Results overview: Found 3 records in 0.01 seconds.
Articles, 3 records found
Articles 3 records found  
1.
18 p, 8.3 MB Suppression of endogenous lipogenesis induces reversion of the malignant phenotype and normalized differentiation in breast cancer / Gonzalez-Guerrico, Anatilde M. (Department of Laboratory Medicine and Pathology, Division of Experimental Pathology, Mayo Clinic, Rochester, MN, USA) ; Espinoza, Ingrid (Department of Biochemistry, University of Mississippi Medical Center, Jackson, MS, USA) ; Schroeder, Barbara (Department of Laboratory Medicine and Pathology, Division of Experimental Pathology, Mayo Clinic, Rochester, MN, USA) ; Park, Cheol Hong (Department of Laboratory Medicine and Pathology, Division of Experimental Pathology, Mayo Clinic, Rochester, MN, USA) ; Chandra Mohan, KVP (Department of Laboratory Medicine and Pathology, Division of Experimental Pathology, Mayo Clinic, Rochester, MN, USA) ; Khurana, Ashwani (Department of Laboratory Medicine and Pathology, Division of Experimental Pathology, Mayo Clinic, Rochester, MN, USA) ; Corominas-Faja, Bruna (Molecular Oncology Group, Girona Biomedical Research Institute (IDIBGI), Girona, Spain) ; Cuyàs, Elisabet (Molecular Oncology Group, Girona Biomedical Research Institute (IDIBGI), Girona, Spain) ; Alarcón, Tomás (Universitat Autònoma de Barcelona. Departament de Matemàtiques) ; Kleer, Celina (Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA) ; Menendez, Javier A. (Molecular Oncology Group, Girona Biomedical Research Institute (IDIBGI), Girona, Spain) ; Lupu, Ruth (Mayo Clinic Cancer Center, Rochester, MN, USA)
The correction of specific signaling defects can reverse the oncogenic phenotype of tumor cells by acting in a dominant manner over the cancer genome. Unfortunately, there have been very few successful attempts at identifying the primary cues that could redirect malignant tissues to a normal phenotype. [...]
2016 - 10.18632/oncotarget.9463
Oncotarget, Vol. 7 (may 2016) , p. 71151-71168  
2.
11 p, 2.4 MB Oncometabolic nuclear reprogramming of cancer stemness / Menendez, Javier A. (Institut Català d'Oncologia) ; Corominas-Faja, Bruna (Institut d'Investigació Biomèdica de Girona) ; Cuyàs, Elisabet (Institut d'Investigació Biomèdica de Girona) ; García, María G. (Instituto Universitario de Oncología del Principado de Asturias) ; Fernández-Arroyo, Salvador (Hospital Universitari de Sant Joan) ; Fernández, Agustín F. (Instituto Universitario de Oncología del Principado de Asturias) ; Joven, Jorge (Hospital Universitari de Sant Joan) ; Fraga, Mario F. (Instituto Universitario de Oncología del Principado de Asturias) ; Alarcón Cor, Tomás (Centre de Recerca Matemàtica)
By impairing histone demethylation and locking cells into a reprogramming-prone state, oncometabolites can partially mimic the process of induced pluripotent stem cell generation. Using a systems biology approach, combining mathematical modeling, computation, and proof-of-concept studies with live cells, we found that an oncometabolite-driven pathological version of nuclear reprogramming increases the speed and efficiency of dedifferentiating committed epithelial cells into stem-like states with only a minimal core of stemness transcription factors. [...]
2016 - 10.1016/j.stemcr.2015.12.012
Stem cell reports, Vol. 6, issue 3 (March 2016) , p. 273-283  
3.
4 p, 1.6 MB Metabostemness : metaboloepigenetic reprogramming of cancer stem-cell functions / Menendez, Javier A. (Institut Català d'Oncologia) ; Corominas-Faja, Bruna (Institut Català d'Oncologia) ; Cuyàs Navarro, Elisabet (Institut Català d'Oncologia) ; Alarcón Cor, Tomás (Centre de Recerca Matematica)
Cancer researchers are currently embarking on one of their field's biggest challenges, namely the understanding of how cellular metabolism or certain classes of elite metabolites (e. g. , oncometabolites) can directly influence chromatin structure and the functioning of epi-transcriptional circuits to causally drive tumour formation. [...]
2014
Oncoscience, Vol. 1 (Dec. 2014) , p. 803-806  

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