任瑞寶

中文名：任瑞寶

英文名：Ruibao Ren

性別：男

學(xué)位：博士（M.D./Ph.D.）

1992 u20131994 博士后，美國洛克菲勒大學(xué)David Baltimore 實(shí)驗(yàn)室。期間， 1994,7-1994,12 在美國麻省理工學(xué) 院。

1988 u20131992 博士研究生, 美國紐約哥侖比亞大學(xué)醫(yī)學(xué)院微生物系Vincent

Racaniello實(shí)驗(yàn)室。

1983 u20131986 中國北京醫(yī)科大學(xué)（現(xiàn)北京大學(xué)醫(yī)學(xué)部）微生物系 ，醫(yī)學(xué)碩士研

究生

1978 u20131983 中國北京醫(yī)學(xué)院（現(xiàn)北京大學(xué)醫(yī)學(xué)部），基礎(chǔ)醫(yī)學(xué)系本科生

1995-2000 美國布蘭戴斯大學(xué)(BrandeisUniversity)生物系助理教授

2000-2008 美國布蘭戴斯大學(xué)生物系副教授(tenured)

2008-2011 美國布蘭戴斯大學(xué)生物系終生教授

2010-2011 美國布蘭戴斯大學(xué)生物系聯(lián)席系主任

1992 獲美國哥侖比亞大學(xué)研究生院優(yōu)秀研究生院長獎(jiǎng)

1992 獲Irvinton研究所博士后獎(jiǎng)學(xué)金

1992-1995 獲腫瘤研究所博士后獎(jiǎng)學(xué)金

1996-1998 獲美國癌癥研究協(xié)會(huì)青年學(xué)者獎(jiǎng)

1996-1998 獲美國March of Dimes, Basil Ou2019Connor 青年學(xué)者獎(jiǎng)

1998-2003 獲美國白血病及淋巴瘤協(xié)會(huì)學(xué)者獎(jiǎng)

2003 獲美國癌癥研究協(xié)會(huì)研究學(xué)者稱號(hào)

1998-至今 美國血液學(xué)協(xié)會(huì)會(huì)員

2002 美國血液學(xué)協(xié)會(huì)2002年年會(huì)慢性髓細(xì)胞白血病分會(huì)主席

2006-至今 美國癌癥研究協(xié)會(huì)會(huì)員

2005-至今 美國國家衛(wèi)生研究院血液學(xué)項(xiàng)目評審委員會(huì)委員

2006-至今 美國白血病及淋巴瘤協(xié)會(huì)評審委員會(huì)委員

2007-至今 美國國防部CML項(xiàng)目評審委員會(huì)主席

2006-至今 北京大學(xué)學(xué)報(bào)醫(yī)學(xué)版特邀編委

2008-至今 美國Journal of Hematology and Oncology雜志常務(wù)副主編

2011-至今 美國Journal of Biological Chemistry雜志編委

2011-至今 醫(yī)學(xué)前沿編委

2017-至今 上海血液研究所所長

任瑞寶教授長期從事分子生物學(xué), 疾病學(xué)及治療學(xué)研究。 在《Cell》, 《Nature》, 《Science》， 《Genes & Development》， 《PNAS》， 《Blood》， 《MCB》, 《Cancer Research》等重要學(xué)術(shù)期刊發(fā)表50多篇論文，引用率達(dá)6000次。 發(fā)表在《Science》雜志上的一篇論文在1993年全世界論文引用次數(shù)最多的十篇論文中排名第三。獲美國國立衛(wèi)生院, 美國國防部及美國腫瘤協(xié)會(huì)的多項(xiàng)研究基金。已培養(yǎng)了超過20名的博士研究生, 博士后和訪問學(xué)者。先后獲美國腫瘤協(xié)會(huì), 美國March of Dimes, Basil Ou2019Connor 和白血病及淋巴瘤協(xié)會(huì)學(xué)者獎(jiǎng)。歷任布蘭戴斯大學(xué)終生教授，生物系聯(lián)席系主任，布蘭戴斯大學(xué)生物安全委員會(huì)主席， 美國國家衛(wèi)生研究院血液學(xué)項(xiàng)目評審委員會(huì)委員， 白血病及淋巴瘤協(xié)會(huì)評審委員會(huì)委員， 美國國防部CML項(xiàng)目評審委員會(huì)主席�，F(xiàn)任美國生物化學(xué)雜志（JBC）編委，美國血液與腫瘤學(xué)雜志（JHO）常務(wù)副主編，醫(yī)學(xué)前沿編委及北京大學(xué)學(xué)報(bào)醫(yī)學(xué)版特邀編委。2011年全職回國任上海交通大學(xué)醫(yī)學(xué)院附屬瑞金醫(yī)院上海血液學(xué)研究所常務(wù)副所長、所長，研究員。

1. 將人小兒麻痹病毒受體轉(zhuǎn)入小鼠而制成了小兒麻痹病毒受體的轉(zhuǎn)基因小鼠模型，并用此模型做了大量深入的小兒麻痹病毒分子生物學(xué)研究。這個(gè)模型對研究小兒麻痹病毒的致病機(jī)理及小兒麻痹病毒疫苗的安全測試具有廣泛的理論及應(yīng)用價(jià)值。該動(dòng)物模型獲美國專利.

2. 首次發(fā)現(xiàn)了存在于許多重要信號(hào)傳導(dǎo)蛋白質(zhì)中的SH3功能基團(tuán)的功能及結(jié)合靶點(diǎn)。發(fā)表在《Science》雜志上的該論文在1993年全世界論文引用次數(shù)最多的十篇論文中排名第三。同時(shí)，在克隆3BP2基因后與Bruce Mayer 一道首次發(fā)現(xiàn)并命名了Pleckstrin homology功能基團(tuán)（PHD）。

3. 研發(fā)了BCR/ABL誘導(dǎo)的人慢性髓細(xì)胞白血�。–ML）及人急性淋巴細(xì)胞白血�。ˋLL），AML1/EVI1誘導(dǎo)的人急性髓細(xì)胞白血病（AML），及RAS誘導(dǎo)的人急性及慢性粒細(xì)胞及單核細(xì)胞白血�。ˋMML，CMML）的小鼠模型。 這些疾病模型對研究白血病致病機(jī)理，研發(fā)及測試白血病治療具有重要的理論及應(yīng)用價(jià)值。

4. 用CML小鼠模型系統(tǒng)的進(jìn)行BCR/ABL功能與結(jié)構(gòu)的研究。揭示了BCR/ABL蛋白質(zhì)激酶活性對其誘導(dǎo)CML的必要性 u2013 為BCR/ABL蛋白質(zhì)激酶抑制劑成功治療CML 提供了理論基礎(chǔ)。同時(shí)發(fā)現(xiàn)BCR/ABL蛋白質(zhì)激酶外的功能集團(tuán)對誘導(dǎo)CML 的重要作用 - 為研發(fā)抗BCR/ABL蛋白質(zhì)激酶抑制劑耐藥性治療提供了理論基礎(chǔ)。

5. RAS是人類最常見的癌基因（RAS基因突變見于30%人類腫瘤）。 任瑞寶教授的實(shí)驗(yàn)室首次建立了NRAS（白血病中最常見的RAS基因突變）誘導(dǎo)的AMML及CMML動(dòng)物模型，并用此模型系統(tǒng)的進(jìn)行NRAS功能與結(jié)構(gòu)的研究。首次發(fā)現(xiàn)棕櫚酰化（Palmitoylation）修飾對NRAS誘導(dǎo)白血病的必要性 u2013 為研發(fā)抗NRAS相關(guān)的白血病及其他癌的治療奠定了理論基礎(chǔ)。

NRAS腫瘤基因存在于25-30% 白血病， 肝癌及黑色素瘤中， 抑制NRAS棕櫚�；�修飾對這些腫瘤應(yīng)有有效的治療作用。雖然很多腫瘤為KRAS4B腫瘤基因陽性， 而KRAS不需棕櫚�；�修飾， 但進(jìn)來發(fā)現(xiàn)KRAS4A （另一KRAS基因剪接產(chǎn)物）在KRAS陽性腫瘤， 如肺癌，發(fā)病過程中起重要作用，而KRAS4A需要棕櫚酰化修飾。同時(shí)我們還發(fā)現(xiàn)抑制NRAS棕櫚�；�修飾對RAS上游腫瘤蛋白有阻斷作用, 因此抑制RAS棕櫚酰化修飾對腫瘤應(yīng)有廣泛的治療效果。該應(yīng)用的專利申請正在審理中。

6. 三氧化二砷成功治療急性早幼粒細(xì)胞白血病（APL）是中國的首創(chuàng)。三氧化二砷主要作用機(jī)理是誘導(dǎo)PML-RARα融合癌蛋白降解。任瑞寶教授的實(shí)驗(yàn)室發(fā)現(xiàn)三氧化二砷也誘導(dǎo)EVI1癌蛋白降解。EVI1的異常表達(dá)見于10%AML病人及90%以上宮頸癌病人。 上述發(fā)現(xiàn)為擴(kuò)大三氧化二砷治療這些疾病提供了理論基礎(chǔ)。

7. 干擾素調(diào)節(jié)因子4（IRF4）最初被發(fā)現(xiàn)為癌蛋白， 對多發(fā)性骨髓癌癌細(xì)胞生存的維系起重要作用。近來，任瑞寶教授的實(shí)驗(yàn)室首次發(fā)現(xiàn)IRF4 在早期B-淋巴細(xì)胞及髓細(xì)胞中的功能為癌抑制蛋白。 這一發(fā)現(xiàn)對發(fā)展多發(fā)性骨髓癌及白血病的治療具有重要指導(dǎo)作用。IRF4癌抑制功能及應(yīng)用的專利申請正在審理中。

1. Racaniello,V.R., C.L. Mendelsohn, M. Morrison, M. Freistadt, G. Kaplan, E. Moss, and R.Ren. 1990. Molecular genetics of cellular receptors forpoliovirus. In: "Positive StrandRNA Viruses" (M.A. Brinton and F.X. Heinz, eds). American Society for Microbiology,Washington, DC. pp. 278-286.

2. Ren,R., E. G. Moss, V. R. Racaniello. 1991. Identification of twodeterminants that attenuate vaccine-related type 2 poliovirus. J. Virol. 65:1377-1382.

3. Newlon,C. S., L. R. Lipchitz, I. Collins, A. Deshpande, R. J. Devenish, R. P. Green,H. L. Klein, T. G Palzkill, R. Ren, S. Synn, and S. T. Woody. 1991. Analysis of a circular derivative ofSaccharomyces cerevisiae chromosome III: A physical map and identification andlocation of ARS elements. Genetics. 129: 343-357.

4. Racaniello,V.R., E. Moss, G. Kaplan, R. Ren. 1991. Interaction of polioviruswith its immunoglobulin-like cell receptor. In: "Microbial Adhesion" (M. Hook and L. Switalski, eds)Springer Verlag, Berlin.

5. Ren,R., V. R. Racaniello. 1992. Humanpoliovirus receptor gene expression and poliovirus tissue tropism in transgenicmice. J. Virol. 66: 296-304.

6. Ren,R., V. R. Racaniello. 1992. Poliovirusspreads from muscle to the central nervous system by neural pathways. J.Infect. Dis. 166: 747-752

7. Racaniello,V.R., R. Ren, M. Bouchard. 1992. Poliovirus attenuation and pathogenesis in atransgenic mouse model for poliomyelitis. Develop. Biol. Standard. 78:105-112.

8. Ren,R., B. J. Mayer, P. Ciccheti, and D. Baltimore. 1993. Identification of a ten-amino acid proline-rich SH3 binding site.Science. 259: 1157-1161. (the third-most-frequently cited paper in 1993,Science Watch. 5[1]:1).

9. Mayer,B. J., R. Ren, K. L. Clark, D. Baltimore. 1993. A putative modular domainpresent in diverse signaling proteins. Cell. 73: 629-630.

10. Ren,R., Z. Ye, D. Baltimore. 1994. Ablprotein-tyrosine kinase selects Crk adapter as a substrate using SH3 bindingsites. Genes Dev. 8: 783-795

11. Songyang,Z., S. E. Shoelson, J. McGlade, P. Olivier, T. Pawson, R. X. Bustelo, H.Hanafusa, T. Yi, R. Ren, D. Baltimore, S. Ratnofsky, R. A. Feldman, L. C.Cantley. 1994. Specific motifs recognized by the SH2 domains of csk, 3BP2,fes/fpd, Grb2, SHPTP1, SHC, Syk and vav. Mol. Cell. Biol. 14: 2777-2785

12. Feller,S. M., R. Ren, H. Hanafusa, and D. Baltimore. 1994. SH2 and SH3 domains insignal transduction - the interactions of Crk and Abl. TIBS. 19:453-458.

13. Racaniello,V.R., R. Ren. 1994. Transgenic mice and the pathogenesis of poliomyelitis. ArchVirol Suppl. 9:79-86.

14. Cohen,G., R. Ren, D. Baltimore. 1995. Modular binding domains in signal transduction.Cell: 80:237-48.

15. BaltimoreD; Ren R; Cheng G; Alexandropoulos K; Cicchetti P. 1995. A nuclear tyrosine kinase becomes acytoplasmic oncogene. Ann N Y Acad Sci 758:339-344.

16. Kharbanda,S., R. Ren (co-first-author), P. Pandey, T. D. Shafman, J. Kyriakis, R. R.Weichselbaum, D. Kufe. 1995. Activation of the c-Abl tyrosine kinase in the stress response toDNA-damage agents. Nature. 376: 785-788

17. Racaniello,V. R., R. Ren. 1996. Poliovirus biology and pathogenesis. In: “Transgenic Model of Human Viral and ImmunologicalDisease” (F. V. Chisari and M. B. A. Oldstane, eds). Springer-Verlag, Berlin Heidelberg New York.pp. 305-326.

18. Freeman,N. L., K. A. Mintzer, T. Lila, Z. Chen, A. J. Pahk, R. Ren, and J. Field. 1996. A domain containing a conserved SH3 binding site on the Saccharomycescerevisiae cyclase associated proteinmodulates cytoskeletal interactions and RAS signaling. Mol. Cell. Biol. 16:548-556

19. KharbandaS; P. Pandey; R. Ren; B. Mayer; L. Zon; D. Kufe. 1996. c-Abl activation regulates induction of theSEK1/stress-activated protein kinase pathway in the cellular response to1-beta-D-arabinofuranosylcytosine. J Biol. Chem. 270: 30278-81

20. Kharbanda,S., A. Bharti, D. Pei, J. Wang, P. Pandey, R. Ren, R. Weichselbaum, C. Walsh,and D. Kufe. 1996. The stress responseto ionizing radiation involves c-Abl-Dependent phosphorylation of SHPTP1. Proc. Natl. Acad. Sci. USA. 93: 6898-901

21. Holmes,T. C., D. A. Fadool, R. Ren, and I. B. Levitan. 1996. Association of Src tyrosine kinase with a human potassium channelmediated by SH3 domain. Science. 274: 2089-91

22. Chen,M., H., She, E. M., Davis, C. M., Spicer, L., Kim, R., Ren, M. M., Le Beau, W.,Li. 1998. Identification of Nck family genes, chromosomal localization,expression, and signaling specificity. J. Biol. Chem. 273: 25171

23. Zhang,X. and R. Ren. 1998. Bcr-Abl efficiently induces a myeloproliferative diseaseand production of excess IL-3 and GM-CSF in mice: a novel model for chronicmyelogenous leukemia. Blood. 92: 3829-3840

24. Skourides,P. A., Perera, S. A., and R. Ren. 1999. Polarized distribution of Bcr-Abl inmigrating myeloid cells and co-localization of Bcr-Abl and its target proteins.Oncogene. 18: 1165-1176

25. Gross,A., X. Zhang, and R. Ren. 1999. Bcr-Ablwith an SH3 deletion retains the ability to induce a myeloproliferative diseasein mice, yet c-Abl activated by SH3 deletion induces only lymphoid malignancy.Mol. Cell. Biol. 19: 6918-6928

26. Hao,S. X., and R. Ren. 2000. Expression of ICSBP is downregulated in Bcr-Abl-inducedmurine CML-like disease, and forced coexpression of ICSBP inhibits theBcr-Abl-induced myeloproliferative disorder. Mol. Cell. Biol. 20: 1149-1161.

27. Cuenco,G. M., G. Nucifora, and R. Ren. 2000.Human AML1/MDS1/EVI1 fusion protein induces an acute myelogenous leukemia (AML)in mice: a novel model for human AML. Proc. Natl. Acad. Sci. USA. 97:1760-1765.

28. GrossA. W. and R. Ren. 2000. Bcr-Abl has a greater intrinsic capacity than v-Abl toinduce the neoplastic expansion of myeloid cells in vivo. Oncogene. 19:6286-6296

29. ZhangX, R. Wong, S. X. Hao, W. S. Pear, and R. Ren. 2001. The SH2 domain of Bcr-Abl is not required to induce a murinemyeloproliferative disease; however, SH2 signaling influences disease latencyand phenotype. Blood. 97: 277-287.

30. ZhangX, R. Subrahmanyam, R. Wong, A. W. Gross and R. Ren. 2001. The NH2-terminalcoiled-coil domain and tyrosine 177 play important roles in induction of amyeloproliferative disease in mice by Bcr-Abl. Mol. Cell. Biol. 21: 840-853

31. Cuenco,M. G. and R. Ren. 2001. Cooperation of BCR-ABL and AML1/MDS1/EVI1 in blockingmyeloid differentiation and rapid induction of an Acute Myelogenous Leukemia.Oncogene. 20:8236-8248

32. He,Y., J. A. Wertheim, L. Xu, J. P. Miller, F. G. Karnell, J. K. Choi, R. Ren, andW. S. Pear. 2002. The coiled-coildomain and Tyr177 of bcr are required to induce a murine chronic myelogenousleukemia-like disease by bcr/abl. Blood.99: 2957-2968.

33. Ren,R. 2002. Dissecting the molecular mechanism of chronic myelogenous leukemiausing murine models. Leukemia and Lymphoma. 8: 1549-1561

34. Ren,R. 2002. The molecular mechanism of chronic myelogenous leukemia and itstherapeutic implications: studies in a murine model. Oncogene. 21: 8629-8642.

35. Wertheim,J. A., S. A. Perera, D. Hammer, R. Ren, D. Boettiger and W. S. Pear. 2003. Localization of BCR-ABL to F-actinregulates cell adhesion but does not attenuate CML development. Blood.102:2220-8

36. Dinulescu,D. M., L. J. Wood, L. Shen, M. Loriaux, C. L. Corless, A. W. Gross, R. Ren, M.W..N. Deininger & B. J. Druker. 2003. c-CBL is not required for leukemiainduction by Bcr-Abl in mice. Oncogene. 22:8852-60

37. Ren,R. 2003. Overriding BCR/ABL mitotic signal by ICSBP-induced differentiation.Inside blood, Blood. 102:4251-52

38. Cuenco,G. M. and R. Ren. 2004. Both AML1 andEVI1 oncogenic components are required to the cooperation of AML1/MDS1/EVI1with BCR/ABL in induction of acute myelogenous leukemia in mice. Oncogene.23:569-79

39. Ren,R. 2004. Modeling the dosage effect of oncogenes in leukemogenesis. CurrentOpinion in Hematology. 11:25-34

40. Ren,R. 2004. Restraing CML by adhesives. Blood. 104:1917-18

41. Ren,R. 2005. Mechanisms of BCR-ABL in the pathogenesis of chronic myelogenousleukaemia. Nature Reviews Cancer. 5(3):172-83.

42. Ren,R. 2005. Oncogenic forms of Abl family kinases. in "Abl family kinases indevelopment and disease" (A. Koleske, ed). Landes Publishing.

43. Parikh,C. R. Subrahmanyam and R. Ren. 2006. Oncogenic NRAS rapidly and efficientlyinduces CMML- and AML-like diseases in mice. Blood. 108:2349-57.

44. Cuiffo,B. and R. Ren. 2006. Models of hematopoietic malignancies: chronic myeloidleukemia. Drug Discovery Today: Disease Models. 3:183-189

45. Shackelford,D., C. Kenific, A. Blusztajn, S. Waxman and R. Ren. 2006. Targeted Degradationof the AML1/MDS1/EVI1 oncoprotein by Arsenic Trioxide. Cancer Research.66:11360-11369

46. YanM, JK Luo, KJ Ritchie, I Sakai, K Takeuchi, R Ren, DE Zhang. 2007. Ubp43regulates BCR-ABL leukemogenesis via the Type I interferon receptor signaling.Blood. 110:305-12.

47. Parikh,C., R. Subrahmanyam and R. Ren. 2007. Oncogenic NRAS, KRAS and HRAS exhibitdifferent leukemogenic potentials in mice. Cancer Research. 67:7139-46

48. Zhang,S. J., L. Y. Ma, Q. H. Huang, G. Li, B. W. Gu, X. D. Gao, J. Y. Shi, Y. Y.Wang, L. Gao, X. Cai, R. Ren, J. Zhu, Z. Chen, S. J. Chen. 2008.Gain-of-function mutation of GATA-2 in acute myeloid transformation of chronicmyeloid leukemia. Proc. Natl. Acad. Sci. USA. 105: 2076-81.

49. Parikh,C. and R. Ren. 2008. Mouse model for NRAS-induced leukemogenesis. MethodsEnzymol. 439:15-24.

50. BaumKJ, R. Ren. 2008. Effect of Ras Inhibition in Hematopoiesis and BCR/ABLLeukemogenesis. J Hematol Oncol. 1:5.

51. Acquaviva,J. X. Chen and R. Ren. 2008. IRF-4 functions as a tumor suppressor in earlyB-cell development. Blood. 110:3798-806.

52. JaganiZ, K. Song, J. L. Kutok, M. R. Dewar, A. Melet, T. Santos, A. Grassian, S.Ghaffari, C. Wu, H. Yeckes-Rodin, R. Ren, K. Miller, R. Khosravi-Far. 2009.Proteasome inhibition causes regression of leukemia and abrogatesBCR-ABL-induced evasion of apoptosis in part through regulation of forkheadtumor suppressors. Cancer Research. 69:6546-55.

53. Cuiffo,B., and R. Ren. 2010. Palmitoylation of oncogenic NRAS is essential forleukemogenesis. Blood. 115:3598-605. PMID: 20200357

54. Jo,S., J. Schatz, J. Acquaviva, H. Singh and R. Ren. 2010. Cooperation betweendeficiencies of IRF-4 and IRF-8 promotes both myeloid and lymphoidtumorigenesis. Blood. 116:2759-67. PMID: 20585039

55. Wang,Y.Y., L.J. Zhao, C.F. Wu, P. Liu, L. Shi, Y. Liang, S.M. Xiong, J.Q. Mi, Z.Chen, R. Ren (co-corresponding author), S.J. Chen. 2011. C-KIT mutation cooperates withfull-length AML1-ETO to induce acute myeloid leukemia in mice. Proc. Natl.Acad. Sci. USA. 108: 2450-5. PMID: 21262832

56. Jo,S. and R. Ren. 2012. IRF-4 suppresses BCR/ABL transformation of myeloid cellsin a DNA binding-independent manner. J Biol Chem. 287:1770-8. PMID:22110133

57. Jiao, B., Z.H. Ren, P. Liu, L.J Chen, J.Y. Shi, Y. Dong, J. Ablain, L. Shi, L. Gao, J.P. Hu, R. Ren, H. de Thé, Z. Chen, and S.J. Chen. 2013. 8-CPT-cAMP/all-trans retinoic acid targets t(11;17) acute promyelocytic leukemia through enhanced cell differentiation and PLZF/RARα degradation.Proc. Natl. Acad. Sci. USA.110:3495-500

58. Liu, Y.J., H.B. Fan, Y. Jin, C.G. Ren, X.E. Jia, L. Wang, Y. Chen, M. Dong, K.Y. Zhu, Z.W. Dong, B.X. Ye, Z. Zhong, M. Deng, T.X. Liu and R. Ren. 2013.Cannabinoid receptor 2suppresses leukocyte inflammatory migration by modulating the JNK/c-Jun/Alox5pathway.J Biol Chem.288:13551-62.

59. Ren C.G., L. Wang, X.E. Jia, Y.J. Liu, Z.W. Dong, Y. Jin, Y. Chen, M. Deng, Y. Zhou, Y. Zhou, R. Ren(co-corresponding author), W.J. Pan and T.X. Liu. 2013. Activated N-Ras signaling regulates arterial-venous specification in zebrafish.J Hematol Oncol.6:34 doi: 10.1186/1756-8722-6-34.

60. Fredericks J. and R. Ren. 2013. The role of RAS effectors in BCR/ABL induced chronic myelogenous leukemia.Front Med.7:452-61.

61.Du T.T., P.F. Xu, Z.W. Dong, H.B. Fan, Y. Jin, M. Dong, Y. Chen, W.J. Pan, R. Ren, T.X. Liu, M. Deng, and Q.H. Huang. 2014. Setdb2 controls convergence and extension movements during zebrafish gastrulation by transcriptional regulation of dvr1.Dev Biol.392:233-44

62. Wang Y., M. Xiao, X. Chen, L. Chen, P. Wang, H. Yang, S. Ma, J. Zhang, B. Jiao, R. Ren, D. Ye, K. Guan and Y. Xiong. 2015. WT1 recruits TET2 to regulate its target gene expression and suppress leukemia cell proliferation.Molecular Cell.57:662-73

63. Zhao H., P. Liu, R. Zhang, M. Wu, D. Li, X. Zhao, C. Zhang, B. Jiao, B. Chen, Z. Chen and R. Ren. 2015. Roles of palmitoylation and the KIKK membrane-targeting motif in leukemogenesis by oncogenic KRAS4A.J Hematol Oncol.8:132:1-14

64. Liu P., B. Jiao, R. Zhang, H. Zhao, C. Zhang, M. Wu, D. Li, X. Zhao, Q. Qiu, J. Li and R. Ren. 2016. Palmitoylacyltransferase Zdhhc9 Inactivation Mitigates Leukemogenic Potential of Oncogenic Nras.Leukemia.30:1225-8

65. Pan MM, Zhang QY, Wang YY, Liu P, Ren RB, Huang JY, Chen LT, Xi XD, Chen Z, Chen SJ. 2016. Human NUP98-IQCG fusion protein induces acute myelomonocytic leukemia in mice by dysregulating the Hox/Pbx3 pathway.Leukemia.30:1590-3.

66. Zhang ZG, Wang Q, Kong J, Chen B, Zhu YM, Weng XQ, Shen ZX, Li JM, Wang J, Yan XJ, Li Y, Liang YM, Liu L, Chen XQ, Zhang WG, Yan JS, Hu JD, Shen SH, Chen J, Gu LJ, Pei D, Li Y, Wu G, Zhou X, Ren RB, Cheng C, Yang JJ, Wang KK, Wang SY, Zhang J, Mi JQ, Pui CH, Tang JY, Chen Z, Chen SJ. 2016. Genomic Profiling of Adult and Pediatric B-cell Acute Lymphoblastic Leukemia.EBioMedicine.8:173-83

67. Jin Y, Zhou J, Xu F, Jin B, Cui L, Wang Y, Du X, Li J, Li P, Ren R, Pan J. 2016 Targeting methyltransferase PRMT5 eliminates leukemia stem cells in chronic myelogenous leukemia.J Clin Invest.126:3961-3980

68. Li D., X. Zhao, R. Zhang, H. Zhao, B. Jiao, Q. Qiu, M. Wu, P. Liu, R. Ren. 2016. BCR/ABL can promote CD19 cell growth but not render them long-term stemness.Stem Cell Investigation.3:85

69. Jiang J, Gui F, He Z, Li L, Li Y, Li S, Wu X, Deng Z, Sun X, Huang X, Huang W, Han S, Zhang T, Wang Z, Jiao B, Song S, Wang HR, Chen L, Zhou D, Liu Q, Ren R (co-corresponding author), Zhang J, Deng X. 2017. Targeting BRK-positive breast cancers with small molecule kinase inhibitors.Cancer Res. 77:175-186

70. Wu M., J. Huang, J. Zhang, C. Benes, B. Jiao, R. Ren. 2017. N-Arachidonoyl Dopamine Inhibits NRAS Neoplastic Transformation by Suppressing Its Plasma Membrane Translocation.Molecular Cancer Therapeutics.16:57-67