Daniel Mertens

ORCID: 0000-0003-0227-7188
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About
Contact & Profiles
Research Areas
  • Chronic Lymphocytic Leukemia Research
  • Lymphoma Diagnosis and Treatment
  • Immunodeficiency and Autoimmune Disorders
  • Cancer Genomics and Diagnostics
  • Epigenetics and DNA Methylation
  • Glycosylation and Glycoproteins Research
  • Acute Lymphoblastic Leukemia research
  • Cancer-related Molecular Pathways
  • RNA modifications and cancer
  • Advanced Breast Cancer Therapies
  • Immune Cell Function and Interaction
  • MicroRNA in disease regulation
  • Cancer-related gene regulation
  • Genomic variations and chromosomal abnormalities
  • Cell death mechanisms and regulation
  • Monoclonal and Polyclonal Antibodies Research
  • Chronic Myeloid Leukemia Treatments
  • Phagocytosis and Immune Regulation
  • PI3K/AKT/mTOR signaling in cancer
  • Galectins and Cancer Biology
  • Ubiquitin and proteasome pathways
  • Acute Myeloid Leukemia Research
  • DNA Repair Mechanisms
  • RNA Interference and Gene Delivery
  • Telomeres, Telomerase, and Senescence

Fraunhofer Society
2024

Heidelberg University
2015-2024

German Cancer Research Center
2015-2024

University Hospital Ulm
2015-2024

Universität Ulm
2014-2023

Medical University of Vienna
2005-2022

DKFZ-ZMBH Alliance
2002-2020

Deutschen Konsortium für Translationale Krebsforschung
2013-2020

Epigenomics (Germany)
2013

National Center for Tumor Diseases
2013

Two mutants of Saccharomyces cerevisiae affected in peroxisomal assembly (pas mutants) have been isolated and characterized. Each strain contains a single mutation that results (i) the inability to grow on oleic acid, (ii) accumulation matrix enzymes cytosol, (iii) absence detectable peroxisomes at ultrastructural level. These lesions (pas1-1 pas2) are shown be nonallelic recessive. Crossing pas1-1 pas2 strains resulted diploid cells had regained ability acid as sole carbon source form...

10.1073/pnas.86.14.5419 article EN Proceedings of the National Academy of Sciences 1989-07-01

ABSTRACT Cdc25 phosphatases play key roles in cell cycle progression by activating cyclin-dependent kinases. In human cells, cdc25 proteins are encoded a multigene family, consisting of cdc25A, cdc25B and cdc25C. While cdc25A plays crucial role at the G 1/S phase transition, cdc25C is involved dephosphorylation activation mitotic kinase, cdc2/cyclinB. addition, itself regulated cdc2/cyclinB which then creates positive feedback loop that controls entry into mitosis. this study we show...

10.1242/jcs.111.16.2445 article EN Journal of Cell Science 1998-08-15

Non-coding RNAs are much more common than previously thought. However, for the vast majority of non-coding RNAs, cellular function remains enigmatic. The two long RNA (lncRNA) genes DLEU1 and DLEU2 map to a critical region at chromosomal band 13q14.3 that is recurrently deleted in solid tumors hematopoietic malignancies like chronic lymphocytic leukemia (CLL). While no point mutations have been found protein coding candidate 13q14.3, they deregulated malignant cells, suggesting an epigenetic...

10.1371/journal.pgen.1003373 article EN cc-by PLoS Genetics 2013-04-04

Although clonal selection by genetic driver aberrations in cancer is well documented, the ability of epigenetic alterations to promote tumor evolution undefined. We used 450k arrays and next-generation sequencing evaluate intratumor heterogeneity DNA methylation chronic lymphocytic leukemia (CLL). CLL cases exhibit vast interpatient differences heterogeneity, with genetically maintaining low up 10% total CpGs a monoallelically methylated state. Increasing correlates advanced subclonal...

10.1158/2159-8290.cd-13-0349 article EN Cancer Discovery 2013-12-20

Increased ZAP-70 expression predicts poor prognosis in chronic lymphocytic leukemia (CLL). Current methods for accurately measuring are problematic, preventing widespread application of these tests clinical decision making. We therefore used comprehensive DNA methylation profiling the regulatory region to identify sites important transcriptional control.High-resolution quantitative analysis entire gene regions was conducted on 247 samples from patients with CLL four independent...

10.1200/jco.2011.39.3090 article EN Journal of Clinical Oncology 2012-05-08

Abstract Epigenetic alterations, such as promoter hypermethylation, may drive cancer through tumor suppressor gene inactivation. However, we have limited ability to differentiate driver DNA methylation (DNAme) changes from passenger events. We developed DNAme inference–MethSig–accounting for the varying stochastic hypermethylation rate across genome and between samples. applied MethSig bisulfite sequencing data of chronic lymphocytic leukemia (CLL), multiple myeloma, ductal carcinoma in...

10.1158/2159-8290.cd-20-1334 article EN Cancer Discovery 2021-05-10

Gene knock down by RNAi is a highly effective approach to silence gene expression in experimental as well therapeutic settings. However, this widely used methodology entails serious pitfalls, especially concerning specificity of the molecules. We tested most control siRNA directed against GFP for off-target effects and found that it deregulates addition set endogenous target genes. The were dependent on amount transfected detected variety cell lines. Since respective molecule specific...

10.1186/1471-2199-9-60 article EN cc-by BMC Molecular Biology 2008-01-01

Programmed death-1 (PD-1) is an immunoreceptor predominantly expressed on exhausted T cells, which through interaction with its ligand (PD-L1), controls peripheral tolerance by limiting effector functions of lymphocytes. qRT-PCR for PD-1, PD-L1 and their splicing forms as well flow cytometric assessment surface expression was performed in a cohort 58 chronic lymphocytic leukemia (CLL) patients. In functional studies, we assessed the influence proliferative response leukemic B-cells induced...

10.1371/journal.pone.0035178 article EN cc-by PLoS ONE 2012-04-19
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