A5018453565- Ubiquitin and proteasome pathways
- Ferroptosis and cancer prognosis
- RNA modifications and cancer
- Protein Kinase Regulation and GTPase Signaling
- Growth Hormone and Insulin-like Growth Factors
- Peptidase Inhibition and Analysis
- Bladder and Urothelial Cancer Treatments
- Neurofibromatosis and Schwannoma Cases
- Chromatin Remodeling and Cancer
- Bioinformatics and Genomic Networks
- interferon and immune responses
- Cancer Immunotherapy and Biomarkers
- Neuropeptides and Animal Physiology
- Autophagy in Disease and Therapy
- Protein Degradation and Inhibitors
- Lung Cancer Treatments and Mutations
- Sarcoma Diagnosis and Treatment
- Immune cells in cancer
- Apelin-related biomedical research
- Cancer, Stress, Anesthesia, and Immune Response
- Erythrocyte Function and Pathophysiology
- Ovarian cancer diagnosis and treatment
- Advanced Glycation End Products research
- Lung Cancer Research Studies
- PI3K/AKT/mTOR signaling in cancer
VIB-KU Leuven Center for Cancer Biology
2023-2024
KU Leuven
2023
Vlaams Instituut voor Biotechnologie
2023
University of Oxford
2020
UConn Health
2020
University of Split
2019-2020
Bladder cancer (BC) is the most common malignant disease of urinary tract. Recurrent high grade non muscle invasive BC carries a serious risk for progression and subsequent metastases. The preclinical mouse model bladder relies on administration N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN) to mice. BBN-induced tumors in mice recapitulate histology human were characterized with an overexpression markers typical basal-like subtype addition mutational burden frequent mutations Trp53, similar...
Blood flow produces shear stress exerted on the endothelial layer of vessels. Spatial characterization proteome is required to uncover mechanisms activation by stress, as blood varies in vasculature. An integrative ubiquitinome and analysis shear-stressed cells demonstrated that non-degradative ubiquitination several GTPases regulated mechano-signaling. reveals increased small GTPase RAP1 descending aorta, a region exposed laminar stress. The ubiquitin ligase WWP2 identified novel regulator...
Abstract Almost 30% of lung adenocarcinomas are driven by activating KRAS mutations. The heterogeneous clinical behavior observed in these cancers could be due to the imbalance wild-type and oncogenic alleles. However, role RAS dysregulation at protein level needs further explored. A genome-wide global stability screen identified CUL3 ubiquitin ligase adaptor LZTR1, as a major proteostatic regulator but not mutant KRAS. In -mutant adenocarcinoma, shallow deletion LZTR1 is up 50% patients...
Abstract Lung adenocarcinomas (LUAD) are frequently driven by activating mutations in the Kirsten rat sarcoma viral oncogene homolog (KRAS). Previous studies have suggested that wild-type (wt)-RAS signaling may modulate cancer progression and drug resistance these tumors. However, interplay between oncogenic KRAS wt-RAS-like GTPases lung biology treatment remains debated. Here, we investigated impact of increased wt-KRAS dosage LUAD harboring mutant on phenotypes response to anti-KRAS...
Abstract Lung cancer is the most frequent with an aggressive clinical course and high mortality rates. About 30% of non-small lung driven by activating mutations in KRAS (Kirsten rat sarcoma virus). signaling tightly controlled through a series post-transcriptional mechanisms, whereas dysregulation activity translated into heterogeneous behavior. We, others, have recently implicated leucine zipper-like transcriptional regulator 1 (LZTR1), adaptor CUL3-containing E3 ligase complex, control...
A total of 30% lung adenocarcinoma are driven by activating KRAS mutations. The treatment options for KRAS-mutant cancer still limited as a challenge therapy is the high heterogeneity within mutant tumors. Co-existing genetic events alter RAS signaling, such alteration ubiquitin ligase leucine zipper-like transcriptional regulator 1 (LZTR1). LZTR1 an adaptor CUL3 E3 that controls localization and expression levels proteins regulating their ubiquitination. Recent studies demonstrated loss...