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Your search keyword '"Croessmann, S"' showing total 3 results
Start Over Author "Croessmann, S" Journal nature communications
3 results on '"Croessmann, S"'

1. Aberrant FGFR signaling mediates resistance to CDK4/6 inhibitors in ER+ breast cancer

Author

Valerie M. Jansen, Yao Lu, Paula Gonzalez Ericsson, Wei He, Luis J. Schwarz, Richard B. Lanman, Dhivya R. Sudhan, Yu Shyr, Teresa C. Dugger, Yan Guo, Carlos L. Arteaga, Marcelo Rocha Cruz, Alberto Servetto, Ingrid A. Mayer, Amir Behdad, Aditya Bardia, Luigi Formisano, Sarah Croessmann, Nadia Solovieff, Angel Guerrero-Zotano, Fei Su, Michelle Miller, Justin M. Balko, Mellissa J. Nixon, Joyce O'Shaughnessy, Ariella B. Hanker, Kyungmin Lee, Melinda E. Sanders, Massimo Cristofanilli, Joshua A. Bauer, Rebecca J. Nagy, Formisano, L, Lu, Y, Servetto, A, Hanker, Ab, Jansen, Vm, Bauer, Ja, Sudhan, Dr, Guerrero-Zotano, Al, Croessmann, S, Guo, Y, Ericsson, Pg, Lee, Km, Nixon, Mj, Schwarz, Lj, Sanders, Me, Dugger, Tc, Cruz, Mr, Behdad, A, Cristofanilli, M, Bardia, A, O'Shaughnessy, J, Nagy, Rj, Lanman, Rb, Solovieff, N, He, W, Miller, M, Su, F, Shyr, Y, Mayer, Ia, Balko, Jm, and Arteaga, Cl.

Subjects
0301 basic medicine, Pyridines, General Physics and Astronomy, Aminopyridines, 02 engineering and technology, Drug resistance, Tyrosine-kinase inhibitor, Piperazines, Circulating Tumor DNA, chemistry.chemical_compound, Mice, Erdafitinib, Antineoplastic Combined Chemotherapy Protocols, Cyclin D1, lcsh:Science, Abemaciclib, Fulvestrant, cancer cell, Multidisciplinary, drug, High-Throughput Nucleotide Sequencing, 021001 nanoscience & nanotechnology, Progression-Free Survival, 3. Good health, inhibitor, Receptors, Estrogen, MCF-7 Cells, Quinolines, Female, biological phenomena, cell phenomena, and immunity, 0210 nano-technology, medicine.drug, Signal Transduction, identification method, Antineoplastic Agents, Hormonal, medicine.drug_class, Science, Breast Neoplasms, Palbociclib, Naphthalenes, General Biochemistry, Genetics and Molecular Biology, Article, resistance, 03 medical and health sciences, Breast cancer, Quinoxalines, medicine, Animals, Humans, Progression-free survival, Receptor, Fibroblast Growth Factor, Type 1, Receptor, Fibroblast Growth Factor, Type 2, Protein Kinase Inhibitors, Proportional Hazards Models, business.industry, Cyclin-Dependent Kinase 4, General Chemistry, DNA, Cyclin-Dependent Kinase 6, medicine.disease, Xenograft Model Antitumor Assays, stomatognathic diseases, 030104 developmental biology, chemistry, Drug Resistance, Neoplasm, Purines, Mutation, Cancer research, Pyrazoles, lcsh:Q, survival tumor, business
Abstract

Using an ORF kinome screen in MCF-7 cells treated with the CDK4/6 inhibitor ribociclib plus fulvestrant, we identified FGFR1 as a mechanism of drug resistance. FGFR1-amplified/ER+ breast cancer cells and MCF-7 cells transduced with FGFR1 were resistant to fulvestrant ± ribociclib or palbociclib. This resistance was abrogated by treatment with the FGFR tyrosine kinase inhibitor (TKI) lucitanib. Addition of the FGFR TKI erdafitinib to palbociclib/fulvestrant induced complete responses of FGFR1-amplified/ER+ patient-derived-xenografts. Next generation sequencing of circulating tumor DNA (ctDNA) in 34 patients after progression on CDK4/6 inhibitors identified FGFR1/2 amplification or activating mutations in 14/34 (41%) post-progression specimens. Finally, ctDNA from patients enrolled in MONALEESA-2, the registration trial of ribociclib, showed that patients with FGFR1 amplification exhibited a shorter progression-free survival compared to patients with wild type FGFR1. Thus, we propose breast cancers with FGFR pathway alterations should be considered for trials using combinations of ER, CDK4/6 and FGFR antagonists., Era+ breast cancer patients often develop resistance to endocrine therapy. Here, the authors show that FGFR1 amplification is a resistance mechanism to CDK4/6 inhibitor and endocrine therapy and that combined treatment with FGFR, CDK4/6, and anti-estrogens is a potential therapeutic strategy in Era+ breast cancer tumors.

Published
2019

2. Single cell analysis of cribriform prostate cancer reveals cell intrinsic and tumor microenvironmental pathways of aggressive disease.

Author

Wong HY, Sheng Q, Hesterberg AB, Croessmann S, Rios BL, Giri K, Jackson J, Miranda AX, Watkins E, Schaffer KR, Donahue M, Winkler E, Penson DF, Smith JA, Herrell SD, Luckenbaugh AN, Barocas DA, Kim YJ, Graves D, Giannico GA, Rathmell JC, Park BH, Gordetsky JB, and Hurley PJ

Subjects
Apolipoproteins E, Extracellular Matrix Proteins, Humans, Ligands, Male, Neoplasm Grading, RNA, Receptors, Antigen, T-Cell, Single-Cell Analysis, Tumor Microenvironment genetics, Carcinoma, Intraductal, Noninfiltrating genetics, Prostatic Neoplasms pathology
Abstract

Cribriform prostate cancer, found in both invasive cribriform carcinoma (ICC) and intraductal carcinoma (IDC), is an aggressive histological subtype that is associated with progression to lethal disease. To delineate the molecular and cellular underpinnings of ICC/IDC aggressiveness, this study examines paired ICC/IDC and benign prostate surgical samples by single-cell RNA-sequencing, TCR sequencing, and histology. ICC/IDC cancer cells express genes associated with metastasis and targets with potential for therapeutic intervention. Pathway analyses and ligand/receptor status model cellular interactions among ICC/IDC and the tumor microenvironment (TME) including JAG1/NOTCH. The ICC/IDC TME is hallmarked by increased angiogenesis and immunosuppressive fibroblasts (CTHRC1 + ASPN + FAP + ENG + ) along with fewer T cells, elevated T cell dysfunction, and increased C1QB + TREM2 + APOE + -M2 macrophages. These findings support that cancer cell intrinsic pathways and a complex immunosuppressive TME contribute to the aggressive phenotype of ICC/IDC. These data highlight potential therapeutic opportunities to restore immune signaling in patients with ICC/IDC that may afford better outcomes., (© 2022. The Author(s).)

Published
2022
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3. Aberrant FGFR signaling mediates resistance to CDK4/6 inhibitors in ER+ breast cancer.

Author

Formisano L, Lu Y, Servetto A, Hanker AB, Jansen VM, Bauer JA, Sudhan DR, Guerrero-Zotano AL, Croessmann S, Guo Y, Ericsson PG, Lee KM, Nixon MJ, Schwarz LJ, Sanders ME, Dugger TC, Cruz MR, Behdad A, Cristofanilli M, Bardia A, O'Shaughnessy J, Nagy RJ, Lanman RB, Solovieff N, He W, Miller M, Su F, Shyr Y, Mayer IA, Balko JM, and Arteaga CL

Subjects
Aminopyridines administration & dosage, Aminopyridines pharmacology, Animals, Antineoplastic Agents, Hormonal administration & dosage, Antineoplastic Agents, Hormonal pharmacology, Breast Neoplasms genetics, Breast Neoplasms metabolism, Cyclin D1 metabolism, Cyclin-Dependent Kinase 4 antagonists & inhibitors, Cyclin-Dependent Kinase 6 antagonists & inhibitors, Drug Resistance, Neoplasm drug effects, Female, Fulvestrant administration & dosage, Fulvestrant pharmacology, High-Throughput Nucleotide Sequencing, Humans, MCF-7 Cells, Mice, Mutation, Naphthalenes pharmacology, Piperazines pharmacology, Progression-Free Survival, Proportional Hazards Models, Protein Kinase Inhibitors administration & dosage, Protein Kinase Inhibitors pharmacology, Purines administration & dosage, Purines pharmacology, Pyrazoles pharmacology, Pyridines pharmacology, Quinolines pharmacology, Quinoxalines pharmacology, Receptor, Fibroblast Growth Factor, Type 1 antagonists & inhibitors, Receptor, Fibroblast Growth Factor, Type 2 antagonists & inhibitors, Receptors, Estrogen metabolism, Signal Transduction, Xenograft Model Antitumor Assays, Antineoplastic Combined Chemotherapy Protocols therapeutic use, Breast Neoplasms drug therapy, Circulating Tumor DNA genetics, Drug Resistance, Neoplasm genetics, Receptor, Fibroblast Growth Factor, Type 1 genetics, Receptor, Fibroblast Growth Factor, Type 2 genetics
Abstract

Using an ORF kinome screen in MCF-7 cells treated with the CDK4/6 inhibitor ribociclib plus fulvestrant, we identified FGFR1 as a mechanism of drug resistance. FGFR1-amplified/ER+ breast cancer cells and MCF-7 cells transduced with FGFR1 were resistant to fulvestrant ± ribociclib or palbociclib. This resistance was abrogated by treatment with the FGFR tyrosine kinase inhibitor (TKI) lucitanib. Addition of the FGFR TKI erdafitinib to palbociclib/fulvestrant induced complete responses of FGFR1-amplified/ER+ patient-derived-xenografts. Next generation sequencing of circulating tumor DNA (ctDNA) in 34 patients after progression on CDK4/6 inhibitors identified FGFR1/2 amplification or activating mutations in 14/34 (41%) post-progression specimens. Finally, ctDNA from patients enrolled in MONALEESA-2, the registration trial of ribociclib, showed that patients with FGFR1 amplification exhibited a shorter progression-free survival compared to patients with wild type FGFR1. Thus, we propose breast cancers with FGFR pathway alterations should be considered for trials using combinations of ER, CDK4/6 and FGFR antagonists.

Published
2019
Full Text
View/download PDF

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