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Article ; Online: Endothelial Dysfunction in Neurodegenerative Diseases.

Fang, Yao-Ching / Hsieh, Yi-Chen / Hu, Chaur-Jong / Tu, Yong-Kwang

International journal of molecular sciences

2023 Volume 24, Issue 3

Abstract: The cerebral vascular system stringently regulates cerebral blood flow (CBF). The components of the blood-brain barrier (BBB) protect the brain from pathogenic infections and harmful substances, efflux waste, and exchange substances; however, diseases ... ...

Abstract	The cerebral vascular system stringently regulates cerebral blood flow (CBF). The components of the blood-brain barrier (BBB) protect the brain from pathogenic infections and harmful substances, efflux waste, and exchange substances; however, diseases develop in cases of blood vessel injuries and BBB dysregulation. Vascular pathology is concurrent with the mechanisms underlying aging, Alzheimer's disease (AD), and vascular dementia (VaD), which suggests its involvement in these mechanisms. Therefore, in the present study, we reviewed the role of vascular dysfunction in aging and neurodegenerative diseases, particularly AD and VaD. During the development of the aforementioned diseases, changes occur in the cerebral blood vessel morphology and local cells, which, in turn, alter CBF, fluid dynamics, and vascular integrity. Chronic vascular inflammation and blood vessel dysregulation further exacerbate vascular dysfunction. Multitudinous pathogenic processes affect the cerebrovascular system, whose dysfunction causes cognitive impairment. Knowledge regarding the pathophysiology of vascular dysfunction in neurodegenerative diseases and the underlying molecular mechanisms may lead to the discovery of clinically relevant vascular biomarkers, which may facilitate vascular imaging for disease prevention and treatment.
MeSH term(s)	Humans ; Neurodegenerative Diseases/pathology ; Alzheimer Disease/pathology ; Brain/pathology ; Dementia, Vascular/pathology ; Blood-Brain Barrier/pathology ; Vascular Diseases/pathology ; Cognitive Dysfunction/pathology
Language	English
Publishing date	2023-02-02
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24032909
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Article: Can chronic kidney disease staging early predict outcome of large-artery ischemic stroke with impaired renal function?

Lian, Ie-Bin / Chiu, Ping-Fang / Hsieh, Yi-Chen / Ou, Yang-Hao / Lin, Chih-Ming

Therapeutic advances in chronic disease

2023 Volume 14, Page(s) 20406223231153564

Abstract: Background: Ischemic stroke poses a major threat to human beings, and a prompt intravenous thrombolytic management remains the gold standard protocol for stroke sufferers. Although the role of thrombolytic therapy (r-tPA) for ischemic stroke patients ... ...

Abstract	Background: Ischemic stroke poses a major threat to human beings, and a prompt intravenous thrombolytic management remains the gold standard protocol for stroke sufferers. Although the role of thrombolytic therapy (r-tPA) for ischemic stroke patients and those with underlying impaired renal function has been advocated as effective treating strategy, there is still a lack of investigation as to finding out baseline important variables that are capable of early outcome prediction. Objectives: In this project, we hypothesize that the change of clinical chronic kidney disease (CKD) staging (delta stage = CKD stage after 3-month follow-up - CKD stage at admission) could serve as a crucial predictor of the prognosis of patients. Design: This is a cohort longitudinal retrospective study. Sources and methods: A total of 765 cerebral artery ischemic stroke patients with impaired renal function were recruited and followed up for 1 year. Among them, 116 had received the thrombolytic treatment (r-tPA) after being evaluated at the triage in the emergency department and the rest had not (non-r-tPA). Propensity-matching was applied to compare the mortality between the r-tPA and non-r-tPA groups. Multiple logistic regression (LR) and decision tree (DT) algorithm were used to identify important prediction factors for mortality as well as the improvement in neurological function. Results: The 1-year mortality rates for r-tPA and non-r-tPA groups were 32.8% and 44.4%, respectively. The propensity-matched odds ratio of mortality for the r-tPA group compared with the non-r-tPA group is 0.469, with Conclusion: Large-artery ischemic stroke patients who received thrombolytic treatment had significantly lower mortality, even when presenting underlying impaired renal function. The change of CKD staging (delta stage) is capable of acting as a powerful clinical baseline surrogate for both r-tPA and non-r-tPA patients in terms of early outcome prediction. Long-term use of diuretics could be potentially harmful to this group of patients. Moreover, delta stage correlates well with clinical long-term neurological functionality assessment (NIHSS, mRS, and Barthel index), which is helpful in aiding urgent clinical decision-making.
Language	English
Publishing date	2023-02-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	2554816-5
ISSN	2040-6231 ; 2040-6223
ISSN (online)	2040-6231
ISSN	2040-6223
DOI	10.1177/20406223231153564
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Article: Plasma extracellular vesicle tau, β-amyloid, and α-synuclein and the progression of Parkinson's disease: a follow-up study.

Chan, Lung / Chung, Chen-Chih / Hsieh, Yi-Chen / Wu, Ruey-Meei / Hong, Chien-Tai

Therapeutic advances in neurological disorders

2023 Volume 16, Page(s) 17562864221150329

Abstract: Background: Plasma extracellular vesicle (EV) contents are promising biomarkers of Parkinson's disease (PD). The pathognomonic proteins of PD, including α-synuclein, tau, and β-amyloid, are altered in people with PD (PwP) and are associated with ... ...

Abstract	Background: Plasma extracellular vesicle (EV) contents are promising biomarkers of Parkinson's disease (PD). The pathognomonic proteins of PD, including α-synuclein, tau, and β-amyloid, are altered in people with PD (PwP) and are associated with clinical presentation in previous cross-sectional studies. However, the dynamic changes in these plasma EV proteins in PwP and their correlation with clinical progression remain unclear. Objective: We investigated the dynamic changes in plasma EV α-synuclein, tau, and β-amyloid and their correlation with/prediction of clinical progression in PwP. Design: A cohort study. Methods: In total, 103 PwP and 37 healthy controls (HCs) completed baseline assessment and 1-year follow-up. Clinical assessments included Unified Parkinson's Disease Rating Scale (UPDRS) parts II and III, Mini-Mental State Examination (MMSE), and Montreal Cognitive Assessment (MoCA). Plasma EVs were isolated, and immunomagnetic reduction-based immunoassay was used to assess α-synuclein, tau, and β-amyloid 1-42 (Aβ1-42) levels within the EVs. Results: Compared with HCs, significant differences were noted in the annual changes in all three EV pathognomonic proteins in PwP. Although the absolute changes in plasma EV pathognomonic proteins did not significantly correlate with clinical changes, PwP with elevated baseline plasma EV tau (upper-half) levels demonstrated significantly greater decline in motor and cognition, and increased plasma EV α-synuclein levels were associated with postural instability and the gait disturbance motor subtype. For PwP with elevated levels of all three biomarkers, clinical deterioration was significant, as indicated by UPDRS-II scores, postural instability and gait disturbance subscores of UPDRS-III, and MMSE score. Conclusion: The combination of plasma EV α-synuclein, tau, and Aβ1-42 may identify PwP with a high risk of deterioration. Our findings can elucidate the interaction between these pathognomonic proteins, and they may serve as treatment response markers and can be applied in treatment approaches for disease modification.
Language	English
Publishing date	2023-02-01
Publishing country	England
Document type	Journal Article
ZDB-ID	2442245-9
ISSN	1756-2864 ; 1756-2856
ISSN (online)	1756-2864
ISSN	1756-2856
DOI	10.1177/17562864221150329
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Article ; Online: Moving beyond amyloid and tau to capture the biological heterogeneity of Alzheimer's disease.

Young-Pearse, Tracy L / Lee, Hyo / Hsieh, Yi-Chen / Chou, Vicky / Selkoe, Dennis J

Trends in neurosciences

2023 Volume 46, Issue 6, Page(s) 426–444

Abstract: Alzheimer's disease (AD) manifests along a spectrum of cognitive deficits and levels of neuropathology. Genetic studies support a heterogeneous disease mechanism, with around 70 associated loci to date, implicating several biological processes that ... ...

Abstract	Alzheimer's disease (AD) manifests along a spectrum of cognitive deficits and levels of neuropathology. Genetic studies support a heterogeneous disease mechanism, with around 70 associated loci to date, implicating several biological processes that mediate risk for AD. Despite this heterogeneity, most experimental systems for testing new therapeutics are not designed to capture the genetically complex drivers of AD risk. In this review, we first provide an overview of those aspects of AD that are largely stereotyped and those that are heterogeneous, and we review the evidence supporting the concept that different subtypes of AD are important to consider in the design of agents for the prevention and treatment of the disease. We then dive into the multifaceted biological domains implicated to date in AD risk, highlighting studies of the diverse genetic drivers of disease. Finally, we explore recent efforts to identify biological subtypes of AD, with an emphasis on the experimental systems and data sets available to support progress in this area.
MeSH term(s)	Alzheimer Disease/drug therapy ; Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Humans ; tau Proteins/genetics ; tau Proteins/metabolism ; Drug Design ; Genetic Loci ; Mutation ; Proteostasis ; Microglia/immunology ; Amyloid beta-Protein Precursor/metabolism ; Animals ; Mice ; Disease Models, Animal
Chemical Substances	tau Proteins ; MAPT protein, human ; Amyloid beta-Protein Precursor
Language	English
Publishing date	2023-04-03
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	282488-7
ISSN	1878-108X ; 0378-5912 ; 0166-2236
ISSN (online)	1878-108X
ISSN	0378-5912 ; 0166-2236
DOI	10.1016/j.tins.2023.03.005
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Article ; Online: Clinical Trials of New Drugs for Vascular Cognitive Impairment and Vascular Dementia.

Linh, Tran Thanh Duy / Hsieh, Yi-Chen / Huang, Li-Kai / Hu, Chaur-Jong

International journal of molecular sciences

2022 Volume 23, Issue 19

Abstract: Population aging has challenged the treatment of cognitive impairment or dementia. Vascular dementia is the second leading cause of dementia after Alzheimer's disease. Cognitive consequences after ischemic brain injury have been recognized as a preferred ...

Abstract	Population aging has challenged the treatment of cognitive impairment or dementia. Vascular dementia is the second leading cause of dementia after Alzheimer's disease. Cognitive consequences after ischemic brain injury have been recognized as a preferred target for therapeutic strategies, prompting the search for potential agents. The keyword "vascular dementia" was used to search ClinicalTrials.gov to determine agents represented in phases I, II, III, and IV. The agents were classified on the basis of their mechanisms. Of the 17 randomized controlled trials meeting our inclusion criteria, 9 were completed in the past 10 years, and 8 are ongoing or in the planning stages. We also identified one trial in phase I, nine in phase II, six in phase III, and one in phase IV. Fewer trials of new drugs for improving cognition or ameliorating the behavioral and psychological symptoms of dementia target vascular dementia than Alzheimer's dementia. Drug trials on vascular dementia overlap with drug trials targeting functional outcomes in cerebrovascular disease. International pharmaceutical companies' investment in new drugs targeting VCI and vascular dementia remains insufficient.
MeSH term(s)	Alzheimer Disease/complications ; Alzheimer Disease/drug therapy ; Cognition Disorders/etiology ; Cognitive Dysfunction/complications ; Cognitive Dysfunction/etiology ; Dementia, Vascular/complications ; Dementia, Vascular/etiology ; Humans ; Pharmaceutical Preparations
Chemical Substances	Pharmaceutical Preparations
Language	English
Publishing date	2022-09-21
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms231911067
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Article ; Online: Timing of symptomatic subsequent vertebral compression fracture associated with different demographic factors.

Hsieh, Yi-Chen / Yang, Yi-Shan / Chien, Li-Nien / Chiang, Yung-Hsiao / Lin, Jiann-Her

European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society

2022 Volume 31, Issue 9, Page(s) 2439–2447

Abstract: Background: Symptomatic subsequent vertebral compression fracture (VCF; SVCF) is a common complication associated with poor outcomes. Accumulating evidence shows that demographic factors and incidences of symptomatic SVCFs differ during different ... ...

Abstract	Background: Symptomatic subsequent vertebral compression fracture (VCF; SVCF) is a common complication associated with poor outcomes. Accumulating evidence shows that demographic factors and incidences of symptomatic SVCFs differ during different periods after the primary vertebroplasty (VP). Purpose: To investigate the incidence and demographic factors of symptomatic SVCFs after the primary VP in different periods using registry data in the Taiwan National Health Insurance Research Database. Methods: This retrospective cohort study included 28,343 patients aged ≥ 50 years with painful VCF treated with VP from 2002 to 2016. Symptomatic SVCF was defined as SVCF requiring another VP or re-admission. During the 2-year follow-up, 1955 patients received subsequent VP while 1,407 were readmitted. Cox proportional hazard models were used to compare the risks of subsequent VP or readmission. Results: The cumulative incident rate of subsequent VP and re-hospitalization was 0.87 [95% confidence interval (CI), 0.82 ~ 0.92] and 0.62 (95% CI, 0.58 ~ 0.66) per 100 person-months, respectively, within the first 6 months after the primary VP, and it decreased over time. A multiple Cox regression model showed that age, osteopenia or osteoporosis, Charlson comorbidity index (CCI) were significant independent risk factors of subsequent VP or readmission within the first 6 months. Conclusions: This study demonstrated that the incidence of symptomatic SVCF peaked in the first 6 months after the primary VP. Age, osteoporosis or osteopenia, and CCI were determined to be risk factors in the first 6 months, but only osteoporosis or osteopenia and CCI were risk factors thereafter.
MeSH term(s)	Fractures, Compression/epidemiology ; Fractures, Compression/surgery ; Humans ; Incidence ; Infant ; Osteoporosis/complications ; Osteoporotic Fractures/complications ; Osteoporotic Fractures/epidemiology ; Osteoporotic Fractures/surgery ; Retrospective Studies ; Risk Factors ; Spinal Fractures/surgery ; Vertebroplasty/adverse effects
Language	English
Publishing date	2022-07-11
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1115375-1
ISSN	1432-0932 ; 0940-6719
ISSN (online)	1432-0932
ISSN	0940-6719
DOI	10.1007/s00586-022-07293-w
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Article: Unveiling the Power of Anticancer Drug Screening: A Clinical Case Study Comparing the Effectiveness of Hollow Fiber Assay Microtube Array Membrane (MTAM-HFA) in Breast Cancer Patients.

Tu, Shih-Hsin / Huang, Wan-Ting / Chew, Chee Ho / Chen, Amanda Lin / Chen, Shou-Tung / Chen, Jin-Hua / Hsieh, Yi-Chen / Chen, Chien-Chung

Cancers

2023 Volume 15, Issue 10

Abstract: Breast cancer is a severe public health problem, and early treatment with powerful anticancer drugs is critical for success. The researchers investigated the clinical results of a novel screening tool termed Microtube Array Membrane Hollow Fiber Assay ( ... ...

Abstract	Breast cancer is a severe public health problem, and early treatment with powerful anticancer drugs is critical for success. The researchers investigated the clinical results of a novel screening tool termed Microtube Array Membrane Hollow Fiber Assay (MTAM-HFA) in breast cancer patients in this clinical investigation. In all trial participants, the MTAM-HFA was utilized to identify active medicines for the treatment of breast cancer. The MTAM-HFA was shown to be extremely useful in predicting patient response to anticancer medication therapy in this study. Furthermore, the substantial association between the MTAM-HFA screening outcome and the clinical outcome of the respective patients emphasizes the promise of this unique screening technology in discovering effective anticancer medication combinations for the treatment of breast cancer. These findings indicate that the MTAM-HFA has clinical significance and might be a valuable tool in the development of tailored therapy for cancer care. This study provides helpful information for physicians and scientists working on breast cancer therapy research. The potential benefits of employing MTAM-HFA to find accurate therapies for breast cancer patients might lead to enhanced personalized medicine approaches to cancer care, resulting in better patient outcomes. Overall, the MTAM-HFA screening approach has the potential to revolutionize customized cancer therapy, providing hope to both patients and physicians.
Language	English
Publishing date	2023-05-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers15102764
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Article ; Online: Tamoxifen for amyotrophic lateral sclerosis: A randomized double-blind clinical trial.

Chen, Po-Chih / Hsieh, Yi-Chen / Huang, Chi-Chen / Hu, Chaur-Jong

Medicine

2020 Volume 99, Issue 22, Page(s) e20423

Abstract: Introduction: Amyotrophic lateral sclerosis (ALS) is the most common cause of motor neuron disease, and effective treatment for ALS is still lacking. Transactive response (TAR) -DNA-binding protein-43 (TDP-43) is aggregated in the neurons of ALS ... ...

Abstract	Introduction: Amyotrophic lateral sclerosis (ALS) is the most common cause of motor neuron disease, and effective treatment for ALS is still lacking. Transactive response (TAR) -DNA-binding protein-43 (TDP-43) is aggregated in the neurons of ALS patients. Animal studies shown TDP-43 aggregation can be attenuated by enhancing autophagy by tamoxifen. However, its beneficial effects for ALS patients remain unknown. Methods: Eighteen patients with ALS without mutations in superoxide dismutase-1 (SOD-1) or fused in sarcoma (FUS) genes were randomly assigned into the tamoxifen 40 mg/day or placebo group in a double-blinded manner and all were given riluzole twice daily. Participants were followed up at 1, 3, 6, and 12 months. The primary end point was time to death or dependence on mechanical ventilation. Secondary end points were decline of the revised ALS Functional Rating Scale (ALSFRS-R) score and pulmonary function measured by forced vital capacity (FVC). Results: Ten participants were randomly assigned in the treatment group with tamoxifen, 7 finished trial, 1 reach primary endpoint; while 8 participants in the placebo group, 2 finished trial and 2 reach primary end point. The proportion of participants reaching the primary end point was lower in the tamoxifen group but did not reach statistical significance. At the 1-, 3-, and 6-month follow-up, the average decline rates of the ALSFRS-R score were slower in the tamoxifen group. No significant difference was observed in FVC and ALSFRS-R score at 12 months between groups. Conclusion: Tamoxifen exerted only a modest effect on attenuate progression for 6 months in this small trial. Additional larger scale studies should be necessary to confirm whether enhancing autophagy can attenuate ALS progression.
MeSH term(s)	Adult ; Amyotrophic Lateral Sclerosis/drug therapy ; Amyotrophic Lateral Sclerosis/genetics ; Autophagy/drug effects ; Disease Progression ; Double-Blind Method ; Female ; Humans ; Male ; Middle Aged ; Neuroprotective Agents/therapeutic use ; Severity of Illness Index ; Tamoxifen/therapeutic use ; Treatment Outcome
Chemical Substances	Neuroprotective Agents ; Tamoxifen (094ZI81Y45)
Language	English
Publishing date	2020-05-29
Publishing country	United States
Document type	Clinical Trial, Phase II ; Journal Article ; Randomized Controlled Trial
ZDB-ID	80184-7
ISSN	1536-5964 ; 0025-7974
ISSN (online)	1536-5964
ISSN	0025-7974
DOI	10.1097/MD.0000000000020423
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Article ; Online: Multiple myeloma driving factor WHSC1 is a transcription target of oncogene HMGA2 that facilitates colon cancer proliferation and metastasis.

Liu, Hou-Hsien / Lee, Chia-Hwa / Hsieh, Yi-Chen / Hsu, Duen-Wei / Cho, Er-Chieh

Biochemical and biophysical research communications

2021 Volume 567, Page(s) 183–189

Abstract: Colon cancer is a common human cancer worldwide. The survival rate of late staged or metastatic colon cancer patients remains low even though the effectiveness of treatment in colon cancer has greatly improved. Research on tumorigenesis mechanisms and ... ...

Abstract	Colon cancer is a common human cancer worldwide. The survival rate of late staged or metastatic colon cancer patients remains low even though the effectiveness of treatment in colon cancer has greatly improved. Research on tumorigenesis mechanisms and discovery of novel molecular target for treating colon cancer is critical. The promotion roles of WHSC1 in multiple myeloma have been demonstrated previously, yet, the regulation of WHSC1 in other cancers is largely unknown, especially in colon cancer. Here, in this study, we analyzed and identified WHSC1 while studying the genetic regulations of HMGA2 in colon cancer cells by microarray analysis, and investigated the HMGA2-WHSC1 interaction. We then applied CRISPR technology to establish stable WHSC1 knockout cells, to address the functional regulation of WHSC1 in colon cancer. In summary, our results for the first time identified the HMGA2-WHSC1 interaction in colon cancer. Moreover, we discovered that WHSC1 promotes cancer proliferation, facilitates resistance of chemotherapy agent, and promotes metastatic capacity of colon cancer.
MeSH term(s)	Cell Proliferation ; Colonic Neoplasms/genetics ; Colonic Neoplasms/pathology ; Gene Expression Regulation, Neoplastic ; HCT116 Cells ; HMGA2 Protein/genetics ; Histone-Lysine N-Methyltransferase/genetics ; Humans ; Multiple Myeloma/genetics ; Neoplasm Invasiveness/genetics ; Neoplasm Invasiveness/pathology ; Repressor Proteins/genetics
Chemical Substances	HMGA2 Protein ; HMGA2 protein, human ; Repressor Proteins ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43) ; NSD2 protein, human (EC 2.1.1.43)
Language	English
Publishing date	2021-06-21
Publishing country	United States
Document type	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.2021.06.034
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Article: Multiple myeloma driving factor WHSC1 is a transcription target of oncogene HMGA2 that facilitates colon cancer proliferation and metastasis

Liu, Hou-Hsien / Lee, Chia-Hwa / Hsieh, Yi-Chen / Hsu, Duen-Wei / Cho, Er-Chieh

Biochemical and biophysical research communications. 2021 Aug. 27, v. 567

2021

Abstract	Colon cancer is a common human cancer worldwide. The survival rate of late staged or metastatic colon cancer patients remains low even though the effectiveness of treatment in colon cancer has greatly improved. Research on tumorigenesis mechanisms and discovery of novel molecular target for treating colon cancer is critical.The promotion roles of WHSC1 in multiple myeloma have been demonstrated previously, yet, the regulation of WHSC1 in other cancers is largely unknown, especially in colon cancer. Here, in this study, we analyzed and identified WHSC1 while studying the genetic regulations of HMGA2 in colon cancer cells by microarray analysis, and investigated the HMGA2-WHSC1 interaction. We then applied CRISPR technology to establish stable WHSC1 knockout cells, to address the functional regulation of WHSC1 in colon cancer. In summary, our results for the first time identified the HMGA2-WHSC1 interaction in colon cancer. Moreover, we discovered that WHSC1 promotes cancer proliferation, facilitates resistance of chemotherapy agent, and promotes metastatic capacity of colon cancer.
Keywords	carcinogenesis ; colorectal neoplasms ; drug therapy ; humans ; metastasis ; microarray technology ; myeloma ; oncogenes ; research ; survival rate
Language	English
Dates of publication	2021-0827
Size	p. 183-189.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2021.06.034
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