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Article ; Online: Independent verification of circulating miRNA as diagnostic biomarkers for urothelial carcinoma.

Urabe, Fumihiko / Matsuzaki, Juntaro / Takeshita, Fumitaka / Kishida, Takeshi / Ochiya, Takahiro / Hirai, Kotaro

2022 Volume 113, Issue 10, Page(s) 3510–3517

Abstract: Urothelial carcinoma (UC) is an umbrella term for bladder cancers (BCa) and upper-tract urothelial carcinoma (UTUC), with BCa and UTUC sometimes detected concomitantly. The methods of detection for UC are often inaccurate or highly invasive, and, ... ...

Abstract	Urothelial carcinoma (UC) is an umbrella term for bladder cancers (BCa) and upper-tract urothelial carcinoma (UTUC), with BCa and UTUC sometimes detected concomitantly. The methods of detection for UC are often inaccurate or highly invasive, and, therefore, are thought to be unsatisfactory. Previously, we reported seven serum miRNAs as diagnostic markers for BCa. Here, we re-evaluated potential diagnostic miRNAs in different institutions. We prospectively analyzed serum samples obtained from 126 UC patients (BCa: 106 samples; UTUC: 14 samples; UTUC with BCa: six samples) and 50 noncancer controls by microarray analysis. We randomly assigned these samples into a training or a validation set. Biomarker candidate miRNAs were selected based on cross-validation scores in the training set of samples, with diagnostic power confirmed in the validation set. Among the diagnostic miRNAs identified in this way, miR-1343-5p and miR-6087 had been identified as potential diagnostic miRNAs in our previous study. In addition, we evaluated the association between the serum levels of identified miRNAs and the presence of UC risk conditions. The expression levels of several miRNAs correlate with the risk factors in participants without UC, which may be explained by the presence of a microscopic tumor or a precancerous lesion. In conclusion, we identified two robust miRNA diagnostic markers for UC detection. Further functional analysis is required to elucidate the mechanism by which alterations in the expression of these miRNAs occur.
MeSH term(s)	Biomarkers, Tumor/genetics ; Carcinoma, Transitional Cell/diagnosis ; Carcinoma, Transitional Cell/genetics ; Carcinoma, Transitional Cell/metabolism ; Circulating MicroRNA ; Humans ; MicroRNAs/genetics ; Urinary Bladder Neoplasms/diagnosis ; Urinary Bladder Neoplasms/genetics
Chemical Substances	Biomarkers, Tumor ; Circulating MicroRNA ; MicroRNAs
Language	English
Publishing date	2022-08-12
Publishing country	England
Document type	Journal Article
ZDB-ID	2115647-5
ISSN	1349-7006 ; 1349-7006
ISSN (online)	1349-7006
ISSN	1349-7006
DOI	10.1111/cas.15496
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Delivery of miR-424-5p via Extracellular Vesicles Promotes the Apoptosis of MDA-MB-231 TNBC Cells in the Tumor Microenvironment.

Zhou, Yueyuan / Yamamoto, Yusuke / Takeshita, Fumitaka / Yamamoto, Tomofumi / Xiao, Zhongdang / Ochiya, Takahiro

International journal of molecular sciences

2021 Volume 22, Issue 2

Abstract: Programmed cell death ligand-1 (PD-L1) overexpressed on cancer cells has emerged as a key inhibitor that maintains the immunosuppressive microenvironment through its interaction with the PD-1 receptor in cancer. Here, we demonstrated that miR-424-5p ... ...

Abstract	Programmed cell death ligand-1 (PD-L1) overexpressed on cancer cells has emerged as a key inhibitor that maintains the immunosuppressive microenvironment through its interaction with the PD-1 receptor in cancer. Here, we demonstrated that miR-424-5p delivery via extracellular vesicles (EVs) derived from adipose tissue-mesenchymal stromal cells (AT-MSCs) partly promotes proinflammation and enhances antitumor cytotoxicity in vitro and in vivo. Triple negative breast cancer (TNBC) exhibits increased expression of
MeSH term(s)	Animals ; Apoptosis ; B7-H1 Antigen/genetics ; Base Sequence ; Cell Line, Tumor ; Cytokines/metabolism ; Exosomes/metabolism ; Extracellular Vesicles/metabolism ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Humans ; Leukocytes, Mononuclear/cytology ; Mesenchymal Stem Cells/metabolism ; Mice ; Mice, Inbred BALB C ; MicroRNAs/genetics ; Neoplasm Recurrence, Local ; Particle Size ; Reverse Transcriptase Polymerase Chain Reaction ; Triple Negative Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/metabolism ; Tumor Microenvironment
Chemical Substances	B7-H1 Antigen ; CD274 protein, human ; Cytokines ; MIRN424 microRNA, mouse ; MIRN424 microrna, human ; MicroRNAs
Language	English
Publishing date	2021-01-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22020844
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Article ; Online: Aurora kinase blockade drives de novo addiction of cervical squamous cell carcinoma to druggable EGFR signalling.

Komatsu, Masayuki / Nakamura, Kanako / Takeda, Takashi / Chiwaki, Fumiko / Banno, Kouji / Aoki, Daisuke / Takeshita, Fumitaka / Sasaki, Hiroki

Oncogene

2022 Volume 41, Issue 16, Page(s) 2326–2339

Abstract: Oncogenic signalling confers tumour-progression advantages; thus, its pharmacological blockade is the best strategy for cancer chemotherapy. However, drug resistance and heterogeneous dependency of tumour hamper their therapeutic potential, suggesting ... ...

Abstract	Oncogenic signalling confers tumour-progression advantages; thus, its pharmacological blockade is the best strategy for cancer chemotherapy. However, drug resistance and heterogeneous dependency of tumour hamper their therapeutic potential, suggesting the necessity for a new ubiquitous modality based on evading drug resistance. Here, we proposed a de novo addiction to oncogenic signalling (Dead-On) concept, wherein specific blockade of target molecules forces cancer cells to develop dependency on an oncogenic signalling. In cervical squamous cell carcinoma cells, Aurora A/B dual blockade elicited rapid addiction to EGFR-Erk signalling, and its pharmacological/genetic inhibition synergistically enhanced anti-cancer activities in vitro, in vivo, and in a patient-derived organoid model. The signal activation was independent of EGFR genetic status, it was triggered by receptor accumulation on the plasma membrane via Rab11-mediated endocytic recycling machinery. These findings support our novel Dead-On concept which may lead to drug discovery as well as expand the adaptation of approved targeted drugs.
MeSH term(s)	Carcinoma, Squamous Cell/drug therapy ; Carcinoma, Squamous Cell/genetics ; Cell Line, Tumor ; Drug Resistance, Neoplasm/genetics ; ErbB Receptors/metabolism ; Female ; Humans ; Oncogenes ; Signal Transduction ; Uterine Cervical Neoplasms/drug therapy ; Uterine Cervical Neoplasms/genetics
Chemical Substances	EGFR protein, human (EC 2.7.10.1) ; ErbB Receptors (EC 2.7.10.1)
Language	English
Publishing date	2022-03-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-022-02256-3
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Article ; Online: ARHGAP-RhoA signaling provokes homotypic adhesion-triggered cell death of metastasized diffuse-type gastric cancer.

Komatsu, Masayuki / Ichikawa, Hitoshi / Chiwaki, Fumiko / Sakamoto, Hiromi / Komatsuzaki, Rie / Asaumi, Makoto / Tsunoyama, Kazuhisa / Fukagawa, Takeo / Matsushita, Hiromichi / Boku, Narikazu / Matsusaki, Keisuke / Takeshita, Fumitaka / Yoshida, Teruhiko / Sasaki, Hiroki

Oncogene

2022 Volume 41, Issue 43, Page(s) 4779–4794

Abstract: Genetic alteration of Rho GTPase-activating proteins (ARHGAP) and GTPase RhoA is a hallmark of diffuse-type gastric cancer and elucidating its biological significance is critical to comprehensively understanding this malignancy. Here, we report that gene ...

Abstract	Genetic alteration of Rho GTPase-activating proteins (ARHGAP) and GTPase RhoA is a hallmark of diffuse-type gastric cancer and elucidating its biological significance is critical to comprehensively understanding this malignancy. Here, we report that gene fusions of ARHGAP6/ARHGAP26 are frequent genetic events in peritoneally-metastasized gastric and pancreatic cancer. From the malignant ascites of patients, we established gastric cancer cell lines that spontaneously gain hotspot RHOA mutations or four different ARHGAP6/ARHGAP26 fusions. These alterations critically downregulate RhoA-ROCK-MLC2 signaling, which elicits cell death. Omics and functional analyses revealed that the downstream signaling initiates actin stress fibers and reinforces intercellular junctions via several types of catenin. E-cadherin-centered homotypic adhesion followed by lysosomal membrane permeabilization is a pivotal mechanism in cell death. These findings support the tumor-suppressive nature of ARHGAP-RhoA signaling and might indicate a new avenue of drug discovery against this refractory cancer.
MeSH term(s)	Humans ; Stomach Neoplasms/genetics ; Stomach Neoplasms/pathology ; Actins/metabolism ; GTPase-Activating Proteins/genetics ; GTPase-Activating Proteins/metabolism ; Cadherins/metabolism ; Catenins/metabolism ; Cell Death ; rhoA GTP-Binding Protein/genetics ; rhoA GTP-Binding Protein/metabolism
Chemical Substances	Actins ; GTPase-Activating Proteins ; Cadherins ; Catenins ; RHOA protein, human (124671-05-2) ; rhoA GTP-Binding Protein (EC 3.6.5.2)
Language	English
Publishing date	2022-09-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-022-02469-6
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Article ; Online: Emerging roles of long non-coding RNA in cancer.

Sanchez Calle, Anna / Kawamura, Yumi / Yamamoto, Yusuke / Takeshita, Fumitaka / Ochiya, Takahiro

Cancer science

2018 Volume 109, Issue 7, Page(s) 2093–2100

Abstract: Since comprehensive analysis of the mammalian genome revealed that the majority of genomic products are transcribed in long non-coding RNA (lncRNA), increasing attention has been paid to these transcripts. The applied next-generation sequencing ... ...

Abstract	Since comprehensive analysis of the mammalian genome revealed that the majority of genomic products are transcribed in long non-coding RNA (lncRNA), increasing attention has been paid to these transcripts. The applied next-generation sequencing technologies have provided accumulating evidence of dysregulated lncRNA in cancer. The implication of this finding can be seen in many forms and at multiple levels. With impacts ranging from integrating chromatin remodeling complexes to regulating transcription and post-transcriptional processes, aberrant expression of lncRNA may have repercussions in cell proliferation, tumor progression or metastasis. lncRNA may act as enhancers, scaffolds or decoys by physically interacting with other RNA species or proteins, resulting in a direct impact on cell signaling cascades. Even though their functional classification is well-established in the context of cancer, clearer characterization in terms of their phenotypic outputs is needed to optimize and identify suitable candidates that enable the development of new therapeutic strategies and the design of novel diagnostic approaches. The present article aims to outline different cancer-associated lncRNA according to their contribution to tumor suppression or tumor promotion based on their most current functional annotations.
MeSH term(s)	Animals ; Humans ; Neoplasms/genetics ; RNA, Long Noncoding/genetics
Chemical Substances	RNA, Long Noncoding
Language	English
Publishing date	2018-06-28
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2115647-5
ISSN	1349-7006 ; 1347-9032
ISSN (online)	1349-7006
ISSN	1347-9032
DOI	10.1111/cas.13642
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Article ; Online: The impact of extracellular vesicle-encapsulated circulating microRNAs in lung cancer research.

Fujita, Yu / Kuwano, Kazuyoshi / Ochiya, Takahiro / Takeshita, Fumitaka

BioMed research international

2014 Volume 2014, Page(s) 486413

Abstract: Lung cancer is the leading cause of cancer-related deaths. Biomarkers for lung cancer have raised great expectations in their clinical applications for early diagnosis, survival, and therapeutic responses. MicroRNAs (miRNAs), a family of short endogenous ...

Abstract	Lung cancer is the leading cause of cancer-related deaths. Biomarkers for lung cancer have raised great expectations in their clinical applications for early diagnosis, survival, and therapeutic responses. MicroRNAs (miRNAs), a family of short endogenous noncoding RNAs, play critical roles in cell growth, differentiation, and the development of various types of cancers. Current studies have shown that miRNAs are present in the extracellular spaces, packaged into various membrane-bound vesicles. Tumor-specific circulating miRNAs have been developed as early diagnostic biomarkers for lung cancer. Remarkably, some studies have succeeded in discovering circulating miRNAs with prognostic or predictive significance. Extracellular vesicles (EVs), such as exosomes and microvesicles, are recognized as novel tools for cell-cell communication and as biomarkers for various diseases. Their vesicle composition and miRNA content have the ability to transfer biological information to recipient cells and play an important role in cancer metastasis and prognosis. This review provides an in-depth summary of current findings on circulating miRNAs in lung cancer patients used as diagnostic biomarkers. We also discuss the role of EV miRNAs in cell-cell communication and explore the effectiveness of these contents as predictive biomarkers for cancer malignancy.
MeSH term(s)	Biomarkers, Tumor/blood ; Cell Communication ; Exosomes/metabolism ; Exosomes/pathology ; Humans ; Lung Neoplasms/blood ; Lung Neoplasms/pathology ; MicroRNAs/blood ; Neoplastic Cells, Circulating/pathology ; Prognosis
Chemical Substances	Biomarkers, Tumor ; MicroRNAs
Language	English
Publishing date	2014-09-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2698540-8
ISSN	2314-6141 ; 2314-6133
ISSN (online)	2314-6141
ISSN	2314-6133
DOI	10.1155/2014/486413
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Article ; Online: MicroRNAs: emerging novel targets of cancer therapies.

Yang, Chengfeng / Jiang, Yiguo / Singh, Ajay P / Takeshita, Fumitaka

BioMed research international

2015 Volume 2015, Page(s) 506323

MeSH term(s)	Animals ; Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism ; MicroRNAs/therapeutic use ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplasms/therapy
Chemical Substances	MicroRNAs
Language	English
Publishing date	2015
Publishing country	United States
Document type	Introductory Journal Article
ZDB-ID	2698540-8
ISSN	2314-6141 ; 2314-6133
ISSN (online)	2314-6141
ISSN	2314-6133
DOI	10.1155/2015/506323
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Article ; Online: Disruption of Circulating Extracellular Vesicles as a Novel Therapeutic Strategy against Cancer Metastasis.

Nishida-Aoki, Nao / Tominaga, Naoomi / Takeshita, Fumitaka / Sonoda, Hikaru / Yoshioka, Yusuke / Ochiya, Takahiro

Molecular therapy : the journal of the American Society of Gene Therapy

2017 Volume 25, Issue 1, Page(s) 181–191

Abstract: Metastasis is the main cause of cancer mortality for many types of cancer; however, difficulties remain in effectively preventing metastasis. It has been recently and widely reported that cancer-derived extracellular vesicles (EVs) contribute to cancer ... ...

Abstract	Metastasis is the main cause of cancer mortality for many types of cancer; however, difficulties remain in effectively preventing metastasis. It has been recently and widely reported that cancer-derived extracellular vesicles (EVs) contribute to cancer metastasis. Thus, therapeutic strategies targeting cancer-derived EVs hold great promise because of the possibility of EVs driving the cancer microenvironment toward metastasis. Here, we provide a novel strategy for therapeutic antibody treatment to target cancer-derived EVs and inhibit the metastasis of breast cancer in a mouse model, establishing a rationale for further clinical investigation. Treatment with human-specific anti-CD9 or anti-CD63 antibodies significantly decreased metastasis to the lungs, lymph nodes, and thoracic cavity, although no obvious effects on primary xenograft tumor growths were observed. In in vitro and in vivo experiments, the EVs incubated with the targeted antibodies were preferentially internalized by macrophages, suggesting that antibody-tagged cancer-derived EVs would be eliminated by macrophages. Our results suggested that therapeutic antibody administration effectively suppresses EV-triggered metastasis in cancer and that the removal of EVs could be a novel strategy for cancer therapy.
MeSH term(s)	Animals ; Antibodies, Monoclonal/pharmacology ; Antineoplastic Agents ; Cell Movement/drug effects ; Cell Proliferation/drug effects ; Cell-Derived Microparticles/metabolism ; Disease Models, Animal ; Extracellular Vesicles/immunology ; Extracellular Vesicles/metabolism ; Humans ; Macrophages/drug effects ; Macrophages/immunology ; Macrophages/metabolism ; Mice ; Neoplasm Metastasis ; Neoplasms/immunology ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplasms/therapy ; Phagocytosis ; Tetraspanin 30/immunology ; Tetraspanin 30/metabolism ; Tetraspanin-29/immunology ; Tetraspanin-29/metabolism ; Tumor Burden/drug effects ; Tumor Burden/immunology ; Xenograft Model Antitumor Assays
Chemical Substances	Antibodies, Monoclonal ; Antineoplastic Agents ; Tetraspanin 30 ; Tetraspanin-29
Language	English
Publishing date	2017-01-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	2010592-7
ISSN	1525-0024 ; 1525-0016
ISSN (online)	1525-0024
ISSN	1525-0016
DOI	10.1016/j.ymthe.2016.10.009
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Article: RNAi Therapeutic Platforms for Lung Diseases.

Fujita, Yu / Takeshita, Fumitaka / Kuwano, Kazuyoshi / Ochiya, Takahiro

Pharmaceuticals (Basel, Switzerland)

2013 Volume 6, Issue 2, Page(s) 223–250

Abstract: RNA interference (RNAi) is rapidly becoming an important method for analyzing gene functions in many eukaryotes and holds promise for the development of therapeutic gene silencing. The induction of RNAi relies on small silencing RNAs, which affect ... ...

Abstract	RNA interference (RNAi) is rapidly becoming an important method for analyzing gene functions in many eukaryotes and holds promise for the development of therapeutic gene silencing. The induction of RNAi relies on small silencing RNAs, which affect specific messenger RNA (mRNA) degradation. Two types of small RNA molecules, i.e. small interfering RNAs (siRNAs) and microRNAs (miRNAs), are central to RNAi. Drug discovery studies and novel treatments of siRNAs are currently targeting a wide range of diseases, including various viral infections and cancers. Lung diseases in general are attractive targets for siRNA therapeutics because of their lethality and prevalence. In addition, the lung is anatomically accessible to therapeutic agents via the intrapulmonary route. Recently, increasing evidence indicates that miRNAs play an important role in lung abnormalities, such as inflammation and oncogenesis. Therefore, miRNAs are being targeted for therapeutic purposes. In this review, we present strategies for RNAi delivery and discuss the current state-of-the-art RNAi-based therapeutics for various lung diseases.
Keywords	covid19
Language	English
Publishing date	2013-02-06
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2193542-7
ISSN	1424-8247
ISSN	1424-8247
DOI	10.3390/ph6020223
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Article ; Online: Establishment and characterization of NCC-ssRMS2-C1: a novel patient-derived cell line of spindle cell/sclerosing rhabdomyosarcoma.

Tsuchiya, Ryuto / Yoshimatsu, Yuki / Noguchi, Rei / Sin, Yooksil / Ono, Takuya / Sei, Akane / Takeshita, Fumitaka / Sugaya, Jun / Nakatani, Fumihiko / Yoshida, Akihiko / Ohtori, Seiji / Kawai, Akira / Kondo, Tadashi

Human cell

2021 Volume 34, Issue 5, Page(s) 1569–1578

Abstract: Spindle cell/sclerosing rhabdomyosarcoma (ssRMS) is a rare subtype of rhabdomyosarcoma (RMS) that has fascicular spindle cell and/or sclerosing morphology. SsRMS has a diverse molecular background and is categorized into three groups: congenital/ ... ...

Abstract	Spindle cell/sclerosing rhabdomyosarcoma (ssRMS) is a rare subtype of rhabdomyosarcoma (RMS) that has fascicular spindle cell and/or sclerosing morphology. SsRMS has a diverse molecular background and is categorized into three groups: congenital/infantile ssRMS with a gene fusion involving the NCOA2 and VGLL2, ssRMS with the MYOD1 mutation, and ssRMS with no recurrent identifiable genetic alterations. Because ssRMS is a newly defined disease concept of RMS, the optimal treatment methods have not been determined. This results in unfavorable prognosis and consequently signals the urgent need for continuous research. Patient-derived cell lines are essential tools in basic and translational research. However, only two ssRMS cell lines with the MYOD1 mutation have been reported to date. Thus, we established a novel ssRMS cell line named NCC-ssRMS2-C1 using a surgically resected tumor tissue from an adult ssRMS patient. NCC-ssRMS2-C1 cells retained the copy number alterations corresponding to the original tumor and are categorized into the group with no recurrent identifiable genetic alterations. NCC-ssRMS2-C1 cells demonstrated constant proliferation, spheroid formation, and capability for invasion in vitro, reflecting the malignant features of the original tumor tissue. In a drug screening test, ssRMS demonstrated remarkable sensitivity to romidepsin, trabectedin, actinomycin D, and bortezomib. Hence, we conclude that the NCC-ssRMS2-C1 cell line is the first ssRMS cell line which belongs to the group with no recurrent identifiable genetic alterations, and it will be a useful resource in both basic and translational studies for ssRMS.
MeSH term(s)	Adult ; Antineoplastic Agents/pharmacology ; Bortezomib/pharmacology ; Cell Line, Tumor ; Dactinomycin/pharmacology ; Depsipeptides/pharmacology ; Gene Fusion ; Head and Neck Neoplasms/classification ; Head and Neck Neoplasms/genetics ; Head and Neck Neoplasms/pathology ; Humans ; Male ; Muscle Proteins/genetics ; Mutation ; MyoD Protein/genetics ; Nuclear Receptor Coactivator 2/genetics ; Rhabdomyosarcoma/classification ; Rhabdomyosarcoma/genetics ; Rhabdomyosarcoma/pathology ; Sarcoma/classification ; Sarcoma/genetics ; Sarcoma/pathology ; Trabectedin/pharmacology ; Transcription Factors/genetics
Chemical Substances	Antineoplastic Agents ; Depsipeptides ; Muscle Proteins ; MyoD Protein ; MyoD1 myogenic differentiation protein ; NCOA2 protein, human ; Nuclear Receptor Coactivator 2 ; Transcription Factors ; VGLL2 protein, human ; Dactinomycin (1CC1JFE158) ; Bortezomib (69G8BD63PP) ; romidepsin (CX3T89XQBK) ; Trabectedin (ID0YZQ2TCP)
Language	English
Publishing date	2021-06-23
Publishing country	Japan
Document type	Journal Article
ZDB-ID	1149134-6
ISSN	1749-0774 ; 0914-7470
ISSN (online)	1749-0774
ISSN	0914-7470
DOI	10.1007/s13577-021-00569-1
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