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Article ; Online: Bioinspired One Cell Culture Isolates Highly Tumorigenic and Metastatic Cancer Stem Cells Capable of Multilineage Differentiation.

Wang, Hai / Agarwal, Pranay / Jiang, Bin / Stewart, Samantha / Liu, Xuanyou / Liang, Yutong / Hancioglu, Baris / Webb, Amy / Fisher, John P / Liu, Zhenguo / Lu, Xiongbin / Tkaczuk, Katherine H R / He, Xiaoming

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

2023 Volume 10, Issue 12, Page(s) e2301726

Language	English
Publishing date	2023-04-26
Publishing country	Germany
Document type	Published Erratum
ZDB-ID	2808093-2
ISSN	2198-3844 ; 2198-3844
ISSN (online)	2198-3844
ISSN	2198-3844
DOI	10.1002/advs.202301726
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Article ; Online: A mathematical model of mitotic exit in budding yeast: the role of Polo kinase.

Hancioglu, Baris / Tyson, John J

PloS one

2012 Volume 7, Issue 2, Page(s) e30810

Abstract: Cell cycle progression in eukaryotes is regulated by periodic activation and inactivation of a family of cyclin-dependent kinases (Cdk's). Entry into mitosis requires phosphorylation of many proteins targeted by mitotic Cdk, and exit from mitosis ... ...

Abstract	Cell cycle progression in eukaryotes is regulated by periodic activation and inactivation of a family of cyclin-dependent kinases (Cdk's). Entry into mitosis requires phosphorylation of many proteins targeted by mitotic Cdk, and exit from mitosis requires proteolysis of mitotic cyclins and dephosphorylation of their targeted proteins. Mitotic exit in budding yeast is known to involve the interplay of mitotic kinases (Cdk and Polo kinases) and phosphatases (Cdc55/PP2A and Cdc14), as well as the action of the anaphase promoting complex (APC) in degrading specific proteins in anaphase and telophase. To understand the intricacies of this mechanism, we propose a mathematical model for the molecular events during mitotic exit in budding yeast. The model captures the dynamics of this network in wild-type yeast cells and 110 mutant strains. The model clarifies the roles of Polo-like kinase (Cdc5) in the Cdc14 early anaphase release pathway and in the G-protein regulated mitotic exit network.
MeSH term(s)	Anaphase ; Anaphase-Promoting Complex-Cyclosome ; Cell Cycle Proteins/metabolism ; Fungal Proteins/metabolism ; GTP-Binding Proteins/metabolism ; Mitosis ; Models, Biological ; Models, Theoretical ; Mutation ; Protein Serine-Threonine Kinases/metabolism ; Protein Tyrosine Phosphatases/metabolism ; Proto-Oncogene Proteins/metabolism ; Saccharomyces cerevisiae/metabolism ; Saccharomyces cerevisiae Proteins/metabolism ; Saccharomycetales ; Software ; Telophase ; Time Factors ; Ubiquitin-Protein Ligase Complexes/metabolism ; Polo-Like Kinase 1
Chemical Substances	CDC14 protein, S cerevisiae ; Cell Cycle Proteins ; Fungal Proteins ; Proto-Oncogene Proteins ; Saccharomyces cerevisiae Proteins ; Ubiquitin-Protein Ligase Complexes (EC 2.3.2.23) ; Anaphase-Promoting Complex-Cyclosome (EC 2.3.2.27) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; CDC5 protein, S cerevisiae (EC 2.7.11.21) ; Protein Tyrosine Phosphatases (EC 3.1.3.48) ; GTP-Binding Proteins (EC 3.6.1.-)
Language	English
Publishing date	2012-02-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0030810
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Article ; Online: Non-monotonic Response to Monotonic Stimulus: Regulation of Glyoxylate Shunt Gene-Expression Dynamics in Mycobacterium tuberculosis.

Ascensao, Joao A / Datta, Pratik / Hancioglu, Baris / Sontag, Eduardo / Gennaro, Maria L / Igoshin, Oleg A

PLoS computational biology

2016 Volume 12, Issue 2, Page(s) e1004741

Abstract: Understanding how dynamical responses of biological networks are constrained by underlying network topology is one of the fundamental goals of systems biology. Here we employ monotone systems theory to formulate a theorem stating necessary conditions for ...

Abstract	Understanding how dynamical responses of biological networks are constrained by underlying network topology is one of the fundamental goals of systems biology. Here we employ monotone systems theory to formulate a theorem stating necessary conditions for non-monotonic time-response of a biochemical network to a monotonic stimulus. We apply this theorem to analyze the non-monotonic dynamics of the σB-regulated glyoxylate shunt gene expression in Mycobacterium tuberculosis cells exposed to hypoxia. We first demonstrate that the known network structure is inconsistent with observed dynamics. To resolve this inconsistency we employ the formulated theorem, modeling simulations and optimization along with follow-up dynamic experimental measurements. We show a requirement for post-translational modulation of σB activity in order to reconcile the network dynamics with its topology. The results of this analysis make testable experimental predictions and demonstrate wider applicability of the developed methodology to a wide class of biological systems.
MeSH term(s)	Bacterial Proteins/genetics ; Gene Expression Regulation, Bacterial/genetics ; Glyoxylates/metabolism ; Metabolic Networks and Pathways/genetics ; Models, Genetic ; Mycobacterium tuberculosis/genetics ; Systems Biology/methods ; Transcription Factors/genetics
Chemical Substances	Bacterial Proteins ; Glyoxylates ; Transcription Factors ; glyoxylic acid (JQ39C92HH6)
Language	English
Publishing date	2016-02-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2193340-6
ISSN	1553-7358 ; 1553-734X
ISSN (online)	1553-7358
ISSN	1553-734X
DOI	10.1371/journal.pcbi.1004741
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Article: Bioinspired One Cell Culture Isolates Highly Tumorigenic and Metastatic Cancer Stem Cells Capable of Multilineage Differentiation.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

2020 Volume 7, Issue 11, Page(s) 2000259

Abstract: Cancer stem cells (CSCs) are rare cancer cells that are postulated to be responsible for cancer relapse and metastasis. However, CSCs are difficult to isolate and poorly understood. Here, a bioinspired approach for label-free isolation and culture of ... ...

Abstract	Cancer stem cells (CSCs) are rare cancer cells that are postulated to be responsible for cancer relapse and metastasis. However, CSCs are difficult to isolate and poorly understood. Here, a bioinspired approach for label-free isolation and culture of CSCs, by microencapsulating one cancer cell in the nanoliter-scale hydrogel core of each prehatching embryo-like core-shell microcapsule, is reported. Only a small percentage of the individually microencapsulated cancer cells can proliferate into a cell colony. Gene and protein expression analyses indicate high stemness of the cells in the colonies. Importantly, the colony cells are capable of cross-tissue multilineage (e.g., endothelial, cardiac, neural, and osteogenic) differentiation, which is not observed for "CSCs" isolated using other contemporary approaches. Further studies demonstrate the colony cells are highly tumorigenic, metastatic, and drug resistant. These data show the colony cells obtained with the bioinspired one-cell-culture approach are truly CSCs. Significantly, multiple pathways are identified to upregulate in the CSCs and enrichment of genes related to the pathways is correlated with significantly decreased survival of breast cancer patients. Collectively, this study may provide a valuable method for isolating and culturing CSCs, to facilitate the understanding of cancer biology and etiology and the development of effective CSC-targeted cancer therapies.
Language	English
Publishing date	2020-04-28
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2808093-2
ISSN	2198-3844
ISSN	2198-3844
DOI	10.1002/advs.202000259
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Article ; Online: Mutational Mechanisms That Activate Wnt Signaling and Predict Outcomes in Colorectal Cancer Patients.

Hankey, William / McIlhatton, Michael A / Ebede, Kenechi / Kennedy, Brian / Hancioglu, Baris / Zhang, Jie / Brock, Guy N / Huang, Kun / Groden, Joanna

Cancer research

2017 Volume 78, Issue 3, Page(s) 617–630

Abstract: ... ...

Abstract	APC
MeSH term(s)	Adenoma/genetics ; Adenoma/metabolism ; Adenoma/mortality ; Adenoma/pathology ; Animals ; Apc1 Subunit, Anaphase-Promoting Complex-Cyclosome/physiology ; Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/metabolism ; Colorectal Neoplasms/mortality ; Colorectal Neoplasms/pathology ; Gene Expression Profiling ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mutation ; Prognosis ; Survival Rate ; Wnt Proteins/genetics ; Wnt Proteins/metabolism ; beta Catenin/physiology
Chemical Substances	Anapc1 protein, mouse ; Apc1 Subunit, Anaphase-Promoting Complex-Cyclosome ; Biomarkers, Tumor ; CTNNB1 protein, mouse ; Wnt Proteins ; beta Catenin
Language	English
Publishing date	2017-12-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-17-1357
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Article ; Online: MYH9 binds to lncRNA gene PTCSC2 and regulates FOXE1 in the 9q22 thyroid cancer risk locus.

Wang, Yanqiang / He, Huiling / Li, Wei / Phay, John / Shen, Rulong / Yu, Lianbo / Hancioglu, Baris / de la Chapelle, Albert

Proceedings of the National Academy of Sciences of the United States of America

2017 Volume 114, Issue 3, Page(s) 474–479

Abstract: A locus on chromosome 9q22 harbors a SNP (rs965513) firmly associated with risk of papillary thyroid carcinoma (PTC). The locus also comprises the forkhead box E1 (FOXE1) gene, which is implicated in thyroid development, and a long noncoding RNA (lncRNA) ...

Abstract	A locus on chromosome 9q22 harbors a SNP (rs965513) firmly associated with risk of papillary thyroid carcinoma (PTC). The locus also comprises the forkhead box E1 (FOXE1) gene, which is implicated in thyroid development, and a long noncoding RNA (lncRNA) gene, papillary thyroid cancer susceptibility candidate 2 (PTCSC2). How these might interact is not known. Here we report that PTCSC2 binds myosin-9 (MYH9). In a bidirectional promoter shared by FOXE1 and PTCSC2, MYH9 inhibits the promoter activity in both directions. This inhibition can be reversed by PTCSC2, which acts as a suppressor. RNA knockdown of FOXE1 in primary thyroid cells profoundly interferes with the p53 pathway. We propose that the interaction between the lncRNA, its binding protein MYH9, and the coding gene FOXE1 underlies the predisposition to PTC triggered by rs965513.
MeSH term(s)	Binding Sites/genetics ; Carcinoma, Papillary/genetics ; Carcinoma, Papillary/metabolism ; Cell Line, Tumor ; Chromosomes, Human, Pair 9/genetics ; Forkhead Transcription Factors/antagonists & inhibitors ; Forkhead Transcription Factors/genetics ; Gene Knockdown Techniques ; Genetic Predisposition to Disease ; Humans ; Molecular Motor Proteins/metabolism ; Myosin Heavy Chains/metabolism ; Promoter Regions, Genetic ; Protein Binding ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; Thyroid Cancer, Papillary ; Thyroid Neoplasms/genetics ; Thyroid Neoplasms/metabolism
Chemical Substances	FOXE1 protein, human ; Forkhead Transcription Factors ; MYH9 protein, human ; Molecular Motor Proteins ; RNA, Long Noncoding ; Myosin Heavy Chains (EC 3.6.4.1)
Language	English
Publishing date	2017-01-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1619917114
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Zs.A 1148: Show issues

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Article ; Online: Chromatin-associated APC regulates gene expression in collaboration with canonical WNT signaling and AP-1.

Hankey, William / Chen, Zhong / Bergman, Maxwell J / Fernandez, Max O / Hancioglu, Baris / Lan, Xun / Jegga, Anil G / Zhang, Jie / Jin, Victor X / Aronow, Bruce J / Wang, Qianben / Groden, Joanna

Oncotarget

2018 Volume 9, Issue 58, Page(s) 31214–31230

Abstract: Mutation of ... ...

Abstract	Mutation of the
Language	English
Publishing date	2018-07-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.25781
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Article: A dynamical model of human immune response to influenza A virus infection.

Hancioglu, Baris / Swigon, David / Clermont, Gilles

Journal of theoretical biology

2007 Volume 246, Issue 1, Page(s) 70–86

Abstract: We present a simplified dynamical model of immune response to uncomplicated influenza A virus (IAV) infection, which focuses on the control of the infection by the innate and adaptive immunity. Innate immunity is represented by interferon-induced ... ...

Abstract	We present a simplified dynamical model of immune response to uncomplicated influenza A virus (IAV) infection, which focuses on the control of the infection by the innate and adaptive immunity. Innate immunity is represented by interferon-induced resistance to infection of respiratory epithelial cells and by removal of infected cells by effector cells (cytotoxic T-cells and natural killer cells). Adaptive immunity is represented by virus-specific antibodies. Similar in spirit to the recent model of Bocharov and Romanyukha [1994. Mathematical model of antiviral immune response. III. Influenza A virus infection. J. Theor. Biol. 167, 323-360], the model is constructed as a system of 10 ordinary differential equations with 27 parameters characterizing the rates of various processes contributing to the course of disease. The parameters are derived from published experimental data or estimated so as to reproduce available data about the time course of IAV infection in a naïve host. We explore the effect of initial viral load on the severity and duration of the disease, construct a phase diagram that sheds insight into the dynamics of the disease, and perform sensitivity analysis on the model parameters to explore which ones influence the most the onset, duration and severity of infection. To account for the variability and speed of adaptation of the adaptive response to a particular virus strain, we introduce a variable that quantifies the antigenic compatibility between the virus and the antibodies currently produced by the organism. We find that for small initial viral load the disease progresses through an asymptomatic course, for intermediate value it takes a typical course with constant duration and severity of infection but variable onset, and for large initial viral load the disease becomes severe. This behavior is robust to a wide range of parameter values. The absence of antibody response leads to recurrence of disease and appearance of a chronic state with nontrivial constant viral load.
MeSH term(s)	Antibodies, Viral/immunology ; Antigen-Presenting Cells/immunology ; Computer Simulation ; Humans ; Immunologic Memory ; Influenza A virus ; Influenza, Human/immunology ; Interferons/immunology ; Models, Immunological ; Recurrence ; Respiratory Mucosa/immunology ; Respiratory Mucosa/virology ; T-Lymphocytes/immunology ; Viral Load
Chemical Substances	Antibodies, Viral ; Interferons (9008-11-1)
Language	English
Publishing date	2007-05-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2972-5
ISSN	1095-8541 ; 0022-5193
ISSN (online)	1095-8541
ISSN	0022-5193
DOI	10.1016/j.jtbi.2006.12.015
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Zs.A 923: Show issues

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Article ; Online: Whole-exome tumor sequencing study in biliary cancer patients with a response to MEK inhibitors.

Ahn, Daniel H / Ozer, Hatice Gulcin / Hancioglu, Baris / Lesinski, Gregory B / Timmers, Cynthia / Bekaii-Saab, Tanios

Oncotarget

2015 Volume 7, Issue 5, Page(s) 5306–5312

Abstract: We previously conducted a phase-II study with selumetinib (AZD6244), a small molecule inhibitor of MEK1/2, in advanced biliary tract cancers (BTC), where the primary endpoint was response rate. Several patients experienced objective response. These ... ...

Abstract	We previously conducted a phase-II study with selumetinib (AZD6244), a small molecule inhibitor of MEK1/2, in advanced biliary tract cancers (BTC), where the primary endpoint was response rate. Several patients experienced objective response. These findings were confirmed with MEK162 in a similar patient population. To assess for tumor-specific genetic variants that mediate sensitivity to MEK inhibition in BTC, we performed whole-exome sequencing in patients with an objective response to selumetinib. Normal and tumor DNA from FFPE tissue from two patients who experienced an objective response underwent whole-exome sequencing. Raw sequence reads were processed with GATK workflow and tumor specific variants were identified using MuTect and VarScan2. Ensemble Variant Effect Predictor was used to determine functional consequences of these variants. Copy number changes and potential gene fusion events were also screened. Findings were compared to assess for any commonality between the two tumor samples, and whether the identified variants were intrinsic to the MAPK pathway. 1169 and 628 tumor-specific variants were identified in the two samples. Further analysis demonstrated 60 and 53 functional and novel variants, respectively. Of the identified tumor-specific variants, fusion events or copy number changes, no commonality was seen. Several variants in genes associated with ERK signaling were present in each tumor sample. Although there were no common tumor-specific variants in the two patients who exhibited an objective response to selumetinib, several genes associated with ERK signaling were identified. Confirmatory studies investigating the role of the identified genes and other potential tumor independent factors need further investigation.
MeSH term(s)	Biliary Tract Neoplasms/genetics ; Biliary Tract Neoplasms/pathology ; Female ; Genetic Variation ; Humans ; MAP Kinase Kinase 1/antagonists & inhibitors ; Male ; Mutation ; Sequence Analysis, DNA/methods
Chemical Substances	MAP Kinase Kinase 1 (EC 2.7.12.2)
Language	English
Publishing date	2015-12-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.6632
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Article: Laser Capture Microdissection of Pancreatic Acinar Cells to Identify Proteomic Alterations in a Murine Model of Caerulein-Induced Pancreatitis.

Shapiro, John P / Komar, Hannah M / Hancioglu, Baris / Yu, Lianbo / Jin, Ming / Ogata, Yuko / Hart, Phil A / Cruz-Monserrate, Zobeida / Lesinski, Gregory B / Conwell, Darwin L

Clinical and translational gastroenterology

2017 Volume 8, Issue 4, Page(s) e89

Abstract: Objectives: Chronic pancreatitis (CP) is characterized by inflammation and fibrosis of the pancreas, leading to pain, parenchymal damage, and loss of exocrine and endocrine function. There are currently no curative therapies; diagnosis remains difficult ...

Abstract	Objectives: Chronic pancreatitis (CP) is characterized by inflammation and fibrosis of the pancreas, leading to pain, parenchymal damage, and loss of exocrine and endocrine function. There are currently no curative therapies; diagnosis remains difficult and aspects of pathogenesis remain unclear. Thus, there is a need to identify novel biomarkers to improve diagnosis and understand pathophysiology. We hypothesize that pancreatic acinar regions contain proteomic signatures relevant to disease processes, including secreted proteins that could be detected in biofluids. Methods: Acini from pancreata of mice injected with or without caerulein were collected using laser capture microdissection followed by mass spectrometry analysis. This protocol enabled high-throughput analysis that captured altered protein expression throughout the stages of CP. Results: Over 2,900 proteins were identified, whereas 331 were significantly changed ≥2-fold by mass spectrometry spectral count analysis. Consistent with pathogenesis, we observed increases in proteins related to fibrosis (e.g., collagen, P<0.001), several proteases (e.g., trypsin 1, P<0.001), and altered expression of proteins associated with diminished pancreas function (e.g., lipase, amylase, P<0.05). In comparison with proteomic data from a public data set of CP patients, a significant correlation was observed between proteomic changes in tissue from both the caerulein model and CP patients (r=0.725, P<0.001). Conclusions: This study illustrates the ability to characterize proteome changes of acinar cells isolated from pancreata of caerulein-treated mice and demonstrates a relationship between signatures from murine and human CP.
Language	English
Publishing date	2017-04-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	2581516-7
ISSN	2155-384X
ISSN	2155-384X
DOI	10.1038/ctg.2017.15
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