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(ANN 118119, A.C) and the MedinProt Program of the Hungarian Academy of Sciences (L.B.). The work of V.V. was supported by a János Bolyai Research Scholarship of the Hungarian Academy of Sciences.\nInstitute of Enzymology, Research Centre for Natural Sciences, Budapest, Hungary \n Department of Medical Chemistry, Semmelweis University Medical School, Budapest, Hungary \n Export Date: 4 January 2021 \n CODEN: CMRED \n Correspondence Address: Vas, V.; Institute of Enzymology, Research Centre for Natural SciencesHungary; email: vas.virag@ttk.hu \n Funding details: Magyar Tudományos Akadémia, MTA \n Funding details: K 124045, HunProEx 2018-1.2.1-NKP-2018-00005, ANN 118119, FIEK_16-1-2016-0005 \n Funding text 1: Open access funding provided by ELKH Research Centre for Natural Sciences. This work was supported by the grants from the National Research, Development and Innovation Fund of Hungary (K 124045, FIEK_16-1-2016-0005, HunProEx 2018-1.2.1-NKP-2018-00005, L.B.) 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Ras is a key molecule that controls several tumorigenesis-related processes, and mutations in RAS genes often lead to unbiased intensification of signaling networks that fuel cancer progression. In this article, we review recent studies that describe mutant Ras-regulated signaling routes and their cross-talk. In addition to the two main Ras-driven signaling pathways, i.e., the RAF/MEK/ERK and PI3K/AKT/mTOR pathways, we have also collected emerging data showing the importance of Ras in other signaling pathways, including the RAC/PAK, RalGDS/Ral, and PKC/PLC signaling pathways. Moreover, microRNA-regulated Ras-associated signaling pathways are also discussed to highlight the importance of Ras regulation in cancer. Finally, emerging data show that the signal alterations in specific cell types, such as cancer stem cells, could promote cancer development. 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