A5077306787- DNA Repair Mechanisms
- Cervical Cancer and HPV Research
- Radiation Therapy and Dosimetry
- Mitochondrial Function and Pathology
- Cancer-related Molecular Pathways
- Cancer, Hypoxia, and Metabolism
- Adenosine and Purinergic Signaling
- Neutropenia and Cancer Infections
- Polyomavirus and related diseases
- Ubiquitin and proteasome pathways
- Cell death mechanisms and regulation
- Effects of Radiation Exposure
- Cancer Immunotherapy and Biomarkers
- Genetics and Neurodevelopmental Disorders
- CRISPR and Genetic Engineering
- Microscopic Colitis
- PI3K/AKT/mTOR signaling in cancer
- Advanced Radiotherapy Techniques
- Respiratory viral infections research
- 14-3-3 protein interactions
- Head and Neck Cancer Studies
- Protein Degradation and Inhibitors
- Clostridium difficile and Clostridium perfringens research
- RNA modifications and cancer
- Colorectal and Anal Carcinomas
Anderson University - South Carolina
2025
The University of Texas MD Anderson Cancer Center
2020-2022
Essen University Hospital
2018-2021
University of Duisburg-Essen
2018-2021
Technical improvements in clinical radiotherapy for maximizing cytotoxicity to the tumor while limiting negative impact on co-irradiated healthy tissues include increasing use of particle therapy (e.g., proton therapy) worldwide. Yet potential differences biology DNA damage induction and repair between irradiation with X-ray photons protons remain elusive. We compared double strand break (DSB) survival cells compromised non-homologous end joining (NHEJ), homologous recombination (HRR) or...
Exploiting cancer vulnerabilities is critical for the discovery of anticancer drugs. However, tumor suppressors cannot be directly targeted because their loss function. To uncover specific cells with deficiency in any given suppressor(s), we performed genome-scale CRISPR loss-of-function screens using a panel isogenic knockout generated 12 common suppressors. Here, provide comprehensive and comparative dataset genetic interactions between whole-genome protein-coding genes suppressor genes,...
<title>Abstract</title> <bold>Introduction</bold>: Immune checkpoint inhibitors have revolutionized cancer therapy; however, adverse events from an unchecked immune system such as inhibitor mediated diarrhea and colitis (IMDC) can develop. Fecal microbiota transplantation (FMT) remains option for patients with refractory colitis, but has not been tested in upfront setting. <bold>Methods</bold>: From open-label, phase I/II clinical trial (NCT0403861) starting June 2021, we report analysis of...
Abstract Because of essential roles DNA damage response (DDR) in the maintenance genomic integrity, cellular homeostasis, and tumor suppression, targeting DDR has become a promising therapeutic strategy for cancer treatment. However, benefits therapy are limited mainly due to lack predictive biomarkers. To address this challenge, we performed CRISPR screens search genetic vulnerabilities that affect cells’ inhibition. By undertaking with inhibitors key mediators, i.e. ATR, ATM, DNAPK CHK1,...
Proton beam therapy is increasingly applied for the treatment of human cancer, as it promises to reduce normal tissue damage. However, little known about relationship between linear energy transfer (LET), type DNA damage, and cellular repair mechanisms, particularly cells irradiated with protons. We cultured delivering equal doses X-ray photons, Bragg-peak protons, or plateau protons used this set-up quantitate initial damage (mainly double strand breaks (DSBs)), analyze kinetics by...
Cancer bioenergetics fuel processes necessary to maintain viability and growth under stress conditions. We hypothesized that cancer metabolism supports the repair of radiation-induced DNA double-stranded breaks (DSBs). combined systematic collection metabolic radiobiological data from a panel irradiated cell lines with mathematical modeling identified common response impact on DSB kinetics, including mitochondrial shutdown followed by compensatory glycolysis resumption function. Combining...
The survival kinase protein B (Akt) participates in the regulation of essential subcellular processes, e.g., proliferation, growth, survival, and apoptosis, has a documented role promoting resistance against genotoxic stress including radiotherapy, presumably by influencing DNA damage response double-strand break (DSB) repair. However, its exact DSB repair requires further elucidation. We used genetic approach to explore consequences impaired phosphorylation Akt1 at one or both key sites,...
The ectonucleoside triphosphate diphosphohydrolase (CD39)/5' ectonuclotidase (CD73)-dependent purinergic pathway emerges as promising cancer target. Yet, except for own previous work revealing a pathogenic role of CD73 and adenosine in radiation-induced lung fibrosis, the signaling radiotherapy outcome remained elusive. Here we used C57BL/6 wild-type (WT), CD39 knockout (CD39-/-), (CD73-/-) mice hind-leg tumors syngeneic murine Lewis carcinoma cells (LLC1) to elucidate how host shapes growth...
<h3>Background</h3> Human papillomavirus (HPV) infection causes at least 650,000 anogenital and oropharyngeal cancers (OPC) worldwide annually. Despite the viral immunological target, immune checkpoint inhibitors produce responses only in a minority of patients, cancer therapies that directly target HPV-antigens represent an attractive alternative therapeutic approach. With this work, we introduce high-throughput epitope-agnostic pipeline for HPV16-reactive T cell discovery validation....
Human papillomavirus (HPV) infection causes at least 650,000 anogenital and oropharyngeal cancers (OPC) worldwide annually.A prophylactic vaccine against high-risk HPV types was approved in 2006 by the FDA, but still, burden of HPV-related is constantly increasing.Thus, therapies that directly target HPV-antigens represent an attractive alternative therapeutic approach.However, current research' focus on epitopes E6 E7 proteins despite a high expression other tumors.Large efforts targeting...
Abstract Flexibility and reprogramming of cancer metabolism supports progression therapy resistance. In previous work we described opportunities for overcoming environment-induced resistance to ionizing radiation (IR) by pharmacologic inhibition metabolic processes [1,2,3]. Here, hypothesized that certain aspects will support the repair radiation-induced DNA double-strand breaks (DSBs) identification pathways critical damage cell survival allow enhance sensitivity cells IR interfering with...