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| 1 | Application of next-generation sequencing technology to precision medicine in cancer: joint consensus of the Tumor Biomarker Committee of the Chinese Society of Clinical Oncology显示文摘Next-generation sequencing(NGS) technology is capable of sequencing millions or billions of DNA molecules simultaneously.Therefore, it represents a promising tool for the analysis of molecular targets for the initial diagnosis of disease, monitoring of disease progression, and identifying the mechanism of drug resistance. On behalf of the Tumor Biomarker Committee of the Chinese Society of Clinical Oncology(CSCO) and the China Actionable Genome Consortium(CAGC), the present expert group hereby proposes advisory guidelines on clinical applications of NGS technology for the analysis of cancer driver genes for precision cancer therapy. This group comprises an assembly of laboratory cancer geneticists, clinical oncologists, bioinformaticians,pathologists, and other professionals. After multiple rounds of discussions and revisions, the expert group has reached a preliminary consensus on the need of NGS in clinical diagnosis, its regulation, and compliance standards in clinical sample collection. Moreover, it has prepared NGS criteria, the sequencing standard operation procedure(SOP), data analysis, report, and NGS platform certification and validation. | Xuchao Zhang Zhiyong Liang Shengyue Wang Shun Lu Yong Song Ying Cheng Jianming Ying Weiping Liu Yingyong Hou Yangqiu Li Yi Liu Jun Hou Xiufeng Liu Jianyong Shao Yanhong Tai Zheng Wang Li Fu Hui Li Xiaojun Zhou Hua Bai Mengzhao Wang You Lu Jinji Yang Wenzhao Zhong Qing Zhou Xuening Yang Jie Wang Cheng Huang Xiaoqing Liu Xiaoyan Zhou Shirong Zhang Hongxia Tian Yu Chen Ruibao Ren Ning Liao Chunyan Wu Zhongzheng Zhu Hongming Pan Yanhong Gu Liwei Wang Yunpeng Liu Suzhan Zhang Tianshu Liu Gong Chen Zhimin Shao Binghe Xu Qingyuan Zhang Ruihua Xu Lin Shen Yilong Wu | 2019 | Cancer Biology & Medicine2019，16，1： | 14 |
| 2 | Biomarkers of aging显示文摘Aging biomarkers are a combination of biological parameters to(i)assess age-related changes,(ii)track the physiological aging process,and(iii)predict the transition into a pathological status.Although a broad spectrum of aging biomarkers has been developed,their potential uses and limitations remain poorly characterized.An immediate goal of biomarkers is to help us answer the following three fundamental questions in aging research:How old are we?Why do we get old?And how can we age slower?This review aims to address this need.Here,we summarize our current knowledge of biomarkers developed for cellular,organ,and organismal levels of aging,comprising six pillars:physiological characteristics,medical imaging,histological features,cellular alterations,molecular changes,and secretory factors.To fulfill all these requisites,we propose that aging biomarkers should qualify for being specific,systemic,and clinically relevant. | Aging Biomarker Consortium Hainan Bao Jiani Cao Mengting Chen Min Chen Wei Chen Xiao Chen Yanhao Chen Yu Chen Yutian Chen Zhiyang Chen Jagadish K Chhetri Yingjie Ding Junlin Feng Jun Guo Mengmeng Guo Chuting He Yujuan Jia Haiping Jiang Ying Jing Dingfeng Li Jiaming Li Jingyi Li Qinhao Liang Rui Liang Feng Liu Xiaoqian Liu Zuojun Liu Oscar Junhong Luo Jianwei Lv Jingyi Ma Kehang Mao Jiawei Nie Xinhua Qiao Xinpei Sun Xiaoqiang Tang Jianfang Wang Qiaoran Wang Siyuan Wang Xuan Wang Yaning Wang Yuhan Wang Rimo Wu Kai Xia Fu-Hui Xiao Lingyan Xu Yingying Xu Haoteng Yan Liang Yang Ruici Yang Yuanxin Yang Yilin Ying Le Zhang Weiwei Zhang Wenwan Zhang Xing Zhang Zhuo Zhang Min Zhou Rui Zhou Qingchen Zhu Zhengmao Zhu Feng Cao Zhongwei Cao Piu Chan Chang Chen Guobing Chen Hou-Zao Chen Jun Chen Weimin Ci Bi-Sen Ding Qiurong Ding Feng Gao Jing-Dong JHan Kai Huang Zhenyu Ju Qing-Peng Kong Ji Li Jian Li Xin Li Baohua Liu Feng Liu Lin Liu Qiang Liu Qiang Liu Xingguo Liu Yong Liu Xianghang Luo Shuai Ma Xinran Ma Zhiyong Mao Jing Nie Yaojin Peng Jing Qu Jie Ren Ruibao Ren Moshi Song Zhou Songyang Yi Eve Sun Yu Sun Mei Tian Shusen Wang Si Wang Xia Wang Xiaoning Wang Yan-Jiang Wang Yunfang Wang Catherine CL Wong Andy Peng Xiang Yichuan Xiao Zhengwei Xie Daichao Xu Jing Ye Rui Yue Cuntai Zhang Hongbo Zhang Liang Zhang Weiqi Zhang Yong Zhang Yun-Wu Zhang Zhuohua Zhang Tongbiao Zhao Yuzheng Zhao Dahai Zhu Weiguo Zou Gang Pei Guang-Hui Liu | 2023 | Science China(Life Sciences)2023，66，5： | 2 |
| 3 | The molecular mechanism of chronic myelogenous leukemia and its therapeutic implications:studies in a murine model显示文摘 | Ruibao Ren | | Oncogene0，，： | 1 |
| 4 | Zfyve16 regulates the proliferation of β-lymphoid cells显示文摘Zfyvel6 (a.k.a. endofin or endosome-associated _FYVE-domain protein), a member of the FYVE-domain protein family, is involved in endosomal trafficking and in TGF-β, BMP, and EGFR signaling. The FYVEprotein SARA regulates the TGF-β signaling pathway by recruiting Smad2/3 and accelerating theirphosphorylation, thereby altering their susceptibility to TGF-β-mediated T cell suppression. Zfyvel6 binds toSmad4 and their binding affects the formation of Smad2/3-Smad4 complex in TGF-β signaling. However, the invivo function of Zfyvel6 remains unknown. In this study, we generated a Zfyvel6 knockout mouse strain(Zfyve16^KO) and examined its hematopoietic phenotypes and hematopoietic reconstruction ability. The proportionof T cells in the peripheral blood of Zfyve16^KO mice increases compared with that in wild-type mice. This finding isconsistent with the role of Zfyvel6 in facilitating TGF-β signaling. Unpredictably, B cell proliferation is inhibited inZfyvel6^KO mice. The proliferation potential of Zfyvel6^KO B-lymphoid cells also significantly decreases in vitro.These results suggest that Zfyve16 inhibits the proliferation of T cells, possibly through the TGF-β signaling, butupregulates the proliferation of B-lymphoid cells. | Xuemei Zhao Donghe Li Qingsong Qiu Bo Jiao Ruihong Zhang Ping Liu Ruibao Ren | 2018 | Frontiers of Medicine2018，12，5： | 0 |
| 5 | Palmitoylation of GNAQ/11 is critical for tumor cell proliferation and survival in GNAQ/11-mutant uveal melanoma显示文摘More than 85%of patients with uveal melanoma(UM)carry a GNAQ or GNA11 mutation at a hotspot codon(Q209)that encodes G proteinαsubunit q/11 polypeptides(Gα_(q/11)).GNAQ/11 relies on palmitoylation for membrane association and signal transduction.Despite the palmitoylation of GNAQ/11 was discovered long before,its implication in UM remains unclear.Here,results of palmitoylation-targeted mutagenesis and chemical interference approaches revealed that the loss of GNAQ/11 palmitoylation substantially affected tumor cell proliferation and survival in UM cells.Palmitoylation inhibition through the mutation of palmitoylation sites suppressed GNAQ/11^(Q209L)-induced malignant transformation in NIH3T3 cells.Importantly,the palmitoylation-deficient oncogenic GNAQ/11 failed to rescue the cell death initiated by the knock down of endogenous GNAQ/11 oncogenes in UM cells,which are much more dependent on Gα_(q/11) signaling for cell survival and proliferation than other melanoma cells without GNAQ/11 mutations.Furthermore,the palmitoylation inhibitor,2-bromopalmitate,also specifically disrupted Gα_(q/11) downstream signaling by interfering with the MAPK pathway and BCL2 survival pathway in GNAQ/11-mutant UM cells and showed a notable synergistic effect when applied in combination with the BCL2 inhibitor,ABT-199,in vitro.The findings validate that GNAQ/11 palmitoylation plays a critical role in UM and may serve as a promising therapeutic target for GNAQ/11-driven UM. | Yan Zhang Baoyuan Zhang Yongyun Li Yuting Dai Jiaoyang Li Donghe Li Zhizhou Xia Jianming Zhang Ping Liu Ming Chen Bo Jiao Ruibao Ren | 2022 | Frontiers of Medicine2022，16，5： | 0 |
| 6 | DDB1-and CUL4-associated factor 8 plays a critical role in spermatogenesis显示文摘Cullin-RING E3 ubiquitin ligase(CRL)-4 is a member of the large CRL family in eukaryotes.It plays important roles in a wide range of cellular processes,organismal development,and physiological and pathological conditions.DDB1-and CUL4-associated factor 8(DCAF8)is a WD40 repeat-containing protein,which serves as a substrate receptor for CRL4.The physiological role of DCAF8 is unknown.In this study,we constructed Dcaf8 knockout mice.Homozygous mice were viable with no noticeable abnormalities.However,the fertility of Dcaf8-deficient male mice was markedly impaired,consistent with the high expression of DCAF8 in adult mouse testis.Sperm movement characteristics,including progressive motility,path velocity,progressive velocity,and track speed,were significantly lower in Dcaf8 knockout mice than in wild-type(WT)mice.However,the total motility was similar between WT and Dcaf8 knockout sperm.More than 40%of spermatids in Dcaf8 knockout mice showed pronounced morphological abnormalities with typical bent head malformation.The acrosome and nucleus of Dcaf8 knockout sperm looked similar to those of WT sperm.In vitro tests showed that the fertilization rate of Dcaf8 knockout mice was significantly reduced.The results demonstrated that DCAF8 plays a critical role in spermatogenesis,and DCAF8 is a key component of CRL4 function in the reproductive system. | Xiuli Zhang Zhizhou Xia Xingyu Lv Donghe Li Mingzhu Liu Ruihong Zhang Tong Ji Ping Liu Ruibao Ren | 2021 | Frontiers of Medicine2021，15，2： | 0 |
| 7 | The role of RAS effectors in BCR/ABL induced chronic myelogenous leukemia显示文摘BCR/ABL is the causative agent of chronic myelogenous leukemia(CML).Through structure/function analysis,several protein motifs have been determined to be important for the development of leukemogenesis.Tyrosine177 of BCR is a Grb2 binding site required for BCR/ABL-induced CML in mice.In the current study,we use a mouse bone marrow transduction/transplantation system to demonstrate that addition of oncogenic NRAS(NRASG12D)to a vector containing a BCR/ABL^(Y177F)mutant“rescues”the CML phenotype rapidly and efficiently.To further narrow down the pathways downstream of RAS that are responsible for this rescue effect,we utilize well-characterized RAS effector loop mutants and determine that the RAL pathway is important for rapid induction of CML.Inhibition of this pathway by a dominant negative RAL is capable of delaying disease progression.Results from the present study support the notion of RAL inhibition as a potential therapy for BCR/ABL-induced CML. | Jessica Fredericks Ruibao Ren | 2013 | Frontiers of Medicine2013，7，4： | 0 |
| 8 | IRF4 and IRF8 expression are associated with clinical phenotype and clinico-hematological response to hydroxyurea in essential thrombocythemia显示文摘The morbidity and mortality of myeloproliferative neoplasms(MPNs)are primarily caused by arterial and venous complications,progression to myelofibrosis,and transformation to acute leukemia.However,identifying molecular-based biomarkers for risk stratification of patients with MPNs remains a challenge.We have previously shown that interferon regulatory factor-8(IRF8)and IRF4 serve as tumor suppressors in myeloid cells.In this study,we evaluated the expression of IRF4 and IRF8 and the JAK2V617F mutant allele burden in patients with MPNs.Patients with decreased IRF4 expression were correlated with a more developed MPN phenotype in myelofibrosis(MF)and secondary AML(sAML)transformed from MPNs versus essential thrombocythemia(ET).Negative correlations between the JAK2V617F allele burden and the expression of IRF8(P<0.05)and IRF4(P<0.001)and between white blood cell(WBC)count and IRF4 expression(P<0.05)were found in ET patients.IRF8 expression was negatively correlated with the JAK2V617F allele burden(P<0.05)in polycythemia vera patients.Complete response(CR),partial response(PR),and no response(NR)were observed in 67.5%,10%,and 22.5%of ET patients treated with hydroxyurea(HU),respectively,in 12 months.At 3 months,patients in the CR group showed high IRF4 and IRF8 expression compared with patients in the PR and NR groups.In the 12-month therapy period,low IRF4 and IRF8 expression were independently associated with the unfavorable response to HU and high WBC count.Our data indicate that the expression of IRF4 and IRF8 was associated with the MPN phenotype,which may serve as biomarkers for the response to HU in ET. | Xiao Huang Tingting Ma Yongmei Zhu Bo Jiao Shanhe Yu Kankan Wang Jian-Qing Mi Ruibao Ren | 2022 | Frontiers of Medicine2022，16，3： | 0 |
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