A hotspot mutation targeting the R-RAS2 GTPase acts as a potent oncogenic driver in a wide spectrum of tumors.
Isabel Fernández-Pisonero, Laura Clavaín, Javier Robles-Valero, L Francisco Lorenzo-Martín, Rubén Caloto, Blanca Nieto, Carmen García-Macías, Clara L Oeste, Manuel Sánchez-Martín, Antonio Abad, Alejandro Hortal, Dolores Caballero, Marcos González, Mercedes Dosil, Balbino Alarcón
March 2022 Cell RepSynopsis of Social media discussions
The discussions strongly support the publication’s findings, with posts describing the RRAS2 mutation as a 'potent oncogenic driver' and discussing its implications for therapy, indicating high agreement and perceived impact. The tone is enthusiastic, with words like 'advance' and 'potent,' and examples include mentions of how this discovery opens new treatment avenues, reflecting deep engagement and recognition of the research's significance.
Agreement
Strong agreementMost discussions express strong approval, highlighting the significance of the findings and their potential impact on cancer research.
Interest
High level of interestPosts show high curiosity and enthusiasm, often referencing exciting breakthroughs and advances in understanding tumor drivers.
Engagement
Moderate level of engagementMany comments reference detailed aspects such as the mutation’s role and therapeutic potential, indicating active and thoughtful engagement.
Impact
High level of impactThe discussions consistently emphasize the importance of the research, suggesting it could influence future cancer therapies and understanding of oncogenic processes.
Social Mentions
YouTube
4 Videos
25 Posts
News
4 Articles
Metrics
Video Views
3,306
Total Likes
75
Extended Reach
239,652
Social Features
33
Timeline: Posts about article
Top Social Media Posts
Posts referencing the article
New Oncogenic Gene RRAS2 and Its Therapeutic Vulnerabilities
This video summarizes a scientific article published by Xos Bustelo's team in Cell Reports, March 2022, identifying the RRAS2 gene mutation that promotes various cancers and exploring its mechanisms and potential treatments, with implications for other diseases like Noonan syndrome.
RRAS2 Mutation as a Potent Oncogenic Driver in Various Tumors
A mutation in the RRAS2 gene acts as a strong oncogenic driver across multiple tumor types. Recent research using a mouse model shows RRAS2 causes rapid tumor formation, primarily relying on the mTORC1 pathway for growth, offering potential therapeutic targets.
RRAS2 Mutation as a Broad-Oncogenic Driver in Tumors
A mutation in the RRAS2 gene acts as a potent oncogenic driver across various tumor types by promoting rapid tumor formation, primarily through the mTORC1 pathway. These tumors show unique responses to targeted therapies, offering potential treatment avenues.
RRAS2 Mutation as a Potent Oncogenic Driver in Tumors
This video summarizes a study published in Cell Reports revealing how mutations in the RRAS2 gene promote various cancers. Using a mouse model, the research shows RRAS2-driven tumors rely on the mTORC1 pathway, highlighting potential targeted therapies.
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RT @XRBustelo:
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Xose R Bustelo
@XRBustelo (Twitter)RT @XRBustelo:
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Xose R Bustelo
@XRBustelo (Twitter)RT @XRBustelo:
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Revista SEBBM
@SEBBM_Revista (Twitter)En @SEBBM_Revista n°212 -junio | Una mutación de RRAS2 actúa como potente inductor oncogénico | Fernández-Pisonero et al. @usal https://t.co/ApSRW6MxL3
view full postJuly 7, 2022
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Pablo Hortal
@PixVideos_ (Twitter)Identification of R-RAS2 as a new oncogenic driver https://t.co/4JjnogNvfV
view full postJune 4, 2022
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Xose R Bustelo
@XRBustelo (Twitter)RT @XRBustelo:
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Xose R Bustelo
@XRBustelo (Twitter)RT @XRBustelo:
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Xose R Bustelo
@XRBustelo (Twitter)RT @CICancer_com: Compartimos el vídeo que explica el avance del laboratorio de @XRBustelo que difundimos en https://t.co/T9iqZozLRd que es…
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Centro de Investigación del Cáncer/CSIC-USAL-FICUS
@ciccancer (Twitter)Compartimos el vídeo que explica el avance del laboratorio de @XRBustelo que difundimos en https://t.co/T9iqZozLRd que está disponible en nuestro canal de YouTube https://t.co/ZqtLfH3Odr
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BruzosAliciaL, Dr. (she/her)
@BruzosAliciaL (Twitter)RT @XRBustelo:
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Toni Celia-Terrassa
@TCeliaTerrassa (Twitter)RT @XRBustelo:
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Laura Quevedo
@lauriquepa (Twitter)RT @XRBustelo:
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Juan Rodriguez Vita
@J_RodriguezVita (Twitter)RT @XRBustelo:
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Luis Paz-Ares
@LuisPaz_Ares (Twitter)RT @XRBustelo:
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Marisol Soengas
@msmelanoma (Twitter)RT @XRBustelo:
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Grupo R Comunicación
@GrupoRComunica (Twitter)RT @XRBustelo:
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RamonReyes
@RamonReyesCC (Twitter)RT @XRBustelo:
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Javier Robles
@JaviRoblesV (Twitter)RT @XRBustelo:
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Conexión Cáncer CSIC
@CancerCSIC (Twitter)RT @XRBustelo:
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Xose R Bustelo
@XRBustelo (Twitter)May 26, 2022
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Xose R Bustelo
@XRBustelo (Twitter)May 26, 2022
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QiDa
@fast04050146 (Twitter)RT @CellReports: A hotspot mutation targeting the R-RAS2 GTPase acts as a potent oncogenic driver in a wide spectrum of tumors https://t.co…
view full postMarch 17, 2022
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Victoria Hendry
@HendryVictoria (Twitter)RT @CellReports: A hotspot mutation targeting the R-RAS2 GTPase acts as a potent oncogenic driver in a wide spectrum of tumors https://t.co…
view full postMarch 17, 2022
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Cell Reports
@CellReports (Twitter)A hotspot mutation targeting the R-RAS2 GTPase acts as a potent oncogenic driver in a wide spectrum of tumors https://t.co/DGGCSBaj6r
view full postMarch 17, 2022
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Xose R Bustelo
@XRBustelo (Twitter)❓Do you want to see the actual data ? If so, use this link
view full postMarch 16, 2022
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Abstract Synopsis
- A mutation in the RRAS2 gene, similar to known cancer-driving mutations in RAS proteins, acts as a strong oncogenic driver across various tumor types, but its specific role in tumor development in living organisms was previously unclear.
- Using a mouse model with an inducible RRAS2 mutation, researchers found that RRAS2 causes rapid tumor formation, which differs from tumors caused by classical RAS genes, and these tumors can be grouped based on their response to treatments.
- The study reveals that tumors driven by RRAS2 rely heavily on the mTORC1 pathway for growth, making it a promising target for therapy, especially since these tumors are independent of other common signaling pathways like PI3K, MEK, and Ral.]
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