Cathinka Boedicker

ORCID: 0000-0003-4668-3516
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About
Contact & Profiles
Research Areas
  • Protein Degradation and Inhibitors
  • Cancer-related Molecular Pathways
  • Hedgehog Signaling Pathway Studies
  • Multiple Myeloma Research and Treatments
  • Epigenetics and DNA Methylation
  • Immune Cell Function and Interaction
  • Histone Deacetylase Inhibitors Research
  • Ubiquitin and proteasome pathways
  • Nanoparticles: synthesis and applications
  • Cancer Mechanisms and Therapy
  • Cancer-related gene regulation
  • Cell death mechanisms and regulation
  • Immunotherapy and Immune Responses
  • Genomics and Chromatin Dynamics
  • RNA Interference and Gene Delivery
  • Melanoma and MAPK Pathways
  • Neuroblastoma Research and Treatments
  • Environmental Toxicology and Ecotoxicology
  • CAR-T cell therapy research
  • Sarcoma Diagnosis and Treatment

Goethe University Frankfurt
2013-2022

Frankfurt Cancer Institute
2016-2022

Deutschen Konsortium für Translationale Krebsforschung
2016-2019

German Cancer Research Center
2016-2019

Heidelberg University
2016-2019

The antibacterial properties of nanosilver have led to a versatile application spectrum including medical purposes and personal care products. However, the increasing use has raised concerns about its environmental impacts. Long-term exposure studies with aquatic invertebrates are essential assess possible adverse effects on ecosystems. In present study, acute (48 h), chronic (21 d) long-term (primary size 15 nm) five successive generations three Daphnia species (D. magna, D. pulex, galeata)...

10.1371/journal.pone.0075026 article EN cc-by PLoS ONE 2013-10-07

A range of studies has addressed possible environmental impacts nanosilver, but most focused on acute effects in few species. Moreover, it remains unclear if toxic are particle-specific or mediated by released silver ions. We investigated chronic nanosilver and soluble (AgNO3) the freshwater bivalve Sphaerium corneum. Animals were exposed to (0–500 μg Ag L−1) AgNO3 (0–318 over 28 days, reproduction behavioral changes assessed. To explore mechanisms, we evaluated intracellular levels reactive...

10.3109/17435390.2014.963723 article EN Nanotoxicology 2014-09-30

The induction of apoptosis is a direct way to eliminate tumor cells and improve cancer therapy. Apoptosis tightly controlled by the balance pro- antiapoptotic Bcl-2 proteins. BH3 mimetics neutralize function proteins are highly promising compounds inducing in several entities including pediatric malignancies. However, clinical application solid tumors impeded frequent resistance single anticipated toxicity high concentrations or combination treatments. One potential avenue increase potency...

10.1038/s41420-021-00812-6 article EN cc-by Cell Death Discovery 2022-01-10

Rhabdomyosarcoma (RMS), the most common cancer of connective tissues in pediatrics, is often resistant to conventional therapies. One underlying mechanism this resistance overexpression Inhibitor Apoptosis (IAP) proteins, leading a dysfunctional cell death program within tumor cells. Smac mimetics (SM) are small molecules that can reactivate by antagonizing IAP proteins and thereby compensating their overexpression. Here, we report SM sensitize two RMS lines (RD RH30) toward natural killer...

10.3389/fimmu.2017.00202 article EN cc-by Frontiers in Immunology 2017-03-07

The RAS/MEK/ERK genetic axis is commonly altered in rhabdomyosarcoma (RMS), indicating high activity of downstream effector ERK1/2 kinase. Previously, we have demonstrated that inhibition the signaling pathway RMS insufficient to induce cell death due residual pro-survival MCL-1 activity. Here, show combination inhibitor Ulixertinib and S63845 highly synergistic induces apoptotic vitro vivo. Importantly, Ulixertinib/S63845 co-treatment suppresses long-term survival cells, rapid caspase...

10.1016/j.tranon.2021.101313 article EN cc-by-nc-nd Translational Oncology 2021-12-11

BH3 mimetics are promising novel anticancer therapeutics. By selectively inhibiting BCL-2, BCL-xL, or MCL-1 (i.e. ABT-199, A-1331852, S63845) they shift the balance of pro- and anti-apoptotic proteins in favor apoptosis. As Bromodomain Extra Terminal (BET) protein inhibitors promote pro-apoptotic rebalancing, we evaluated potential BET inhibitor JQ1 combination with A-1331852 S63845 rhabdomyosarcoma (RMS) cells. The strongest synergistic interaction was identified for JQ1/A-1331852...

10.1016/j.neo.2021.11.012 article EN cc-by-nc-nd Neoplasia 2021-12-24
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