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Article ; Online: Stem cell signature in glioblastoma: therapeutic development for a moving target.

Nakano, Ichiro

2015 Volume 122, Issue 2, Page(s) 324–330

Abstract: Tumor heterogeneity of adult high-grade glioma (HGG) is recognized in 3 major subtypes based on core gene signatures. However, the molecular signatures and clinical implications of glioma stem cells (GSCs) in individual HGG subtypes remain poorly ... ...

Abstract	Tumor heterogeneity of adult high-grade glioma (HGG) is recognized in 3 major subtypes based on core gene signatures. However, the molecular signatures and clinical implications of glioma stem cells (GSCs) in individual HGG subtypes remain poorly characterized. Recently genome-wide transcriptional analysis identified two mutually exclusive GSC subtypes with distinct dysregulated signaling and metabolic pathways. Analysis of genetic profiles and phenotypic assays distinguished proneural (PN) from mesenchymal (MES) GSCs and revealed a striking correlation with the corresponding PN or MES HGGs. Similar to HGGs with a MES signature, MES GSCs display more aggressive phenotypes both in vitro and in vivo. Furthermore, MES GSCs are markedly resistant to radiation as compared with PN GSCs, consistent with the relative radiation resistance of MES GBM compared with other subtypes. A systems biology approach has identified a set of transcription factors as the master regulators for the MES signature. Metabolic reprogramming in MES GSCs has also been noticed with the prominent activation of the glycolytic pathway, comprising aldehyde dehydrogenase (ALDH) family genes. This review summarizes recent progress in the characterization of the molecular signature in distinct HGG and GSC subtypes and plasticity between different GSC subtypes as well as between GSCs and non-GSCs in HGG tumors. Clinical implications of the translational GSC research are also discussed.
MeSH term(s)	Brain Neoplasms/classification ; Brain Neoplasms/pathology ; Brain Neoplasms/therapy ; Cellular Reprogramming ; Glioblastoma/classification ; Glioblastoma/pathology ; Glioblastoma/therapy ; Humans ; Mesoderm/pathology ; Neoplastic Stem Cells/pathology ; Neuronal Plasticity ; Neurons/pathology ; Phenotype ; Systems Biology ; Translational Medical Research/trends
Language	English
Publishing date	2015-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	3089-2
ISSN	1933-0693 ; 0022-3085
ISSN (online)	1933-0693
ISSN	0022-3085
DOI	10.3171/2014.9.JNS132253
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Article ; Online: Therapeutic potential of targeting glucose metabolism in glioma stem cells.

Nakano, Ichiro

Expert opinion on therapeutic targets

2014 Volume 18, Issue 11, Page(s) 1233–1236

Abstract: Glioblastoma is a highly lethal cancer. Glioma stem cells (GSCs) are potentially an attractive therapeutic target and eradication of GSCs may impact tumor growth and sensitize tumors to conventional therapies. The brain is one of the most metabolically ... ...

Abstract	Glioblastoma is a highly lethal cancer. Glioma stem cells (GSCs) are potentially an attractive therapeutic target and eradication of GSCs may impact tumor growth and sensitize tumors to conventional therapies. The brain is one of the most metabolically active organs with glucose representing the most important, but not the only, source of energy and carbon. Like all other cancers, glioblastoma requires a continuous source of energy and molecular resources for new cell production with a preferential use of aerobic glycolysis, recognized as the Warburg effect. As selected metabolic nodes are amenable to therapeutic targeting, we observed that the Warburg effect may causally contribute to glioma heterogeneity. This Editorial summarizes recent studies that examine the relationship between GSCs and metabolism and briefly provides our views for the future directions. The ultimate goal is to establish a new concept by incorporating both the cellular hierarchical theory and the cellular evolution theory to explain tumor heterogeneity. Such concept may better elucidate the mechanisms of how tumors gain cellular and molecular complexity and guide us develop novel and effective targeted therapies.
MeSH term(s)	Brain/metabolism ; Brain/pathology ; Brain Neoplasms/pathology ; Brain Neoplasms/therapy ; Glioblastoma/pathology ; Glioblastoma/therapy ; Glioma/pathology ; Glioma/therapy ; Glucose/metabolism ; Glycolysis/physiology ; Humans ; Molecular Targeted Therapy ; Neoplastic Stem Cells/metabolism
Chemical Substances	Glucose (IY9XDZ35W2)
Language	English
Publishing date	2014-11
Publishing country	England
Document type	Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2055208-7
ISSN	1744-7631 ; 1472-8222
ISSN (online)	1744-7631
ISSN	1472-8222
DOI	10.1517/14728222.2014.944899
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Article ; Online: Transcription factors as master regulator for cancer stemness: remove milk from fox?

Nakano, Ichiro

Expert review of anticancer therapy

2014 Volume 14, Issue 8, Page(s) 873–875

Abstract: Some cancers display a cellular hierarchy of varying differentiation states, as if they phenocopy the normal organ development processes. Accumulating evidence suggests that the molecular signals that control carcinogenesis, at least partially, overlap ... ...

Abstract	Some cancers display a cellular hierarchy of varying differentiation states, as if they phenocopy the normal organ development processes. Accumulating evidence suggests that the molecular signals that control carcinogenesis, at least partially, overlap with those involved in organogenesis. Cancer stem cells (CSCs) at the apex of cellular hierarchy are likely one, if not the only, critical therapeutic target in cancers. The proto-oncogene FOXM1 is a transcription factor (TF) defined as a master regulator for a broad array of genes required for CSCs and therefore FOXM1 is overexpressed in various cancers. In general, therapeutic development for TFs is a challenging task. Recently, on the other hand, novel insight has been brought by the discovery of a protein complex of FOXM1 with the mitotic kinase MELK in CSCs in brain cancers, as this protein complex appears to be cancer-specific. This editorial describes FOXM1 signaling in cancers and its potential therapeutic development.
MeSH term(s)	Animals ; Brain Neoplasms/genetics ; Brain Neoplasms/pathology ; Cell Differentiation/genetics ; Forkhead Box Protein M1 ; Forkhead Transcription Factors/genetics ; Gene Expression Regulation, Neoplastic ; Humans ; Neoplasms/genetics ; Neoplasms/pathology ; Neoplastic Stem Cells/cytology ; Protein-Serine-Threonine Kinases/genetics
Chemical Substances	FOXM1 protein, human ; Forkhead Box Protein M1 ; Forkhead Transcription Factors ; MELK protein, human (EC 2.7.1.-) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2014-07-14
Publishing country	England
Document type	Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2112544-2
ISSN	1744-8328 ; 1473-7140
ISSN (online)	1744-8328
ISSN	1473-7140
DOI	10.1586/14737140.2014.940324
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Article ; Online: Engulfing losers by winners in cancer: do cancer stem cells catch eat-me signals from noncancer stem cells?

Nakano, Ichiro

Future oncology (London, England)

2014 Volume 10, Issue 8, Page(s) 1335–1338

MeSH term(s)	Animals ; Cell Communication ; Humans ; Neoplastic Stem Cells/metabolism ; Phagocytosis ; Stem Cells/metabolism
Language	English
Publishing date	2014-07-23
Publishing country	England
Document type	Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2274956-1
ISSN	1744-8301 ; 1479-6694
ISSN (online)	1744-8301
ISSN	1479-6694
DOI	10.2217/fon.14.66
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Article ; Online: Proneural-mesenchymal transformation of glioma stem cells: do therapies cause evolution of target in glioblastoma?

Nakano, Ichiro

Future oncology (London, England)

2014 Volume 10, Issue 9, Page(s) 1527–1530

MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Brain Neoplasms/drug therapy ; Brain Neoplasms/pathology ; Cell Transdifferentiation ; Glioblastoma/drug therapy ; Glioblastoma/pathology ; Humans ; Neoplastic Stem Cells/drug effects ; Neoplastic Stem Cells/physiology ; Signal Transduction
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2014-08-22
Publishing country	England
Document type	Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2274956-1
ISSN	1744-8301 ; 1479-6694
ISSN (online)	1744-8301
ISSN	1479-6694
DOI	10.2217/fon.14.86
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Article ; Online: [Frontotemporal lobar degeneration (FTLD) concept and classification update].

Nakano, Imaharu

Rinsho shinkeigaku = Clinical neurology

2012 Volume 51, Issue 11, Page(s) 844–847

Abstract: FTLD is a neuroanatomical disease concept defined only by the presence of degeneration of the frontal and temporal lobes regardless of the underlying histopathological features, and therefore inevitably includes heterogeneous diseases that affect those ... ...

Abstract	FTLD is a neuroanatomical disease concept defined only by the presence of degeneration of the frontal and temporal lobes regardless of the underlying histopathological features, and therefore inevitably includes heterogeneous diseases that affect those cerebral regions. The ambiguous idea of Pick disease, the prototype of FTLD, constantly caused great nosological confusion as to FTLD. Progress in molecular neuropathology aimed at clarification of the protein constituents of the inclusion bodies seen in conditions causing FTLD, however, has resolved this problem by providing FTLD with a new concise nomenclature and classification based on the inclusion body proteins. The substances in inclusions in FTLD with ubiquitin-only inclusions (FTLD-U) have been discovered one after another; TDP-43 was the first, being found in inclusions in ALS and ALS with dementia (ALSD) too, and soon FUS/TLS was identified in some TDP-43-negative FTLD-U groups. Thus, FTLD has been divided into three main subgroups; 1) FTLD-tau, which includes Pick disease, PSP, CBD, etc., 2) FTLD-TDP, which is further divided to types A-D, ALSD belonging to type B, and 3) FTLD-FUS, which includes aFTLD-U, NIFID, and BIBD. Further deciphering of yet-unidentified proteins of some FTLD-U subsets will add more subclasses.
MeSH term(s)	Frontotemporal Lobar Degeneration/classification ; Humans
Language	Japanese
Publishing date	2012-01-03
Publishing country	Japan
Document type	English Abstract ; Journal Article ; Review
ZDB-ID	604200-4
ISSN	1882-0654 ; 0009-918X
ISSN (online)	1882-0654
ISSN	0009-918X
DOI	10.5692/clinicalneurol.51.844
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Article ; Online: [Frontotemporal lobar degeneration (FTLD) - changes of its concept and classification based on aggregated proteins].

Nakano, Imaharu

Rinsho shinkeigaku = Clinical neurology

2012 Volume 52, Issue 11, Page(s) 1218–1220

Abstract: FTLD is a purely anatomically defined concept, being unrelated to the underling cellular pathology; the sine qua non is only the presence of main lesions in the frontal and temporal lobes. FTLD, therefore, is destined to include various maladies that ... ...

Abstract	FTLD is a purely anatomically defined concept, being unrelated to the underling cellular pathology; the sine qua non is only the presence of main lesions in the frontal and temporal lobes. FTLD, therefore, is destined to include various maladies that involve the two areas. Cases reported by Arnold Pick, "Pick's disease", are a prototype of FTLD. Because of lack of histopathological description of the brains in his reports, however, the nomenclature brought about a great confusion in its nosology; the history of establishing the concept of FTLD was that of how to seperate genuine Pick's disease. After a long chaos, the present molecular neuropathology has ultimately resolved this problem by clarifying protein constituents of neuronal and glial aggregates in FTLD. TDP-43 was first found in ALS and ALS with dementia (ALSD), and soon FUS/TLS was detected in some TDP-43-negative FTLD-U groups. At the present time, FTLD consists of three main subgroups; 1) FTLD-tau, which includes Pick disease, PSP, CBD, etc., 2) FTLD-TDP, which is subdivided into types A-D, with ALSD belonging to type B, and 3) FTLD-FUS, the members of which are aFTLD-U, NIFID, and BIBD. Further discovery of yet-undetected proteins of some FTLD-U subsets will add more subclasses.
MeSH term(s)	Brain Chemistry ; Frontotemporal Dementia/metabolism ; Frontotemporal Lobar Degeneration/classification ; Humans ; Nerve Tissue Proteins/analysis
Chemical Substances	Nerve Tissue Proteins
Language	Japanese
Publishing date	2012-11-08
Publishing country	Japan
Document type	English Abstract ; Journal Article
ZDB-ID	604200-4
ISSN	1882-0654 ; 0009-918X
ISSN (online)	1882-0654
ISSN	0009-918X
DOI	10.5692/clinicalneurol.52.1218
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Article ; Online: Angiocrine extracellular vesicles impose mesenchymal reprogramming upon proneural glioma stem cells.

Adnani, Lata / Kassouf, Jordan / Meehan, Brian / Spinelli, Cristiana / Tawil, Nadim / Nakano, Ichiro / Rak, Janusz

Nature communications

2022 Volume 13, Issue 1, Page(s) 5494

Abstract: Glioblastoma (GBM) is an incurable form of primary astrocytic brain tumor driven by glioma stem cell (GSC) compartment closely associated with the vascular niche. GSC phenotypes are heterogeneous and range from proneural to mesenchymal-like, the latter ... ...

Abstract	Glioblastoma (GBM) is an incurable form of primary astrocytic brain tumor driven by glioma stem cell (GSC) compartment closely associated with the vascular niche. GSC phenotypes are heterogeneous and range from proneural to mesenchymal-like, the latter characterised by greater invasiveness. Here we document the secretory (angiocrine) role of endothelial cells and their derived extracellular vesicles (EVs) as drivers of proneural-to-mesenchymal reprogramming of GSCs. These changes involve activation of matrix metalloproteinases (MMPs) and NFκB, and inactivation of NOTCH, while altering responsiveness to chemotherapy and driving infiltrative growth in the brain. Our findings suggest that EV-mediated angiocrine interactions impact the nature of cellular stemness in GBM with implications for disease biology and therapy.
MeSH term(s)	Endothelial Cells/pathology ; Extracellular Vesicles/pathology ; Glioblastoma/pathology ; Glioma/pathology ; Humans ; Neoplastic Stem Cells/pathology
Language	English
Publishing date	2022-09-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-33235-7
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Article ; Online: Symptomatology and Neuropathology of patients presenting with focal cortical signs.

Ishihara, Kenji / Fukui, Toshiya / Kawamura, Mitsuru / Shiota, Jun-Ichi / Nakano, Imaharu

Neuropathology : official journal of the Japanese Society of Neuropathology

2022 Volume 43, Issue 1, Page(s) 27–43

Abstract: Here, we describe two patients who presented with focal cortical signs and underwent neuropathological examination. Case 1 was a 73-year-old woman with progressive speech disorder and abnormal behavior. She showed agraphia of the frontal lobe type, ... ...

Abstract	Here, we describe two patients who presented with focal cortical signs and underwent neuropathological examination. Case 1 was a 73-year-old woman with progressive speech disorder and abnormal behavior. She showed agraphia of the frontal lobe type, featured by the omission of kana letters when writing, other than pyramidal tract signs, pseudobulbar palsy, and frontal lobe dementia. Neuropathological examination, including TAR DNA-binding protein 43 (TDP-43) immunohistochemistry, revealed bilateral frontal and anterior temporal lobe lesions accentuated in the precentral gyrus and posterior part of the middle frontal gyrus. Both upper and lower motor neurons showed pathological changes compatible with amyotrophic lateral sclerosis. Case 2 was a 62-year-old man with progressive speech disorder and hand clumsiness. He had a motor speech disorder, compatible with apraxia of speech, and limb apraxia of the limb-kinetic and ideomotor type. Neuropathological examination revealed degeneration in the left frontal lobe, including the precentral gyrus, anterior temporal, and parietal lobe cortices. Moreover, numerous argyrophilic neuronal intracytoplasmic inclusions (Pick body) and ballooned neurons were observed in these lesions and the limbic system. The pathological diagnosis was Pick disease involving the peri-Rolandic area and parietal lobe. In these two cases, the distribution of neuropathological changes in the cerebral cortices correlated with the clinical symptoms observed.
MeSH term(s)	Male ; Female ; Humans ; Aged ; Middle Aged ; Amyotrophic Lateral Sclerosis/pathology ; Motor Neurons/pathology ; Dementia/pathology ; Temporal Lobe/pathology ; Apraxias/pathology
Language	English
Publishing date	2022-11-03
Publishing country	Australia
Document type	Case Reports ; Journal Article ; Review
ZDB-ID	1483794-8
ISSN	1440-1789 ; 0919-6544
ISSN (online)	1440-1789
ISSN	0919-6544
DOI	10.1111/neup.12854
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Article: [Classification of dementia with Lewy body and frontotemporal lobar degeneration].

Nakano, Imaharu

Brain and nerve = Shinkei kenkyu no shinpo

2010 Volume 62, Issue 12, Page(s) 1352–1354

MeSH term(s)	Brain/metabolism ; Brain/pathology ; DNA-Binding Proteins/metabolism ; Frontotemporal Lobar Degeneration/classification ; Frontotemporal Lobar Degeneration/metabolism ; Frontotemporal Lobar Degeneration/pathology ; Humans ; Lewy Body Disease/classification ; Lewy Body Disease/diagnosis ; Lewy Body Disease/pathology ; Lewy Body Disease/physiopathology ; tau Proteins/metabolism
Chemical Substances	DNA-Binding Proteins ; tau Proteins
Language	English
Publishing date	2010-12
Publishing country	Japan
Document type	Journal Article
ZDB-ID	390389-8
ISSN	1344-8129 ; 1881-6096 ; 0006-8969
ISSN (online)	1344-8129
ISSN	1881-6096 ; 0006-8969
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