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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
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Article ; Online: [Clinical and long-term characteristics of the subtypes of chronic inflammatory demyelinating polyneuropathy].

Shimizu, Fumitaka / Nemoto, Jo / Takeshita, Yukio / Maeda, Toshihiko / Koga, Michiaki / Kanda, Takashi

Rinsho shinkeigaku = Clinical neurology

2022 Volume 62, Issue 3, Page(s) 173–177

Abstract: Objective: To clarify the clinical and long-term characteristic of each subtype of chronic inflammatory demyelinating polyneuropathy (CIDP).: Methods: We evaluated data from 30 consecutive CIDP patients who met the criteria proposed by the European ... ...

Abstract	Objective: To clarify the clinical and long-term characteristic of each subtype of chronic inflammatory demyelinating polyneuropathy (CIDP). Methods: We evaluated data from 30 consecutive CIDP patients who met the criteria proposed by the European Federation of Neurological Societies and the Peripheral Nerve Society. Results: Patients were classified as having typical CIDP (t-‍CIDP) (10/30, 33%), multifocal acquired demyelinating sensory and motor (MADSAM) (12/30, 40%), DADS (4/30, 13%), sensory CIDP (3/30, 10%) or motor CIDP (1/30, 3%). Nerve conduction studies showed more prolonged distal motor latencies/F-wave latencies and slower motor nerve conduction in the typical CIDP group than in the MADSAM group. Intravenous immunoglobulin (IVIg) was effective in 80% (8/10) of t-‍CIDP, 100% (12/12) of MADSAM, 100% (4/4) of DADS, and 100% (3/3) of sensory CIDP cases. Maintenance therapy with immunoglobulin was administered in patients with t-‍CIDP (5/10, 50%), MADSAM (9/12, 75%), DADS (1/4, 25%), and sensory CIDP (2/3, 67%). There were no patients with CIDP, in whom CIDP subtype was transformed from the initial diagnosis during five years of follow-up. Discussion: Percentage of MADSAM was the most common phenotype in our cohort of CIDP patients, and IVIg/immunoglobulin maintenance was effective for MADSAM as well as t-‍CIDP in contrast to findings from the previous reports.
MeSH term(s)	Humans ; Immunoglobulins, Intravenous ; Neural Conduction ; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating/diagnosis ; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating/drug therapy
Chemical Substances	Immunoglobulins, Intravenous
Language	Japanese
Publishing date	2022-03-25
Publishing country	Japan
Document type	Journal Article
ZDB-ID	604200-4
ISSN	1882-0654 ; 0009-918X
ISSN (online)	1882-0654
ISSN	0009-918X
DOI	10.5692/clinicalneurol.cn-001667
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Article ; Online: Jo-1 Antibodies From Myositis Induce Complement-Dependent Cytotoxicity and TREM-1 Upregulation in Muscle Endothelial Cells.

Honda, Masaya / Shimizu, Fumitaka / Sato, Ryota / Mizukami, Yoichi / Watanabe, Kenji / Takeshita, Yukio / Maeda, Toshihiko / Koga, Michiaki / Kanda, Takashi

Neurology(R) neuroimmunology & neuroinflammation

2023 Volume 10, Issue 4

Abstract: Background and objectives: Muscle microangiopathy due to dysfunction of endothelial cells because of inflammation is a critical hallmark of dermatomyositis (DM); however, its pathomechanism remains unclear. The aim of this study was to evaluate the ... ...

Abstract	Background and objectives: Muscle microangiopathy due to dysfunction of endothelial cells because of inflammation is a critical hallmark of dermatomyositis (DM); however, its pathomechanism remains unclear. The aim of this study was to evaluate the effect of immunogloblin G (IgG) from patients with idiopathic inflammatory myopathies (IIM) on muscle endothelial cells in vitro. Methods: Using a high-content imaging system, we analyzed whether IgG purified from sera from patients with IIM (n = 15), disease controls (DCs: n = 7), and healthy controls (HCs: n = 7) can bind to muscle endothelial cells and induce complement-dependent cellular cytotoxicity. Results: IgGs from Jo-1 antibody myositis could bind to muscle endothelial cells and caused complement-dependent cell cytotoxicity. RNA-seq demonstrated the upregulation of genes associated with tumor necrosis factor (TNF)-α, triggering receptor expressed on myeloid cells-1 (TREM-1), CD25, and mitochondria pathways after exposure to IgG from the Jo-1, signal recognition particle (SRP), and polymyositis (PM) groups. The high-content imaging system showed that TREM-1 expression in the Jo-1, SRP, and PM groups was increased in comparison with DCs and HCs and that the TNF-α expression in the Jo-1 group was higher in comparison with the SRP, PM, DC, and HC groups. The expression of TREM-1 was observed in biopsied capillaries and the muscle membrane from patients with Jo-1 and in biopsied muscle fiber and capillaries from patients with DM and SRP. The depletion of Jo-1 antibodies by IgG of patients with Jo-1 antibody myositis reduced the Jo-1 antibody-induced complement-dependent cellular cytotoxicity in muscle endothelial cells. Discussion: Jo-1 antibodies from Jo-1 antibody myositis show complement-dependent cellular cytotoxicity in muscle endothelial cells. IgGs from patients with Jo-1, SRP, and DM increase the TREM-1 expression in endothelial cells and muscles.
MeSH term(s)	Humans ; Triggering Receptor Expressed on Myeloid Cells-1 ; Endothelial Cells ; Up-Regulation ; Myositis ; Polymyositis ; Muscles/pathology ; Immunoglobulin G
Chemical Substances	Jo-1 antibody ; Triggering Receptor Expressed on Myeloid Cells-1 ; Immunoglobulin G
Language	English
Publishing date	2023-05-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2767740-0
ISSN	2332-7812 ; 2332-7812
ISSN (online)	2332-7812
ISSN	2332-7812
DOI	10.1212/NXI.0000000000200116
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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: Delivery of miR-424-5p via Extracellular Vesicles Promotes the Apoptosis of MDA-MB-231 TNBC Cells in the Tumor Microenvironment

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

International Journal of Molecular Sciences, Vol 22, Iss 2, p

2021 Volume 844

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 PD-L1 , and PD-L1 is positively correlated with the overall survival of patients with TNBC. PD-L1 shows relatively higher expression in MDA-MB-231 (MM231) cells and can be downregulated by miR-424-5p. Furthermore, miR-424-5p transported by EVs can increase the secretion of proinflammatory cytokines, decrease the secretion of anti-inflammatory cytokines and promote the apoptosis of tumor cells. The intratumoral administration of miR-424-5p-EVs significantly slowed tumor growth. In conclusion, these results demonstrate that EVs may serve as a delivery system for novel immunotherapies for TNBC through the miR-424-5p/PD-L1 pathway.
Keywords	exosome ; miR-424-5p ; PD-L1 ; triple-negative breast cancer ; mesenchymal stromal cell ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	610
Language	English
Publishing date	2021-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Autocrine TNF-α Increases Penetration of Myelin-Associated Glycoprotein Antibodies Across the Blood-Nerve Barrier in Anti-MAG Neuropathy.

Sato, Ryota / Shimizu, Fumitaka / Kuwahara, Motoi / Mizukami, Yoichi / Watanabe, Kenji / Maeda, Toshihiko / Sano, Yasuteru / Takeshita, Yukio / Koga, Michiaki / Kusunoki, Susumu / Kanda, Takashi

Neurology(R) neuroimmunology & neuroinflammation

2023 Volume 10, Issue 3

Abstract: Background and objectives: Deposition of myelin-associated glycoprotein (MAG) immunoglobulin M (IgM) antibodies in the sural nerve is a key feature in anti-MAG neuropathy. Whether the blood-nerve barrier (BNB) is disrupted in anti-MAG neuropathy remains ...

Abstract	Background and objectives: Deposition of myelin-associated glycoprotein (MAG) immunoglobulin M (IgM) antibodies in the sural nerve is a key feature in anti-MAG neuropathy. Whether the blood-nerve barrier (BNB) is disrupted in anti-MAG neuropathy remains elusive.We aimed to evaluate the effect of sera from anti-MAG neuropathy at the molecular level using our in vitro human BNB model and observe the change of BNB endothelial cells in the sural nerve of anti-MAG neuropathy. Methods: Diluted sera from patients with anti-MAG neuropathy (n = 16), monoclonal gammopathies of undetermined significance (MGUS) neuropathy (n = 7), amyotrophic lateral sclerosis (ALS, n = 10), and healthy controls (HCs, n = 10) incubated with human BNB endothelial cells to identify the key molecule of BNB activation using RNA-seq and a high-content imaging system, and exposed with a BNB coculture model to evaluate small molecule/IgG/IgM/anti-MAG antibody permeability. Results: RNA-seq and the high-content imaging system showed the significant upregulation of tumor necrosis factor (TNF-α) and nuclear factor-kappa B (NF-κB) in BNB endothelial cells after exposure to sera from patients with anti-MAG neuropathy, whereas the serum TNF-α concentration was not changed among the MAG/MGUS/ALS/HC groups. Sera from patients with anti-MAG neuropathy did not increase 10-kDa dextran or IgG permeability but enhanced IgM and anti-MAG antibody permeability. Sural nerve biopsy specimens from patients with anti-MAG neuropathy showed higher TNF-α expression levels in BNB endothelial cells and preservation of the structural integrity of the tight junctions and the presence of more vesicles in BNB endothelial cells. Neutralization of TNF-α reduces IgM/anti-MAG antibody permeability. Discussion: Sera from individuals with anti-MAG neuropathy increased transcellular IgM/anti-MAG antibody permeability via autocrine TNF-α secretion and NF-κB signaling in the BNB.
MeSH term(s)	Humans ; Myelin-Associated Glycoprotein ; Tumor Necrosis Factor-alpha ; Blood-Nerve Barrier ; Endothelial Cells ; Amyotrophic Lateral Sclerosis ; NF-kappa B ; Peripheral Nervous System Diseases ; Autoantibodies ; Immunoglobulin M ; Monoclonal Gammopathy of Undetermined Significance ; Immunoglobulin G
Chemical Substances	Myelin-Associated Glycoprotein ; Tumor Necrosis Factor-alpha ; NF-kappa B ; Autoantibodies ; Immunoglobulin M ; Immunoglobulin G
Language	English
Publishing date	2023-02-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2767740-0
ISSN	2332-7812 ; 2332-7812
ISSN (online)	2332-7812
ISSN	2332-7812
DOI	10.1212/NXI.0000000000200086
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Article ; Online: Exploring lipophilic compounds that induce BDNF secretion in astrocytes beyond the BBB using a new multi-cultured human in vitro BBB model.

Fujisawa, Miwako / Takeshita, Yukio / Fujikawa, Susumu / Matsuo, Kinya / Okamoto, Masashi / Tamada, Masaya / Shimizu, Fumitaka / Sano, Yasuteru / Koga, Michiaki / Kanda, Takashi

Journal of neuroimmunology

2021 Volume 362, Page(s) 577783

Abstract: Brain-derived neurotrophic factor (BDNF) cannot cross the blood-brain barrier (BBB) when administered peripherally, which hinders its therapeutic potential. We utilized an in vitro BBB model-a tri-culture of a human endothelial cell line, a pericyte cell ...

Abstract	Brain-derived neurotrophic factor (BDNF) cannot cross the blood-brain barrier (BBB) when administered peripherally, which hinders its therapeutic potential. We utilized an in vitro BBB model-a tri-culture of a human endothelial cell line, a pericyte cell line, and an astrocyte cell line-to study the effect of twenty candidate lipophilic compounds on stimulating BDNF secretion in pericytes and astrocytes. The prostaglandin E2 receptor 4 agonist and sphingosine-1-phosphate receptor 5 agonist facilitated secretion of BDNF in the astrocyte, but did not decrease the transendothelial electrical resistance. These compounds may be promising agents for neurodegenerative and neuroinflammatory diseases.
MeSH term(s)	Astrocytes/metabolism ; Blood-Brain Barrier ; Brain-Derived Neurotrophic Factor/biosynthesis ; Cells, Cultured ; Coculture Techniques/methods ; Humans ; Receptors, Prostaglandin E, EP4 Subtype/agonists ; Sphingosine-1-Phosphate Receptors/agonists
Chemical Substances	Brain-Derived Neurotrophic Factor ; Receptors, Prostaglandin E, EP4 Subtype ; Sphingosine-1-Phosphate Receptors ; BDNF protein, human (7171WSG8A2)
Language	English
Publishing date	2021-12-06
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	8335-5
ISSN	1872-8421 ; 0165-5728
ISSN (online)	1872-8421
ISSN	0165-5728
DOI	10.1016/j.jneuroim.2021.577783
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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: Radiogenomics predicts the expression of microRNA-1246 in the serum of esophageal cancer patients.

Hoshino, Isamu / Yokota, Hajime / Ishige, Fumitaka / Iwatate, Yosuke / Takeshita, Nobuyoshi / Nagase, Hiroki / Uno, Takashi / Matsubara, Hisahiro

Scientific reports

2020 Volume 10, Issue 1, Page(s) 2532

Abstract: Radiogenomics is a new field that provides clinically useful prognostic predictions by linking molecular characteristics such as the genetic aberrations of malignant tumors with medical images. The abnormal expression of serum microRNA-1246 (miR-1246) ... ...

Abstract	Radiogenomics is a new field that provides clinically useful prognostic predictions by linking molecular characteristics such as the genetic aberrations of malignant tumors with medical images. The abnormal expression of serum microRNA-1246 (miR-1246) has been reported as a prognostic factor of esophageal squamous cell carcinoma (ESCC). To evaluate the power of the miR-1246 level predicted with radiogenomics techniques as a predictor of the prognosis of ESCC patients. The real miR-1246 expression (miR-1246
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Biomarkers, Tumor/blood ; Disease-Free Survival ; Esophageal Squamous Cell Carcinoma/blood ; Esophageal Squamous Cell Carcinoma/diagnostic imaging ; Esophageal Squamous Cell Carcinoma/pathology ; Female ; Gene Expression Regulation, Neoplastic/genetics ; Humans ; Kaplan-Meier Estimate ; Male ; MicroRNAs/blood ; Middle Aged ; Prognosis ; Radiography/methods
Chemical Substances	Biomarkers, Tumor ; MIRN1246 microRNA, human ; MicroRNAs
Language	English
Publishing date	2020-02-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-59500-7
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