RAS proto-oncogenes (HRAS, KRAS, and NRAS) are mutated in approximately 30% of human cancers and commonly associated with bad prognosis and resistance to frontline standard therapies. The dogma describing RAS as “undruggable” has been recently questioned by the development of pharmacological agents that specifically target the KRAS(G12C) mutant protein. However, the complexity of RAS downstream signaling and feedback mechanisms, the limited applicability of these inhibitors to G12C-mutant tumors, the different response rates observed between different cancer types and the early progression observed in some patients suggest that targeting a single pathway component might be not effective. To this purpose 1) better deciphering mutant RAS-regulated pathways and their cross-talk; 2) understanding the contribution of WT RAS to Mutant RAS-Driven Cancers; 3) investigating the effects of cancer clonal evolution on the positive and negative selection of RAS mutant subclones, 4) elucidating the relationship between cancer stem cells and RAS and 5) depicting RAS interactions with immunosuppressive microenvironment are some crucial points that still need to be addressed.
In this Research Topic, we welcome articles with a focus on (but not limited to) the following themes:
1) RAS dysregulated pathways in cancer
2) distinct roles of each Ras mutation in signal transduction;
3) novel therapeutic approaches that target RAS activation, including studies of drug combinations
4) Clonal evolution of RAS mutant cancers as assessed through liquid biopsies.
5) contribution of WT RAS clones to proliferation in RAS-mutated cancers
6) new approaches in HRAS-dependent cancers
7) Immune modulatory effects of oncogenic RAS in cancer
8) Metabolic reprogramming mediated by oncogenic RAS
We welcome submissions of Review, Mini-review, Original Research, Case reports and Clinical Trial articles which provide novel information about RAS driven cancers, mechanisms of resistance to new RAS inhibitors as assessed through liquid biopsy and new therapeutic strategies.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
RAS proto-oncogenes (HRAS, KRAS, and NRAS) are mutated in approximately 30% of human cancers and commonly associated with bad prognosis and resistance to frontline standard therapies. The dogma describing RAS as “undruggable” has been recently questioned by the development of pharmacological agents that specifically target the KRAS(G12C) mutant protein. However, the complexity of RAS downstream signaling and feedback mechanisms, the limited applicability of these inhibitors to G12C-mutant tumors, the different response rates observed between different cancer types and the early progression observed in some patients suggest that targeting a single pathway component might be not effective. To this purpose 1) better deciphering mutant RAS-regulated pathways and their cross-talk; 2) understanding the contribution of WT RAS to Mutant RAS-Driven Cancers; 3) investigating the effects of cancer clonal evolution on the positive and negative selection of RAS mutant subclones, 4) elucidating the relationship between cancer stem cells and RAS and 5) depicting RAS interactions with immunosuppressive microenvironment are some crucial points that still need to be addressed.
In this Research Topic, we welcome articles with a focus on (but not limited to) the following themes:
1) RAS dysregulated pathways in cancer
2) distinct roles of each Ras mutation in signal transduction;
3) novel therapeutic approaches that target RAS activation, including studies of drug combinations
4) Clonal evolution of RAS mutant cancers as assessed through liquid biopsies.
5) contribution of WT RAS clones to proliferation in RAS-mutated cancers
6) new approaches in HRAS-dependent cancers
7) Immune modulatory effects of oncogenic RAS in cancer
8) Metabolic reprogramming mediated by oncogenic RAS
We welcome submissions of Review, Mini-review, Original Research, Case reports and Clinical Trial articles which provide novel information about RAS driven cancers, mechanisms of resistance to new RAS inhibitors as assessed through liquid biopsy and new therapeutic strategies.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
