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Search Results to Marsha Rosner

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overview Cancer is the second leading cause of death but, unlike heart disease, it has been a difficult disease to effectively understand or treat. The reason relates to the complexity and heterogeneity of the disease. Most tumors have complicated origins and are driven by rare mutations. Furthermore, different tissues have distinct cancers, individual tissues have multiple cancer subtypes, and tumors are composed of cells that are both genetically and phenotypically diverse. Thus, every tumor is unique and dynamic. The cause of lethality in most solid tumors such as breast cancer is the metastatic dissemination of tumor cells throughout the body. Metastasis is characterized by many distinct properties that are driven by changing stresses in the tumor microenvironment. Underlying all of these events are subcellular signaling pathways within tumor and environmental cells that are ultimately responsible for driving cells to a tumorigenic state. The current focus of my laboratory is to understand fundamental signaling mechanisms leading to the generation of tumor cells and their progression to metastatic disease, particularly in triple-negative breast cancer that lacks targeted therapies. We use systems level approaches including activity-based proteomics, RNAseq, ChIPseq, and mass spectrometry as well as computational, molecular, biophysical, cellular and mouse model-based methodologies to identify and characterize key regulators of tumor growth and metastasis. As an additional tool, we have utilized a specific physiological suppressor of metastasis, Raf Kinase Inhibitory Protein (RKIP or PEBP1), and a downstream target of RKIP in cells, BACH1, to identify both molecular and cellular mediators of metastasis. Our recent studies have shown that regulators of metastasis control multiple processes within the tumor cell microenvironment including metabolism, redox state, extracellular matrix, and recruitment and programming of tumor-associated macrophages. These factors also direct extracellular vesicles (exosomes) secreted by tumor cells to reprogram other cells in the body toward a pro-metastatic phenotype. Correlating omic-generated data from these studies with clinical data from cancer patients led to the identification of novel signaling modules that we used to build gene signatures that predict the metastatic potential of a tumor. More recently, our studies have led us to potential therapeutic treatments based on the concept of targeting key regulators of tumorigenesis, mimicking the action of metastasis suppressors such as RKIP or reprogramming signaling networks in cells to sensitize tumors to therapeutic agents.

One or more keywords matched the following items that are connected to Rosner, Marsha

Item TypeName
Concept Transcription Factors
Concept E2F Transcription Factors
Concept Basic-Leucine Zipper Transcription Factors
Concept Gene Regulatory Networks
Concept Transcription Factor RelA
Academic Article Signalling pathway for RKIP and Let-7 regulates and predicts metastatic breast cancer.
Academic Article WT1 suppresses synthesis of the epidermal growth factor receptor and induces apoptosis.
Academic Article CDKL5/Stk9 kinase inactivation is associated with neuronal developmental disorders.
Academic Article A proline- and glutamine-rich protein promotes apoptosis in neuronal cells.
Academic Article mTOR phosphorylated at S2448 binds to raptor and rictor.
Academic Article Structural changes in intermediate filament networks alter the activity of insulin-degrading enzyme.
Academic Article Regulation of airway smooth muscle cyclin D1 transcription by protein kinase C-delta.
Academic Article NF-kappaB is required for UV-induced JNK activation via induction of PKCdelta.
Academic Article MicroRNA-regulated feed forward loop network.
Academic Article Embryoid body formation of human amniotic fluid stem cells depends on mTOR.
Academic Article Cyclin D1 is required for S phase traversal in bovine tracheal myocytes.
Academic Article Raf and fibroblast growth factor phosphorylate Elk1 and activate the serum response element of the immediate early gene pip92 by mitogen-activated protein kinase-independent as well as -dependent signaling pathways.
Academic Article An integrated view of cyclin E function and regulation.
Academic Article A prognostic gene signature for metastasis-free survival of triple negative breast cancer patients.
Academic Article Network of mutually repressive metastasis regulators can promote cell heterogeneity and metastatic transitions.
Academic Article Raf kinase inhibitory protein (RKIP) as a metastasis suppressor: regulation of signaling networks in cancer.
Academic Article Effective breast cancer combination therapy targeting BACH1 and mitochondrial metabolism.

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