Peter Schmezer

SRSF2 safeguards efficient transcription of DNA damage and repair genes

Rebecca E. Wagner, Leonie Arnetzl, Thiago Britto‐Borges, Anke Heit-Mondrzyk et autres

The serine-/arginine-rich splicing factor 2 (SRSF2) plays pivotal roles in pre-mRNA processing and gene transcription. Recurrent mutations, particularly a proline-to-histidine substitution at position 95 (P95H), are common in neoplastic diseases. Here, we assess SRSF2's diverse functions in squamous cell carcinoma. We show …

de, gb (code pays fourni par la source)

SRSF2 transcriptional function maintains genome integrity during cell division

Rebecca E. Wagner, Leonie Arnetzl, Thiago Britto‐Borges, Anke Heit-Mondrzyk et autres

Abstract Recurrent mutations in serine / arginine-rich splicing factor 2 (SRSF2), particularly the proline-to-histidine substitution at position 95 (P95H), have been proposed to drive neoplastic diseases. SRSF2 plays pivotal roles in pre-mRNA processing and gene transcription. However, the precise impact of these …

de, be, gb (code pays fourni par la source)

ARID1A regulates DNA repair through chromatin organization and its deficiency triggers DNA damage-mediated anti-tumor immune response

Ali Bakr, G Corte, Olivera Veselinov, Simge Kelekçi et autres

AT-rich interaction domain protein 1A (ARID1A), a SWI/SNF chromatin remodeling complex subunit, is frequently mutated across various cancer entities. Loss of ARID1A leads to DNA repair defects. Here, we show that ARID1A plays epigenetic roles to promote both DNA double-strand breaks (DSBs) …

de (code pays fourni par la source)

Deposition of onco‐histone H3 . 3‐G34W leads to DNA repair deficiency and activates cGAS / STING ‐mediated immune responses

Daniela Mancarella, Henrik Ellinghaus, Gianluca Sigismondo, Olivera Veselinov et autres

Mutations in histone H3.3-encoding genes causing mutant histone tails are associated with specific cancers such as pediatric glioblastomas (H3.3-G34R/V) and giant cell tumor of the bone (H3.3-G34W). The mechanisms by which these mutations promote malignancy are not completely understood. Here we show …

de (code pays fourni par la source)

Data from Specialty Supplement Use and Biologic Measures of Oxidative Stress and DNA Damage

Elizabeth D. Kantor, Cornelia M. Ulrich, Robert Wyn Owen, Peter Schmezer et autres

Abstract Background: Oxidative stress and resulting cellular damage have been suggested to play a role in the etiology of several chronic diseases, including cancer and cardiovascular disease. Identifying factors associated with reduced oxidative stress and resulting damage may guide future disease-prevention strategies. …

Editorial from Specialty Supplement Use and Biologic Measures of Oxidative Stress and DNA Damage

Elizabeth D. Kantor, Cornelia M. Ulrich, Robert Wyn Owen, Peter Schmezer et autres

Editorial from Specialty Supplement Use and Biologic Measures of Oxidative Stress and DNA Damage

Editorial from Specialty Supplement Use and Biologic Measures of Oxidative Stress and DNA Damage

Elizabeth D. Kantor, Cornelia M. Ulrich, Robert Wyn Owen, Peter Schmezer et autres

Editorial from Specialty Supplement Use and Biologic Measures of Oxidative Stress and DNA Damage

Data from Specialty Supplement Use and Biologic Measures of Oxidative Stress and DNA Damage

Elizabeth D. Kantor, Cornelia M. Ulrich, Robert Wyn Owen, Peter Schmezer et autres

Abstract Background: Oxidative stress and resulting cellular damage have been suggested to play a role in the etiology of several chronic diseases, including cancer and cardiovascular disease. Identifying factors associated with reduced oxidative stress and resulting damage may guide future disease-prevention strategies. …

Data from Integrative Genome-Scale Analysis Identifies Epigenetic Mechanisms of Transcriptional Deregulation in Unfavorable Neuroblastomas

Kai‐Oliver Henrich, Sebastian Bender, Maral Saadati, Daniel Dreidax et autres

Abstract The broad clinical spectrum of neuroblastoma ranges from spontaneous regression to rapid progression despite intensive multimodal therapy. This diversity is not fully explained by known genetic aberrations, suggesting the possibility of epigenetic involvement in pathogenesis. In pursuit of this hypothesis, we …

Data from Integrative Genome-Scale Analysis Identifies Epigenetic Mechanisms of Transcriptional Deregulation in Unfavorable Neuroblastomas

Kai‐Oliver Henrich, Sebastian Bender, Maral Saadati, Daniel Dreidax et autres

Abstract The broad clinical spectrum of neuroblastoma ranges from spontaneous regression to rapid progression despite intensive multimodal therapy. This diversity is not fully explained by known genetic aberrations, suggesting the possibility of epigenetic involvement in pathogenesis. In pursuit of this hypothesis, we …

Supplementary Methods and References from Integrative Genome-Scale Analysis Identifies Epigenetic Mechanisms of Transcriptional Deregulation in Unfavorable Neuroblastomas

Kai‐Oliver Henrich, Sebastian Bender, Maral Saadati, Daniel Dreidax et autres

Description of additional methods and procedures used in the study. Also includes Supplementary References.

Table S8 from Integrative Genome-Scale Analysis Identifies Epigenetic Mechanisms of Transcriptional Deregulation in Unfavorable Neuroblastomas

Kai‐Oliver Henrich, Sebastian Bender, Maral Saadati, Daniel Dreidax et autres

Genes whose hypermethylation and downregulation are associated with high-risk disease (HyperDownHR) are de-repressed upon combination treatment with epigenetically active drugs