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6鏈堜唤锛孨ature Communications涓婂彂琛ㄧ殑棰樹负鈥淚dentification of metabolic vulnerabilities of receptor tyrosine kinases-driven cancer鈥濈殑鏂囩珷涓紝鐮旂┒鑰呬互闈炲皬缁嗚優鑲虹檶閲嶈鐨勫垎瀛愬垎鍨婨GFR绐佸彉鍜孎GFR鎵╁涓轰緥锛屼粠鍙椾綋閰皑閰告縺閰讹紙Receptor tyrosine kinase锛孯TK锛夊叆鎵嬶紝 杩愮敤澶氱绋冲畾鍚屼綅绱犳爣璁扮殑浠h阿缁勫鍜岃浆褰曠粍瀛︽妧鏈槓鏄庝簡涓嶅悓RTK椹卞姩鑲跨槫鐨勪唬璋緷璧栨€у強鍏惰浆褰曡皟鎺х殑鍒嗗瓙鏈哄埗锛岀郴缁熻瘉瀹炰簡EGFR绐佸彉鍜孎GFR鎵╁椹卞姩鑲跨槫鐨勪唬璋㈠急鐐广€傚叾涓紝EGFR绐佸彉鑲跨槫楂樺害渚濊禆涓濇皑閰稿悎鎴愰€氳矾锛岃€孎GFR鎵╁鑲跨槫渚濊禆涔抽吀鍚堟垚銆?/p>
鐮旂┒杩樺埄鐢ㄤ汉婧愯偪鐦ょ粍缁囨潵婧愮Щ妞嶇槫PDX妯″瀷锛岃瘉瀹炰簡EGFR绐佸彉鍜孎GFR鎵╁浣滀负涓濇皑閰镐唬璋㈠拰涔抽吀鍚堟垚鎶戝埗鍓傛晱鎰熸爣蹇楃墿鐨勫彲琛屾€э紝涓哄悓绫讳唬璋㈡姂鍒跺墏鐨勪釜鎬у寲娌荤枟鎻愪緵浜嗛噸瑕佷俊鎭紝涓轰唬璋㈡姂鍒跺墏鏁忔劅缇や綋鐮旂┒鎻愪緵浜嗘柊鐨勬€濊矾銆?/p>
1.p53 regulation of ammonia metabolism through urea cycle controls polyamine biosynthesis.
2.Extracellular Vesicle-packaged HIF-1伪-stabilizing LncRNA from Tumour-associated Macrophages Regulates Aerobic Glycolysis of Breast Cancer Cells.
3.Loss of BCAA Catabolism during Carcinogenesis Enhances mTORC1 Activity and Promotes Tumor Development and Progression.
4.Metagenomic and metabolomic analyses reveal distinct stage-specific phenotypes of the gut microbiota in colorectal cancer.
5.https://doi.org/10.1038/s41591-019-0423-5.
6.Identification of metabolic vulnerabilities of receptor tyrosine kinases-driven cancer
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璧炲姪鍚堜綔
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liushihao@360zhyx.com
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