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Article ; Online: CAR T-Cell Therapy in Hematological Malignancies.

Haslauer, Theresa / Greil, Richard / Zaborsky, Nadja / Geisberger, Roland

International journal of molecular sciences

2021 Volume 22, Issue 16

Abstract: Chimeric antigen receptor (CAR) T-cells (CAR T-cells) are a promising therapeutic approach in treating hematological malignancies. CAR T-cells represent engineered autologous T-cells, expressing a synthetic CAR, targeting tumor-associated antigens (TAAs) ...

Abstract	Chimeric antigen receptor (CAR) T-cells (CAR T-cells) are a promising therapeutic approach in treating hematological malignancies. CAR T-cells represent engineered autologous T-cells, expressing a synthetic CAR, targeting tumor-associated antigens (TAAs) independent of major histocompatibility complex (MHC) presentation. The most common target is CD19 on B-cells, predominantly used for the treatment of lymphoma and acute lymphocytic leukemia (ALL), leading to approval of five different CAR T-cell therapies for clinical application. Despite encouraging clinical results, treatment of other hematological malignancies such as acute myeloid leukemia (AML) remains difficult. In this review, we focus especially on CAR T-cell application in different hematological malignancies as well as strategies for overcoming CAR T-cell dysfunction and increasing their efficacy.
MeSH term(s)	Antigens, Neoplasm/immunology ; Hematologic Neoplasms/metabolism ; Hematologic Neoplasms/pathology ; Hematologic Neoplasms/therapy ; Humans ; Immunotherapy/methods ; Immunotherapy, Adoptive/methods ; Immunotherapy, Adoptive/trends ; Leukemia/immunology ; Leukemia/therapy ; Lymphoma/immunology ; Lymphoma/therapy ; Receptors, Antigen, T-Cell/immunology ; Receptors, Chimeric Antigen/immunology ; T-Lymphocytes/immunology
Chemical Substances	Antigens, Neoplasm ; Receptors, Antigen, T-Cell ; Receptors, Chimeric Antigen
Language	English
Publishing date	2021-08-20
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/ijms22168996
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Article ; Online: Re-Sensitizing Tumor Cells to Cancer Drugs with Epigenetic Regulators.

Rauscher, Stefanie / Greil, Richard / Geisberger, Roland

Current cancer drug targets

2021 Volume 21, Issue 4, Page(s) 353–359

Abstract: Cancer drug resistance is a major problem for cancer therapy. While many drugs can be effective in first-line treatments, cancer cells can become resistant due to genetic (mutations and chromosomal aberrations) but also epigenetic changes. Hence, many ... ...

Abstract	Cancer drug resistance is a major problem for cancer therapy. While many drugs can be effective in first-line treatments, cancer cells can become resistant due to genetic (mutations and chromosomal aberrations) but also epigenetic changes. Hence, many research studies addressed epigenetic drugs in circumventing resistance to conventional therapeutics in different tumor entities and in increasing the efficiency of immune checkpoint therapies. Furthermore, repositioning of already approved drugs in combination with epigenetic modifiers could potentiate their efficacy and thus could be an attractive strategy for cancer treatment. Summarizing, we recapitulate current data on epigenetic drugs and their targets in modulating sensitivity towards conventional and immune therapies, providing evidence that altering expression profiles by epigenetic modifiers holds great potential to improve the clinical outcome of cancer patients.
MeSH term(s)	Antineoplastic Agents/classification ; Antineoplastic Agents/pharmacology ; Drug Discovery ; Drug Repositioning ; Drug Resistance, Neoplasm/genetics ; Drug Therapy, Combination/methods ; Drug Therapy, Combination/trends ; Epigenesis, Genetic/drug effects ; Gene Expression Regulation, Neoplastic ; Histone Code/drug effects ; Histone Code/physiology ; Humans ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2021-01-12
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2064824-8
ISSN	1873-5576 ; 1568-0096
ISSN (online)	1873-5576
ISSN	1568-0096
DOI	10.2174/1568009620666210108102723
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Article: miRNA-Based Therapeutics in the Era of Immune-Checkpoint Inhibitors.

Huemer, Florian / Leisch, Michael / Geisberger, Roland / Zaborsky, Nadja / Greil, Richard

Pharmaceuticals (Basel, Switzerland)

2021 Volume 14, Issue 2

Abstract: MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression by binding to complementary target regions on gene transcripts. Thus, miRNAs fine-tune gene expression profiles in a cell-type-specific manner and thereby regulate important ... ...

Abstract	MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression by binding to complementary target regions on gene transcripts. Thus, miRNAs fine-tune gene expression profiles in a cell-type-specific manner and thereby regulate important cellular functions, such as cell growth, proliferation and cell death. MiRNAs are frequently dysregulated in cancer cells by several mechanisms, which significantly affect the course of the disease. In this review, we summarize the current knowledge on how dysregulated miRNAs contribute to cancer and how miRNAs can be exploited as predictive factors and therapeutic targets, particularly in regard to immune-checkpoint inhibitor therapies.
Language	English
Publishing date	2021-01-26
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2193542-7
ISSN	1424-8247
ISSN	1424-8247
DOI	10.3390/ph14020089
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Article ; Online: Detecting Bacterial-Human Lateral Gene Transfer in Chronic Lymphocytic Leukemia.

Akimova, Ekaterina / Gassner, Franz Josef / Greil, Richard / Zaborsky, Nadja / Geisberger, Roland

International journal of molecular sciences

2022 Volume 23, Issue 3

Abstract: Chronic lymphocytic leukemia (CLL) is a very common and mostly incurable B-cell malignancy. Recent studies revealed high interpatient mutational heterogeneity and worsened therapy response and survival of patients with complex genomic aberrations. In ... ...

Abstract	Chronic lymphocytic leukemia (CLL) is a very common and mostly incurable B-cell malignancy. Recent studies revealed high interpatient mutational heterogeneity and worsened therapy response and survival of patients with complex genomic aberrations. In line with this, a better understanding of the underlying mechanisms of specific genetic aberrations would reveal new prognostic factors and possible therapeutic targets. It is known that chromosomal rearrangements including DNA insertions often play a role during carcinogenesis. Recently it was reported that bacteria (microbiome)-human lateral gene transfer occurs in somatic cells and is enriched in cancer samples. To further investigate this mechanism in CLL, we analyzed paired-end RNA sequencing data of 45 CLL patients and 9 healthy donors, in which we particularly searched for bacterial DNA integrations into the human somatic genome. Applying the Burrows-Wheeler aligner (BWA) first on a human genome and then on bacterial genome references, we differentiated between sequencing reads mapping to the human genome, to the microbiome or to bacterial integrations into the human genome. Our results indicate that CLL samples featured bacterial DNA integrations more frequently (approx. two-fold) compared to normal samples, which corroborates the latest findings in other cancer entities. Moreover, we determined common integration sites and recurrent integrated bacterial transcripts. Finally, we investigated the contribution of bacterial integrations to oncogenesis and disease progression.
MeSH term(s)	Bacteria/genetics ; Bacteria/growth & development ; Case-Control Studies ; Chromosome Aberrations ; Gene Transfer, Horizontal ; Genome, Bacterial ; Genome, Human ; Humans ; Leukemia, Lymphocytic, Chronic, B-Cell/genetics ; Leukemia, Lymphocytic, Chronic, B-Cell/microbiology ; Leukemia, Lymphocytic, Chronic, B-Cell/pathology ; Microbiota
Language	English
Publishing date	2022-01-20
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/ijms23031094
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Article ; Online: Validation of genetic variants from NGS data using deep convolutional neural networks.

Vaisband, Marc / Schubert, Maria / Gassner, Franz Josef / Geisberger, Roland / Greil, Richard / Zaborsky, Nadja / Hasenauer, Jan

BMC bioinformatics

2023 Volume 24, Issue 1, Page(s) 158

Abstract: Accurate somatic variant calling from next-generation sequencing data is one most important tasks in personalised cancer therapy. The sophistication of the available technologies is ever-increasing, yet, manual candidate refinement is still a necessary ... ...

Abstract	Accurate somatic variant calling from next-generation sequencing data is one most important tasks in personalised cancer therapy. The sophistication of the available technologies is ever-increasing, yet, manual candidate refinement is still a necessary step in state-of-the-art processing pipelines. This limits reproducibility and introduces a bottleneck with respect to scalability. We demonstrate that the validation of genetic variants can be improved using a machine learning approach resting on a Convolutional Neural Network, trained using existing human annotation. In contrast to existing approaches, we introduce a way in which contextual data from sequencing tracks can be included into the automated assessment. A rigorous evaluation shows that the resulting model is robust and performs on par with trained researchers following published standard operating procedure.
MeSH term(s)	Humans ; Reproducibility of Results ; Neural Networks, Computer ; Machine Learning ; High-Throughput Nucleotide Sequencing/methods
Language	English
Publishing date	2023-04-20
Publishing country	England
Document type	Journal Article
ZDB-ID	2041484-5
ISSN	1471-2105 ; 1471-2105
ISSN (online)	1471-2105
ISSN	1471-2105
DOI	10.1186/s12859-023-05255-7
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Article: Risks and chances of aberrant DNA repair in cancer.

Schubert, Maria / Greil, Richard / Geisberger, Roland

Oncoscience

2018 Volume 5, Issue 9-10, Page(s) 256–257

Language	English
Publishing date	2018-08-22
Publishing country	United States
Document type	Journal Article
ISSN	2331-4737
ISSN	2331-4737
DOI	10.18632/oncoscience.459
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Article ; Online: AIDing cancer treatment: Reducing AID activity via HSP90 inhibition.

Rebhandl, Stefan / Geisberger, Roland

European journal of immunology

2015 Volume 45, Issue 8, Page(s) 2208–2211

Abstract: The activation induced deaminase (AID) catalyses the two key events underlying humoral adaptive immunity: class switch recombination and somatic hypermutation of antibody genes in B lymphocytes. AID accomplishes this task by directly deaminating ... ...

Abstract	The activation induced deaminase (AID) catalyses the two key events underlying humoral adaptive immunity: class switch recombination and somatic hypermutation of antibody genes in B lymphocytes. AID accomplishes this task by directly deaminating cytosines within the genomic immunoglobulin locus, thereby triggering a complex mutagenic process eventually leading to improved effector function of antibodies. However, it has long been noticed that AID can be aberrantly expressed in cancer and that its activity is not absolutely restricted to antibody genes, as substantial genome-wide off-target mutations have been observed, which contribute to tumorigenesis and clonal evolution of AID-expressing malignancies. In this issue of the European Journal of Immunology, Montamat-Sicotte et al. [Eur. J. Immunol. 2015. 45: 2365-2376] investigate the feasibility and efficacy of in vivo inhibition of AID with HSP90 inhibitors in a mouse model of B-cell leukemia and in vitro with a human breast cancer cell line, thereby demonstrating that cancer patients may benefit from preventing noncanonical AID functions.
MeSH term(s)	Animals ; B-Lymphocytes/immunology ; Breast Neoplasms/immunology ; Cytidine Deaminase/immunology ; Female ; HSP90 Heat-Shock Proteins/immunology ; Humans ; Neoplasm Proteins/immunology ; Neoplasms, Experimental/immunology ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/immunology
Chemical Substances	HSP90 Heat-Shock Proteins ; Neoplasm Proteins ; Cytidine Deaminase (EC 3.5.4.5)
Language	English
Publishing date	2015-07-07
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.201545832
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Zs.A 489: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Oncogenic MTOR signaling axis compensates BTK inhibition in a Chronic Lymphocytic Leukemia patient with Richter Transformation: A Case Report and Review of the Literature.

Parigger, Thomas / Drothler, Stephan / Scherhäufl, Christian / Gassner, Franz Josef / Schubert, Maria / Steiner, Markus / Höpner, Jan Philip / Hödlmoser, Alexandra / Schultheis, Lena / Abu Bakar, Aryunni / Neureiter, Daniel / Pleyer, Lisa / Egle, Alexander / Greil, Richard / Geisberger, Roland / Zaborsky, Nadja

Acta haematologica

2024

Abstract: Introduction: Targeting the B cell receptor (BCR) pathway via ibrutinib, a specific inhibitor of Bruton's tyrosine kinase, has shown marked clinical efficacy in treatment of patients with chronic lymphocytic leukemia (CLL), thus becoming a preferred ... ...

Abstract	Introduction: Targeting the B cell receptor (BCR) pathway via ibrutinib, a specific inhibitor of Bruton's tyrosine kinase, has shown marked clinical efficacy in treatment of patients with chronic lymphocytic leukemia (CLL), thus becoming a preferred first line option independent of risk factors. However, acquired resistance to ibrutinib poses a major clinical problem and requires the development of novel treatment combinations to increase efficacy and counteract resistance development and clinical relapse rates. Case presentation: In this study, we performed exome and transcriptome analyses of an ibrutinib resistant CLL patient in order to investigate genes and expression patterns associated with ibrutinib resistance. Here we provide evidence that ibrutinib resistance can be attributed to aberrant mammalian target of rapamycin (MTOR) signaling. Conclusion: Thus, our study proposes that combined use of MTOR inhibitors with ibrutinib could be a possible option to overcome therapy resistance in ibrutinib treated patients.
Language	English
Publishing date	2024-02-24
Publishing country	Switzerland
Document type	Case Reports
ZDB-ID	80008-9
ISSN	1421-9662 ; 0001-5792
ISSN (online)	1421-9662
ISSN	0001-5792
DOI	10.1159/000537791
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Article: RNA Editing Alters miRNA Function in Chronic Lymphocytic Leukemia.

Gassner, Franz J / Zaborsky, Nadja / Feldbacher, Daniel / Greil, Richard / Geisberger, Roland

Cancers

2020 Volume 12, Issue 5

Abstract: Chronic lymphocytic leukemia (CLL) is a high incidence B cell leukemia with a highly variable clinical course, leading to survival times ranging from months to several decades. MicroRNAs (miRNAs) are small non-coding RNAs that regulate the expression ... ...

Abstract	Chronic lymphocytic leukemia (CLL) is a high incidence B cell leukemia with a highly variable clinical course, leading to survival times ranging from months to several decades. MicroRNAs (miRNAs) are small non-coding RNAs that regulate the expression levels of genes by binding to the untranslated regions of transcripts. Although miRNAs have been previously shown to play a crucial role in CLL development, progression and treatment resistance, their further processing and diversification by RNA editing (specifically adenosine to inosine or cytosine to uracil deamination) has not been addressed so far. In this study, we analyzed next generation sequencing data to provide a detailed map of adenosine to inosine and cytosine to uracil changes in miRNAs from CLL and normal B cells. Our results reveal that in addition to a CLL-specific expression pattern, there is also specific RNA editing of many miRNAs, particularly miR-3157 and miR-6503, in CLL. Our data draw further light on how miRNAs and miRNA editing might be implicated in the pathogenesis of the disease.
Language	English
Publishing date	2020-05-05
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers12051159
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Article ; Online: Combination Strategies for Immune-Checkpoint Blockade and Response Prediction by Artificial Intelligence.

Huemer, Florian / Leisch, Michael / Geisberger, Roland / Melchardt, Thomas / Rinnerthaler, Gabriel / Zaborsky, Nadja / Greil, Richard

International journal of molecular sciences

2020 Volume 21, Issue 8

Abstract: The therapeutic concept of unleashing a pre-existing immune response against the tumor by the application of immune-checkpoint inhibitors (ICI) has resulted in long-term survival in advanced cancer patient subgroups. However, the majority of patients do ... ...

Abstract	The therapeutic concept of unleashing a pre-existing immune response against the tumor by the application of immune-checkpoint inhibitors (ICI) has resulted in long-term survival in advanced cancer patient subgroups. However, the majority of patients do not benefit from single-agent ICI and therefore new combination strategies are eagerly necessitated. In addition to conventional chemotherapy, kinase inhibitors as well as tumor-specific vaccinations are extensively investigated in combination with ICI to augment therapy responses. An unprecedented clinical outcome with chimeric antigen receptor (CAR-)T cell therapy has led to the approval for relapsed/refractory diffuse large B cell lymphoma and B cell acute lymphoblastic leukemia whereas response rates in solid tumors are unsatisfactory. Immune-checkpoints negatively impact CAR-T cell therapy in hematologic and solid malignancies and as a consequence provide a therapeutic target to overcome resistance. Established biomarkers such as programmed death ligand 1 (PD-L1) and tumor mutational burden (TMB) help to select patients who will benefit most from ICI, however, biomarker negativity does not exclude responses. Investigating alterations in the antigen presenting pathway as well as radiomics have the potential to determine tumor immunogenicity and response to ICI. Within this review we summarize the literature about specific combination partners for ICI and the applicability of artificial intelligence to predict ICI therapy responses.
MeSH term(s)	Animals ; Antineoplastic Agents, Immunological/pharmacology ; Antineoplastic Agents, Immunological/therapeutic use ; Artificial Intelligence ; Biomarkers, Tumor ; Cancer Vaccines/adverse effects ; Cancer Vaccines/immunology ; Cancer Vaccines/therapeutic use ; Combined Modality Therapy ; Humans ; Immune Checkpoint Inhibitors/pharmacology ; Immune Checkpoint Inhibitors/therapeutic use ; Immunotherapy/adverse effects ; Immunotherapy/methods ; Molecular Targeted Therapy ; Neoplasms/etiology ; Neoplasms/metabolism ; Neoplasms/therapy ; T-Lymphocyte Subsets/drug effects ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism ; Treatment Outcome
Chemical Substances	Antineoplastic Agents, Immunological ; Biomarkers, Tumor ; Cancer Vaccines ; Immune Checkpoint Inhibitors
Language	English
Publishing date	2020-04-19
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/ijms21082856
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