克拉斯
结直肠癌
癌症研究
突变
癌症
医学
生物
靶向治疗
基因
生物信息学
遗传学
作者
Alessandro Ottaiano,Francesco Sabbatino,Francesco Perri,Marco Cascella,Roberto Sirica,Renato Patrone,Maurizio Capuozzo,Giovanni Savarese,Monica Ianniello,Nadia Petrillo,Luisa Circelli,Vincenza Granata,Massimiliano Berretta,Mariachiara Santorsola,Guglielmo Nasti
出处
期刊:Cancers
[MDPI AG]
日期:2023-07-12
卷期号:15 (14): 3579-3579
被引量:4
标识
DOI:10.3390/cancers15143579
摘要
KRAS is frequently mutated in tumors. It is mutated in approximately 30% of all cancer cases and in nearly 50% of cases of metastatic colorectal cancer (CRC), which is the third leading cause of cancer-related deaths worldwide. Recent advancements in understanding CRC biology and genetics have highlighted the significance of KRAS mutations in the progression of CRC. The KRAS gene encodes a small GTPase (Guanosine TriPhosphatases) that plays a key role in signaling pathways associated with important proteins involved in amplifying growth factor and receptor signals. Mutations in KRAS are frequently observed in codons 12 and 13, and these mutations have oncogenic properties. Abnormal activation of KRAS proteins strongly stimulates signals associated with various cancer-related processes in CRC, including cell proliferation, migration and neoangiogenesis. In this review, we explore the distinct prognostic implications of KRAS mutations. Specifically, the KRAS p.G12C mutation is associated with a worse prognosis in metastatic CRC. The correlation between structure, conformation and mutations is visually presented to emphasize how alterations in individual amino acids at the same position in a single protein can unexpectedly exhibit complex involvement in cancer. Last, KRAS p.G12C is discussed as an emerging and promising therapeutic target in metastatic CRC, providing a concise overview of available clinical data regarding the use of new inhibitors.
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