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27 p, 3.0 MB |
A multiscale model of epigenetic heterogeneity-driven cell fate decision-making
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Folguera Blasco, Núria (Universitat Autònoma de Barcelona. Departament de Matemàtiques) ;
Pérez Carrasco, Rubén (University College London. Department of Mathematics) ;
Cuyàs, Elisabet (Institut d'Investigació Biomèdica de Girona) ;
Menendez, Javier A. (Institut d'Investigació Biomèdica de Girona) ;
Alarcón Cor, Tomás (Universitat Autònoma de Barcelona. Departament de Matemàtiques) ;
Universitat Autònoma de Barcelona.
Centre de Recerca Matemàtica
The inherent capacity of somatic cells to switch their phenotypic status in response to damage stimuli in vivo might have a pivotal role in ageing and cancer. However, how the entryexit mechanisms of phenotype reprogramming are established remains poorly understood. [...]
2019 -  10.1371/journal.pcbi.1006592
PLoS computational biology, Vol. 15, Issue 4 (April 2019) , art. e1006592
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19 p, 13.4 MB |
Germline BRCA1 mutation reprograms breast epithelial cell metabolism towards mitochondrial-dependent biosynthesis : evidence for metformin-based "starvation" strategies in BRCA1 carriers
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Cuyàs, Elisabet (Molecular Oncology Group, Girona Biomedical Research Institute (IDIBGI), Girona, Catalonia, Spain) ;
Fernández-Arroyo, Salvador (Hospital Universitari Sant Joan de Reus) ;
Alarcón, Tomás (Universitat Autònoma de Barcelona. Departament de Matemàtiques) ;
Joven, Jorge (Hospital Universitari Sant Joan de Reus) ;
Menendez, Javier A. (Molecular Oncology Group, Girona Biomedical Research Institute (IDIBGI), Girona, Catalonia, Spain)
We hypothesized that women inheriting one germline mutation of the BRCA1 gene ("one-hit") undergo cell-type-specific metabolic reprogramming that supports the high biosynthetic requirements of breast epithelial cells to progress to a fully malignant phenotype. [...]
2016 - 10.18632/oncotarget.9732
Oncotarget, Vol. 7 (may 2016) , p. 52974-52992
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18 p, 8.3 MB |
Suppression of endogenous lipogenesis induces reversion of the malignant phenotype and normalized differentiation in breast cancer
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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
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4.
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13 p, 3.9 MB |
Accelerated geroncogenesis in hereditary breast-ovarian cancer syndrome
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Menendez, Javier A. (Institut d'Investigació Biomèdica de Girona) ;
Folguera-Blasco, Núria (Centre de Recerca Matemàtica) ;
Cuyàs Navarro, Elisabet (Institut d'Investigació Biomèdica de Girona) ;
Fernández-Arroyo, Salvador (Hospital Universitari de Sant Joan) ;
Joven, Jorge (Hospital Universitari de Sant Joan) ;
Alarcón Cor, Tomás (Universitat Autònoma de Barcelona. Departament de Matemàtiques)
The geroncogenesis hypothesis postulates that the decline in metabolic cellular health that occurs naturally with aging drives a "field effect" predisposing normal tissues for cancer development. We propose that mutations in the cancer susceptibility genes BRCA1/2 might trigger "accelerated geroncogenesis" in breast and ovarian epithelia. [...]
2016 - 10.18632/oncotarget.7867
Oncotarget, Vol. 7, issue 11 (March 2016) , p. 11959-11971
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11 p, 2.4 MB |
Oncometabolic nuclear reprogramming of cancer stemness
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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
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