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Article ; Online: Di-n-butyl phthalate promotes the neural differentiation of mouse embryonic stem cells through neurogenic differentiation 1.

Lin, Ying-Chu / Wuputra, Kenly / Kato, Kohsuke / Ku, Chia-Chen / Saito, Shigeo / Noguchi, Michiya / Nakamura, Yukio / Hsiao, Michael / Lin, Chang-Shen / Wu, Deng-Chyang / Kawaguchi, Atsushi / Yu, Hsin-Su / Yokoyama, Kazunari K

Environmental pollution (Barking, Essex : 1987)

2024 Volume 347, Page(s) 123722

Abstract: An understanding of the risk of gene deletion and mutation posed by endocrine-disrupting chemicals (EDCs) is necessary for the identification of etiological reagents for many human diseases. Therefore, the characterization of the genetic traits caused by ...

Abstract	An understanding of the risk of gene deletion and mutation posed by endocrine-disrupting chemicals (EDCs) is necessary for the identification of etiological reagents for many human diseases. Therefore, the characterization of the genetic traits caused by developmental exposure to EDCs is an important research subject. A new regenerative approach using embryonic stem cells (ESCs) holds promise for the development of stem-cell-based therapies and the identification of novel therapeutic agents against human diseases. Here, we focused on the characterization of the genetic traits and alterations in pluripotency/stemness triggered by phthalate ester derivatives. Regarding their in vitro effects, we reported the abilities of ESCs regarding proliferation, cell-cycle control, and neural ectoderm differentiation. The expression of their stemness-related genes and their genetic changes toward neural differentiation were examined, which led to the observation that the tumor suppressor gene product p53/retinoblastoma protein 1 and its related cascades play critical functions in cell-cycle progression, cell death, and neural differentiation. In addition, the expression of neurogenic differentiation 1 was affected by exposure to di-n-butyl phthalate in the context of cell differentiation into neural lineages. The nervous system is one of the most sensitive tissues to exposure to phthalate ester derivatives. The present screening system provides a good tool for studying the mechanisms underlying the effects of EDCs on the developmental regulation of humans and rodents, especially on the neuronal development of ESCs.
MeSH term(s)	Animals ; Humans ; Mice ; Mouse Embryonic Stem Cells ; Dibutyl Phthalate/toxicity ; Cell Differentiation ; Esters ; Phthalic Acids
Chemical Substances	phthalic acid (6O7F7IX66E) ; Dibutyl Phthalate (2286E5R2KE) ; Esters ; Phthalic Acids
Language	English
Publishing date	2024-03-07
Publishing country	England
Document type	Journal Article
ZDB-ID	280652-6
ISSN	1873-6424 ; 0013-9327 ; 0269-7491
ISSN (online)	1873-6424
ISSN	0013-9327 ; 0269-7491
DOI	10.1016/j.envpol.2024.123722
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Article: Biomarkers of Cancer Stem Cells for Experimental Research and Clinical Application.

Saito, Shigeo / Ku, Chia-Chen / Wuputra, Kenly / Pan, Jia-Bin / Lin, Chang-Shen / Lin, Ying-Chu / Wu, Deng-Chyang / Yokoyama, Kazunari K

Journal of personalized medicine

2022 Volume 12, Issue 5

Abstract: The use of biomarkers in cancer diagnosis, therapy, and prognosis has been highly effective over several decades. Studies of biomarkers in cancer patients pre- and post-treatment and during cancer progression have helped identify cancer stem cells (CSCs) ...

Abstract	The use of biomarkers in cancer diagnosis, therapy, and prognosis has been highly effective over several decades. Studies of biomarkers in cancer patients pre- and post-treatment and during cancer progression have helped identify cancer stem cells (CSCs) and their related microenvironments. These analyses are critical for the therapeutic application of drugs and the efficient targeting and prevention of cancer progression, as well as the investigation of the mechanism of the cancer development. Biomarkers that characterize CSCs have thus been identified and correlated to diagnosis, therapy, and prognosis. However, CSCs demonstrate elevated levels of plasticity, which alters their functional phenotype and appearance by interacting with their microenvironments, in response to chemotherapy and radiotherapeutics. In turn, these changes induce different metabolic adaptations of CSCs. This article provides a review of the most frequently used CSCs and stem cell markers.
Language	English
Publishing date	2022-04-29
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2662248-8
ISSN	2075-4426
ISSN	2075-4426
DOI	10.3390/jpm12050715
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Article ; Online: Translational models of 3-D organoids and cancer stem cells in gastric cancer research.

Wuputra, Kenly / Ku, Chia-Chen / Kato, Kohsuke / Wu, Deng-Chyang / Saito, Shigeo / Yokoyama, Kazunari K

Stem cell research & therapy

2021 Volume 12, Issue 1, Page(s) 492

Abstract: It is postulated as a general concept of cancer stem cells (CSCs) that they can produce cancer cells overtly and repopulate cancer progenitor cells indefinitely. The CSC niche is part of a specialized cancer microenvironment that is important to keep the ...

Abstract	It is postulated as a general concept of cancer stem cells (CSCs) that they can produce cancer cells overtly and repopulate cancer progenitor cells indefinitely. The CSC niche is part of a specialized cancer microenvironment that is important to keep the phenotypes of CSCs. Stem cell- and induced pluripotent stem cell (iPSC)-derived organoids with genetic manipulation are beneficial to the investigation of the regulation of the microenvironment of CSCs. It would be useful to assess the efficiency of the cancer microenvironment on initiation and progression of cancers. To identify CSCs in cancer tissues, normal cell organoids and gastric cancer organoids from the cancerous areas, as well as iPSCs, were established several years ago. However, many questions remain about the extent to which these cultures recapitulate the development of the gastrointestinal tract and the mechanism of Helicobacter pylori-induced cancer progression. To clarify the fidelity of human organoid models, we have noted several key issues for the cultivation of, and differences between, normal and cancerous organoids. We developed precise culture conditions for gastric organoids in vitro to improve the accuracy of the generation of organoid models for therapeutic and medical applications. In addition, the current knowledge on gastrointestinal CSC research, including the topic of CSC markers, cancer cell reprogramming, and application to target cancer cell plasticity through niches, should be reinforced. We discuss the progression of cancers derived from human gastric organoids and the identification of CSCs.
MeSH term(s)	Humans ; Induced Pluripotent Stem Cells ; Neoplastic Stem Cells ; Organoids ; Stomach Neoplasms/genetics ; Tumor Microenvironment
Language	English
Publishing date	2021-09-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2548671-8
ISSN	1757-6512 ; 1757-6512
ISSN (online)	1757-6512
ISSN	1757-6512
DOI	10.1186/s13287-021-02521-4
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Article ; Online: Independent Signaling of Hepatoma Derived Growth Factor and Tumor Necrosis Factor-Alpha in Human Gastric Cancer Organoids Infected by

Wuputra, Kenly / Ku, Chia-Chen / Pan, Jia-Bin / Liu, Chung-Jung / Kato, Kohsuke / Lin, Ying-Chu / Liu, Yi-Chang / Lin, Chang-Shen / Hsiao, Michael / Tai, Ming-Hong / Chong, Inn-Wen / Hu, Huang-Ming / Kuo, Chao-Hung / Wu, Deng-Chyang / Yokoyama, Kazunari K

International journal of molecular sciences

2023 Volume 24, Issue 7

Abstract: We prepared three-dimensional (3-D) organoids of human stomach cancers and examined the correlation between the tumorigenicity and cytotoxicity ... ...

Abstract	We prepared three-dimensional (3-D) organoids of human stomach cancers and examined the correlation between the tumorigenicity and cytotoxicity of
MeSH term(s)	Humans ; Stomach Neoplasms/pathology ; Tumor Necrosis Factor-alpha/metabolism ; Helicobacter pylori/metabolism ; Antigens, Bacterial/metabolism ; Carcinoma, Hepatocellular ; Intercellular Signaling Peptides and Proteins/metabolism ; Liver Neoplasms ; Organoids/metabolism ; Helicobacter Infections/metabolism ; Bacterial Proteins/genetics ; Bacterial Proteins/pharmacology ; Bacterial Proteins/metabolism
Chemical Substances	Tumor Necrosis Factor-alpha ; hepatoma-derived growth factor ; Antigens, Bacterial ; Intercellular Signaling Peptides and Proteins ; Bacterial Proteins
Language	English
Publishing date	2023-03-31
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/ijms24076567
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Article ; Online: Generation of Human Stomach Cancer iPSC-Derived Organoids Induced by

Ku, Chia-Chen / Wuputra, Kenly / Pan, Jia-Bin / Li, Chia-Pei / Liu, Chung-Jung / Liu, Yi-Chang / Saito, Shigeo / Chan, Te-Fu / Lin, Chang-Shen / Wu, Deng-Chyang / Yokoyama, Kazunari K

Cells

2022 Volume 11, Issue 2

Abstract: There is considerable cellular diversity in the human stomach, which has helped to clarify cell plasticity in normal development and tumorigenesis. Thus, the stomach is an interesting model for understanding cellular plasticity and for developing ... ...

Abstract	There is considerable cellular diversity in the human stomach, which has helped to clarify cell plasticity in normal development and tumorigenesis. Thus, the stomach is an interesting model for understanding cellular plasticity and for developing prospective anticancer therapeutic agents. However, many questions remain regarding the development of cancers in vivo and in vitro in two- or three-dimensional (2D/3D) cultures, as well as the role of
MeSH term(s)	Biomedical Research ; Helicobacter Infections/pathology ; Humans ; Induced Pluripotent Stem Cells/physiology ; Organoids/pathology ; Stomach Neoplasms/genetics ; Stomach Neoplasms/microbiology ; Stomach Neoplasms/pathology ; Tissue Culture Techniques
Language	English
Publishing date	2022-01-06
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11020184
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Article ; Online: Prevention of tumor risk associated with the reprogramming of human pluripotent stem cells.

Wuputra, Kenly / Ku, Chia-Chen / Wu, Deng-Chyang / Lin, Ying-Chu / Saito, Shigeo / Yokoyama, Kazunari K

Journal of experimental & clinical cancer research : CR

2020 Volume 39, Issue 1, Page(s) 100

Abstract: Human pluripotent embryonic stem cells have two special features: self-renewal and pluripotency. It is important to understand the properties of pluripotent stem cells and reprogrammed stem cells. One of the major problems is the risk of reprogrammed ... ...

Abstract	Human pluripotent embryonic stem cells have two special features: self-renewal and pluripotency. It is important to understand the properties of pluripotent stem cells and reprogrammed stem cells. One of the major problems is the risk of reprogrammed stem cells developing into tumors. To understand the process of differentiation through which stem cells develop into cancer cells, investigators have attempted to identify the key factors that generate tumors in humans. The most effective method for the prevention of tumorigenesis is the exclusion of cancer cells during cell reprogramming. The risk of cancer formation is dependent on mutations of oncogenes and tumor suppressor genes during the conversion of stem cells to cancer cells and on the environmental effects of pluripotent stem cells. Dissecting the processes of epigenetic regulation and chromatin regulation may be helpful for achieving correct cell reprogramming without inducing tumor formation and for developing new drugs for cancer treatment. This review focuses on the risk of tumor formation by human pluripotent stem cells, and on the possible treatment options if it occurs. Potential new techniques that target epigenetic processes and chromatin regulation provide opportunities for human cancer modeling and clinical applications of regenerative medicine.
MeSH term(s)	Animals ; Cell Differentiation ; Cellular Reprogramming ; Epigenesis, Genetic ; Humans ; Neoplasms/genetics ; Neoplasms/pathology ; Neoplasms/prevention & control ; Pluripotent Stem Cells/cytology
Language	English
Publishing date	2020-06-03
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	803138-1
ISSN	1756-9966 ; 0392-9078
ISSN (online)	1756-9966
ISSN	0392-9078
DOI	10.1186/s13046-020-01584-0
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Zs.A 2065: Show issues

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Article ; Online: Heterogeneity of Phase II Enzyme Ligands on Controlling the Progression of Human Gastric Cancer Organoids as Stem Cell Therapy Model.

Wu, Deng-Chyang / Ku, Chia-Chen / Pan, Jia-Bin / Wuputra, Kenly / Yang, Ya-Han / Liu, Chung-Jung / Liu, Yi-Chang / Kato, Kohsuke / Saito, Shigeo / Lin, Ying-Chu / Chong, Inn-Wen / Hsiao, Michael / Hu, Huang-Ming / Kuo, Chao-Hung / Kuo, Kung-Kai / Lin, Chang-Shen / Yokoyama, Kazunari K

International journal of molecular sciences

2023 Volume 24, Issue 21

Abstract: Gastric cancer (GC) organoids are frequently used to examine cell proliferation and death as well as cancer development. Invasion/migration assay, xenotransplantation, and reactive oxygen species (ROS) production were used to examine the effects of ... ...

Abstract	Gastric cancer (GC) organoids are frequently used to examine cell proliferation and death as well as cancer development. Invasion/migration assay, xenotransplantation, and reactive oxygen species (ROS) production were used to examine the effects of antioxidant drugs, including perillaldehyde (PEA), cinnamaldehyde (CA), and sulforaphane (SFN), on GC. PEA and CA repressed the proliferation of human GC organoids, whereas SFN enhanced it. Caspase 3 activities were also repressed on treatment with PEA and CA. Furthermore, the tumor formation and invasive activities were repressed on treatment with PEA and CA, whereas they were enhanced on treatment with SFN. These results in three-dimensional (3D)-GC organoids showed the different cancer development of phase II enzyme ligands in 2D-GC cells. ROS production and the expression of TP53, nuclear factor erythroid 2-related factor (NRF2), and Jun dimerization protein 2 were also downregulated on treatment with PEA and CA, but not SFN. NRF2 knockdown reversed the effects of these antioxidant drugs on the invasive activities of the 3D-GC organoids. Moreover, ROS production was also inhibited by treatment with PEA and CA, but not SFN. Thus, NRF2 plays a key role in the differential effects of these antioxidant drugs on cancer progression in 3D-GC organoids. PEA and CA can potentially be new antitumorigenic therapeutics for GC.
MeSH term(s)	Humans ; Antioxidants/pharmacology ; Apoptosis ; Cell- and Tissue-Based Therapy ; Isothiocyanates/pharmacology ; Isothiocyanates/metabolism ; NF-E2-Related Factor 2/metabolism ; Organoids/metabolism ; Oxidative Stress ; Reactive Oxygen Species/metabolism ; Stomach Neoplasms/drug therapy ; Stomach Neoplasms/metabolism ; Sulfoxides/pharmacology
Chemical Substances	Antioxidants ; Isothiocyanates ; NF-E2-Related Factor 2 ; Reactive Oxygen Species ; sulforaphane (GA49J4310U) ; Sulfoxides
Language	English
Publishing date	2023-11-02
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/ijms242115911
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Article: Jdp2 is a spatiotemporal transcriptional activator of the AhR via the Nrf2 gene battery.

Wuputra, Kenly / Tsai, Ming-Ho / Kato, Kohsuke / Ku, Chia-Chen / Pan, Jia-Bin / Yang, Ya-Han / Saito, Shigeo / Wu, Chun-Chieh / Lin, Ying-Chu / Cheng, Kuang-Hung / Kuo, Kung-Kai / Noguchi, Michiya / Nakamura, Yukio / Yoshioka, Tohru / Wu, Deng-Chyang / Lin, Chang-Shen / Yokoyama, Kazunari K

Inflammation and regeneration

2023 Volume 43, Issue 1, Page(s) 42

Abstract: Background: Crosstalk between the aryl hydrocarbon receptor (AhR) and nuclear factor (erythroid-derived 2)-like 2 (Nrf2) signaling is called the "AhR-Nrf2 gene battery", which works synergistically in detoxification to support cell survival. Nrf2- ... ...

Abstract	Background: Crosstalk between the aryl hydrocarbon receptor (AhR) and nuclear factor (erythroid-derived 2)-like 2 (Nrf2) signaling is called the "AhR-Nrf2 gene battery", which works synergistically in detoxification to support cell survival. Nrf2-dependent phase II gene promoters are controlled by coordinated recruitment of the AhR to adjacent dioxin responsive element (DRE) and Nrf2 recruitment to the antioxidative response element (ARE). The molecular interaction between AhR and Nrf2 members, and the regulation of each target, including phase I and II gene complexes, and their mediators are poorly understood. Methods: Knockdown and forced expression of AhR-Nrf2 battery members were used to examine the molecular interactions between the AhR-Nrf2 axis and AhR promoter activation. Sequential immunoprecipitation, chromatin immunoprecipitation, and histology were used to identify each protein complex recruited to their respective cis-elements in the AhR promoter. Actin fiber distribution, cell spreading, and invasion were examined to identify functional differences in the AhR-Jdp2 axis between wild-type and Jdp2 knockout cells. The possible tumorigenic role of Jdp2 in the AhR-Nrf2 axis was examined in mutant Kras-Trp53-driven pancreatic tumors. Results: Crosstalk between AhR and Nrf2 was evident at the transcriptional level. The AhR promoter was activated by phase I ligands such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) through the AhR-Jdp2-Nrf2 axis in a time- and spatial transcription-dependent manner. Jdp2 was a bifunctional activator of DRE- and ARE-mediated transcription in response to TCDD. After TCDD exposure, Jdp2 activated the AhR promoter at the DRE and then moved to the ARE where it activated the promoter to increase reactive oxygen species (ROS)-mediated functions such as cell spreading and invasion in normal cells, and cancer regression in mutant Kras-Trp53-driven pancreatic tumor cells. Conclusions: Jdp2 plays a critical role in AhR promoter activation through the AhR-Jdp2-Nrf2 axis in a spatiotemporal manner. The AhR functions to maintain ROS balance and cell spreading, invasion, and cancer regression in a mouse model of mutant Kras-Trp53 pancreatic cancer. These findings provide new insights into the roles of Jdp2 in the homeostatic regulation of oxidative stress and in the antioxidation response in detoxification, inflammation, and cancer progression.
Language	English
Publishing date	2023-08-18
Publishing country	England
Document type	Journal Article
ZDB-ID	2051471-2
ISSN	1880-9693 ; 0389-4290
ISSN	1880-9693 ; 0389-4290
DOI	10.1186/s41232-023-00290-6
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Zs.B 2929: Show issues

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Article ; Online: FOXM1-CD44 Signaling Is Critical for the Acquisition of Regorafenib Resistance in Human Liver Cancer Cells.

Wuputra, Kenly / Hsiao, Pi-Jung / Chang, Wen-Tsan / Wu, Po-Hsuan / Chen, Lin-Ann / Huang, Jian-Wei / Su, Wen-Lung / Yang, Ya-Han / Wu, Deng-Chyang / Yokoyama, Kazunari K / Kuo, Kung-Kai

International journal of molecular sciences

2022 Volume 23, Issue 14

Abstract: Regorafenib is a multikinase inhibitor that was approved by the US Food and Drug administration in 2017. Cancer stem cells (CSCs) are a small subset of cancer-initiating cells that are thought to contribute to therapeutic resistance. The forkhead box ... ...

Abstract	Regorafenib is a multikinase inhibitor that was approved by the US Food and Drug administration in 2017. Cancer stem cells (CSCs) are a small subset of cancer-initiating cells that are thought to contribute to therapeutic resistance. The forkhead box protein M1 (FOXM1) plays an important role in the regulation of the stemness of CSCs and mediates resistance to chemotherapy. However, the relationship between FOXM1 and regorafenib resistance in liver cancer cells remains unknown. We found that regorafenib-resistant HepG2 clones overexpressed FOXM1 and various markers of CSCs. Patients with hepatocellular carcinoma also exhibited an upregulation of FOXM1 and resistance to regorafenib, which were correlated with a poor survival rate. We identified a close relationship between FOXM1 expression and regorafenib resistance, which was correlated with the survival of patients with hepatocellular carcinoma. Thus, a strategy that antagonizes FOXM1-CD44 signaling would enhance the therapeutic efficacy of regorafenib in these patients.
MeSH term(s)	Carcinoma, Hepatocellular/drug therapy ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/metabolism ; Cell Line, Tumor ; Cell Proliferation ; Drug Resistance, Neoplasm ; Forkhead Box Protein M1/genetics ; Forkhead Box Protein M1/metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; Hyaluronan Receptors/metabolism ; Liver Neoplasms/drug therapy ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; Phenylurea Compounds ; Pyridines
Chemical Substances	CD44 protein, human ; FOXM1 protein, human ; Forkhead Box Protein M1 ; Hyaluronan Receptors ; Phenylurea Compounds ; Pyridines ; regorafenib (24T2A1DOYB)
Language	English
Publishing date	2022-07-14
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/ijms23147782
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Article ; Online: Translational models of 3-D organoids and cancer stem cells in gastric cancer research

Kenly Wuputra / Chia-Chen Ku / Kohsuke Kato / Deng-Chyang Wu / Shigeo Saito / Kazunari K. Yokoyama

Stem Cell Research & Therapy, Vol 12, Iss 1, Pp 1-

2021 Volume 16

Abstract: Abstract It is postulated as a general concept of cancer stem cells (CSCs) that they can produce cancer cells overtly and repopulate cancer progenitor cells indefinitely. The CSC niche is part of a specialized cancer microenvironment that is important to ...

Abstract	Abstract It is postulated as a general concept of cancer stem cells (CSCs) that they can produce cancer cells overtly and repopulate cancer progenitor cells indefinitely. The CSC niche is part of a specialized cancer microenvironment that is important to keep the phenotypes of CSCs. Stem cell- and induced pluripotent stem cell (iPSC)-derived organoids with genetic manipulation are beneficial to the investigation of the regulation of the microenvironment of CSCs. It would be useful to assess the efficiency of the cancer microenvironment on initiation and progression of cancers. To identify CSCs in cancer tissues, normal cell organoids and gastric cancer organoids from the cancerous areas, as well as iPSCs, were established several years ago. However, many questions remain about the extent to which these cultures recapitulate the development of the gastrointestinal tract and the mechanism of Helicobacter pylori-induced cancer progression. To clarify the fidelity of human organoid models, we have noted several key issues for the cultivation of, and differences between, normal and cancerous organoids. We developed precise culture conditions for gastric organoids in vitro to improve the accuracy of the generation of organoid models for therapeutic and medical applications. In addition, the current knowledge on gastrointestinal CSC research, including the topic of CSC markers, cancer cell reprogramming, and application to target cancer cell plasticity through niches, should be reinforced. We discuss the progression of cancers derived from human gastric organoids and the identification of CSCs.
Keywords	Cancer microenvironment ; Cancer stem cells ; Human gastric organoids ; Gastric cancer ; Translational research ; Tumor suppressor genes ; Medicine (General) ; R5-920 ; Biochemistry ; QD415-436
Language	English
Publishing date	2021-09-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
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