Colorectal cancer

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Specific inhibition of p110α subunit of PI3K: putative therapeutic strategy for KRAS mutant colorectal cancers

Authors and Affiliations:

Maria Sofia Fernandes1,2, Soraia Melo1,2,3, Sérgia Velho1,2, Patrícia Carneiro1,2, Fátima Carneiro1,2,3,4, Raquel Seruca1,2,3

8th European Multidisciplinary Colorectal Cancer Congress

RAI Amsterdam, Forum Centre, Amsterdam, Netherlands

 

11 - 13 December, 2016

 

See more informations here: http://www.emccc2016.org/en/Home_10_6_12.html

8th European Multidisciplinary Colorectal Cancer Congress

RAI Amsterdam, Forum Centre, Amsterdam, Netherlands

 

11 - 13 December, 2016

 

See more informations here: http://www.emccc2016.org/en/Home_10_6_12.html

Targeting the serrated pathway of colorectal cancer with mutation in BRAF

Paulo Matos (1-3), Vânia Gonçalves (2,3), Peter Jordan (2,3)

1. Department of Chemistry and Biochemistry, Faculty of Sciences, University of Lisbon, Portugal

2. BioISI — Biosystems & Integrative Sciences Institute, Faculty of Sciences, University of Lisbon, Portugal

3. Department of Human Genetics, National Health Institute ‘Dr. Ricardo Jorge’, Lisbon, Portugal

8th European Multidisciplinary Colorectal Cancer Congress

RAI, Amsterdam, Netherlands

 

11 - 13 December, 2016

 

See more informations here: http://www.emccc2016.org/en/Home_10_6_12.html

 

 

8th European Multidisciplinary Colorectal Cancer Congress

RAI, Amsterdam, Netherlands

 

11 - 13 December, 2016

 

See more informations here: http://www.emccc2016.org/en/Home_10_6_12.html

 

 

Colorectal cancer-related mutant KRAS alleles function as positive regulators of autophagy

O recente interesse para modular a autofagia na terapêutica do cancro tem sido dificultado pelo papel duplo deste processo catabólico no cancro, destacando a necessidade de abordagens personalizadas. Uma vez que as isoformas do RAS têm sido implicadas na regulação da autofagia e a mutação do oncogene KRAS é muito frequente no cancro colorretal (CCR), questionamos se/como os alelos mutados do KRAS regulam a autofagia no CCR e quais as suas implicações.

Expression of tumor-related Rac1b antagonizes BRAF-induced senescence in colorectal cells

Tumour initiation results from a mutation acquired, for example, in a cell proliferation-regulating oncogene, for example the MAP kinase BRAF in melanoma, thyroid, ovarian and colorectal cancer. As a protective response to this initial proliferative stimulus, tissues induce a growth-arrest program termed oncogene-induced senescence (OIS). It remains largely unknown by which mechanisms the initiated cells eventually escape from the dormant OIS state.

Expression of tumor-related Rac1b antagonizes BRAF-induced senescence in colorectal cells

Tumour initiation results from a mutation acquired, for example, in a cell proliferation-regulating oncogene, for example the MAP kinase BRAF in melanoma, thyroid, ovarian and colorectal cancer. As a protective response to this initial proliferative stimulus, tissues induce a growth-arrest program termed oncogene-induced senescence (OIS). It remains largely unknown by which mechanisms the initiated cells eventually escape from the dormant OIS state.

Cathepsin D protects colorectal cancer cells from acetate-induced apoptosis through degradation of damaged mitochondria

Authors and Affiliations:

Cláudia Suellen F. Oliveira (1,2), Helena Pereira (1), Sara Alves (1), Lisandra Castro (1), Fátima Baltazar (3,4), Susana R. Chaves (1), Ana Preto (1*), Manuela Côrte-Real (1*#)

(1) CBMA- Centro de Biologia Molecular e Ambiental. Departamento de Biologia, Universidade do Minho, Campus de Gualtar, 4710-057, Braga, Portugal.

(2) ICBAS - Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, 4050-313, Porto, Portugal.