Dr. Yijun Gao is a Professor and Principal Investigator at the State Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center. She received her Ph.D. from the Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, under the mentorship of Dr. Hongbin Ji. She subsequently completed her postdoctoral training with Dr. Neal Rosen at Memorial Sloan Kettering Cancer Center, where she later served as an Associate Research Scientist.

Dr. Gao’s research focuses on understanding how tumors adapt to RAS/MAPK-targeted therapies and progress from initial response through minimal residual disease to acquired resistance and relapse. Her laboratory investigates three interconnected stages of non-genetic resistance: therapy-induced lineage plasticity that enables tumor cells to enter drug-tolerant states; state-specific metabolic, epigenetic, and stress-response dependencies that sustain residual-cell survival and can be therapeutically exploited; and the mechanisms that enable residual persister cells to re-enter the cell cycle, expand under continued therapy, and progress toward acquired resistance. By integrating patient-derived organoids, patient-derived xenografts, genetically engineered mouse models, single-cell multi-omics, lineage tracing, functional genomic screening, and targeted perturbation, her team aims to constrain entry into drug tolerance, convert residual-cell tolerance into lethality, and block proliferative persister outgrowth before clinically established resistance emerges. Her work has been published in leading journals, including Cancer Cell, Nature Medicine, Cancer Discovery, Nature Communications, Cell Research, Signal Transduction and Targeted Therapy, and PNAS.

1. Zhang Y, Chen J, She Y, Zhang Y, Guo W, Liao J, Fang W, Pan X, Kang W,Wang Z, Wu Y, Deng R, Tian L, Wang L, Huang H, Zheng J, Yaeger R, Zhao Q#, Liao W#, Wang F#, Gao Y# . Paneth-like transition drives resistance to KRAS/EGER Dual Therapy in Colorectal Cancer. Cancer Cell. 2026 Jan 12;44(1):77-93.e8.

2. Guo Y, Zhong Y, Hu P, Chen Y, Guo W, Chen J, Guan P, Zhou Z, Zhu F, Zeng X, Gao J, Xiong Q, Yu Z, Hu C, Cai Z, Xie X, Hong J, Chan JY, Wang W, Diao D, Xia X, Yu Q, Ong CK, Gao Y# , Wu X# , Tan J# . Mevalonate pathway rewiring driven by enhancer remodelling confers resistance to KRAS inhibitors in colorectal cancer. Nat Commun. 2026 Jun 2. doi: 10.1038/s41467-026-73805-7. 

3. Yin G#, Huang J, Petela J, Jiang H, Zhang Y, Gong S, Wu J, Lv Q, Yang Z, Li D, Hou X, Yang  H, Sun Z, Yang Y, Cai N, Huang Y, Yi C, Xue H, Chen J, Ding P, Zhang X, Zhu X, Liu B, Shi J#, and Gao Y# . Targeting small GTPases: Emerging grasps on previously untamable targets, pioneered by KRAS. Signal Transduct Target Ther. 2023 May 23;8(1):212. doi:10.1038/s41392-023-01441-4.

4. Gao Y, Maria A, Na N, Paula A, Gorelick AN, Hechtman JF, Carson J, Lefkowitz RA, Weigelt B, Taylor BS, Zhao H, Reis-Filho JS, de Stanchina E, Rosen N, Yao Z and Yaeger R. V211D mutation in MEK1 causes resistance to MEK inhibitors  in colon cancer. Cancer Discov. 2019, DOI:10.1158/2159-8290.

5. Yao Z*, Gao Y*, Su W*, Yaeger R, Tao J, Na N, Zhang Y, Zhang C, Rymar A, Tao A, Timaul NM, Mcgriskin R, Outmezguine NA, Zhao H, Chang Q, Qeriqi B, Barbacid M, de  Stanchina E, Hyman DM, Bollag G, Rosen N. RAF inhibitor PLX8394 selectively disrupts BRAF dimers and RAS-independent BRAF-mutant-driven signaling. Nat Med. 2019, 25(2):284-291.

6. Gao Y, Chang MT, McKay D, Na N, Zhou B, Yaeger RD, Torres NM, Muniz K, Drosten M, Barbacid  M, Caponigro G, Stuart  D, Moebitz H, Solit DB, Abdel-Wahab O, Taylor BS, Yao Z, Rosen N. Allele-specific mechanisms of activation of MEK1 mutants determine their properties.  Cancer Discov. 2018, 8(5):648-661.

7. Zhang W*, Gao Y*, Li F, Tong X, Ren Y, Han X, Yao S, Long F, Yang Z, Fan H, Zhang L, Ji H. YAP promotes malignant progression of Lkb1-deficient lung adenocarcinoma through downstream regulation of survivin. Cancer Res. 2015, 75(21):4450-7.

8. Gao Y*, Zhang W*, Han X, Li F, Wang X, Wang R, Fang Z, Tong X, Yao S, Li F, Feng Y, Sun Y, Hou Y, Yang Z, Guan K, Chen H, Zhang L, Ji H. YAP inhibits squamous  transdifferentiation  of  Lkb1-deficient  lung  adenocarcinoma  through ZEB2-dependent DNp63 repression. Nat Commun. 2014 Aug  13;  5:4629. doi: 10.1038/ncomms5629.

9. Zhang W*, Gao Y*, Li P*, Shi Z, Guo T, Li F, Han X, Feng Y, Zheng C, Wang Z, Li  F,  Chen H, Zhou Z, Zhang L, Ji H.  VGLL4  functions  as  a  new  tumor suppressor in lung cancer by negatively regulating the YAP-TEAD transcriptional complex. Cell Res. 2014 Mar; 24(3):331-43.

10. Gao Y, Ge G, Ji H. LKB1 in lung cancerigenesis: a serine/threonine kinase as tumor suppressor. Protein & Cell. 2011, 2(2):99-107.

11. Gao Y*, Xiao Q*, Ma H*, Li L, Liu J, Feng Y, Fang Z, Wu J, Han X, Zhang J, Sun Y, Wu G, Padera R, Chen H, Wong KK, Ge G, Ji H. LKB1 inhibits lung cancer progression through  lysyl  oxidase  and  extracellular  matrix  remodeling. Proc Natl Acad Sci USA. 2010, 107(44):18892-7.