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Artikel ; Online: Activated T cell therapy targeting glioblastoma cancer stem cells.

Miyaguchi, Ken / Wang, Hongqiang / Black, Keith L / Shiao, Stephen L / Wang, Rongfu / Yu, John S

2023 Band 13, Heft 1, Seite(n) 196

Abstract: Naïve T cells become effector T cells following stimulation by antigen-loaded dendritic cells (DCs) and sequential cytokine activation. We aimed to develop procedures to efficiently activate T cells with tumor-associated antigens (TAAs) to glioblastoma ( ... ...

Abstract	Naïve T cells become effector T cells following stimulation by antigen-loaded dendritic cells (DCs) and sequential cytokine activation. We aimed to develop procedures to efficiently activate T cells with tumor-associated antigens (TAAs) to glioblastoma (GBM) stem cells. To remove antigen presentation outside of the immunosuppressive tumor milieu, three different glioma stem cell (GSC) specific antigen sources to load DCs were compared in their ability to stimulate lymphocytes. An activated T cell (ATC) protocol including cytokine activation and expansion in culture to target GSCs was generated and optimized for a planned phase I clinical trial. We compared three different antigen-loading methods on DCs to effectively activate T cells, which were GBM patient-derived GSC-lysate, acid-eluate of GSCs and synthetic peptides derived from proteins expressed in GSCs. DCs derived from HLA-A2 positive blood sample were loaded with TAAs. Autologous T cells were activated by co-culturing with loaded DCs. Efficiency and cytotoxicity of ATCs were evaluated by targeting TAA-pulsed DCs or T2 cells, GSCs, or autologous PHA-blasts. Characteristics of ATCs were evaluated by Flow Cytometry and ELISpot assay, which showed increased number of ATCs secreting IFN-γ targeting GSCs as compared with non-activated T cells and unloaded target cells. Neither GSC-lysate nor acid-eluate loading showed enhancement in response of ATCs but the synthetic peptide pool showed significantly increased IFN-γ secretion and increased cytotoxicity towards target cells. These results demonstrate that ATCs activated using a TAA synthetic peptide pool efficiently enhance cytotoxicity specifically to target cells including GSC.
Mesh-Begriff(e)	Humans ; T-Lymphocytes, Cytotoxic ; Glioblastoma/therapy ; Glioblastoma/metabolism ; Interferon-gamma/metabolism ; Antigens, Neoplasm ; Peptides/metabolism ; Neoplastic Stem Cells/metabolism ; Cell- and Tissue-Based Therapy ; Dendritic Cells
Chemische Substanzen	Interferon-gamma (82115-62-6) ; Antigens, Neoplasm ; Peptides
Sprache	Englisch
Erscheinungsdatum	2023-01-05
Erscheinungsland	England
Dokumenttyp	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-27184-w
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Tumor Microenvironment Is Critical for the Maintenance of Cellular States Found in Primary Glioblastomas.

Pine, Allison R / Cirigliano, Stefano M / Nicholson, James G / Hu, Yang / Linkous, Amanda / Miyaguchi, Ken / Edwards, Lincoln / Singhania, Richa / Schwartz, Theodore H / Ramakrishna, Rohan / Pisapia, David J / Snuderl, Matija / Elemento, Olivier / Fine, Howard A

Cancer discovery

2020 Band 10, Heft 7, Seite(n) 964–979

Abstract: Glioblastoma (GBM), an incurable tumor, remains difficult to model and more importantly to treat due to its genetic/epigenetic heterogeneity and plasticity across cellular states. The ability of current tumor models to recapitulate the cellular states ... ...

Abstract	Glioblastoma (GBM), an incurable tumor, remains difficult to model and more importantly to treat due to its genetic/epigenetic heterogeneity and plasticity across cellular states. The ability of current tumor models to recapitulate the cellular states found in primary tumors remains unexplored. To address this issue, we compared single-cell RNA sequencing of tumor cells from 5 patients across four patient-specific glioblastoma stem cell (GSC)-derived model types, including glioma spheres, tumor organoids, glioblastoma cerebral organoids (GLICO), and patient-derived xenografts. We find that GSCs within the GLICO model are enriched for a neural progenitor-like cell subpopulation and recapitulate the cellular states and their plasticity found in the corresponding primary parental tumors. These data demonstrate how the contribution of a neuroanatomically accurate human microenvironment is critical and sufficient for recapitulating the cellular states found in human primary GBMs, a principle that may likely apply to other tumor models. SIGNIFICANCE: It has been unclear how well different patient-derived GBM models are able to recreate the full heterogeneity of primary tumors. Here, we provide a complete transcriptomic characterization of the major model types. We show that the microenvironment is crucial for recapitulating GSC cellular states, highlighting the importance of tumor-host cell interactions.
Mesh-Begriff(e)	Glioblastoma/physiopathology ; Humans ; Tumor Microenvironment/genetics
Sprache	Englisch
Erscheinungsdatum	2020-04-06
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-20-0057
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Elevated Asparagine Biosynthesis Drives Brain Tumor Stem Cell Metabolic Plasticity and Resistance to Oxidative Stress.

Thomas, Tom M / Miyaguchi, Ken / Edwards, Lincoln A / Wang, Hongqiang / Wollebo, Hassen / Aiguo, Li / Murali, Ramachandran / Wang, Yizhou / Braas, Daniel / Michael, Justin S / Andres, Allen M / Zhang, Miqin / Khalili, Kamel / Gottlieb, Roberta A / Perez, J Manuel / Yu, John S

Molecular cancer research : MCR

2021 Band 19, Heft 8, Seite(n) 1375–1388

Abstract: Asparagine synthetase (ASNS) is a gene on the long arm of chromosome 7 that is copy-number amplified in the majority of glioblastomas. ASNS copy-number amplification is associated with a significantly decreased survival. Using patient-derived glioma stem ...

Abstract	Asparagine synthetase (ASNS) is a gene on the long arm of chromosome 7 that is copy-number amplified in the majority of glioblastomas. ASNS copy-number amplification is associated with a significantly decreased survival. Using patient-derived glioma stem cells (GSC), we showed that significant metabolic alterations occur in gliomas when perturbing the expression of ASNS, which is not merely restricted to amino acid homeostasis. ASNS-high GSCs maintained a slower basal metabolic profile yet readily shifted to a greatly increased capacity for glycolysis and oxidative phosphorylation when needed. This led ASNS-high cells to a greater ability to proliferate and spread into brain tissue. Finally, we demonstrate that these changes confer resistance to cellular stress, notably oxidative stress, through adaptive redox homeostasis that led to radiotherapy resistance. Furthermore, ASNS overexpression led to modifications of the one-carbon metabolism to promote a more antioxidant tumor environment revealing a metabolic vulnerability that may be therapeutically exploited. IMPLICATIONS: This study reveals a new role for ASNS in metabolic control and redox homeostasis in glioma stem cells and proposes a new treatment strategy that attempts to exploit one vulnerable metabolic node within the larger multilayered tumor network.
Mesh-Begriff(e)	Animals ; Asparagine/biosynthesis ; Aspartate-Ammonia Ligase/metabolism ; Brain/metabolism ; Brain Stem Neoplasms/metabolism ; Glioma/metabolism ; HEK293 Cells ; Humans ; Mice ; Neoplastic Stem Cells/metabolism ; Oxidative Stress/physiology ; Retrospective Studies
Chemische Substanzen	Asparagine (7006-34-0) ; Aspartate-Ammonia Ligase (EC 6.3.1.1)
Sprache	Englisch
Erscheinungsdatum	2021-04-16
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-20-0086
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: Centrosomal BRCA2 is a target protein of membrane type-1 matrix metalloproteinase (MT1-MMP)

Wali, Nadila / Hosokawa, Kana / Malik, Sadiya / Saito, Hiroko / Miyaguchi, Ken / Imajoh-Ohmi, Shinobu / Miki, Yoshio / Nakanishi, Akira

Biochemical and biophysical research communications. 2014 Jan. 24, v. 443

2014

Abstract: BRCA2 localizes to centrosomes between G1 and prophase and is removed from the centrosomes during mitosis, but the underlying mechanism is not clear. Here we show that BRCA2 is cleaved into two fragments by membrane type-1 matrix metalloproteinase (MT1- ... ...

Abstract	BRCA2 localizes to centrosomes between G1 and prophase and is removed from the centrosomes during mitosis, but the underlying mechanism is not clear. Here we show that BRCA2 is cleaved into two fragments by membrane type-1 matrix metalloproteinase (MT1-MMP), and that knockdown of MT1-MMP prevents the removal of BRCA2 from centrosomes during metaphase. Mass spectrometry mapping revealed that the MT1-MMP cleavage site of human BRCA2 is between Asn-2135 and Leu-2136 (2132LSNN/LNVEGG2141), and the point mutation L2136D abrogated MT1-MMP cleavage. Our data demonstrate that MT1-MMP proteolysis of BRCA2 regulates the abundance of BRCA2 on centrosomes.
Schlagwörter	centrosomes ; humans ; mass spectrometry ; membrane proteins ; metalloproteinases ; metaphase ; mitosis ; point mutation ; prophase ; proteolysis ; tumor suppressor proteins
Sprache	Englisch
Erscheinungsverlauf	2014-0124
Umfang	p. 1148-1154.
Erscheinungsort	Elsevier Inc.
Dokumenttyp	Artikel
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2013.12.103
Datenquelle	NAL Katalog (AGRICOLA)

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Artikel ; Online: Modeling Patient-Derived Glioblastoma with Cerebral Organoids.

Cell reports

2019 Band 26, Heft 12, Seite(n) 3203–3211.e5

Abstract: The prognosis of patients with glioblastoma (GBM) remains dismal, with a median survival of approximately 15 months. Current preclinical GBM models are limited by the lack of a "normal" human microenvironment and the inability of many tumor cell lines to ...

Abstract	The prognosis of patients with glioblastoma (GBM) remains dismal, with a median survival of approximately 15 months. Current preclinical GBM models are limited by the lack of a "normal" human microenvironment and the inability of many tumor cell lines to accurately reproduce GBM biology. To address these limitations, we have established a model system whereby we can retro-engineer patient-specific GBMs using patient-derived glioma stem cells (GSCs) and human embryonic stem cell (hESC)-derived cerebral organoids. Our cerebral organoid glioma (GLICO) model shows that GSCs home toward the human cerebral organoid and deeply invade and proliferate within the host tissue, forming tumors that closely phenocopy patient GBMs. Furthermore, cerebral organoid tumors form rapidly and are supported by an interconnected network of tumor microtubes that aids in the invasion of normal host tissue. Our GLICO model provides a system for modeling primary human GBM ex vivo and for high-throughput drug screening.
Mesh-Begriff(e)	Brain Neoplasms/metabolism ; Brain Neoplasms/pathology ; Glioblastoma/metabolism ; Glioblastoma/pathology ; Humans ; Models, Biological ; Neoplasm Invasiveness ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/pathology ; Organoids/metabolism ; Organoids/pathology
Sprache	Englisch
Erscheinungsdatum	2019-03-20
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2019.02.063
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Involvement of MAP3K8 and miR-17-5p in poor virologic response to interferon-based combination therapy for chronic hepatitis C.

Tsubota, Akihito / Mogushi, Kaoru / Aizaki, Hideki / Miyaguchi, Ken / Nagatsuma, Keisuke / Matsudaira, Hiroshi / Kushida, Tatsuya / Furihata, Tomomi / Tanaka, Hiroshi / Matsuura, Tomokazu

PloS one

2014 Band 9, Heft 5, Seite(n) e97078

Abstract: Despite advances in chronic hepatitis C treatment, a proportion of patients respond poorly to treatment. This study aimed to explore hepatic mRNA and microRNA signatures involved in hepatitis C treatment resistance. Global hepatic mRNA and microRNA ... ...

Abstract	Despite advances in chronic hepatitis C treatment, a proportion of patients respond poorly to treatment. This study aimed to explore hepatic mRNA and microRNA signatures involved in hepatitis C treatment resistance. Global hepatic mRNA and microRNA expression profiles were compared using microarray data between treatment responses. Quantitative real-time polymerase chain reaction validated the gene signatures from 130 patients who were infected with hepatitis C virus genotype 1b and treated with pegylated interferon-alpha and ribavirin combination therapy. The correlation between mRNA and microRNA was evaluated using in silico analysis and in vitro siRNA and microRNA inhibition/overexpression experiments. Multivariate regression analysis identified that the independent variables IL28B SNP rs8099917, hsa-miR-122-5p, hsa-miR-17-5p, and MAP3K8 were significantly associated with a poor virologic response. MAP3K8 and miR-17-5p expression were inversely correlated with treatment response. Furthermore, miR-17-5p repressed HCV production by targeting MAP3K8. Collectively, the data suggest that several molecules and the inverse correlation between mRNA and microRNA contributed to a host genetic refractory hepatitis C treatment response.
Mesh-Begriff(e)	Base Sequence ; Cell Line, Tumor ; Drug Interactions ; Drug Resistance, Viral/genetics ; Genotype ; Hepacivirus/drug effects ; Hepacivirus/genetics ; Hepacivirus/physiology ; Hepatitis C, Chronic/drug therapy ; Hepatitis C, Chronic/enzymology ; Hepatitis C, Chronic/genetics ; Humans ; Interferon-alpha/pharmacology ; Interferon-alpha/therapeutic use ; Liver/drug effects ; Liver/virology ; MAP Kinase Kinase Kinases/metabolism ; MicroRNAs/genetics ; Proto-Oncogene Proteins/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Treatment Outcome
Chemische Substanzen	Interferon-alpha ; MIRN17 microRNA, human ; MicroRNAs ; Proto-Oncogene Proteins ; RNA, Messenger ; MAP Kinase Kinase Kinases (EC 2.7.11.25) ; MAP3K8 protein, human (EC 2.7.11.25)
Sprache	Englisch
Erscheinungsdatum	2014-05-12
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0097078
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Centrosomal BRCA2 is a target protein of membrane type-1 matrix metalloproteinase (MT1-MMP).

Wali, Nadila / Hosokawa, Kana / Malik, Sadiya / Saito, Hiroko / Miyaguchi, Ken / Imajoh-Ohmi, Shinobu / Miki, Yoshio / Nakanishi, Akira

Biochemical and biophysical research communications

2014 Band 443, Heft 4, Seite(n) 1148–1154

Abstract	BRCA2 localizes to centrosomes between G1 and prophase and is removed from the centrosomes during mitosis, but the underlying mechanism is not clear. Here we show that BRCA2 is cleaved into two fragments by membrane type-1 matrix metalloproteinase (MT1-MMP), and that knockdown of MT1-MMP prevents the removal of BRCA2 from centrosomes during metaphase. Mass spectrometry mapping revealed that the MT1-MMP cleavage site of human BRCA2 is between Asn-2135 and Leu-2136 ((2132)LSNN/LNVEGG(2141)), and the point mutation L2136D abrogated MT1-MMP cleavage. Our data demonstrate that MT1-MMP proteolysis of BRCA2 regulates the abundance of BRCA2 on centrosomes.
Mesh-Begriff(e)	Amino Acid Sequence ; Amino Acid Substitution ; BRCA2 Protein/chemistry ; BRCA2 Protein/genetics ; BRCA2 Protein/metabolism ; Binding Sites/genetics ; Cell Cycle ; Cell Division ; Centrosome/metabolism ; Gene Knockdown Techniques ; HeLa Cells ; Humans ; Matrix Metalloproteinase 14/genetics ; Matrix Metalloproteinase 14/metabolism ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; Recombinant Fusion Proteins/chemistry ; Recombinant Fusion Proteins/genetics ; Recombinant Fusion Proteins/metabolism
Chemische Substanzen	BRCA2 Protein ; BRCA2 protein, human ; Recombinant Fusion Proteins ; MMP14 protein, human (EC 3.4.24.80) ; Matrix Metalloproteinase 14 (EC 3.4.24.80)
Sprache	Englisch
Erscheinungsdatum	2014-01-24
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2013.12.103
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: Identification of pathogenesis-related microRNAs in hepatocellular carcinoma by expression profiling.

Katayama, Yuki / Maeda, Moegi / Miyaguchi, Ken / Nemoto, Shota / Yasen, Mahmut / Tanaka, Shinji / Mizushima, Hiroshi / Fukuoka, Yutaka / Arii, Shigeki / Tanaka, Hiroshi

Oncology letters

2012 Band 4, Heft 4, Seite(n) 817–823

Abstract: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors of the liver. Since postoperative recurrence and intrahepatic metastases occur frequently, the postoperative 5-year survival rate is low. To investigate the molecular mechanisms of ...

Abstract	Hepatocellular carcinoma (HCC) is one of the most common malignant tumors of the liver. Since postoperative recurrence and intrahepatic metastases occur frequently, the postoperative 5-year survival rate is low. To investigate the molecular mechanisms of HCC progression, mRNA as well as microRNA (miRNA) expression levels have been profiled in various studies. However, no previous study has comprehensively compared the expression of miRNAs in HCC patients with various clinical features using the tumor and surrounding non-tumor tissues and normal liver samples. In this study, we profiled the expression of miRNAs in tumor and non-tumor tissues from 40 HCC patients with heterogeneous pathogenesis and 6 surrounding non-tumor tissues from patients with metastatic liver cancer. To identify miRNAs specific to each disease state, we comprehensively compared the expression of miRNAs in various combinations. The results indicate that the expression of many known as well as novel miRNAs was altered in patients with the hepatitis C virus infection compared with those with the hepatitis B virus and without any virus infection. The following miRNAs were downregulated in the tumor and non-tumor tissues, and thus could serve as novel biomarkers for chronic liver diseases: miR-18b, miR-296-5p, miR-557, miR-581, miR-625, miR-1228, miR-1249 and miR-2116. Similarly, miR-129, miR-146b-3p and miR-448 are novel candidates for HCC biomarkers regardless of virus infection.
Sprache	Englisch
Erscheinungsdatum	2012-07-18
Erscheinungsland	Greece
Dokumenttyp	Journal Article
ZDB-ID	2573196-8
ISSN	1792-1082 ; 1792-1074
ISSN (online)	1792-1082
ISSN	1792-1074
DOI	10.3892/ol.2012.810
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: The high-temperature requirement factor A3 (HtrA3) is associated with acquisition of the invasive phenotype in oral squamous cell carcinoma cells.

Moriya, Yujiro / Uzawa, Narikazu / Morita, Takuma / Mogushi, Kaoru / Miyaguchi, Ken / Takahashi, Ken-Ichiro / Michikawa, Chieko / Sumino, Jun / Tanaka, Hiroshi / Harada, Kiyoshi

Oral oncology

2015 Band 51, Heft 1, Seite(n) 84–89

Abstract: Objectives: Previous studies have identified several genes involved in the carcinogenesis of oral cancer; however, the detailed mechanisms underlying this process have not been elucidated. Previously, we established a database of the transcriptional ... ...

Abstract	Objectives: Previous studies have identified several genes involved in the carcinogenesis of oral cancer; however, the detailed mechanisms underlying this process have not been elucidated. Previously, we established a database of the transcriptional progression profile of oral carcinogenesis and identified 15 candidate genes with continuously increasing or decreasing expression (Sumino et al., 2013). Materials and methods: In the present study, using this database, we attempted to identify genes that may specifically contribute to progression from oral dysplastic lesions to invasive tumours. Results: We identified 4 candidate genes. Using a literature survey, we narrowed down the candidates and focused on the high-temperature requirement factor A3 (HtrA3). Quantitative real-time reverse transcription polymerase chain reaction and immunohistochemical analysis confirmed that HtrA3 expression significantly increased during this process. In addition, high HtrA3 expression was significantly associated with decreased disease-free survival (P=0.045) and overall survival (P=0.003). Multivariate Cox proportional hazards analysis found that high HtrA3 expression significantly correlated with overall survival (P=0.018). Conclusion: The findings of this study demonstrated that the HtrA3 is likely to be associated with the acquisition of the invasive phenotype in oral squamous cell carcinoma cells and may be a potential prognostic marker for oral cancer.
Mesh-Begriff(e)	Base Sequence ; Biomarkers, Tumor/metabolism ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/pathology ; Cell Line, Tumor ; DNA Primers ; Hot Temperature ; Humans ; Mouth Neoplasms/genetics ; Mouth Neoplasms/pathology ; Phenotype ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Serine Endopeptidases/genetics ; Serine Endopeptidases/physiology
Chemische Substanzen	Biomarkers, Tumor ; DNA Primers ; HTRA3 protein, human (EC 3.4.21.-) ; Serine Endopeptidases (EC 3.4.21.-)
Sprache	Englisch
Erscheinungsdatum	2015-01
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1120465-5
ISSN	1879-0593 ; 0964-1955 ; 1368-8375
ISSN (online)	1879-0593
ISSN	0964-1955 ; 1368-8375
DOI	10.1016/j.oraloncology.2014.10.001
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Gene expression changes in initiation and progression of oral squamous cell carcinomas revealed by laser microdissection and oligonucleotide microarray analysis.

Sumino, Jun / Uzawa, Narikazu / Okada, Norihiko / Miyaguchi, Ken / Mogushi, Kaoru / Takahashi, Ken-Ichiro / Sato, Hiroaki / Michikawa, Chieko / Nakata, Yoshimi / Tanaka, Hiroshi / Amagasa, Teruo

International journal of cancer

2013 Band 132, Heft 3, Seite(n) 540–548

Abstract: Oral carcinogenesis is a complex process involving multiple genes. However, the genetic changes involved in this process are not apparent in identical oral squamous cell carcinomas (OSCCs). According to pathological characteristics, samples of normal ... ...

Abstract	Oral carcinogenesis is a complex process involving multiple genes. However, the genetic changes involved in this process are not apparent in identical oral squamous cell carcinomas (OSCCs). According to pathological characteristics, samples of normal tissue, oral dysplastic lesions (ODLs), and invasive cancers were obtained from identical OSCCs using laser microdissection (LMD). Large-scale gene expression profiling was carried out on 33 samples derived from 11 OSCCs. We analyzed genes differentially expressed in normal tissues vs. ODLs and in ODLs vs. invasive tumors and identified 15 candidate genes with continuously increasing or decreasing expression during oral carcinogenesis. One of these genes, ISG15, was chosen for further characterization. Real-time quantitative reverse transcription-polymerase chain reaction and immunohistochemical analysis confirmed that ISG15 expression consistently increased during oral tumorigenesis. An ISG15 high-expression level was significantly associated with poor prognosis (p = 0.027). In addition, patients with high-expression tumors had a poorer 5-year survival rate than patients with low expression levels (p = 0.019). In conclusion, we identified 15 genes with continuously increasing or decreasing expression during oral carcinogenesis. One of these, ISG15, is likely to be associated with both dysgenesis and tumorigenesis and may be a potential prognostic marker for oral cancer.
Mesh-Begriff(e)	Biomarkers, Tumor/genetics ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/metabolism ; Carcinoma, Squamous Cell/mortality ; Carcinoma, Squamous Cell/pathology ; Cell Transformation, Neoplastic ; Cytokines/biosynthesis ; Cytokines/genetics ; Disease Progression ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Humans ; Laser Capture Microdissection ; Male ; Middle Aged ; Mouth Neoplasms/genetics ; Mouth Neoplasms/metabolism ; Mouth Neoplasms/mortality ; Mouth Neoplasms/pathology ; Oligonucleotide Array Sequence Analysis ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Ubiquitins/biosynthesis ; Ubiquitins/genetics
Chemische Substanzen	Biomarkers, Tumor ; Cytokines ; RNA, Messenger ; Ubiquitins ; ISG15 protein, human (60267-61-0)
Sprache	Englisch
Erscheinungsdatum	2013-02-01
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218257-9
ISSN	1097-0215 ; 0020-7136
ISSN (online)	1097-0215
ISSN	0020-7136
DOI	10.1002/ijc.27702
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Verfügbar in ZB MED Bonn

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Verfügbar in ZB MED Köln/Königswinter

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Verfügbar in ZB MED Köln/Königswinter

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Verfügbar in ZB MED Köln/Königswinter

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