%0 Journal Article %1 noauthororeditor %A Konishi, Takuma Hayashi | Nobuo Yaegashi | Ikuo %D 2023 %J INTERNATIONAL JOURNAL OF TREND IN SCIENTIFIC RESEARCH AND DEVELOPMENT %K Cancer EGFR Genome KRAS Medicine oncogenic variant %N 7 %P 457-460 %T RAS Mutations that Become Nonfunctional Kinase Activity %U https://www.ijtsrd.com/medicine/other/52365/ras-mutations-that-become-nonfunctional-kinase-activity/takuma-hayashi %V 6 %X The rat sarcoma viral oncogene homolog RAS family of closely related oncogenes KRAS, HRAS, and NRAS are the most frequently mutated drivers of malignant transformation. RAS family highly associates the epidermal growth factor receptor EGFR mainly. EGF selectively binds to EGFR and triggers the receptor to form a dimer that activates RAS. RAS transmits signals from activated trans membrane receptor EGFR to effectors in the B raf proto oncogene BRAF mitogen activated protein kinase MEK extracellular signal regulated kinase ERK signaling pathway in the cytoplasm. The status of RAS proteins is a negative predictive biomarker for anti EGFR therapy in metastatic colon cancer or other malignant tumors. In here, we report that our clinical studies revealed that splicing caused by the RAS mutations, which were considered oncogenic, generates unfunctional RAS family. Especially, Kirsten Rat Sarcoma KRAS silent variants are of concern to be a serious problem in genomic cancer medicine.The status of rat sarcoma viral oncogene homolog RAS proteins is a negative predictive biomarker for anti epidermal growth factor receptor EGFR therapy in metastatic colon cancer. In the phase 2 CHRONOS trial, patients with mutant gene s are ineligible for anti EGFR therapy.1,2 However, our studies revealed that splicing caused by the RAS mutations, which were considered oncogenic, generates unfunctional RAS family. Especially, Kirsten Rat Sarcoma KRAS silent variants are of concern to be a serious problem in genomic cancer medicine. Takuma Hayashi | Nobuo Yaegashi | Ikuo Konishi "RAS Mutations that Become Nonfunctional Kinase Activity" Published in International Journal of Trend in Scientific Research and Development (ijtsrd), ISSN: 2456-6470, Volume-6 | Issue-7 , December 2022, URL: https://www.ijtsrd.com/papers/ijtsrd52365.pdf Paper URL: https://www.ijtsrd.com/medicine/other/52365/ras-mutations-that-become-nonfunctional-kinase-activity/takuma-hayashi

@article{noauthororeditor, abstract = {The rat sarcoma viral oncogene homolog RAS family of closely related oncogenes KRAS, HRAS, and NRAS are the most frequently mutated drivers of malignant transformation. RAS family highly associates the epidermal growth factor receptor EGFR mainly. EGF selectively binds to EGFR and triggers the receptor to form a dimer that activates RAS. RAS transmits signals from activated trans membrane receptor EGFR to effectors in the B raf proto oncogene BRAF mitogen activated protein kinase MEK extracellular signal regulated kinase ERK signaling pathway in the cytoplasm. The status of RAS proteins is a negative predictive biomarker for anti EGFR therapy in metastatic colon cancer or other malignant tumors. In here, we report that our clinical studies revealed that splicing caused by the RAS mutations, which were considered oncogenic, generates unfunctional RAS family. Especially, Kirsten Rat Sarcoma KRAS silent variants are of concern to be a serious problem in genomic cancer medicine.The status of rat sarcoma viral oncogene homolog RAS proteins is a negative predictive biomarker for anti epidermal growth factor receptor EGFR therapy in metastatic colon cancer. In the phase 2 CHRONOS trial, patients with mutant gene s are ineligible for anti EGFR therapy.1,2 However, our studies revealed that splicing caused by the RAS mutations, which were considered oncogenic, generates unfunctional RAS family. Especially, Kirsten Rat Sarcoma KRAS silent variants are of concern to be a serious problem in genomic cancer medicine. Takuma Hayashi | Nobuo Yaegashi | Ikuo Konishi "RAS Mutations that Become Nonfunctional Kinase Activity" Published in International Journal of Trend in Scientific Research and Development (ijtsrd), ISSN: 2456-6470, Volume-6 | Issue-7 , December 2022, URL: https://www.ijtsrd.com/papers/ijtsrd52365.pdf Paper URL: https://www.ijtsrd.com/medicine/other/52365/ras-mutations-that-become-nonfunctional-kinase-activity/takuma-hayashi }, added-at = {2023-01-07T13:14:00.000+0100}, author = {Konishi, Takuma Hayashi | Nobuo Yaegashi | Ikuo}, biburl = {https://www.bibsonomy.org/bibtex/200a86adfffc42fecd705b2f80f473829/ijtsrd}, interhash = {975b0304b34bf32ee9d6af09ee70b7a2}, intrahash = {00a86adfffc42fecd705b2f80f473829}, issn = {2456-6470}, journal = {INTERNATIONAL JOURNAL OF TREND IN SCIENTIFIC RESEARCH AND DEVELOPMENT}, keywords = {Cancer EGFR Genome KRAS Medicine oncogenic variant}, language = {english}, month = jan, number = 7, pages = {457-460}, timestamp = {2023-01-07T13:14:00.000+0100}, title = {RAS Mutations that Become Nonfunctional Kinase Activity }, url = {https://www.ijtsrd.com/medicine/other/52365/ras-mutations-that-become-nonfunctional-kinase-activity/takuma-hayashi}, volume = 6, year = 2023 }