AI Article Synopsis
- The study found that mutations in oncNRAS, when induced at an early stage of embryonal rhabdomyosarcoma (ERMS), accelerate tumor growth but do not change tumor differentiation or initiate tumors.
- Earlier induction of oncNRAS at 2 weeks leads to shorter ERMS-free survival and a higher incidence of tumors compared to later induction.
- The research highlights that the impact of oncRAS mutations varies based on the specific isoform and the timing of their occurrence during tumor development.
Article Abstract
In the mouse model for embryonal rhabdomyosarcoma (ERMS), we recently showed that oncogenic (onc) H-, K- or NRAS mutations do not influence tumor growth when induced at the advanced, full-blown tumor stage. However, when induced at the invisible ERMS precursor stage at 4 weeks of age, tumor development was enforced upon oncHRAS and oncKRAS but not by oncNRAS, which instead initiated tumor differentiation. These data indicate that oncRAS-associated processes differ from each other in dependency on the isoform and their occurrence during tumor development. Here, we investigated the outcome of oncNRAS induction at an earlier ERMS precursor stage at 2 weeks of age. In this setting, oncNRAS accelerates tumor growth because it significantly shortens the ERMS-free survival and increases the ERMS incidence. However, it does not seem to alter the differentiation of the tumors. It is also not involved in tumor initiation. Together, these data show that oncNRAS mutations can accelerate tumor growth when targeting immature ERMS precursors within a specific time window, in which the precursors are permissive to the mutation and show that oncNRAS-associated processes differ from each other in dependency on their occurrence during tumor development.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8703790 | PMC |
| http://dx.doi.org/10.3390/ijms222413377 | DOI Listing |
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