PET compatible bioreactor approach to efficiently explore cell and tissue metabolism, the understanding of which is critical for developing clinically translatable biomarkers of disease states and responses to therapeutics.

Published
2015

9. Preclinical efficacy of MEK inhibition in Nras-mutant AML

Author

Burgess, Michael R, Hwang, Eugene, Firestone, Ari J, Huang, Tannie, Xu, Jin, Zuber, Johannes, Bohin, Natacha, Wen, Tiffany, Kogan, Scott C, Haigis, Kevin M, Sampath, Deepak, Lowe, Scott, Shannon, Kevin, and Li, Qing

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Biological Sciences, Childhood Leukemia, Pediatric Cancer, Stem Cell Research - Nonembryonic - Non-Human, Stem Cell Research, Rare Diseases, Hematology, Cancer, Stem Cell Research - Nonembryonic - Human, Orphan Drug, Genetics, Regenerative Medicine, Pediatric, Aetiology, Development of treatments and therapeutic interventions, 2.1 Biological and endogenous factors, 5.1 Pharmaceuticals, Animals, Apoptosis, Cell Line, Tumor, Cell Proliferation, Cell Survival, Genes, ras, Hematopoietic Stem Cells, Humans, Leukemia, Myeloid, Acute, MAP Kinase Kinase Kinases, MAP Kinase Signaling System, Mice, Mice, Inbred C57BL, Monomeric GTP-Binding Proteins, Mutation, Protein Kinase Inhibitors, RNA, Small Interfering, Signal Transduction, Stem Cells, Transgenes, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Paediatrics and Reproductive Medicine, Immunology, Biochemistry and cell biology, Cardiovascular medicine and haematology, Paediatrics
Abstract

Oncogenic NRAS mutations are highly prevalent in acute myeloid leukemia (AML). Genetic analysis supports the hypothesis that NRAS mutations cooperate with antecedent molecular lesions in leukemogenesis, but have limited independent prognostic significance. Using short hairpin RNA-mediated knockdown in human cell lines and primary mouse leukemias, we show that AML cells with NRAS/Nras mutations are dependent on continued oncogene expression in vitro and in vivo. Using the Mx1-Cre transgene to inactivate a conditional mutant Nras allele, we analyzed hematopoiesis and hematopoietic stem and progenitor cells (HSPCs) under normal and stressed conditions and found that HSPCs lacking Nras expression are functionally equivalent to normal HSPCs in the adult mouse. Treating recipient mice transplanted with primary Nras(G12D) AMLs with 2 potent allosteric mitogen-activated protein kinase kinase (MEK) inhibitors (PD0325901 or trametinib/GlaxoSmithKline 1120212) significantly prolonged survival and reduced proliferation but did not induce apoptosis, promote differentiation, or drive clonal evolution. The phosphatidylinositol 3-kinase inhibitor GDC-0941 was ineffective as a single agent and did not augment the activity of PD0325901. All mice ultimately succumbed to progressive leukemia. Together, these data validate oncogenic N-Ras signaling as a therapeutic target in AML and support testing combination regimens that include MEK inhibitors.

Published
2014

11. Loss of oncogenic Notch1 with resistance to a PI3K inhibitor in T-cell leukaemia

Author

Dail, Monique, Wong, Jason, Lawrence, Jessica, O’Connor, Daniel, Nakitandwe, Joy, Chen, Shann-Ching, Xu, Jin, Lee, Leslie B, Akagi, Keiko, Li, Qing, Aster, Jon C, Pear, Warren S, Downing, James R, Sampath, Deepak, and Shannon, Kevin

Subjects
Pediatric, Cancer, Rare Diseases, Pediatric Cancer, Childhood Leukemia, Hematology, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, Animals, Benzamides, Clone Cells, Diphenylamine, Down-Regulation, Drug Resistance, Neoplasm, Drug Synergism, Genes, ras, Indazoles, Male, Mice, Mice, Inbred C57BL, Mitogen-Activated Protein Kinase Kinases, Phosphoinositide-3 Kinase Inhibitors, Precursor T-Cell Lymphoblastic Leukemia-Lymphoma, Protein Kinase Inhibitors, Protein Structure, Tertiary, Proto-Oncogene Proteins c-akt, Receptor, Notch1, Signal Transduction, Sulfonamides, General Science & Technology
Abstract

Mutations that deregulate Notch1 and Ras/phosphoinositide 3 kinase (PI3K)/Akt signalling are prevalent in T-cell acute lymphoblastic leukaemia (T-ALL), and often coexist. Here we show that the PI3K inhibitor GDC-0941 is active against primary T-ALLs from wild-type and Kras(G12D) mice, and addition of the MEK inhibitor PD0325901 increases its efficacy. Mice invariably relapsed after treatment with drug-resistant clones, most of which unexpectedly had reduced levels of activated Notch1 protein, downregulated many Notch1 target genes, and exhibited cross-resistance to γ-secretase inhibitors. Multiple resistant primary T-ALLs that emerged in vivo did not contain somatic Notch1 mutations present in the parental leukaemia. Importantly, resistant clones upregulated PI3K signalling. Consistent with these data, inhibiting Notch1 activated the PI3K pathway, providing a likely mechanism for selection against oncogenic Notch1 signalling. These studies validate PI3K as a therapeutic target in T-ALL and raise the unexpected possibility that dual inhibition of PI3K and Notch1 signalling could promote drug resistance in T-ALL.

Published
2014

12. PLC-γ and PI3K Link Cytokines to ERK Activation in Hematopoietic Cells with Normal and Oncogenic Kras

Author

Diaz-Flores, Ernesto, Goldschmidt, Hana, Depeille, Philippe, Ng, Victor, Akutagawa, Jon, Krisman, Kimberly, Crone, Michael, Burgess, Michael R, Williams, Olusegun, Houseman, Benjamin, Shokat, Kevan, Sampath, Deepak, Bollag, Gideon, Roose, Jeroen P, Braun, Benjamin S, and Shannon, Kevin

Subjects
Biochemistry and Cell Biology, Biological Sciences, Cancer, Rare Diseases, Hematology, Stem Cell Research, 1.1 Normal biological development and functioning, Underpinning research, Amino Acid Substitution, Animals, Cells, Cultured, Cytokines, Extracellular Signal-Regulated MAP Kinases, Hematopoietic Stem Cells, Leukemia, MAP Kinase Signaling System, Mice, Mutation, Missense, Neoplastic Stem Cells, Phosphatidylinositol 3-Kinases, Phospholipase C gamma, Proto-Oncogene Proteins p21(ras), Second Messenger Systems, TOR Serine-Threonine Kinases, Biochemistry and cell biology
Abstract

Oncogenic K-Ras proteins, such as K-Ras(G12D), accumulate in the active, guanosine triphosphate (GTP)-bound conformation and stimulate signaling through effector kinases. The presence of the K-Ras(G12D) oncoprotein at a similar abundance to that of endogenous wild-type K-Ras results in only minimal phosphorylation and activation of the canonical Raf-mitogen-activated or extracellular signal-regulated protein kinase kinase (MEK)-extracellular signal-regulated kinase (ERK) and phosphoinositide 3-kinase (PI3K)-Akt-mammalian target of rapamycin (mTOR) signaling cascades in primary hematopoietic cells, and these pathways remain dependent on growth factors for efficient activation. We showed that phospholipase C-γ (PLC-γ), PI3K, and their generated second messengers link activated cytokine receptors to Ras and ERK signaling in differentiated bone marrow cells and in a cell population enriched for leukemia stem cells. Cells expressing endogenous oncogenic K-Ras(G12D) remained dependent on the second messenger diacylglycerol for the efficient activation of Ras-ERK signaling. These data raise the unexpected possibility of therapeutically targeting proteins that function upstream of oncogenic Ras in cancer.

Published
2013

13. Pan-Cancer Metabolic Signature Predicts Co-Dependency on Glutaminase and De Novo Glutathione Synthesis Linked to a High-Mesenchymal Cell State

Author

Daemen, Anneleen, Liu, Bonnie, Song, Kyung, Kwong, Mandy, Gao, Min, Hong, Rebecca, Nannini, Michelle, Peterson, David, Liederer, Bianca M., de la Cruz, Cecile, Sangaraju, Dewakar, Jaochico, Allan, Zhao, Xiaofeng, Sandoval, Wendy, Hunsaker, Thomas, Firestein, Ron, Latham, Sheerin, Sampath, Deepak, Evangelista, Marie, and Hatzivassiliou, Georgia

Published
2018
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17. Supplementary Table 1 from Bcl-2/Bcl-xL Inhibition Increases the Efficacy of MEK Inhibition Alone and in Combination with PI3 Kinase Inhibition in Lung and Pancreatic Tumor Models

Author

Tan, Nguyen, primary, Wong, Maureen, primary, Nannini, Michelle A., primary, Hong, Rebecca, primary, Lee, Leslie B., primary, Price, Stephen, primary, Williams, Karen, primary, Savy, Pierre Pascal, primary, Yue, Peng, primary, Sampath, Deepak, primary, Settleman, Jeffrey, primary, Fairbrother, Wayne J., primary, and Belmont, Lisa D., primary

Published
2023
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18. Supplementary Figure 1 from Bcl-2/Bcl-xL Inhibition Increases the Efficacy of MEK Inhibition Alone and in Combination with PI3 Kinase Inhibition in Lung and Pancreatic Tumor Models

Author

Tan, Nguyen, primary, Wong, Maureen, primary, Nannini, Michelle A., primary, Hong, Rebecca, primary, Lee, Leslie B., primary, Price, Stephen, primary, Williams, Karen, primary, Savy, Pierre Pascal, primary, Yue, Peng, primary, Sampath, Deepak, primary, Settleman, Jeffrey, primary, Fairbrother, Wayne J., primary, and Belmont, Lisa D., primary

Published
2023
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19. Supplementary Figure 1 from Expression Profile of BCL-2, BCL-XL, and MCL-1 Predicts Pharmacological Response to the BCL-2 Selective Antagonist Venetoclax in Multiple Myeloma Models

Author

Punnoose, Elizabeth A., primary, Leverson, Joel D., primary, Peale, Franklin, primary, Boghaert, Erwin R., primary, Belmont, Lisa D., primary, Tan, Nguyen, primary, Young, Amy, primary, Mitten, Michael, primary, Ingalla, Ellen, primary, Darbonne, Walter C., primary, Oleksijew, Anatol, primary, Tapang, Paul, primary, Yue, Peng, primary, Oeh, Jason, primary, Lee, Leslie, primary, Maiga, Sophie, primary, Fairbrother, Wayne J., primary, Amiot, Martine, primary, Souers, Andrew J., primary, and Sampath, Deepak, primary

Published
2023
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21. Data from Venetoclax Increases Intratumoral Effector T Cells and Antitumor Efficacy in Combination with Immune Checkpoint Blockade

Author

Kohlhapp, Frederick J., primary, Haribhai, Dipica, primary, Mathew, Rebecca, primary, Duggan, Ryan, primary, Ellis, Paul A., primary, Wang, Rui, primary, Lasater, Elisabeth A., primary, Shi, Yan, primary, Dave, Nimita, primary, Riehm, Jacob J., primary, Robinson, Valerie A., primary, Do, An D., primary, Li, Yijin, primary, Orr, Christine J., primary, Sampath, Deepak, primary, Raval, Aparna, primary, Merchant, Mark, primary, Bhathena, Anahita, primary, Salem, Ahmed Hamed, primary, Hamel, Keith M., primary, Leverson, Joel D., primary, Donawho, Cherrie, primary, Pappano, William N., primary, and Uziel, Tamar, primary

Published
2023
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22. Table S7 from Machine-Learning and Chemicogenomics Approach Defines and Predicts Cross-Talk of Hippo and MAPK Pathways

Author

Pham, Trang H., primary, Hagenbeek, Thijs J., primary, Lee, Ho-June, primary, Li, Jason, primary, Rose, Christopher M., primary, Lin, Eva, primary, Yu, Mamie, primary, Martin, Scott E., primary, Piskol, Robert, primary, Lacap, Jennifer A., primary, Sampath, Deepak, primary, Pham, Victoria C., primary, Modrusan, Zora, primary, Lill, Jennie R., primary, Klijn, Christiaan, primary, Malek, Shiva, primary, Chang, Matthew T., primary, and Dey, Anwesha, primary

Published
2023
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23. Data from An Anti-GDNF Family Receptor Alpha 1 (GFRA1) Antibody–Drug Conjugate for the Treatment of Hormone Receptor–Positive Breast Cancer

Author

Bhakta, Sunil, primary, Crocker, Lisa M., primary, Chen, Yvonne, primary, Hazen, Meredith, primary, Schutten, Melissa M., primary, Li, Dongwei, primary, Kuijl, Coenraad, primary, Ohri, Rachana, primary, Zhong, Fiona, primary, Poon, Kirsten A., primary, Go, Mary Ann T., primary, Cheng, Eric, primary, Piskol, Robert, primary, Firestein, Ron, primary, Fourie-O'Donohue, Aimee, primary, Kozak, Katherine R., primary, Raab, Helga, primary, Hongo, Jo-Anne, primary, Sampath, Deepak, primary, Dennis, Mark S., primary, Scheller, Richard H., primary, Polakis, Paul, primary, and Junutula, Jagath R., primary

Published
2023
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24. Legends for Tables S1 to S3 and Figures S1 to S5 from Expression Profile of BCL-2, BCL-XL, and MCL-1 Predicts Pharmacological Response to the BCL-2 Selective Antagonist Venetoclax in Multiple Myeloma Models

Author

Punnoose, Elizabeth A., primary, Leverson, Joel D., primary, Peale, Franklin, primary, Boghaert, Erwin R., primary, Belmont, Lisa D., primary, Tan, Nguyen, primary, Young, Amy, primary, Mitten, Michael, primary, Ingalla, Ellen, primary, Darbonne, Walter C., primary, Oleksijew, Anatol, primary, Tapang, Paul, primary, Yue, Peng, primary, Oeh, Jason, primary, Lee, Leslie, primary, Maiga, Sophie, primary, Fairbrother, Wayne J., primary, Amiot, Martine, primary, Souers, Andrew J., primary, and Sampath, Deepak, primary

Published
2023
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25. Data from Phase I Dose-Escalation Study of Taselisib, an Oral PI3K Inhibitor, in Patients with Advanced Solid Tumors

Author

Juric, Dejan, primary, Krop, Ian, primary, Ramanathan, Ramesh K., primary, Wilson, Timothy R., primary, Ware, Joseph A., primary, Sanabria Bohorquez, Sandra M., primary, Savage, Heidi M., primary, Sampath, Deepak, primary, Salphati, Laurent, primary, Lin, Ray S., primary, Jin, Huan, primary, Parmar, Hema, primary, Hsu, Jerry Y., primary, Von Hoff, Daniel D., primary, and Baselga, José, primary

Published
2023
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26. Data from RTK-Dependent Inducible Degradation of Mutant PI3Kα Drives GDC-0077 (Inavolisib) Efficacy

Author

Song, Kyung W., primary, Edgar, Kyle A., primary, Hanan, Emily J., primary, Hafner, Marc, primary, Oeh, Jason, primary, Merchant, Mark, primary, Sampath, Deepak, primary, Nannini, Michelle A., primary, Hong, Rebecca, primary, Phu, Lilian, primary, Forrest, William F., primary, Stawiski, Eric, primary, Schmidt, Stephen, primary, Endres, Nicholas, primary, Guan, Jane, primary, Wallin, Jeffrey J., primary, Cheong, Jonathan, primary, Plise, Emile G., primary, Lewis Phillips, Gail D., primary, Salphati, Laurent, primary, Heffron, Timothy P., primary, Olivero, Alan G., primary, Malek, Shiva, primary, Staben, Steven T., primary, Kirkpatrick, Donald S., primary, Dey, Anwesha, primary, and Friedman, Lori S., primary

Published
2023
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27. Supplementary Figure S5 from Combined MEK and BCL-2/XL Inhibition Is Effective in High-Grade Serous Ovarian Cancer Patient–Derived Xenograft Models and BIM Levels Are Predictive of Responsiveness

Author

Iavarone, Claudia, primary, Zervantonakis, Ioannis K., primary, Selfors, Laura M., primary, Palakurthi, Sangeetha, primary, Liu, Joyce F., primary, Drapkin, Ronny, primary, Matulonis, Ursula A., primary, Hallberg, Dorothy, primary, Velculescu, Victor E., primary, Leverson, Joel D., primary, Sampath, Deepak, primary, Mills, Gordon B., primary, and Brugge, Joan S., primary

Published
2023
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28. Supplementary Figures 1-4, Tables 1-8 from GDC-0980 Is a Novel Class I PI3K/mTOR Kinase Inhibitor with Robust Activity in Cancer Models Driven by the PI3K Pathway

Author

Wallin, Jeffrey J., primary, Edgar, Kyle A., primary, Guan, Jane, primary, Berry, Megan, primary, Prior, Wei Wei, primary, Lee, Leslie, primary, Lesnick, John D., primary, Lewis, Cristina, primary, Nonomiya, Jim, primary, Pang, Jodie, primary, Salphati, Laurent, primary, Olivero, Alan G., primary, Sutherlin, Daniel P., primary, O'Brien, Carol, primary, Spoerke, Jill M., primary, Patel, Sonal, primary, Lensun, Letitia, primary, Kassees, Robert, primary, Ross, Leanne, primary, Lackner, Mark R., primary, Sampath, Deepak, primary, Belvin, Marcia, primary, and Friedman, Lori S., primary

Published
2023
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30. Supplementary Figure 1 from The Bcl-2/Bcl-XL/Bcl-w Inhibitor, Navitoclax, Enhances the Activity of Chemotherapeutic Agents In Vitro and In Vivo

Author

Chen, Jun, primary, Jin, Sha, primary, Abraham, Vivek, primary, Huang, Xiaoli, primary, Liu, Bernard, primary, Mitten, Michael J., primary, Nimmer, Paul, primary, Lin, Xiaoyu, primary, Smith, Morey, primary, Shen, Yu, primary, Shoemaker, Alexander R., primary, Tahir, Stephen K., primary, Zhang, Haichao, primary, Ackler, Scott L., primary, Rosenberg, Saul H., primary, Maecker, Heather, primary, Sampath, Deepak, primary, Leverson, Joel D., primary, Tse, Chris, primary, and Elmore, Steven W., primary

Published
2023
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31. Figure S1 from Machine-Learning and Chemicogenomics Approach Defines and Predicts Cross-Talk of Hippo and MAPK Pathways

Author

Pham, Trang H., primary, Hagenbeek, Thijs J., primary, Lee, Ho-June, primary, Li, Jason, primary, Rose, Christopher M., primary, Lin, Eva, primary, Yu, Mamie, primary, Martin, Scott E., primary, Piskol, Robert, primary, Lacap, Jennifer A., primary, Sampath, Deepak, primary, Pham, Victoria C., primary, Modrusan, Zora, primary, Lill, Jennie R., primary, Klijn, Christiaan, primary, Malek, Shiva, primary, Chang, Matthew T., primary, and Dey, Anwesha, primary

Published
2023
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32. Data from The Bcl-2/Bcl-XL/Bcl-w Inhibitor, Navitoclax, Enhances the Activity of Chemotherapeutic Agents In Vitro and In Vivo

Author

Chen, Jun, primary, Jin, Sha, primary, Abraham, Vivek, primary, Huang, Xiaoli, primary, Liu, Bernard, primary, Mitten, Michael J., primary, Nimmer, Paul, primary, Lin, Xiaoyu, primary, Smith, Morey, primary, Shen, Yu, primary, Shoemaker, Alexander R., primary, Tahir, Stephen K., primary, Zhang, Haichao, primary, Ackler, Scott L., primary, Rosenberg, Saul H., primary, Maecker, Heather, primary, Sampath, Deepak, primary, Leverson, Joel D., primary, Tse, Chris, primary, and Elmore, Steven W., primary

Published
2023
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34. Supplementary Figure 3 from Bcl-2/Bcl-xL Inhibition Increases the Efficacy of MEK Inhibition Alone and in Combination with PI3 Kinase Inhibition in Lung and Pancreatic Tumor Models

Author

Tan, Nguyen, primary, Wong, Maureen, primary, Nannini, Michelle A., primary, Hong, Rebecca, primary, Lee, Leslie B., primary, Price, Stephen, primary, Williams, Karen, primary, Savy, Pierre Pascal, primary, Yue, Peng, primary, Sampath, Deepak, primary, Settleman, Jeffrey, primary, Fairbrother, Wayne J., primary, and Belmont, Lisa D., primary

Published
2023
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35. Data from Expression Profile of BCL-2, BCL-XL, and MCL-1 Predicts Pharmacological Response to the BCL-2 Selective Antagonist Venetoclax in Multiple Myeloma Models

Author

Punnoose, Elizabeth A., primary, Leverson, Joel D., primary, Peale, Franklin, primary, Boghaert, Erwin R., primary, Belmont, Lisa D., primary, Tan, Nguyen, primary, Young, Amy, primary, Mitten, Michael, primary, Ingalla, Ellen, primary, Darbonne, Walter C., primary, Oleksijew, Anatol, primary, Tapang, Paul, primary, Yue, Peng, primary, Oeh, Jason, primary, Lee, Leslie, primary, Maiga, Sophie, primary, Fairbrother, Wayne J., primary, Amiot, Martine, primary, Souers, Andrew J., primary, and Sampath, Deepak, primary

Published
2023
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36. Supplementary Table 1, Figure Legends 1-2 from The Bcl-2/Bcl-XL/Bcl-w Inhibitor, Navitoclax, Enhances the Activity of Chemotherapeutic Agents In Vitro and In Vivo

Author

Chen, Jun, primary, Jin, Sha, primary, Abraham, Vivek, primary, Huang, Xiaoli, primary, Liu, Bernard, primary, Mitten, Michael J., primary, Nimmer, Paul, primary, Lin, Xiaoyu, primary, Smith, Morey, primary, Shen, Yu, primary, Shoemaker, Alexander R., primary, Tahir, Stephen K., primary, Zhang, Haichao, primary, Ackler, Scott L., primary, Rosenberg, Saul H., primary, Maecker, Heather, primary, Sampath, Deepak, primary, Leverson, Joel D., primary, Tse, Chris, primary, and Elmore, Steven W., primary

Published
2023
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37. Supplementary Figure 5 from Expression Profile of BCL-2, BCL-XL, and MCL-1 Predicts Pharmacological Response to the BCL-2 Selective Antagonist Venetoclax in Multiple Myeloma Models

Author

Punnoose, Elizabeth A., primary, Leverson, Joel D., primary, Peale, Franklin, primary, Boghaert, Erwin R., primary, Belmont, Lisa D., primary, Tan, Nguyen, primary, Young, Amy, primary, Mitten, Michael, primary, Ingalla, Ellen, primary, Darbonne, Walter C., primary, Oleksijew, Anatol, primary, Tapang, Paul, primary, Yue, Peng, primary, Oeh, Jason, primary, Lee, Leslie, primary, Maiga, Sophie, primary, Fairbrother, Wayne J., primary, Amiot, Martine, primary, Souers, Andrew J., primary, and Sampath, Deepak, primary

Published
2023
Full Text
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38. Data from Bcl-2/Bcl-xL Inhibition Increases the Efficacy of MEK Inhibition Alone and in Combination with PI3 Kinase Inhibition in Lung and Pancreatic Tumor Models

Author

Tan, Nguyen, primary, Wong, Maureen, primary, Nannini, Michelle A., primary, Hong, Rebecca, primary, Lee, Leslie B., primary, Price, Stephen, primary, Williams, Karen, primary, Savy, Pierre Pascal, primary, Yue, Peng, primary, Sampath, Deepak, primary, Settleman, Jeffrey, primary, Fairbrother, Wayne J., primary, and Belmont, Lisa D., primary

Published
2023
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39. Supplementary Figure 2 from Expression Profile of BCL-2, BCL-XL, and MCL-1 Predicts Pharmacological Response to the BCL-2 Selective Antagonist Venetoclax in Multiple Myeloma Models

Author

Punnoose, Elizabeth A., primary, Leverson, Joel D., primary, Peale, Franklin, primary, Boghaert, Erwin R., primary, Belmont, Lisa D., primary, Tan, Nguyen, primary, Young, Amy, primary, Mitten, Michael, primary, Ingalla, Ellen, primary, Darbonne, Walter C., primary, Oleksijew, Anatol, primary, Tapang, Paul, primary, Yue, Peng, primary, Oeh, Jason, primary, Lee, Leslie, primary, Maiga, Sophie, primary, Fairbrother, Wayne J., primary, Amiot, Martine, primary, Souers, Andrew J., primary, and Sampath, Deepak, primary

Published
2023
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40. Supplementary Tables 1 through 4 and Supplementary Figures 1 through 7 from Phase I Dose-Escalation Study of Taselisib, an Oral PI3K Inhibitor, in Patients with Advanced Solid Tumors

Author

Juric, Dejan, primary, Krop, Ian, primary, Ramanathan, Ramesh K., primary, Wilson, Timothy R., primary, Ware, Joseph A., primary, Sanabria Bohorquez, Sandra M., primary, Savage, Heidi M., primary, Sampath, Deepak, primary, Salphati, Laurent, primary, Lin, Ray S., primary, Jin, Huan, primary, Parmar, Hema, primary, Hsu, Jerry Y., primary, Von Hoff, Daniel D., primary, and Baselga, José, primary

Published
2023
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41. Data from Machine-Learning and Chemicogenomics Approach Defines and Predicts Cross-Talk of Hippo and MAPK Pathways

Author

Pham, Trang H., primary, Hagenbeek, Thijs J., primary, Lee, Ho-June, primary, Li, Jason, primary, Rose, Christopher M., primary, Lin, Eva, primary, Yu, Mamie, primary, Martin, Scott E., primary, Piskol, Robert, primary, Lacap, Jennifer A., primary, Sampath, Deepak, primary, Pham, Victoria C., primary, Modrusan, Zora, primary, Lill, Jennie R., primary, Klijn, Christiaan, primary, Malek, Shiva, primary, Chang, Matthew T., primary, and Dey, Anwesha, primary

Published
2023
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42. Figure S1 from RTK-Dependent Inducible Degradation of Mutant PI3Kα Drives GDC-0077 (Inavolisib) Efficacy

Author

Song, Kyung W., primary, Edgar, Kyle A., primary, Hanan, Emily J., primary, Hafner, Marc, primary, Oeh, Jason, primary, Merchant, Mark, primary, Sampath, Deepak, primary, Nannini, Michelle A., primary, Hong, Rebecca, primary, Phu, Lilian, primary, Forrest, William F., primary, Stawiski, Eric, primary, Schmidt, Stephen, primary, Endres, Nicholas, primary, Guan, Jane, primary, Wallin, Jeffrey J., primary, Cheong, Jonathan, primary, Plise, Emile G., primary, Lewis Phillips, Gail D., primary, Salphati, Laurent, primary, Heffron, Timothy P., primary, Olivero, Alan G., primary, Malek, Shiva, primary, Staben, Steven T., primary, Kirkpatrick, Donald S., primary, Dey, Anwesha, primary, and Friedman, Lori S., primary

Published
2023
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44. Data from Combined MEK and BCL-2/XL Inhibition Is Effective in High-Grade Serous Ovarian Cancer Patient–Derived Xenograft Models and BIM Levels Are Predictive of Responsiveness

Author

Iavarone, Claudia, primary, Zervantonakis, Ioannis K., primary, Selfors, Laura M., primary, Palakurthi, Sangeetha, primary, Liu, Joyce F., primary, Drapkin, Ronny, primary, Matulonis, Ursula A., primary, Hallberg, Dorothy, primary, Velculescu, Victor E., primary, Leverson, Joel D., primary, Sampath, Deepak, primary, Mills, Gordon B., primary, and Brugge, Joan S., primary

Published
2023
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45. Supplementary Figure 4 from Expression Profile of BCL-2, BCL-XL, and MCL-1 Predicts Pharmacological Response to the BCL-2 Selective Antagonist Venetoclax in Multiple Myeloma Models

Author

Punnoose, Elizabeth A., primary, Leverson, Joel D., primary, Peale, Franklin, primary, Boghaert, Erwin R., primary, Belmont, Lisa D., primary, Tan, Nguyen, primary, Young, Amy, primary, Mitten, Michael, primary, Ingalla, Ellen, primary, Darbonne, Walter C., primary, Oleksijew, Anatol, primary, Tapang, Paul, primary, Yue, Peng, primary, Oeh, Jason, primary, Lee, Leslie, primary, Maiga, Sophie, primary, Fairbrother, Wayne J., primary, Amiot, Martine, primary, Souers, Andrew J., primary, and Sampath, Deepak, primary

Published
2023
Full Text
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46. Supplementary Figures from Venetoclax Increases Intratumoral Effector T Cells and Antitumor Efficacy in Combination with Immune Checkpoint Blockade

Author

Kohlhapp, Frederick J., primary, Haribhai, Dipica, primary, Mathew, Rebecca, primary, Duggan, Ryan, primary, Ellis, Paul A., primary, Wang, Rui, primary, Lasater, Elisabeth A., primary, Shi, Yan, primary, Dave, Nimita, primary, Riehm, Jacob J., primary, Robinson, Valerie A., primary, Do, An D., primary, Li, Yijin, primary, Orr, Christine J., primary, Sampath, Deepak, primary, Raval, Aparna, primary, Merchant, Mark, primary, Bhathena, Anahita, primary, Salem, Ahmed Hamed, primary, Hamel, Keith M., primary, Leverson, Joel D., primary, Donawho, Cherrie, primary, Pappano, William N., primary, and Uziel, Tamar, primary

Published
2023
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47. Figures S1-S4, Tables S1-S2 from An Anti-GDNF Family Receptor Alpha 1 (GFRA1) Antibody–Drug Conjugate for the Treatment of Hormone Receptor–Positive Breast Cancer

Author

Bhakta, Sunil, primary, Crocker, Lisa M., primary, Chen, Yvonne, primary, Hazen, Meredith, primary, Schutten, Melissa M., primary, Li, Dongwei, primary, Kuijl, Coenraad, primary, Ohri, Rachana, primary, Zhong, Fiona, primary, Poon, Kirsten A., primary, Go, Mary Ann T., primary, Cheng, Eric, primary, Piskol, Robert, primary, Firestein, Ron, primary, Fourie-O'Donohue, Aimee, primary, Kozak, Katherine R., primary, Raab, Helga, primary, Hongo, Jo-Anne, primary, Sampath, Deepak, primary, Dennis, Mark S., primary, Scheller, Richard H., primary, Polakis, Paul, primary, and Junutula, Jagath R., primary

Published
2023
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48. Supplementary Figure 3 from Expression Profile of BCL-2, BCL-XL, and MCL-1 Predicts Pharmacological Response to the BCL-2 Selective Antagonist Venetoclax in Multiple Myeloma Models

Author

Punnoose, Elizabeth A., primary, Leverson, Joel D., primary, Peale, Franklin, primary, Boghaert, Erwin R., primary, Belmont, Lisa D., primary, Tan, Nguyen, primary, Young, Amy, primary, Mitten, Michael, primary, Ingalla, Ellen, primary, Darbonne, Walter C., primary, Oleksijew, Anatol, primary, Tapang, Paul, primary, Yue, Peng, primary, Oeh, Jason, primary, Lee, Leslie, primary, Maiga, Sophie, primary, Fairbrother, Wayne J., primary, Amiot, Martine, primary, Souers, Andrew J., primary, and Sampath, Deepak, primary

Published
2023
Full Text
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49. Supplementary Table 1 from Expression Profile of BCL-2, BCL-XL, and MCL-1 Predicts Pharmacological Response to the BCL-2 Selective Antagonist Venetoclax in Multiple Myeloma Models

Author

Punnoose, Elizabeth A., primary, Leverson, Joel D., primary, Peale, Franklin, primary, Boghaert, Erwin R., primary, Belmont, Lisa D., primary, Tan, Nguyen, primary, Young, Amy, primary, Mitten, Michael, primary, Ingalla, Ellen, primary, Darbonne, Walter C., primary, Oleksijew, Anatol, primary, Tapang, Paul, primary, Yue, Peng, primary, Oeh, Jason, primary, Lee, Leslie, primary, Maiga, Sophie, primary, Fairbrother, Wayne J., primary, Amiot, Martine, primary, Souers, Andrew J., primary, and Sampath, Deepak, primary

Published
2023
Full Text
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50. Supplementary Table 1 from Combined MEK and BCL-2/XL Inhibition Is Effective in High-Grade Serous Ovarian Cancer Patient–Derived Xenograft Models and BIM Levels Are Predictive of Responsiveness

Author

Iavarone, Claudia, primary, Zervantonakis, Ioannis K., primary, Selfors, Laura M., primary, Palakurthi, Sangeetha, primary, Liu, Joyce F., primary, Drapkin, Ronny, primary, Matulonis, Ursula A., primary, Hallberg, Dorothy, primary, Velculescu, Victor E., primary, Leverson, Joel D., primary, Sampath, Deepak, primary, Mills, Gordon B., primary, and Brugge, Joan S., primary

Published
2023
Full Text
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