LIVIVO - Search results -

Search results

Result 1 - 9 of total 9

Search options

Article ; Online: Loss of VOPP1 Contributes to BET Inhibitor Acquired Resistance in Non-Small Cell Lung Cancer Cells.

Sun, Lin / Wu, Qian / Huan, Xia-Juan / Tian, Chang-Qing / Wang, Ying-Qing / Miao, Ze-Hong

2022 Volume 20, Issue 12, Page(s) 1785–1798

Abstract: Inhibitors targeting bromodomain and extraterminal (BET) proteins are promising anticancer drugs. The emergence of drug resistance during treatments will impair their therapeutic effectiveness. To investigate the mechanisms of acquired resistance to BET ... ...

Abstract	Inhibitors targeting bromodomain and extraterminal (BET) proteins are promising anticancer drugs. The emergence of drug resistance during treatments will impair their therapeutic effectiveness. To investigate the mechanisms of acquired resistance to BET inhibitors (BETi), we generated a series of drug-resistant sublines by exposing non-small cell lung cancer (NSCLC) NCI-H1975 cells to the BETi ABBV-075. These sublines displayed cross-resistance to other tested BETis, increased migration abilities, reduced growth rates accompanied by an increased proportion of cells in G1 phase and decreased apoptotic responses to BETis. Changes in RNA expression and gene mutation profiles in the resistant variants indicate that emergence of BETi resistance is multifactorial. Importantly, all the tested ABBV-075-resistant variants showed loss of vesicular overexpressed in cancer prosurvival protein 1 (VOPP1) and an increase in the antiapoptotic BCL-2 protein. By knockdown, knockout, and reconstitution of VOPP1 in resistant cells, their parental cells, and other NSCLC cells, we confirmed that the loss of VOPP1 contributed to BETi resistance. Moreover, knockout of VOPP1 in the parental cells caused the increased expression of BCL-2, and the latter directly mediated BETi resistance. Through combined treatments with BETis and BCL-2 inhibitors (BCL-2i), we demonstrated that BCL-2is synergistically sensitized resistant cells to BETis. Implications: Based on these results, for the first time, we establish a causal link from VOPP1 loss to BCL-2 gain and then to BETi resistance, which provides new insights into BETi resistance and paves the way for further testing to circumvent BETi resistance.
MeSH term(s)	Humans ; Antineoplastic Agents/pharmacology ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/genetics ; Cell Line, Tumor ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Proto-Oncogene Proteins c-bcl-2/genetics ; Transcription Factors/genetics
Chemical Substances	Antineoplastic Agents ; mivebresib (VR86R11J7J) ; Proto-Oncogene Proteins c-bcl-2 ; Transcription Factors ; VOPP1 protein, human ; DNER protein, human
Language	English
Publishing date	2022-08-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-21-1000
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 5744: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾

Article ; Online: Proteasome inhibitors reduce CD73 expression partly via decreasing p-ERK in NSCLC cells.

Su, Ai-Ling / Tian, Chang-Qing / Ou, Ying-Jie / Bao, Xu-Bin / Huan, Xia-Juan / Miao, Ze-Hong / Wang, Ying-Qing

Life sciences

2023 Volume 332, Page(s) 122129

Abstract: Ecto-5'-nucleotidase (CD73), encoded by the NT5E gene, mediates tumor immunosuppression and has been targeted for the development of new anticancer drugs. Proteasome inhibitors impair protein degradation by inhibiting proteasome and have been used in the ...

Abstract	Ecto-5'-nucleotidase (CD73), encoded by the NT5E gene, mediates tumor immunosuppression and has been targeted for the development of new anticancer drugs. Proteasome inhibitors impair protein degradation by inhibiting proteasome and have been used in the clinic for cancer therapy. Here we report that proteasome inhibitors reduce the protein and mRNA levels of CD73. Among 127 tested small-molecule drugs, proteasome inhibitors were found to consistently decrease the protein and mRNA levels of CD73 in NSCLC NCI-H1299 cells. This effect was further confirmed in different NSCLC cells exposed to different proteasome inhibitors. In those treated cells, the protein levels of ERK and its active form p-ERK, the vital components in the MAPK pathway, were reduced. Consistently, inhibitors of MEK and ERK, another two members of the MAPK pathway, also lowered the protein and mRNA levels of CD73. Correspondingly, treatments with fibroblast growth factor 2 (FGF2), an activator of the MAPK pathway, enhanced the levels of p-ERK and partly rescued the proteasome inhibitor-driven reduction of CD73 mRNA and protein in NSCLC cells. However, exogenous CD73 overexpression in murine Lewis lung carcinoma (LLC) cells was not lowered either in vitro or in vivo, by the treatments with proteasome inhibitors and basically, did not affect their in vitro proliferative inhibition either. In contrast, CD73 overexpression dramatically reduced the in vivo anticancer activity of Bortezomib in immunocompetent mice, with tumor growth inhibition rates from 52.18 % for LLC/vector down to 8.75 % for LLC/NT5E homografts. These findings give new insights into the anticancer mechanisms of proteasome inhibitors.
Language	English
Publishing date	2023-09-26
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2023.122129
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.368: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Polymerase independent repression of FoxO1 transcription by sequence-specific PARP1 binding to FoxO1 promoter.

Tian, Yu-Nan / Chen, Hua-Dong / Tian, Chang-Qing / Wang, Ying-Qing / Miao, Ze-Hong

Cell death & disease

2020 Volume 11, Issue 1, Page(s) 71

Abstract: Poly(ADP-ribose) polymerase 1 (PARP1) regulates gene transcription in addition to functioning as a DNA repair factor. Forkhead box O1 (FoxO1) is a transcription factor involved in extensive biological processes. Here, we report that PARP1 binds to two ... ...

Abstract	Poly(ADP-ribose) polymerase 1 (PARP1) regulates gene transcription in addition to functioning as a DNA repair factor. Forkhead box O1 (FoxO1) is a transcription factor involved in extensive biological processes. Here, we report that PARP1 binds to two separate motifs on the FoxO1 promoter and represses its transcription in a polymerase-independent manner. Using PARP1-knock out (KO) cells, wild-type-PARP1-complemented cells and catalytic mutant PARP1
MeSH term(s)	Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Proliferation/genetics ; DNA Damage/drug effects ; Forkhead Box Protein O1/genetics ; Forkhead Box Protein O1/metabolism ; Gene Expression Regulation/genetics ; Gene Knockout Techniques ; Humans ; Mutation ; Poly (ADP-Ribose) Polymerase-1/antagonists & inhibitors ; Poly (ADP-Ribose) Polymerase-1/genetics ; Poly (ADP-Ribose) Polymerase-1/metabolism ; Poly(ADP-ribose) Polymerase Inhibitors/pharmacology ; Promoter Regions, Genetic ; Protein Binding ; Sarcoma, Ewing/genetics ; Sarcoma, Ewing/metabolism ; Up-Regulation
Chemical Substances	FOXO1 protein, human ; Forkhead Box Protein O1 ; Poly(ADP-ribose) Polymerase Inhibitors ; PARP1 protein, human (EC 2.4.2.30) ; Poly (ADP-Ribose) Polymerase-1 (EC 2.4.2.30)
Language	English
Publishing date	2020-01-28
Publishing country	England
Document type	Journal Article
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-020-2265-y
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Novel bivalent BET inhibitor N2817 exhibits potent anticancer activity and inhibits TAF1.

Wu, Qian / Chen, Dan-Qi / Sun, Lin / Huan, Xia-Juan / Bao, Xu-Bin / Tian, Chang-Qing / Hu, Jianping / Lv, Kai-Kai / Wang, Ying-Qing / Xiong, Bing / Miao, Ze-Hong

Biochemical pharmacology

2021 Volume 185, Page(s) 114435

Abstract: Bromodomain and extra-terminal domain (BET) family proteins are promising anticancer targets. Most BET inhibitors in clinical trials are monovalent. They competitively bind to one of the bromodomains (BD1 and BD2) in BET proteins and exhibit relatively ... ...

Abstract	Bromodomain and extra-terminal domain (BET) family proteins are promising anticancer targets. Most BET inhibitors in clinical trials are monovalent. They competitively bind to one of the bromodomains (BD1 and BD2) in BET proteins and exhibit relatively weak anticancer activity, poor pharmacokinetics, and low metabolic stability. Here, we evaluated the anticancer activity of a novel bivalent BET inhibitor, N2817, which consists of two molecules of the monovalent BET inhibitor 8124-053 connected by a common piperazine ring, rendering a long linker unnecessary. Compared with ABBV-075, one of the potent monovalent BET inhibitors reported to date, N2817 showed greater potency in inhibiting proliferation, arresting cell-cycle, inducing apoptosis, and suppressing the growth of tumor xenografts. Moreover, N2817 showed high metabolic stability, a relatively long half-life, and no brain penetration after oral administration. Additionally, N2817 directly bound and inhibited another BD-containing protein, TAF1 (BD2), as evidenced by a reduction in mRNA and protein levels. TAF1 inhibition contributed to the anticancer effect of N2817. Therefore, this study offers a new paradigm for designing bivalent BET inhibitors and introduces a novel potent bivalent BET inhibitor and a new anticancer mechanism.
MeSH term(s)	A549 Cells ; Animals ; Antineoplastic Agents/pharmacology ; Dose-Response Relationship, Drug ; Female ; HCT116 Cells ; Histone Acetyltransferases/antagonists & inhibitors ; Histone Acetyltransferases/metabolism ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Inbred ICR ; Mice, Nude ; Proteins/antagonists & inhibitors ; Proteins/metabolism ; TATA-Binding Protein Associated Factors/antagonists & inhibitors ; TATA-Binding Protein Associated Factors/metabolism ; Transcription Factor TFIID/antagonists & inhibitors ; Transcription Factor TFIID/metabolism ; Tumor Burden/drug effects ; Tumor Burden/physiology ; Xenograft Model Antitumor Assays/methods
Chemical Substances	Antineoplastic Agents ; Proteins ; TATA-Binding Protein Associated Factors ; Transcription Factor TFIID ; bromodomain and extra-terminal domain protein, human ; Histone Acetyltransferases (EC 2.3.1.48) ; TATA-binding protein associated factor 250 kDa (EC 2.7.11.1)
Language	English
Publishing date	2021-02-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2021.114435
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 19: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: A Novel Type II NAD+-Specific Isocitrate Dehydrogenase from the Marine Bacterium Congregibacter litoralis KT71.

Wu, Ming-Cai / Tian, Chang-Qing / Cheng, Hong-Mei / Xu, Lei / Wang, Peng / Zhu, Guo-Ping

PloS one

2015 Volume 10, Issue 5, Page(s) e0125229

Abstract: In most living organisms, isocitrate dehydrogenases (IDHs) convert isocitrate into ɑ-ketoglutarate (ɑ-KG). Phylogenetic analyses divide the IDH protein family into two subgroups: types I and II. Based on cofactor usage, IDHs are either NAD+-specific (NAD- ...

Abstract	In most living organisms, isocitrate dehydrogenases (IDHs) convert isocitrate into ɑ-ketoglutarate (ɑ-KG). Phylogenetic analyses divide the IDH protein family into two subgroups: types I and II. Based on cofactor usage, IDHs are either NAD+-specific (NAD-IDH) or NADP+-specific (NADP-IDH); NADP-IDH evolved from NAD-IDH. Type I IDHs include NAD-IDHs and NADP-IDHs; however, no type II NAD-IDHs have been reported to date. This study reports a novel type II NAD-IDH from the marine bacterium Congregibacter litoralis KT71 (ClIDH, GenBank accession no. EAQ96042). His-tagged recombinant ClIDH was produced in Escherichia coli and purified; the recombinant enzyme was NAD+-specific and showed no detectable activity with NADP+. The Km values of the enzyme for NAD+ were 262.6±7.4 μM or 309.1±11.2 μM with Mg2+ or Mn2+ as the divalent cation, respectively. The coenzyme specificity of a ClIDH Asp487Arg/Leu488His mutant was altered, and the preference of the mutant for NADP+ was approximately 24-fold higher than that for NAD+, suggesting that ClIDH is an NAD+-specific ancestral enzyme in the type II IDH subgroup. Gel filtration and analytical ultracentrifugation analyses revealed the homohexameric structure of ClIDH, which is the first IDH hexamer discovered thus far. A 163-amino acid segment of CIIDH is essential to maintain its polymerization structure and activity, as a truncated version lacking this region forms a non-functional monomer. ClIDH was dependent on divalent cations, the most effective being Mn2+. The maximal activity of purified recombinant ClIDH was achieved at 35°C and pH 7.5, and a heat inactivation experiment showed that a 20-min incubation at 33°C caused a 50% loss of ClIDH activity. The discovery of a NAD+-specific, type II IDH fills a gap in the current classification of IDHs, and sheds light on the evolution of type II IDHs.
MeSH term(s)	Amino Acid Sequence ; Enzyme Activation ; Gammaproteobacteria/enzymology ; Gammaproteobacteria/genetics ; Gene Expression ; Isocitrate Dehydrogenase/chemistry ; Isocitrate Dehydrogenase/genetics ; Isocitrate Dehydrogenase/metabolism ; Kinetics ; Molecular Sequence Data ; Mutation ; NAD/metabolism ; Protein Multimerization ; Recombinant Proteins/genetics ; Recombinant Proteins/isolation & purification ; Recombinant Proteins/metabolism ; Sequence Alignment
Chemical Substances	Recombinant Proteins ; NAD (0U46U6E8UK) ; Isocitrate Dehydrogenase (EC 1.1.1.41) ; isocitrate dehydrogenase (NADP+) (EC 1.1.1.42)
Language	English
Publishing date	2015
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0125229
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Full text

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Details ▾
- Full text online
- Order with fees

Article ; Online: Inhibition of the BET family reduces its new target gene IDO1 expression and the production of L-kynurenine.

Tian, Chang-Qing / Chen, Lin / Chen, Hua-Dong / Huan, Xia-Juan / Hu, Jian-Ping / Shen, Jing-Kang / Xiong, Bing / Wang, Ying-Qing / Miao, Ze-Hong

Cell death & disease

2019 Volume 10, Issue 8, Page(s) 557

Abstract: The bromodomain and extra terminal domain (BET) family members, including BRD2, BRD3, and BRD4, act as epigenetic readers to regulate gene expression. Indoleamine 2,3-dioxygenase 1 (IDO1) is an enzyme that participates in tumor immune escape primarily by ...

Abstract	The bromodomain and extra terminal domain (BET) family members, including BRD2, BRD3, and BRD4, act as epigenetic readers to regulate gene expression. Indoleamine 2,3-dioxygenase 1 (IDO1) is an enzyme that participates in tumor immune escape primarily by catalyzing tryptophan to L-kynurenine. Here, we report that IDO1 is a new target gene of the BET family. RNA profiling showed that compound 9, a new BET inhibitor, reduced IDO1 mRNA up to seven times in Ty-82 cells. IDO1 differentially expressed in tumor cells and its expression could be induced with interferon gamma (IFN-γ). BET inhibitors (ABBV-075, JQ1, and OTX015) inhibited both constitutive and IFN-γ-inducible expression of IDO1. Similarly, reduction of BRD2, BRD3, or BRD4 decreased IDO1 expression. All these BET family members bound to the IDO1 promoter via the acetylated histone H3. JQ1 led to their release and reduced enrichment of RNA polymerase II (Pol II) on the promoter. IFN-γ increased the binding of BRD2, BRD3, BRD4, and Pol II on the IDO1 promoter by increasing the acetylation of histone H3, which could be prevented by JQ1 partially or even completely. Furthermore, both JQ1 and OTX015 decreased the production of L-kynurenine. The combination of BET inhibitors with the IDO1 inhibitor further reduced L-kynurenine, though only marginally. Importantly, the BET inhibitor ABBV-075 significantly inhibited the growth of human Ty-82 xenografts in nude mice and reduced both protein and mRNA levels of IDO1 in the xenografts. This finding lays a basis for the potential combination of BET inhibitors and IDO1 inhibitors for the treatment of IDO1-expressing cancers.
MeSH term(s)	A549 Cells ; Acetylation ; Animals ; Cell Cycle Proteins/antagonists & inhibitors ; Cell Cycle Proteins/genetics ; Female ; Gene Expression/drug effects ; HL-60 Cells ; HeLa Cells ; Histones/metabolism ; Humans ; Indoleamine-Pyrrole 2,3,-Dioxygenase/antagonists & inhibitors ; Indoleamine-Pyrrole 2,3,-Dioxygenase/genetics ; Indoleamine-Pyrrole 2,3,-Dioxygenase/metabolism ; Kynurenine/biosynthesis ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Promoter Regions, Genetic ; Pyridones/pharmacology ; RNA, Messenger/genetics ; Sulfonamides/pharmacology ; Transcription Factors/antagonists & inhibitors ; Transcription Factors/genetics ; Transfection ; Tumor Burden/drug effects ; Xenograft Model Antitumor Assays
Chemical Substances	BRD2 protein, human ; BRD3 protein, human ; BRD4 protein, human ; Cell Cycle Proteins ; Histones ; IDO1 protein, human ; Indoleamine-Pyrrole 2,3,-Dioxygenase ; Pyridones ; RNA, Messenger ; Sulfonamides ; Transcription Factors ; Kynurenine (343-65-7) ; mivebresib (VR86R11J7J)
Language	English
Publishing date	2019-07-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-019-1793-9
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: A new BET inhibitor, 171, inhibits tumor growth through cell proliferation inhibition more than apoptosis induction.

Damaneh, Mohammadali Soleimani / Hu, Jian-Ping / Huan, Xia-Juan / Song, Shan-Shan / Tian, Chang-Qing / Chen, Dan-Qi / Meng, Tao / Chen, Yue-Lei / Shen, Jing-Kang / Xiong, Bing / Miao, Ze-Hong / Wang, Ying-Qing

Investigational new drugs

2019 Volume 38, Issue 3, Page(s) 700–713

Abstract: The bromodomain and extra-terminal domain (BET) family of proteins, especially bromodomain-containing protein 4 (BRD4), has emerged as exciting anti-tumor targets due to their important roles in epigenetic regulation. Therefore, the discovery of BET ... ...

Abstract	The bromodomain and extra-terminal domain (BET) family of proteins, especially bromodomain-containing protein 4 (BRD4), has emerged as exciting anti-tumor targets due to their important roles in epigenetic regulation. Therefore, the discovery of BET inhibitors with promising anti-tumor efficacy will provide a novel approach to epigenetic anticancer therapy. Recently, we discovered the new BET inhibitor compound 171, which is derived from a polo-like kinase 1 (PLK1)-BRD4 dual inhibitor based on our previous research. Compound 171 was found to maintain BET inhibition ability without PLK1 inhibition, and there was no selectivity among BET family members. The in vitro and in vivo results both indicated that the overall anti-tumor activity of compound 171 was improved compared with the (+)-JQ-1 or OTX-015 BET inhibitors. Furthermore, we found that compound 171 could regulate the expression of cell cycle-regulating proteins including c-Myc and p21 and induce cell cycle arrest in the G
MeSH term(s)	A549 Cells ; Animals ; Apoptosis/drug effects ; Cell Cycle Checkpoints/drug effects ; Cell Death/drug effects ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Epigenesis, Genetic/drug effects ; G1 Phase/drug effects ; Gene Expression Regulation, Neoplastic/drug effects ; HT29 Cells ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; PC-3 Cells ; Proteins/antagonists & inhibitors ; Resting Phase, Cell Cycle/drug effects ; Xenograft Model Antitumor Assays
Chemical Substances	Proteins ; bromodomain and extra-terminal domain protein, human
Language	English
Publishing date	2019-07-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604895-x
ISSN	1573-0646 ; 0167-6997
ISSN (online)	1573-0646
ISSN	0167-6997
DOI	10.1007/s10637-019-00818-z
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 1823: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Monostotic fibrous dysplasia of the thoracic spine: A case report.

Ren, Kai / Lan, Tao / Yu, Zheng / Chen, Yang / Tian, Chang-Qing / Gu, Hu-Sheng / Yang, Xin-Jian

Journal of back and musculoskeletal rehabilitation

2016 Volume 29, Issue 2, Page(s) 387–391

Abstract: Background and objective: Fibrous dysplasia (FD) is a benign bone lesion manifested by local pain, swelling and deformity change. We report a case of monostotic fibrous dysplasia of the first thoracic vertebrae that treated by radical removal and ... ...

Abstract	Background and objective: Fibrous dysplasia (FD) is a benign bone lesion manifested by local pain, swelling and deformity change. We report a case of monostotic fibrous dysplasia of the first thoracic vertebrae that treated by radical removal and reconstruction. Case report: A 29-year-old man with monostotic fibrous dysplasia of the first thoracic vertebrae was admitted to our department because of persistent, dull back pain for 3 months. Radical removal of the first thoracic vertebrae and reconstruction were performed in a combined posterior-anterior approach. This patient experienced complete pain relief without any complication. Conclusion: This report presents a rare case of monostotic fibrous dysplasia of the first thoracic vertebrae, with symptoms of chronic back pain that was successfully treated with radical excision and reconstruction, providing a good option to the patient.
MeSH term(s)	Adult ; Fibrous Dysplasia, Monostotic/diagnosis ; Fibrous Dysplasia, Monostotic/surgery ; Humans ; Male ; Orthopedic Procedures/methods ; Spinal Diseases/diagnosis ; Spinal Diseases/surgery ; Thoracic Vertebrae/diagnostic imaging ; Thoracic Vertebrae/surgery ; Tomography, X-Ray Computed/methods
Language	English
Publishing date	2016-04-27
Publishing country	Netherlands
Document type	Case Reports ; Journal Article
ZDB-ID	1184721-9
ISSN	1878-6324 ; 1053-8127
ISSN (online)	1878-6324
ISSN	1053-8127
DOI	10.3233/BMR-150647
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 4580: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Structure-Based Discovery and Development of a Series of Potent and Selective Bromodomain and Extra-Terminal Protein Inhibitors.

Hu, Jianping / Tian, Chang-Qing / Damaneh, Mohammadali Soleimani / Li, Yanlian / Cao, Danyan / Lv, Kaikai / Yu, Ting / Meng, Tao / Chen, Danqi / Wang, Xin / Chen, Lin / Li, Jian / Song, Shan-Shan / Huan, Xia-Juan / Qin, Lihuai / Shen, Jingkang / Wang, Ying-Qing / Miao, Ze-Hong / Xiong, Bing

Journal of medicinal chemistry

2019 Volume 62, Issue 18, Page(s) 8642–8663

Abstract: BRD4 has recently emerged as a promising drug target. Therefore, identifying novel inhibitors with distinct properties could enrich their use in anticancer treatment. Guided by the cocrystal structure of hit ... ...

Abstract	BRD4 has recently emerged as a promising drug target. Therefore, identifying novel inhibitors with distinct properties could enrich their use in anticancer treatment. Guided by the cocrystal structure of hit compound
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Cell Cycle Proteins/metabolism ; Cell Proliferation ; Crystallography, X-Ray ; Drug Design ; Drug Discovery ; Humans ; Inhibitory Concentration 50 ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred ICR ; Mice, Nude ; Mice, SCID ; Microsomes, Liver/metabolism ; Molecular Structure ; Neoplasm Transplantation ; Neoplasms/drug therapy ; Nuclear Proteins/antagonists & inhibitors ; Peptides/chemistry ; Protein Domains ; Proteins/antagonists & inhibitors ; Transcription Factors/antagonists & inhibitors
Chemical Substances	Antineoplastic Agents ; Cell Cycle Proteins ; Nuclear Proteins ; Peptides ; Proteins ; Transcription Factors ; bromodomain and extra-terminal domain protein, human
Language	English
Publishing date	2019-09-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218133-2
ISSN	1520-4804 ; 0022-2623
ISSN (online)	1520-4804
ISSN	0022-2623
DOI	10.1021/acs.jmedchem.9b01094
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.B 151: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MB 1: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito