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Full-Text Articles in Medicine and Health Sciences
Molecular Mechanisms Of Resistance To Kinase Inhibitors And Redifferentiation In Thyroid Cancers, Marie-Claude Hofmann, Muthusamy Kunnimalaiyaan, Jennifer R Wang, Naifa L Busaidy, Steven I Sherman, Stephen Y Lai, Mark Zafereo, Maria E Cabanillas
Molecular Mechanisms Of Resistance To Kinase Inhibitors And Redifferentiation In Thyroid Cancers, Marie-Claude Hofmann, Muthusamy Kunnimalaiyaan, Jennifer R Wang, Naifa L Busaidy, Steven I Sherman, Stephen Y Lai, Mark Zafereo, Maria E Cabanillas
Student and Faculty Publications
Protein kinases play critical roles in cell survival, proliferation and motility. Their dysregulation is therefore a common feature in the pathogenesis of a number of solid tumors, including thyroid cancers. Inhibiting activated protein kinases has revolutionized thyroid cancer therapy, offering a promising strategy in treating tumors refractory to radioactive iodine treatment or cytotoxic chemotherapies. However, despite satisfactory early responses, these drugs are not curative and most patients inevitably progress due to drug resistance. This review summarizes up-to-date knowledge on various mechanisms that thyroid cancer cells develop to bypass protein kinase inhibition and outlines strategies that are being explored to overcome …
Ros And Mirna Dysregulation In Ovarian Cancer Development, Angiogenesis And Therapeutic Resistance, David C Stieg, Yifang Wang, Ling-Zhi Liu, Bing-Hua Jiang
Ros And Mirna Dysregulation In Ovarian Cancer Development, Angiogenesis And Therapeutic Resistance, David C Stieg, Yifang Wang, Ling-Zhi Liu, Bing-Hua Jiang
Kimmel Cancer Center Faculty Papers
The diverse repertoires of cellular mechanisms that progress certain cancer types are being uncovered by recent research and leading to more effective treatment options. Ovarian cancer (OC) is among the most difficult cancers to treat. OC has limited treatment options, especially for patients diagnosed with late-stage OC. The dysregulation of miRNAs in OC plays a significant role in tumorigenesis through the alteration of a multitude of molecular processes. The development of OC can also be due to the utilization of endogenously derived reactive oxygen species (ROS) by activating signaling pathways such as PI3K/AKT and MAPK. Both miRNAs and ROS are …
Met Inhibition Sensitizes Rhabdomyosarcoma Cells To Notch Signaling Suppression, Clara Perrone, Silvia Pomella, Matteo Cassandri, Michele Pezzella, Giuseppe Maria Milano, Marta Colletti, Cristina Cossetti, Giulia Pericoli, Angela Di Giannatale, Emmanuel De Billy, Maria Vinci, Stefania Petrini, Francesco Marampon, Concetta Quintarelli, Riccardo Taulli, Josep Roma, Soledad Gallego, Simona Camero, Paolo Mariottini, Manuela Cervelli, Roberta Maestro, Lucio Miele, Biagio De Angelis, Franco Locatelli, Rossella Rota
Met Inhibition Sensitizes Rhabdomyosarcoma Cells To Notch Signaling Suppression, Clara Perrone, Silvia Pomella, Matteo Cassandri, Michele Pezzella, Giuseppe Maria Milano, Marta Colletti, Cristina Cossetti, Giulia Pericoli, Angela Di Giannatale, Emmanuel De Billy, Maria Vinci, Stefania Petrini, Francesco Marampon, Concetta Quintarelli, Riccardo Taulli, Josep Roma, Soledad Gallego, Simona Camero, Paolo Mariottini, Manuela Cervelli, Roberta Maestro, Lucio Miele, Biagio De Angelis, Franco Locatelli, Rossella Rota
School of Medicine Faculty Publications
Rhabdomyosarcoma (RMS) is a pediatric myogenic soft tissue sarcoma. The Fusion-Positive (FP) subtype expresses the chimeric protein PAX3-FOXO1 (P3F) while the Fusion-Negative (FN) is devoid of any gene translocation. FP-RMS and metastatic FN-RMS are often unresponsive to conventional therapy. Therefore, novel therapeutic approaches are needed to halt tumor progression. NOTCH signaling has oncogenic functions in RMS and its pharmacologic inhibition through γ-secretase inhibitors blocks tumor growth in vitro and in vivo. Here, we show that NOTCH signaling blockade resulted in the up-regulation and phosphorylation of the MET oncogene in both RH30 (FP-RMS) and RD (FN-RMS) cell lines. Pharmacologic inhibition of …
Ras-Mediated Tumor Stress Adaptation And The Targeting Opportunities It Presents, Alexandra Redding, A E Aplin, Elda Grabocka
Ras-Mediated Tumor Stress Adaptation And The Targeting Opportunities It Presents, Alexandra Redding, A E Aplin, Elda Grabocka
Department of Cancer Biology Faculty Papers
Cellular stress is known to function in synergistic cooperation with oncogenic mutations during tumorigenesis to drive cancer progression. Oncogenic RAS is a strong inducer of a variety of pro-tumorigenic cellular stresses, and also enhances the ability of cells to tolerate these stresses through multiple mechanisms. Many of these oncogenic, RAS-driven, stress-adaptive mechanisms have also been implicated in tolerance and resistance to chemotherapy and to therapies that target the RAS pathway. Understanding how oncogenic RAS shapes cellular stress adaptation and how this functions in drug resistance is of vital importance for identifying new therapeutic targets and therapeutic combinations to treat RAS-driven …