0000000000331532

AUTHOR

Steffen Emmert

showing 3 related works from this author

Baseline factors affecting closure of venous leg ulcers

2017

Objective: The objective of this study was to characterize factors associated with closure of venous leg ulcers (VLUs) in a pooled analysis of subjects from three randomized clinical trials. Methods: Closure of VLUs after treatment with HP802-247, an allogeneic living cell therapy consisting of growth-arrested human keratinocytes and fibroblasts, vs standard therapy with compression bandaging was evaluated in three phase 3 clinical trials of similar design. Two trials enrolled subjects with VLUs ranging from 2 cm2 to 12 cm2 in area with 12-week treatment periods; the third trial enrolled subjects with VLUs between >12 cm2 and #36 cm2 with a 16-week treatment period. The first trial went to …

Malemedicine.medical_specialtyCell- and Tissue-Based Therapy030204 cardiovascular system & hematologyPlaceboVaricose Ulcerlaw.invention030207 dermatology & venereal diseases03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRandomized controlled triallawCompression BandagesInternal medicineDiabetes mellitusmedicineHumansProspective StudiesClosure (psychology)Prospective cohort studyWound Healingbusiness.industryMiddle AgedPrognosismedicine.diseaseClinical trialTreatment OutcomechemistryFemaleSurgeryHuman medicineGlycated hemoglobinCardiology and Cardiovascular MedicinebusinessBody mass indexDiabetic AngiopathiesJournal of Vascular Surgery: Venous and Lymphatic Disorders
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Nucleotide excision repair of abasic DNA lesions

2019

AbstractApurinic/apyrimidinic (AP) sites are a class of highly mutagenic and toxic DNA lesions arising in the genome from a number of exogenous and endogenous sources. Repair of AP lesions takes place predominantly by the base excision pathway (BER). However, among chemically heterogeneous AP lesions formed in DNA, some are resistant to the endonuclease APE1 and thus refractory to BER. Here, we employed two types of reporter constructs accommodating synthetic APE1-resistant AP lesions to investigate the auxiliary repair mechanisms in human cells. By combined analyses of recovery of the transcription rate and suppression of transcriptional mutagenesis at specifically positioned AP lesions, w…

DNA RepairTranscription GeneticDNA damageDNA repairGenome Integrity Repair and ReplicationGene Knockout Techniques03 medical and health sciencesEndonucleasechemistry.chemical_compoundTranscription (biology)CRISPR-Associated Protein 9DNA-(Apurinic or Apyrimidinic Site) LyaseGeneticsHumansAP siteCell Line TransformedSkin030304 developmental biologyGene Editing0303 health sciencesBase SequencebiologyGenome Human030302 biochemistry & molecular biologyDNABase excision repairFibroblastsMolecular biologyXeroderma Pigmentosum Group A ProteinDNA-Binding ProteinschemistryMutationbiology.proteinCRISPR-Cas SystemsDNADNA DamageProtein BindingNucleotide excision repairNucleic Acids Research
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Alterations of DNA Repair in Melanoma Cell Lines Resistant to Cisplatin, Fotemustine, or Etoposide

2000

Resistance to chemotherapy is a common phenomenon in malignant melanoma. In order to assess the role of altered DNA repair in chemoresistant melanoma, we investigated different DNA repair pathways in one parental human melanoma line (MeWo) and in sublines of MeWo selected in vitro for drug resistance against four commonly used drugs (cisplatin, fotemustine, etoposide, and vindesine). Host cell reactivation assays with the plasmid pRSVcat were used to assess processing of different DNA lesions. With ultraviolet-irradiated plasmids, no significant differences were found, indicating a normal (nucleotide excision) repair of DNA photoproducts. With singlet oxygen-treated plasmid, the fotemustine…

DNA RepairUltraviolet RaysDNA repairDNA damageDrug ResistanceAntineoplastic AgentsDermatologyBiologyHost-Cell Reactivationbase excision repairBiochemistryNitrosourea Compounds03 medical and health sciencesOrganophosphorus Compounds0302 clinical medicineTumor Cells CulturedmedicineHumansMelanomaMolecular BiologyEtoposide030304 developmental biology0303 health scienceschemoresistanceMicrosatellite instabilityDNA NeoplasmBase excision repairCell BiologyDNA repair protein XRCC4nucleotide excision repairmedicine.diseaseAntineoplastic Agents PhytogenicMolecular biology3. Good healthOxygenmismatch repair030220 oncology & carcinogenesisDNA mismatch repairCisplatinMicrosatellite RepeatsNucleotide excision repairJournal of Investigative Dermatology
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