The live and fresh characteristics of life and the complexity of the laws of its activities make any new discoveries to attract worldwide attention. Research advances in the field of life sciences in 2016 have been soul-stirring. This paper selects several cases from the research results, which are too numerous to enumerate, to review the typical study progress in this year. The selected cases are:cancer cell induced death of endothelial cells, new type of ectopic inhibitor against drug resistance gene mutation lung cancers, gene targeting scheme that may greatly reduce off-targeting phenomenon, accurate tumor-killing therapy using modified T cells with dual receptor high efficient tumor immunological, therapy, high efficient AIDS immunological therapy, with HIV universal effect anti-virus antibodies, the therapy of autoimmune diseases with the removal of lymphocytes which attacking the patients' own tissues, as well as the crystal regeneration innovation, the resolution of the mechanism of synaptic pruning. Extraordinarily, the problems of tumor treatment, gene editing and so on, have maintained a constant heat, and in 2016, outstanding achievements were still made.
[1] Strilic B, Yang L, Albarrán-Juárez J, et al. Tumour-cell-induced endothelial cell necroptosis via death receptor 6 promotes metastasis[J]. Nature, 2016, 536(7615):215-218.
[2] Jia Y, Yun C H, Park E, et al. Overcoming EGFR (T790M) and EGFR (C797S) resistance with mutant-selective allosteric inhibitors[J]. Nature, 2016, 534(7605):129-132.
[3] Finlay M R V, Anderton M, Ashton S, et al. Discovery of a potent and selective EGFR inhibitor (AZD9291) of both sensitizing and T790M resistance mutations that spares the wild type form of the receptor[J]. Journal of Medicinal Chemistry, 2014, 57:8249-8267.
[4] Thress K S, Paweletz C P, Felip E, et al. Acquired EGFR C797S mutation mediates resistance to AZD9291 in non-small cell lung cancer harboring EG-FR T790M[J]. Nayure Medicine, 2015, 21:560-562.
[5] Gilbert L A, Larson M H, Morsut L, et al. CRISPR-mediated modular RNA-guided regulation of transcription in eukaryotes[J]. Cell, 2013, 154(2):442-451.
[6] 吴晓丽. 2015年生命科学热点回眸[J]. 科技导报, 2016, 34(1):23-35.
[7] Tan T, Chen Z, Lei Y, et al. A regulatory effect of INMAP on centromere proteins:antisense INMAP induces CENP-B variation and centromeric halo[J]. PLoS One, 2014, 9(3):e91937.
[8] Kleinstiver B P, Pattanayak V, Prew M S, et al. High-fidelity CRISPR-Cas9 nucleases with no detectable genome-wide off-target effects[J]. Nature, 2016, 529(7587):490-495.
[9] Morsut L, Roybal K T, Xiong X, et al. Engineering customized cell sensing and response behaviors using synthetic notch receptors[J]. Cell, 2016, 164(4):780-791.
[10] Escolano A, Steichen J M, Dosenovic P, et al. Sequential immunization elicits broadly neutralizing anti-HIV-1 antibodies in Ig knockin mice[J]. Cell, 2016, 166(6):1445-1458.
[11] Ellebrecht C T, Bhoj V G, Nace A, et al. Reengineering chimeric antigen receptor T cells for targeted therapy of autoimmune disease[J]. Science, 2016, 353(6295):179-184.
[12] Clemente-Casares X, Blanco J, Ambalavanan P, et al. Expanding antigen-specific regulatory networks to treat autoimmunity[J]. Nature, 2016, 530:434-440.
[13] Wei Y, Shen E, Zhao N, et al. Identification of a novel centrosomal protein CrpF46 involved in cell cycle progression and mitosis[J]. Expeirimental Cell Research, 2008, 314(8):1693-1707.
[14] Shen E, Lei Y, Liu Q, et al. Identification and characterization of INMAP, a novel interphase nucleus and mitotic apparatus protein that is involved in spindle formation and cell cycle progression[J]. Expeirimental Cell Research, 2009, 315(7):1100-1116.
[15] Zhou Y L, Chen Z, Lei Y, et al. INMAP, a novel truncated version of POLR3B, represses AP-1 and p53 transcriptional activity[J]. Molecular and Cellular Biochemistry, 2013, 374(1/2):81-89.
[16] Tan T, Chen Z, Lei Y, et al. A regulatory effect of INMAP on centromere proteins:Antisense INMAP induces CENP-B variation and centromeric halo[J]. PLoS One, 2014, 9(3):e91937.
[17] Zhu Y, Lei Y, Du B C, et al. INMAP overexpression inhibits cell proliferation, induces genomic instability and functions through p53/p21 pathways[J]. PLoS One, 2015, 10(1):e0115704.
[18] Lin H, Ouyang H, Zhu J, et al. Lens regeneration using endogenous stem cells with gain of visual function[J]. Nature, 2016, 531(7594):323-328.
[19] Sekar A, Bialas A R, de Rivera H, et al. Schizophrenia risk from complex variation of complement component 4[J]. Nature, 2016, 530(7589):177-183.
[20] Hong S, Beja-Glasser V F, Nfonoyim B M, et al. Complement and microglia mediate early synapse loss in Alzheimer mouse models[J]. Science, 2016, 352(6286):712-716.
[21] Lui H, Zhang J, Makinson S R, et al. Progranulin deficiency promotes circuit-specific synaptic pruning by microglia via complement activation[J]. Cell, 2016, 165(4):921-935.