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  1. Article ; Online: Observation of Three Charmoniumlike States with J^{PC}=1^{--} in e^{+}e^{-}→D^{*0}D^{*-}π^{+}.

    Ablikim, M / Achasov, M N / Adlarson, P / Aliberti, R / Amoroso, A / An, M R / An, Q / Bai, Y / Bakina, O / Balossino, I / Ban, Y / Batozskaya, V / Begzsuren, K / Berger, N / Bertani, M / Bettoni, D / Bianchi, F / Bianco, E / Bloms, J /
    Bortone, A / Boyko, I / Briere, R A / Brueggemann, A / Cai, H / Cai, X / Calcaterra, A / Cao, G F / Cao, N / Cetin, S A / Chang, J F / Chang, T T / Chang, W L / Che, G R / Chelkov, G / Chen, C / Chen, Chao / Chen, G / Chen, H S / Chen, M L / Chen, S J / Chen, S M / Chen, T / Chen, X R / Chen, X T / Chen, Y B / Chen, Y Q / Chen, Z J / Cheng, W S / Choi, S K / Chu, X / Cibinetto, G / Coen, S C / Cossio, F / Cui, J J / Dai, H L / Dai, J P / Dbeyssi, A / de Boer, R E / Dedovich, D / Deng, Z Y / Denig, A / Denysenko, I / Destefanis, M / De Mori, F / Ding, B / Ding, X X / Ding, Y / Dong, J / Dong, L Y / Dong, M Y / Dong, X / Du, S X / Duan, Z H / Egorov, P / Fan, Y L / Fang, J / Fang, S S / Fang, W X / Fang, Y / Farinelli, R / Fava, L / Feldbauer, F / Felici, G / Feng, C Q / Feng, J H / Fischer, K / Fritsch, M / Fritzsch, C / Fu, C D / Fu, Y W / Gao, H / Gao, Y N / Gao, Yang / Garbolino, S / Garzia, I / Ge, P T / Ge, Z W / Geng, C / Gersabeck, E M / Gilman, A / Goetzen, K / Gong, L / Gong, W X / Gradl, W / Gramigna, S / Greco, M / Gu, M H / Gu, Y T / Guan, C Y / Guan, Z L / Guo, A Q / Guo, L B / Guo, R P / Guo, Y P / Guskov, A / H, X T / Han, W Y / Hao, X Q / Harris, F A / He, K K / He, K L / Heinsius, F H / Heinz, C H / Heng, Y K / Herold, C / Holtmann, T / Hong, P C / Hou, G Y / Hou, Y R / Hou, Z L / Hu, H M / Hu, J F / Hu, T / Hu, Y / Huang, G S / Huang, K X / Huang, L Q / Huang, X T / Huang, Y P / Hussain, T / Hüsken, N / Imoehl, W / Irshad, M / Jackson, J / Jaeger, S / Janchiv, S / Jeong, J H / Ji, Q / Ji, Q P / Ji, X B / Ji, X L / Ji, Y Y / Jia, Z K / Jiang, P C / Jiang, S S / Jiang, T J / Jiang, X S / Jiang, Y / Jiao, J B / Jiao, Z / Jin, S / Jin, Y / Jing, M Q / Johansson, T / K, X / Kabana, S / Kalantar-Nayestanaki, N / Kang, X L / Kang, X S / Kappert, R / Kavatsyuk, M / Ke, B C / Khoukaz, A / Kiuchi, R / Kliemt, R / Koch, L / Kolcu, O B / Kopf, B / Kuessner, M / Kupsc, A / Kühn, W / Lane, J J / Lange, J S / Larin, P / Lavania, A / Lavezzi, L / Lei, T T / Lei, Z H / Leithoff, H / Lellmann, M / Lenz, T / Li, C / Li, C H / Li, Cheng / Li, D M / Li, F / Li, G / Li, H / Li, H B / Li, H J / Li, H N / Li, Hui / Li, J R / Li, J S / Li, J W / Li, Ke / Li, L J / Li, L K / Li, Lei / Li, M H / Li, P R / Li, S X / Li, T / Li, W D / Li, W G / Li, X H / Li, X L / Li, Xiaoyu / Li, Y G / Li, Z J / Li, Z X / Li, Z Y / Liang, C / Liang, H / Liang, Y F / Liang, Y T / Liao, G R / Liao, L Z / Libby, J / Limphirat, A / Lin, D X / Lin, T / Liu, B X / Liu, B J / Liu, C / Liu, C X / Liu, D / Liu, F H / Liu, Fang / Liu, Feng / Liu, G M / Liu, H / Liu, H B / Liu, H M / Liu, Huanhuan / Liu, Huihui / Liu, J B / Liu, J L / Liu, J Y / Liu, K / Liu, K Y / Liu, Ke / Liu, L / Liu, L C / Liu, Lu / Liu, M H / Liu, P L / Liu, Q / Liu, S B / Liu, T / Liu, W K / Liu, W M / Liu, X / Liu, Y / Liu, Y B / Liu, Z A / Liu, Z Q / Lou, X C / Lu, F X / Lu, H J / Lu, J G / Lu, X L / Lu, Y / Lu, Y P / Lu, Z H / Luo, C L / Luo, M X / Luo, T / Luo, X L / Lyu, X R / Lyu, Y F / Ma, F C / Ma, H L / Ma, J L / Ma, L L / Ma, M M / Ma, Q M / Ma, R Q / Ma, R T / Ma, X Y / Ma, Y / Maas, F E / Maggiora, M / Maldaner, S / Malde, S / Mangoni, A / Mao, Y J / Mao, Z P / Marcello, S / Meng, Z X / Messchendorp, J G / Mezzadri, G / Miao, H / Min, T J / Mitchell, R E / Mo, X H / Muchnoi, N Yu / Nefedov, Y / Nerling, F / Nikolaev, I B / Ning, Z / Nisar, S / Niu, Y / Olsen, S L / Ouyang, Q / Pacetti, S / Pan, X / Pan, Y / Pathak, A / Pei, Y P / Pelizaeus, M / Peng, H P / Peters, K / Ping, J L / Ping, R G / Plura, S / Pogodin, S / Prasad, V / Qi, F Z / Qi, H / Qi, H R / Qi, M / Qi, T Y / Qian, S / Qian, W B / Qiao, C F / Qin, J J / Qin, L Q / Qin, X P / Qin, X S / Qin, Z H / Qiu, J F / Qu, S Q / Redmer, C F / Ren, K J / Rivetti, A / Rodin, V / Rolo, M / Rong, G / Rosner, Ch / Ruan, S N / Salone, N / Sarantsev, A / Schelhaas, Y / Schoenning, K / Scodeggio, M / Shan, K Y / Shan, W / Shan, X Y / Shangguan, J F / Shao, L G / Shao, M / Shen, C P / Shen, H F / Shen, W H / Shen, X Y / Shi, B A / Shi, H C / Shi, J Y / Shi, Q Q / Shi, R S / Shi, X / Song, J J / Song, T Z / Song, W M / Song, Y X / Sosio, S / Spataro, S / Stieler, F / Su, Y J / Sun, G B / Sun, G X / Sun, H / Sun, H K / Sun, J F / Sun, K / Sun, L / Sun, S S / Sun, T / Sun, W Y / Sun, Y / Sun, Y J / Sun, Y Z / Sun, Z T / Tan, Y X / Tang, C J / Tang, G Y / Tang, J / Tang, Y A / Tao, L Y / Tao, Q T / Tat, M / Teng, J X / Thoren, V / Tian, W H / Tian, Y / Tian, Z F / Uman, I / Wang, B / Wang, B L / Wang, Bo / Wang, C W / Wang, D Y / Wang, F / Wang, H J / Wang, H P / Wang, K / Wang, L L / Wang, M / Wang, Meng / Wang, S / Wang, T / Wang, T J / Wang, W / Wang, W H / Wang, W P / Wang, X / Wang, X F / Wang, X J / Wang, X L / Wang, Y / Wang, Y D / Wang, Y F / Wang, Y H / Wang, Y N / Wang, Y Q / Wang, Yaqian / Wang, Yi / Wang, Z / Wang, Z L / Wang, Z Y / Wang, Ziyi / Wei, D / Wei, D H / Weidner, F / Wen, S P / Wenzel, C W / Wiedner, U / Wilkinson, G / Wolke, M / Wollenberg, L / Wu, C / Wu, J F / Wu, L H / Wu, L J / Wu, X / Wu, X H / Wu, Y / Wu, Y J / Wu, Z / Xia, L / Xian, X M / Xiang, T / Xiao, D / Xiao, G Y / Xiao, H / Xiao, S Y / Xiao, Y L / Xiao, Z J / Xie, C / Xie, X H / Xie, Y / Xie, Y G / Xie, Y H / Xie, Z P / Xing, T Y / Xu, C F / Xu, C J / Xu, G F / Xu, H Y / Xu, Q J / Xu, W L / Xu, X P / Xu, Y C / Xu, Z P / Xu, Z S / Yan, F / Yan, L / Yan, W B / Yan, W C / Yan, X Q / Yang, H J / Yang, H L / Yang, H X / Yang, Tao / Yang, Y / Yang, Y F / Yang, Y X / Yang, Yifan / Ye, M / Ye, M H / Yin, J H / You, Z Y / Yu, B X / Yu, C X / Yu, G / Yu, T / Yu, X D / Yuan, C Z / Yuan, L / Yuan, S C / Yuan, X Q / Yuan, Y / Yuan, Z Y / Yue, C X / Zafar, A A / Zeng, F R / Zeng, X / Zeng, Y / Zeng, Y J / Zhai, X Y / Zhan, Y H / Zhang, A Q / Zhang, B L / Zhang, B X / Zhang, D H / Zhang, G Y / Zhang, H / Zhang, H H / Zhang, H Q / Zhang, H Y / Zhang, J J / Zhang, J L / Zhang, J Q / Zhang, J W / Zhang, J X / Zhang, J Y / Zhang, J Z / Zhang, Jiawei / Zhang, L M / Zhang, L Q / Zhang, Lei / Zhang, P / Zhang, Q Y / Zhang, Shuihan / Zhang, Shulei / Zhang, X D / Zhang, X M / Zhang, X Y / Zhang, Y / Zhang, Y T / Zhang, Y H / Zhang, Yan / Zhang, Yao / Zhang, Z H / Zhang, Z L / Zhang, Z Y / Zhao, G / Zhao, J / Zhao, J Y / Zhao, J Z / Zhao, Lei / Zhao, Ling / Zhao, M G / Zhao, S J / Zhao, Y B / Zhao, Y X / Zhao, Z G / Zhemchugov, A / Zheng, B / Zheng, J P / Zheng, W J / Zheng, Y H / Zhong, B / Zhong, X / Zhou, H / Zhou, L P / Zhou, X / Zhou, X K / Zhou, X R / Zhou, X Y / Zhou, Y Z / Zhu, J / Zhu, K / Zhu, K J / Zhu, L / Zhu, L X / Zhu, S H / Zhu, S Q / Zhu, T J / Zhu, W J / Zhu, Y C / Zhu, Z A / Zou, J H / Zu, J

    Physical review letters

    2023  Volume 130, Issue 12, Page(s) 121901

    Abstract: ... observed in the e^{+}e^{-}→K^{+}K^{-}J/ψ process. These three charmoniumlike ψ states are observed ... The Born cross sections of the process e^{+}e^{-}→D^{*0}D^{*-}π^{+} at center-of-mass energies ... in the e^{+}e^{-}→D^{*0}D^{*-}π^{+} process for the first time. ...

    Abstract The Born cross sections of the process e^{+}e^{-}→D^{*0}D^{*-}π^{+} at center-of-mass energies from 4.189 to 4.951 GeV are measured for the first time. The data samples used correspond to an integrated luminosity of 17.9  fb^{-1} and were collected by the BESIII detector operating at the BEPCII storage ring. Three enhancements around 4.20, 4.47, and 4.67 GeV are visible. The resonances have masses of 4209.6±4.7±5.9  MeV/c^{2}, 4469.1±26.2±3.6  MeV/c^{2}, and 4675.3±29.5±3.5  MeV/c^{2} and widths of 81.6±17.8±9.0  MeV, 246.3±36.7±9.4  MeV, and 218.3±72.9±9.3  MeV, respectively, where the first uncertainties are statistical and the second systematic. The first and third resonances are consistent with the ψ(4230) and ψ(4660) states, respectively, while the second one is compatible with the ψ(4500) observed in the e^{+}e^{-}→K^{+}K^{-}J/ψ process. These three charmoniumlike ψ states are observed in the e^{+}e^{-}→D^{*0}D^{*-}π^{+} process for the first time.
    Language English
    Publishing date 2023-04-06
    Publishing country United States
    Document type Journal Article
    ZDB-ID 208853-8
    ISSN 1079-7114 ; 0031-9007
    ISSN (online) 1079-7114
    ISSN 0031-9007
    DOI 10.1103/PhysRevLett.130.121901
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: A universal in silico V(D)J recombination strategy for developing humanized monoclonal antibodies.

    Hsieh, Yuan-Chin / Liao, Jun-Min / Chuang, Kuo-Hsiang / Ho, Kai-Wen / Hong, Shih-Ting / Liu, Hui-Ju / Huang, Bo-Cheng / Chen, I-Ju / Liu, Yen-Ling / Wang, Jaw-Yuan / Tsai, Hsiang-Lin / Su, Yu-Cheng / Wang, Yen-Tseng / Cheng, Tian-Lu

    Journal of nanobiotechnology

    2022  Volume 20, Issue 1, Page(s) 58

    Abstract: ... We developed an in silico V(D)J recombination platform in which we used V(D)J human germline gene sequences ... Conclusions: Our in silico V(D)J recombination platform can facilitate the development of humanized mAbs ...

    Abstract Background: Humanization of mouse monoclonal antibodies (mAbs) is crucial for reducing their immunogenicity in humans. However, humanized mAbs often lose their binding affinities. Therefore, an in silico humanization method that can prevent the loss of the binding affinity of mAbs is needed.
    Methods: We developed an in silico V(D)J recombination platform in which we used V(D)J human germline gene sequences to design five humanized candidates of anti-tumor necrosis factor (TNF)-α mAbs (C1-C5) by using different human germline templates. The candidates were subjected to molecular dynamics simulation. In addition, the structural similarities of their complementarity-determining regions (CDRs) to those of original mouse mAbs were estimated to derive the weighted interatomic root mean squared deviation (wRMSD
    Results: The R
    Conclusions: Our in silico V(D)J recombination platform can facilitate the development of humanized mAbs with low immunogenicity and high binding affinities. This platform can directly transform numerous mAbs with therapeutic potential to humanized or even human therapeutic Abs for clinical use.
    MeSH term(s) Animals ; Antibodies, Monoclonal/chemistry ; Antibodies, Monoclonal, Humanized ; Mice ; Tumor Necrosis Factor Inhibitors ; Tumor Necrosis Factor-alpha ; V(D)J Recombination
    Chemical Substances Antibodies, Monoclonal ; Antibodies, Monoclonal, Humanized ; Tumor Necrosis Factor Inhibitors ; Tumor Necrosis Factor-alpha
    Language English
    Publishing date 2022-01-31
    Publishing country England
    Document type Journal Article
    ZDB-ID 2100022-0
    ISSN 1477-3155 ; 1477-3155
    ISSN (online) 1477-3155
    ISSN 1477-3155
    DOI 10.1186/s12951-022-01259-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Molecular Mechanism of V(D)J Recombination from Synaptic RAG1-RAG2 Complex Structures.

    Ru, Heng / Chambers, Melissa G / Fu, Tian-Min / Tong, Alexander B / Liao, Maofu / Wu, Hao

    Cell

    2015  Volume 163, Issue 5, Page(s) 1138–1152

    Abstract: ... segments by V(D)J recombination are hallmarks of vertebrate immunity. The (RAG1-RAG2)2 recombinase (RAG ...

    Abstract Diverse repertoires of antigen-receptor genes that result from combinatorial splicing of coding segments by V(D)J recombination are hallmarks of vertebrate immunity. The (RAG1-RAG2)2 recombinase (RAG) recognizes recombination signal sequences (RSSs) containing a heptamer, a spacer of 12 or 23 base pairs, and a nonamer (12-RSS or 23-RSS) and introduces precise breaks at RSS-coding segment junctions. RAG forms synaptic complexes only with one 12-RSS and one 23-RSS, a dogma known as the 12/23 rule that governs the recombination fidelity. We report cryo-electron microscopy structures of synaptic RAG complexes at up to 3.4 Å resolution, which reveal a closed conformation with base flipping and base-specific recognition of RSSs. Distortion at RSS-coding segment junctions and base flipping in coding segments uncover the two-metal-ion catalytic mechanism. Induced asymmetry involving tilting of the nonamer-binding domain dimer of RAG1 upon binding of HMGB1-bent 12-RSS or 23-RSS underlies the molecular mechanism for the 12/23 rule.
    MeSH term(s) Amino Acid Sequence ; Animals ; Cryoelectron Microscopy ; DNA-Binding Proteins/chemistry ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/ultrastructure ; Homeodomain Proteins/chemistry ; Homeodomain Proteins/genetics ; Homeodomain Proteins/ultrastructure ; Humans ; Mice ; Molecular Sequence Data ; Multiprotein Complexes/chemistry ; Multiprotein Complexes/ultrastructure ; Mutation ; Sequence Alignment ; V(D)J Recombination ; Zebrafish
    Chemical Substances DNA-Binding Proteins ; Homeodomain Proteins ; Multiprotein Complexes ; V(D)J recombination activating protein 2 ; RAG-1 protein (128559-51-3)
    Language English
    Publishing date 2015-11-19
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2015.10.055
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Molecular Mechanism of V(D)J Recombination from Synaptic RAG1-RAG2 Complex Structures

    Ru, Heng / Melissa G. Chambers / Tian-Min Fu / Alexander B. Tong / Maofu Liao / Hao Wu

    Cell. 2015 Nov. 19, v. 163

    2015  

    Abstract: ... segments by V(D)J recombination are hallmarks of vertebrate immunity. The (RAG1-RAG2)2 recombinase (RAG ...

    Abstract Diverse repertoires of antigen-receptor genes that result from combinatorial splicing of coding segments by V(D)J recombination are hallmarks of vertebrate immunity. The (RAG1-RAG2)2 recombinase (RAG) recognizes recombination signal sequences (RSSs) containing a heptamer, a spacer of 12 or 23 base pairs, and a nonamer (12-RSS or 23-RSS) and introduces precise breaks at RSS-coding segment junctions. RAG forms synaptic complexes only with one 12-RSS and one 23-RSS, a dogma known as the 12/23 rule that governs the recombination fidelity. We report cryo-electron microscopy structures of synaptic RAG complexes at up to 3.4 Å resolution, which reveal a closed conformation with base flipping and base-specific recognition of RSSs. Distortion at RSS-coding segment junctions and base flipping in coding segments uncover the two-metal-ion catalytic mechanism. Induced asymmetry involving tilting of the nonamer-binding domain dimer of RAG1 upon binding of HMGB1-bent 12-RSS or 23-RSS underlies the molecular mechanism for the 12/23 rule.
    Keywords cryo-electron microscopy ; genes ; immunity ; signal peptide ; vertebrates
    Language English
    Dates of publication 2015-1119
    Size p. 1138-1152.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2015.10.055
    Database NAL-Catalogue (AGRICOLA)

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  5. Article: No requirement for V(D)J recombination in p53-deficient thymic lymphoma.

    Liao, M J / Zhang, X X / Hill, R / Gao, J / Qumsiyeh, M B / Nichols, W / Van Dyke, T

    Molecular and cellular biology

    1998  Volume 18, Issue 6, Page(s) 3495–3501

    Abstract: ... inactivation leads to tumorigenesis, several observations suggest that V(D)J recombination of T-cell receptor ... Inactivation of p53 would allow V(D)J driven mutation of additional cancer genes, facilitating tumorigenesis ... Here, we show that mice with a p53 deficiency in thymocytes and unable to carry out V(D)J recombination ...

    Abstract The p53 tumor suppressor is activated in response to a variety of cellular stress signals, although specific in vivo signals that trigger tumor suppression are unknown. In mouse thymocytes, where p53 inactivation leads to tumorigenesis, several observations suggest that V(D)J recombination of T-cell receptor (TCR) loci could provide a DNA damage signal triggering p53-dependent apoptosis and tumor suppression. Inactivation of p53 would allow V(D)J driven mutation of additional cancer genes, facilitating tumorigenesis. Here, we show that mice with a p53 deficiency in thymocytes and unable to carry out V(D)J recombination are not impaired in the development of thymoma. Recombination-activating gene (RAG) deficiencies were introduced into both p53-/- mice and TgTDeltaN transgenic mice, a strain in which 100% of the mice develop thymoma due to thymocyte-specific inactivation of p53 by a simian virus 40 T-antigen variant. V(D)J recombination was dispensable for tumorigenesis since thymomas developed with or without the RAG-1 or RAG-2 gene, although some delay was observed. When V(D)J recombination was suppressed by expression of rearranged TCR transgenes, 100% of the TgTDeltaN mice developed thymoma, surprisingly with reduced latency. Further introduction of a RAG deficiency into these mice had no impact on the timing or frequency of tumorigenesis. Finally, karyotype and chromosome painting analyses showed no evidence for TCR gene translocations in p53-deficient thymomas, although abundant aneuploidy involving frequent duplication of certain chromosomes was present. Thus, contrary to the current hypothesis, these studies indicate that signals other than V(D)J recombination promote p53 tumor suppression in thymocytes and that the mechanism of tumorigenesis is distinct from TCR translocation oncogene activation.
    MeSH term(s) Animals ; Chromosome Aberrations/genetics ; DNA-Binding Proteins/physiology ; Gene Rearrangement, T-Lymphocyte ; Homeodomain Proteins ; Mice ; Mice, Inbred C57BL ; Mice, SCID ; Mice, Transgenic ; Receptors, Antigen, T-Cell/genetics ; Thymoma/genetics ; Thymus Neoplasms/genetics ; Transgenes ; Translocation, Genetic ; Tumor Suppressor Protein p53/deficiency ; Tumor Suppressor Protein p53/genetics
    Chemical Substances DNA-Binding Proteins ; Homeodomain Proteins ; Rag2 protein, mouse ; Receptors, Antigen, T-Cell ; Tumor Suppressor Protein p53 ; V(D)J recombination activating protein 2 ; RAG-1 protein (128559-51-3)
    Language English
    Publishing date 1998-06
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 779397-2
    ISSN 1098-5549 ; 0270-7306
    ISSN (online) 1098-5549
    ISSN 0270-7306
    DOI 10.1128/MCB.18.6.3495
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Critical role for Atm in suppressing V(D)J recombination-driven thymic lymphoma.

    Liao, M J / Van Dyke, T

    Genes & development

    1999  Volume 13, Issue 10, Page(s) 1246–1250

    Abstract: ... from Ataxia telangiectasia (AT) patients and in mouse Atm-/- thymoma, suggesting the involvement of V(D)J recombination ... that V(D)J recombination is critical for thymoma development in these mice. Therefore, aberrant V(D)J ... recombination, normally suppressed by Atm, facilitates tumorigenic events leading to cancer. Because V(D)J ...

    Abstract Chromosome translocations involving T cell receptor (TCR) loci have been found in tumors from Ataxia telangiectasia (AT) patients and in mouse Atm-/- thymoma, suggesting the involvement of V(D)J recombination in these malignancies. By introducing a RAG-1 deficiency into Atm-/- mice in the presence of a TCR transgene, we show that V(D)J recombination is critical for thymoma development in these mice. Therefore, aberrant V(D)J recombination, normally suppressed by Atm, facilitates tumorigenic events leading to cancer. Because V(D)J recombination is dispensable for lymphomagenesis upon p53 deficiency, this study also indicates that Atm and p53 function by distinct mechanisms in suppressing thymoma.
    MeSH term(s) Animals ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins ; DNA-Binding Proteins ; Gene Rearrangement, T-Lymphocyte/genetics ; Genes, T-Cell Receptor beta ; Genes, p53/physiology ; Homeodomain Proteins/physiology ; Immunophenotyping ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Protein-Serine-Threonine Kinases ; Proteins/physiology ; Thymoma/genetics ; Thymus Neoplasms/genetics ; Time Factors ; Tumor Suppressor Proteins
    Chemical Substances Cell Cycle Proteins ; DNA-Binding Proteins ; Homeodomain Proteins ; Proteins ; Tumor Suppressor Proteins ; RAG-1 protein (128559-51-3) ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; Atm protein, mouse (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 1999-05-15
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 806684-x
    ISSN 1549-5477 ; 0890-9369
    ISSN (online) 1549-5477
    ISSN 0890-9369
    DOI 10.1101/gad.13.10.1246
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  7. Article ; Online: Comparison of intravesical chemotherapy regimens after radical nephroureterectomy for upper tract urothelial carcinoma and analysis of risk factors for postoperative recurrence.

    Jiang, S-C / Liao, Y-G / Luo, J / Hu, D / Wang, Y-D / He, K

    European review for medical and pharmacological sciences

    2024  Volume 28, Issue 6, Page(s) 2387–2395

    Abstract: Objective: Upper tract urothelial carcinoma (UTUC) is a relatively rare but aggressive type of urologic cancer that includes renal pelvic tumors and ureteral tumors with a poor prognosis. Full-length nephroureterectomy plus sleeve bladder resection is ... ...

    Abstract Objective: Upper tract urothelial carcinoma (UTUC) is a relatively rare but aggressive type of urologic cancer that includes renal pelvic tumors and ureteral tumors with a poor prognosis. Full-length nephroureterectomy plus sleeve bladder resection is the standard treatment for the disease, but patients are prone to recurrence of bladder tumors after surgery. Intravesical infusion therapy is the main means to prevent the recurrence and progression of bladder cancer. Epirubicin and gemcitabine are widely used in clinical practice as first-line or salvage therapy for intravesical chemotherapy; however, the efficacy of these agents is rarely discussed. The purpose of this study was to investigate the effects of epirubicin and gemcitabine on the occurrence of bladder cancer after radical nephroureterectomy for UTUC and to analyze the risk factors affecting the recurrence of postoperative bladder cancer.
    Patients and methods: A total of 215 patients with diagnosed UTUC and treated in our hospital from June 2019 to August 2021 were retrospectively selected as the research subjects, and they were divided into an observation group (120 cases) and a control group (95 cases) according to different treatment methods. The patients in the control group were treated with epirubicin, while those in the observation group received gemcitabine. All patients were followed up by telephone or outpatient examination for 12 months to record the occurrence of adverse reactions. The occurrence of bladder cancer was recorded at 3 months, 6 months, and 12 months after the surgery. According to the occurrence of bladder cancer after surgery, the patients were divided into a bladder cancer group (63 cases) and a non-bladder cancer group (152 cases). Multivariate Logistic regression analysis was used to analyze the risk factors of bladder cancer after surgery.
    Results: The total incidence of adverse reactions in the control group was 49.47%, which was higher than that in the observation group with 15.00% (p<0.01). The incidence of bladder tumors in the observation group and the control group was 0.00% and 2.11% at 3 months, 5.00% and 8.42% at 6 months, 13.33% and 15.79% at 12 months, without significant difference (p>0.05). After 12 months of perfusion, the levels of acidic fibroblast growth factor (aFGF), basic fibroblast growth factor (bFGF), and vascular endothelial growth factor (VEGF) in the two groups were significantly lower than those before perfusion (p<0.05). In the observation group, the levels of these three factors were slightly decreased compared with those in the control group, without a significant difference (p>0.05). Between the bladder cancer and non-bladder cancer groups, there were significant differences in tumor location, number of lesions, tumor stage, preoperative ureteral examination, and preoperative history of bladder cancer (p<0.05). The above indexes were all risk factors for postoperative bladder cancer (p<0.05).
    Conclusions: Epirubicin and gemcitabine reduced the occurrence of bladder cancer and effectively inhibited tumor angiogenesis after radical nephroureterectomy for UTUC. The tumor location, number of lesions, tumor stage, preoperative ureteral examination, and preoperative history of bladder cancer were risk factors for postoperative bladder cancer.
    MeSH term(s) Humans ; Nephroureterectomy ; Urinary Bladder Neoplasms/drug therapy ; Urinary Bladder Neoplasms/surgery ; Urinary Bladder Neoplasms/pathology ; Carcinoma, Transitional Cell/drug therapy ; Carcinoma, Transitional Cell/surgery ; Retrospective Studies ; Epirubicin/therapeutic use ; Gemcitabine ; Vascular Endothelial Growth Factor A ; Risk Factors ; Neoplasm Recurrence, Local/pathology ; Nephrectomy
    Chemical Substances Epirubicin (3Z8479ZZ5X) ; Gemcitabine ; Vascular Endothelial Growth Factor A
    Language English
    Publishing date 2024-04-04
    Publishing country Italy
    Document type Journal Article
    ZDB-ID 605550-3
    ISSN 2284-0729 ; 1128-3602 ; 0392-291X
    ISSN (online) 2284-0729
    ISSN 1128-3602 ; 0392-291X
    DOI 10.26355/eurrev_202403_35745
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: A Single-Institution Review of the Use of Radiation in the Adjuvant and Definitive Management of Keloids.

    Fernandes, J / Liao, D / Dasgupta, A / Tsao, M N / Barnes, E A

    Clinical oncology (Royal College of Radiologists (Great Britain))

    2024  

    Abstract: Aims: Many individuals suffer from keloids that are refractory to standard treatment modalities, including surgical excision alone. Radiation therapy can be used to reduce the risk of recurrent keloids post-operatively, as well as be used as primary ... ...

    Abstract Aims: Many individuals suffer from keloids that are refractory to standard treatment modalities, including surgical excision alone. Radiation therapy can be used to reduce the risk of recurrent keloids post-operatively, as well as be used as primary treatment for keloids not amenable to surgical resection. The purpose of this study was to review our institutional experience of radiation therapy for keloid management.
    Materials and methods: A retrospective review of patients treated with radiation therapy for keloids between 2014 and 2020 at our institution was performed.
    Results: A total of 70 keloids in 41 patients were treated. For the 55 keloids treated with post-operative radiation therapy (16Gy delivered in 2 fractions), 82.5% (33/40) of evaluable lesions did not recur. Among the 15 keloids treated with definitive radiation therapy (24Gy delivered in 3 fractions), 78.6% (11/14) of evaluable keloids showed complete flattening, and 14.3% (2/14) had partial flattening. Both acute and late toxicities were mild, with only a single instance of grade 3 toxicity (dermatitis).
    Conclusion: Our study confirms that radiation therapy has a role in reducing the risk of keloid recurrence post-operatively, and plays an important role in the definitive management of unresectable keloids.
    Language English
    Publishing date 2024-03-18
    Publishing country England
    Document type Journal Article
    ZDB-ID 1036844-9
    ISSN 1433-2981 ; 0936-6555
    ISSN (online) 1433-2981
    ISSN 0936-6555
    DOI 10.1016/j.clon.2024.03.018
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Letter: Determining optimal ALT cut-off values for predicting significant hepatic histological changes in chronic hepatitis B virus infection.

    Li, Jianrong / Yang, Dalong / Zhong, Jianhong / Liao, Yingyang

    Alimentary pharmacology & therapeutics

    2024  Volume 59, Issue 9, Page(s) 1156–1157

    MeSH term(s) Humans ; Hepatitis B, Chronic/pathology ; Hepatitis B virus/genetics ; Alanine Transaminase ; Hepatitis B e Antigens ; DNA, Viral
    Chemical Substances Alanine Transaminase (EC 2.6.1.2) ; Hepatitis B e Antigens ; DNA, Viral
    Language English
    Publishing date 2024-04-09
    Publishing country England
    Document type Letter
    ZDB-ID 639012-2
    ISSN 1365-2036 ; 0269-2813 ; 0953-0673
    ISSN (online) 1365-2036
    ISSN 0269-2813 ; 0953-0673
    DOI 10.1111/apt.17939
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Inhibition of miR-542-3p augments autophagy to promote diabetic corneal wound healing.

    Liao, Danling / Wei, Shijia / Hu, Jianzhang

    Eye and vision (London, England)

    2024  Volume 11, Issue 1, Page(s) 3

    Abstract: Background: Autophagy has recently been shown to be critical for protecting peripheral nerve regeneration. This study explored the impact of miR-542-3p on diabetic corneal nerve regeneration and epithelial healing through the regulation of autophagy.: ...

    Abstract Background: Autophagy has recently been shown to be critical for protecting peripheral nerve regeneration. This study explored the impact of miR-542-3p on diabetic corneal nerve regeneration and epithelial healing through the regulation of autophagy.
    Methods: A type 1 diabetes model was established in male mice through streptozotocin administration. Immunofluorescence staining of β-Tubulin III and sodium fluorescein staining were performed to observe corneal nerve fiber density and corneal epithelial healing, respectively. Western blotting, immunofluorescence and transmission electron microscopy were used to determine autophagy levels. Subconjunctival injection of RAPA and 3-MA altered autophagy levels; with them, we evaluated the role of autophagy in diabetic keratopathy. miRNA sequencing and bioinformatics analysis were performed to identify miRNA-mRNA networks with potential autophagy-regulating roles, and miR-542-3p was measured by quantitative real-time polymerase chain reaction (qRT-PCR). miR-542-3p antagomir was injected subconjunctivally to assess the role in diabetic corneal neuropathy.
    Results: Our data suggest that autophagy is suppressed in the diabetic corneal nerve and that activation of autophagy promotes diabetic corneal wound healing. We identified a potential autophagy-regulating miRNA-mRNA network in the diabetic trigeminal ganglion, in which miR-542-3p expression was significantly upregulated. Inhibition of miR-542-3p significantly enhanced the level of autophagy in trigeminal ganglion by upregulating ATG4D expression, thereby accelerating diabetic corneal nerve regeneration and epithelial healing.
    Conclusions: Dysregulated autophagy is an important contributor to delayed diabetic corneal injury healing. Inhibiting miR-542-3p promotes diabetic corneal nerve regeneration and epithelial healing through autophagy activation by ATG4D.
    Language English
    Publishing date 2024-01-03
    Publishing country England
    Document type Journal Article
    ZDB-ID 2806610-8
    ISSN 2326-0254
    ISSN 2326-0254
    DOI 10.1186/s40662-023-00370-1
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