CV Lattes
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Secretaria da Saúde (São Paulo - Estado). Instituto Butantan (Institutional affiliation from the last research proposal) Birthplace: Brazil
Dr. Matheus Henrique Dias is a Senior Scientist at the Netherlands Cancer Institute (NKI). A biomedical scientist specializing in cancer research, his work focuses on developing a novel therapeutic strategy that leverages oncogenic signaling overactivation as a cancer treatment. He earned his PhD in Biochemistry from Universidade de São Paulo (USP) and completed postdoctoral training at Instituto Butantan, the University of Liverpool, and NKI.Dr. Dias is pioneering research that challenges conventional cancer therapies by exploiting the intrinsic vulnerabilities of malignant cells through oncogenic overactivation. His work has established a robust theoretical framework and generated substantial preclinical proof-of-concept data, laying the foundation for clinical translation. His research has been widely recognized, earning major publications, conference awards, and media coverage.Beyond his research, Dr. Dias chairs the European Association for Cancer Research (EACR) Early Career Researchers Council, is an active reviewer for scientific grants and awards, delivers lectures and engages in discussions with researchers and professionals in the healthcare and pharmaceutical sectors. Dr. Dias can be reached via email at matheusdias@iric.com.br. (Source: Lattes Curriculum)
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K-Ras, H-Ras e N-Ras are part of a family of small GTPases which work as "molecular switches" converting the activation of membrane receptors into activation of intracellular signaling pathways such as the MAPK pathway. Gain-of-function mutations in Ras proteins are found in about to 20% of all human tumors, frequently leading to bad prognosis. Among other proteins whose activity has been…
We propose that in Ras-driven malignant cells there is a functional interaction between cyclin D1 and this oncogene; in which the main function of cyclin D1 is to guarantee cell survival overcoming the Ras oncogenic stress. We showed in the presented reports that CRISPR-Cas9-mediated cyclin D1 depletion induces p53-independent senescence in Ras-driven carcinoma cells. Moreover, in MEFs cy…
| 1 / 1 | Completed scholarships in Brazil |
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