Results 51 to 60 of about 845,274 (281)

Targeting the eIF4A RNA helicase blocks translation of the MUC1-C oncoprotein [PDF]

, 2012
The oncogenic MUC1-C subunit is aberrantly overexpressed in most human breast cancers by mechanisms that are not well understood. The present studies demonstrate that stimulation of non- malignant MCF-10A cells with epidermal growth factor (EGF) or ...
Jin, Caining, Kufe, Donald, Porco, John A., Rajabi, Hasan, Rodrigo, Christina M.   +4 more
core   +1 more source

Cis‐regulatory and long noncoding RNA alterations in breast cancer – current insights, biomarker utility, and the critical need for functional validation

Molecular Oncology, EarlyView.
The noncoding region of the genome plays a key role in regulating gene expression, and mutations within these regions are capable of altering it. Researchers have identified multiple functional noncoding mutations associated with increased cancer risk in the genome of breast cancer patients.
Arnau Cuy Saqués, Aracele Martinez‐Mendez, John Crown, Alex Eustace   +3 more
wiley   +1 more source

cAMP-PKA/EPAC signaling and cancer: the interplay in tumor microenvironment

Journal of Hematology & Oncology
Cancer is a complex disease resulting from abnormal cell growth that is induced by a number of genetic and environmental factors. The tumor microenvironment (TME), which involves extracellular matrix, cancer-associated fibroblasts (CAF), tumor ...
Hongying Zhang, Yongliang Liu, Jieya Liu, Jinzhu Chen, Jiao Wang, Hui Hua, Yangfu Jiang   +6 more
doaj   +1 more source

Author Correction: Lysyl oxidase drives tumour progression by trapping EGF receptors at the cell surface

Nature Communications, 2019
An amendment to this paper has been published and can be accessed via a link at the top of the paper.
HaoRan Tang, Leo Leung, Grazia Saturno, Amaya Viros, Duncan Smith, Gianpiero Di Leva, Eamonn Morrison, Dan Niculescu-Duvaz, Filipa Lopes, Louise Johnson, Nathalie Dhomen, Caroline Springer, Richard Marais   +12 more
doaj   +1 more source

Emerging Roles of Hydrogen Sulfide in Inflammatory and Neoplastic Colonic Diseases

Frontiers in Physiology, 2016
Hydrogen sulfide (H2S) is a toxic gas that has been recognized as an important mediator of many physiological processes, such as neurodegeneration, regulation of inflammation and blood pressure, and metabolism. In the human colon, H2S is produced by both
Fang fang eGuo, Ta chung eYu, Jie eHong, Jingyuan eFang   +3 more
doaj   +1 more source

Potential therapeutic targeting of BKCa channels in glioblastoma treatment

Molecular Oncology, EarlyView.
This review summarizes current insights into the role of BKCa and mitoBKCa channels in glioblastoma biology, their potential classification as oncochannels, and the emerging pharmacological strategies targeting these channels, emphasizing the translational challenges in developing BKCa‐directed therapies for glioblastoma treatment.
Kamila Maliszewska‐Olejniczak, Karolina Pytlak, Sandra Jaworowska, Bogusz Kulawiak, Piotr Bednarczyk   +4 more
wiley   +1 more source

SUMOylation inhibits FOXM1 activity and delays mitotic transition [PDF]

, 2014
The forkhead box transcription factor FOXM1 is an essential effector of G2/M-phase transition, mitosis and the DNA damage response. As such, it is frequently deregulated during tumorigenesis. Here we report that FOXM1 is dynamically modified by SUMO1 but
Brosens, Jan J., Coombes, R. C., Dunsby, C. W., French, P. M., Gomes, Ana R., Karunarathna, U., Kelly, D. J., Khongkow, P., Kongsema, M., Lam, Eric W.-F., Langer, J. K., Man, Cornelia W-Y., Myatt, Stephen S., Zona, Stefania   +13 more
core   +1 more source

Exploiting metabolic adaptations to overcome dabrafenib treatment resistance in melanoma cells

Molecular Oncology, EarlyView.
We show that dabrafenib‐resistant melanoma cells undergo mitochondrial remodeling, leading to elevated respiration and ROS production balanced by stronger antioxidant defenses. This altered redox state promotes survival despite mitochondrial damage but renders resistant cells highly vulnerable to ROS‐inducing compounds such as PEITC, highlighting redox
Silvia Eller, Susanne Ebner, Carmen Haselrieder, Julia K. Günther, Astrid Drasche, Sophie Strich, Chiara Volani, Andrea Medici, Aleksandar Nikolajevic, Alex Deltedesco, Johannes E. Sigmund, Michael J. Blumer, Martin Hermann, Johanna Vanacker, Gerald Brandacher, Eduard Stefan, Omar Torres‐Quesada, Jakob Troppmair   +17 more
wiley   +1 more source

Acute WNT signalling activation perturbs differentiation within the adult stomach and rapidly leads to tumour formation [PDF]

, 2013
A role for WNT signalling in gastric carcinogenesis has been suggested due to two major observations. First, patients with germline mutations in adenomatous polyposis coli (APC) are susceptible to stomach polyps and second, in gastric cancer, WNT ...
A Gregorieff, A Horii, A Jung, A Novak, AC de Vries, AN Milne, AT Franco, B Kim, B Tycko, C Cavard, D Athineos, D M Pritchard, DM Parkin, E Half, E Tahara, EF Chan, G Gatta, H Guillen-Ahlers, H Ireland, H Luche, H Nagase, H Oshima, H Shibata, H Watanabe, H Zhang, HC Zheng, HJ Freeman, J Cordero, J Neumann, J Parsonnet, J Woodgett, JG Forte, K Miyazawa, K Oien, KF Becker, KW Kinzler, LK Bianchi, M Crabtree, M Iida, M Nakayama, M Shitashige, M Suzuki, M Suzuki, M Torbenson, MG Smith, MP Ebert, N Barker, N Barker, N Barker, N Barker, N Barker, N Harada, N Murata-Kamiya, N Uemura, O J Sansom, O Sokolova, O Tetsu, OJ Sansom, P Blache, P Correa, P Correa, P Lauren, P Salgueiro, P Soriano, PJ Guilford, R A Ridgway, R Kemp, R Poulsom, S Garrean, S Nakatsuru, S Patel, S Patel, S Radulescu, S Segditsas, S Sekine, SC Abraham, SC Abraham, SM Przemeck, SS Ng, T Gnad, T Oda, TC He, WM Clements, WS Park, XC He, Y Miyoshi, Y Park do, Z Spicer, Z Zhao   +88 more
core   +1 more source

Recurrent cancer‐associated ERBB4 mutations are transforming and confer resistance to targeted therapies

Molecular Oncology, EarlyView.
We show that the majority of the 18 analyzed recurrent cancer‐associated ERBB4 mutations are transforming. The most potent mutations are activating, co‐operate with other ERBB receptors, and are sensitive to pan‐ERBB inhibitors. Activating ERBB4 mutations also promote therapy resistance in EGFR‐mutant lung cancer.
Veera K. Ojala, Sini Ahonen, Sara Peltola, Aura Tuohisto‐Kokko, Olaya Esparta, Peppi Suominen, Anne Jokilammi, Iman Farahani, Deepankar Chakroborty, Nikol Dibus, Steffen Boettcher, Tomi T. Airenne, Mark S. Johnson, Lisa D. Eli, Klaus Elenius, Kari J. Kurppa   +15 more
wiley   +1 more source