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Article ; Online: Harnessing natural killer cells for the treatment of multiple myeloma.

Clara, Joseph A / Childs, Richard W

2022 Volume 49, Issue 1, Page(s) 69–85

Abstract: Multiple myeloma (MM) is hematologic malignancy that is associated with profound immune alterations. Myeloma cells are susceptible to killing by natural killer (NK) cells but acquire the ability to elude NK cell surveillance by avoiding recognition and ... ...

Abstract	Multiple myeloma (MM) is hematologic malignancy that is associated with profound immune alterations. Myeloma cells are susceptible to killing by natural killer (NK) cells but acquire the ability to elude NK cell surveillance by avoiding recognition and suppressing NK cell function. Major advances in the treatment of multiple myeloma have been achieved by effective new drugs that redirect NK cells and enhance their function. Despite significant progress, myeloma remains incurable and novel treatment approaches are required. Strategies to take advantage of the intrinsic antitumor properties of NK cells to treat MM represent a novel immunotherapeutic approach. One such strategy is adoptive NK cell therapy that consist of infusions of NK cells that have been propagated ex vivo. Adoptive NK cell therapy encompasses contemporary genetic engineering strategies such as chimeric antigen receptor (CAR)-engineered NK cells. An alternative approach involves the use of pharmacologic agents to enhance NK cell activity against myeloma. NK cell-modulating therapies can be used to bolster the function of endogenous NK cells or to enhance the efficacy of adoptively infused NK cells. Here, we review the mechanistic complexities influencing NK cell activity in MM and highlight a variety of innovative NK cell-based strategies being developed for the treatment of MM.
MeSH term(s)	Humans ; Immunotherapy ; Killer Cells, Natural ; Multiple Myeloma/drug therapy
Language	English
Publishing date	2022-01-21
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	189220-4
ISSN	1532-8708 ; 0093-7754
ISSN (online)	1532-8708
ISSN	0093-7754
DOI	10.1053/j.seminoncol.2022.01.004
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Article ; Online: Current Therapy for Metastatic Urothelial Carcinoma.

Nadal, Rosa / Clara, Joseph A / Valderrama, Begoña P / Bellmunt, Joaquim

Hematology/oncology clinics of North America

2021 Volume 35, Issue 3, Page(s) 469–493

Abstract: Urothelial carcinoma (UC) is a highly lethal malignancy in the metastatic state. Platinum-based chemotherapy regimens have been the backbone treatment for patients with advanced UC in the first-line setting. However, a large subset of patients are ... ...

Abstract	Urothelial carcinoma (UC) is a highly lethal malignancy in the metastatic state. Platinum-based chemotherapy regimens have been the backbone treatment for patients with advanced UC in the first-line setting. However, a large subset of patients are suboptimal candidates for these combinations owing to poor renal function and/or other comorbidities. Patients who are unable to tolerate or who progress after frontline platinum chemotherapy face a poor outcome. Recent insights into UC biology and immunology are being translated into new therapies for metastatic UC (mUC) including immune checkpoint inhibitors (ICIs), erdafitinib, a FGFR inhibitor, and antibody drug conjugates (ADC) such enfortumab vedotin.
MeSH term(s)	Carcinoma, Transitional Cell/drug therapy ; Humans ; Immune Checkpoint Inhibitors/therapeutic use ; Immunoconjugates/therapeutic use ; Protein Kinase Inhibitors/therapeutic use ; Urinary Bladder Neoplasms/drug therapy
Chemical Substances	Immune Checkpoint Inhibitors ; Immunoconjugates ; Protein Kinase Inhibitors
Language	English
Publishing date	2021-04-10
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	93115-9
ISSN	1558-1977 ; 0889-8588
ISSN (online)	1558-1977
ISSN	0889-8588
DOI	10.1016/j.hoc.2021.02.010
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Article ; Online: Integrated transcription factor profiling with transcriptome analysis identifies L1PA2 transposons as global regulatory modulators in a breast cancer model.

Jiang, Jiayue-Clara / Rothnagel, Joseph A / Upton, Kyle R

Scientific reports

2021 Volume 11, Issue 1, Page(s) 8083

Abstract: While transposons are generally silenced in somatic tissues, many transposons escape epigenetic repression in epithelial cancers, become transcriptionally active and contribute to the regulation of human gene expression. We have developed a bioinformatic ...

Abstract	While transposons are generally silenced in somatic tissues, many transposons escape epigenetic repression in epithelial cancers, become transcriptionally active and contribute to the regulation of human gene expression. We have developed a bioinformatic pipeline for the integrated analysis of transcription factor binding and transcriptomic data to identify transposon-derived promoters that are activated in specific diseases and developmental states. We applied this pipeline to a breast cancer model, and found that the L1PA2 transposon subfamily contributes abundant regulatory sequences to co-ordinated transcriptional regulation in breast cancer. Transcription factor profiling demonstrates that over 27% of L1PA2 transposons harbour co-localised binding sites of functionally interacting, cancer-associated transcription factors in MCF7 cells, a cell line used to model breast cancer. Transcriptomic analysis reveals that L1PA2 transposons also contribute transcription start sites to up-regulated transcripts in MCF7 cells, including some transcripts with established oncogenic properties. In addition, we verified the utility of our pipeline on other transposon subfamilies, as well as on leukemia and lung carcinoma cell lines. We demonstrate that the normally quiescent regulatory activities of transposons can be activated and alter the cancer transcriptome. In particular, the L1PA2 subfamily contributes abundant regulatory sequences, and likely plays a global role in modulating breast cancer transcriptional regulation. Understanding the regulatory impact of L1PA2 on breast cancer genomes provides additional insights into cancer genome regulation, and may provide novel biomarkers for disease diagnosis, prognosis and therapy.
MeSH term(s)	Breast Neoplasms ; Female ; Gene Expression Profiling ; Humans ; MCF-7 Cells ; Promoter Regions, Genetic ; Transcription Factors
Chemical Substances	Transcription Factors
Language	English
Publishing date	2021-04-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-86395-9
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Article ; Online: Widespread Exaptation of L1 Transposons for Transcription Factor Binding in Breast Cancer.

Jiang, Jiayue-Clara / Rothnagel, Joseph A / Upton, Kyle R

International journal of molecular sciences

2021 Volume 22, Issue 11

Abstract: L1 transposons occupy 17% of the human genome and are widely exapted for the regulation of human genes, particularly in breast cancer, where we have previously shown abundant cancer-specific transcription factor (TF) binding sites within the L1PA2 ... ...

Abstract	L1 transposons occupy 17% of the human genome and are widely exapted for the regulation of human genes, particularly in breast cancer, where we have previously shown abundant cancer-specific transcription factor (TF) binding sites within the L1PA2 subfamily. In the current study, we performed a comprehensive analysis of TF binding activities in primate-specific L1 subfamilies and identified pervasive exaptation events amongst these evolutionarily related L1 transposons. By motif scanning, we predicted diverse and abundant TF binding potentials within the L1 transposons. We confirmed substantial TF binding activities in the L1 subfamilies using TF binding sites consolidated from an extensive collection of publicly available ChIP-seq datasets. Young L1 subfamilies (L1HS, L1PA2 and L1PA3) contributed abundant TF binding sites in MCF7 cells, primarily via their 5' UTR. This is expected as the L1 5' UTR hosts cis-regulatory elements that are crucial for L1 replication and mobilisation. Interestingly, the ancient L1 subfamilies, where 5' truncation was common, displayed comparable TF binding capacity through their 3' ends, suggesting an alternative exaptation mechanism in L1 transposons that was previously unnoticed. Overall, primate-specific L1 transposons were extensively exapted for TF binding in MCF7 breast cancer cells and are likely prominent genetic players modulating breast cancer transcriptional regulation.
MeSH term(s)	Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Female ; Humans ; Long Interspersed Nucleotide Elements ; MCF-7 Cells ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Response Elements ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transcription, Genetic
Chemical Substances	Neoplasm Proteins ; Transcription Factors
Language	English
Publishing date	2021-05-25
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/ijms22115625
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Article ; Online: In Reply to Levy and Ahmed.

Gonnella, Joseph S / Callahan, Clara A / Erdmann, James B / Veloski, J Jon / Markle, Ronald A / Hojat, Mohammadreza

Academic medicine : journal of the Association of American Medical Colleges

2022 Volume 97, Issue 5, Page(s) 623

Language	English
Publishing date	2022-04-27
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	96192-9
ISSN	1938-808X ; 1040-2446
ISSN (online)	1938-808X
ISSN	1040-2446
DOI	10.1097/ACM.0000000000004617
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Article ; Online: Widespread Exaptation of L1 Transposons for Transcription Factor Binding in Breast Cancer

Jiayue-Clara Jiang / Joseph A. Rothnagel / Kyle R. Upton

International Journal of Molecular Sciences, Vol 22, Iss 5625, p

2021 Volume 5625

Abstract	L1 transposons occupy 17% of the human genome and are widely exapted for the regulation of human genes, particularly in breast cancer, where we have previously shown abundant cancer-specific transcription factor (TF) binding sites within the L1PA2 subfamily. In the current study, we performed a comprehensive analysis of TF binding activities in primate-specific L1 subfamilies and identified pervasive exaptation events amongst these evolutionarily related L1 transposons. By motif scanning, we predicted diverse and abundant TF binding potentials within the L1 transposons. We confirmed substantial TF binding activities in the L1 subfamilies using TF binding sites consolidated from an extensive collection of publicly available ChIP-seq datasets. Young L1 subfamilies (L1HS, L1PA2 and L1PA3) contributed abundant TF binding sites in MCF7 cells, primarily via their 5′ UTR. This is expected as the L1 5′ UTR hosts cis-regulatory elements that are crucial for L1 replication and mobilisation. Interestingly, the ancient L1 subfamilies, where 5′ truncation was common, displayed comparable TF binding capacity through their 3′ ends, suggesting an alternative exaptation mechanism in L1 transposons that was previously unnoticed. Overall, primate-specific L1 transposons were extensively exapted for TF binding in MCF7 breast cancer cells and are likely prominent genetic players modulating breast cancer transcriptional regulation.
Keywords	breast cancer ; transposon ; exaptation ; transcription factor ; transcriptional regulation ; L1 ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	570
Language	English
Publishing date	2021-05-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Integrated transcription factor profiling with transcriptome analysis identifies L1PA2 transposons as global regulatory modulators in a breast cancer model

Jiayue-Clara Jiang / Joseph A. Rothnagel / Kyle R. Upton

Scientific Reports, Vol 11, Iss 1, Pp 1-

2021 Volume 18

Abstract: Abstract While transposons are generally silenced in somatic tissues, many transposons escape epigenetic repression in epithelial cancers, become transcriptionally active and contribute to the regulation of human gene expression. We have developed a ... ...

Abstract	Abstract While transposons are generally silenced in somatic tissues, many transposons escape epigenetic repression in epithelial cancers, become transcriptionally active and contribute to the regulation of human gene expression. We have developed a bioinformatic pipeline for the integrated analysis of transcription factor binding and transcriptomic data to identify transposon-derived promoters that are activated in specific diseases and developmental states. We applied this pipeline to a breast cancer model, and found that the L1PA2 transposon subfamily contributes abundant regulatory sequences to co-ordinated transcriptional regulation in breast cancer. Transcription factor profiling demonstrates that over 27% of L1PA2 transposons harbour co-localised binding sites of functionally interacting, cancer-associated transcription factors in MCF7 cells, a cell line used to model breast cancer. Transcriptomic analysis reveals that L1PA2 transposons also contribute transcription start sites to up-regulated transcripts in MCF7 cells, including some transcripts with established oncogenic properties. In addition, we verified the utility of our pipeline on other transposon subfamilies, as well as on leukemia and lung carcinoma cell lines. We demonstrate that the normally quiescent regulatory activities of transposons can be activated and alter the cancer transcriptome. In particular, the L1PA2 subfamily contributes abundant regulatory sequences, and likely plays a global role in modulating breast cancer transcriptional regulation. Understanding the regulatory impact of L1PA2 on breast cancer genomes provides additional insights into cancer genome regulation, and may provide novel biomarkers for disease diagnosis, prognosis and therapy.
Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2021-04-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Reply to the 'Comment on "Bilayer aggregate microstructure determines viscoelasticity of lung surfactant suspensions"' by J.-F. Berret, DOI: 10.1039/d2sm00653g.

Ciutara, Clara O / Zasadzinski, Joseph A

Soft matter

2022 Volume 18, Issue 44, Page(s) 8520–8523

Abstract: In their comment, Berret suggests that Curosurf, one of three clinical lung surfactant aqueous suspensions examined in ... ...

Abstract	In their comment, Berret suggests that Curosurf, one of three clinical lung surfactant aqueous suspensions examined in the
MeSH term(s)	Suspensions ; Pulmonary Surfactants/chemistry ; Viscosity ; Surface-Active Agents/chemistry ; Lung
Chemical Substances	Suspensions ; Pulmonary Surfactants ; Surface-Active Agents
Language	English
Publishing date	2022-11-16
Publishing country	England
Document type	Journal Article ; Comment
ZDB-ID	2191476-X
ISSN	1744-6848 ; 1744-683X
ISSN (online)	1744-6848
ISSN	1744-683X
DOI	10.1039/d2sm01142e
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Article: RNA-Seq Analysis Reveals CCR5 as a Key Target for CRISPR Gene Editing to Regulate In Vivo NK Cell Trafficking.

Levy, Emily R / Clara, Joseph A / Reger, Robert N / Allan, David S J / Childs, Richard W

Cancers

2021 Volume 13, Issue 4

Abstract: A growing number of natural killer (NK) cell-based immunotherapy trials utilize ex vivo expansion to grow and activate allogenic and autologous NK cells prior to administration to patients with malignancies. Recent data in both murine and macaque models ... ...

Abstract	A growing number of natural killer (NK) cell-based immunotherapy trials utilize ex vivo expansion to grow and activate allogenic and autologous NK cells prior to administration to patients with malignancies. Recent data in both murine and macaque models have shown that adoptively infused ex vivo expanded NK cells have extensive trafficking into liver tissue, with relatively low levels of homing to other sites where tumors often reside, such as the bone marrow or lymph nodes. Here, we evaluated gene and surface expression of molecules involved in cellular chemotaxis in freshly isolated human NK cells compared with NK cells expanded ex vivo using two different feeder cells lines: Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines (LCLs) or K562 cells with membrane-bound (mb) 4-1BB ligand and interleukin (IL)-21. Expanded NK cells had altered expression in a number of genes that encode chemotactic ligands and chemotactic receptors that impact chemoattraction and chemotaxis. Most notably, we observed drastic downregulation of C-X-C chemokine receptor type 4 (CXCR4) and upregulation of C-C chemokine receptor type 5 (CCR5) transcription and phenotypic expression. clustered regularly interspaced short palindromic repeats (CRISPR) gene editing of CCR5 in expanded NK cells reduced cell trafficking into liver tissue and increased NK cell presence in the circulation following infusion into immunodeficient mice. The findings reported here show that ex vivo expansion alters multiple factors that govern NK cell homing and define a novel approach using CRISPR gene editing that reduces sequestration of NK cells by the liver.
Language	English
Publishing date	2021-02-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13040872
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Article ; Online: The effects of acute pain on cognitive skills in emergency department patients.

Marco, Catherine A / Studebaker, Haely / Harrington, Michael / Ganz, Ellie / Boodt, Benjamin / Hunt, Tyler / Costin, Andrea / Joseph, Clara / Ely, Isabelle

The American journal of emergency medicine

2022 Volume 55, Page(s) 72–75

Abstract: Introduction: Effective pain management results in improved patient satisfaction, reduced anxiety, and improved comfort. However, concern exists regarding the effects of pain medications on cognition and patient ability to consent for procedures, ... ...

Abstract	Introduction: Effective pain management results in improved patient satisfaction, reduced anxiety, and improved comfort. However, concern exists regarding the effects of pain medications on cognition and patient ability to consent for procedures, hospital admission, or to refuse recommended medical interventions. Methods: This prospective, case-control study was conducted at a Level 1 Trauma Center. Eligible subjects included ED patients ages 18 and older with a triage pain score of 1 or higher, who received non-narcotic analgesic agents. Cognition was measured before and after non-narcotic pain medication using the Digit Symbol Substitution Test (DSST). A control group consisted of 35 healthy volunteers who completed the DSST at baseline and one hour. Results: Among 46 subjects, the mean age was 33. The mean triage pain score was 7. Before medication, the average DSST score was 39.5. After medication, the average DSST score was 42.9. There was a significant within-subject average change in DSST score (pre-post) of 3.4 (95% confidence interval: 1.6, 5.2), p < 0.001. Among the control group, the mean baseline DSST score was 64.2 (SD 10.7). One hour later the mean DSST score had increased to 71.1 (SD 10.4). Overall, the mean within-subject change over time in DSST was 6.9 (SD 8.0) with 95% CI 4.2 to 9.7. There was not enough evidence to detect relationships between change in DSST scores and age, triage pain, triage HR, triage RR, change in pain scores, gender, ethnicity, mode of arrival nor insurance (all with p > 0.05). Conclusions: We found significant variation in DSST scores among ED patients with pain. Treatment of pain with nonsedating analgesic agents was not associated with improved scores on the Digit Symbol Substitution Test among ED patients with acute painful conditions, compared to control subjects.
MeSH term(s)	Acute Disease ; Acute Pain/drug therapy ; Adolescent ; Adult ; Case-Control Studies ; Cognition ; Emergency Service, Hospital ; Humans ; Prospective Studies
Language	English
Publishing date	2022-03-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	605890-5
ISSN	1532-8171 ; 0735-6757
ISSN (online)	1532-8171
ISSN	0735-6757
DOI	10.1016/j.ajem.2022.03.001
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