Wynand P. Roos Source Confirmed

Affiliation confirmed via AI analysis of OpenAlex, ORCID, and web sources.

High Impact

Researcher

John Brown University

faculty

35 h-index 120 pubs 8,786 cited

Research Areas

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OverviewAI-generated summary

Dr. Wynand P. Roos investigates cancer-related molecular pathways, including DNA repair mechanisms and the efficacy of PARP inhibition in cancer therapy. His research extends to glioma diagnosis and treatment, along with the study of histone deacetylase inhibitors. Recent work has elucidated the cryo-EM structure of the Mre11-Rad50-Nbs1 complex, revealing its scaffolding functions, and has explored the role of Class I HDAC overexpression in promoting temozolomide resistance within glioma cells via RAD18 regulation. Other investigations have focused on epigenetic modifiers such as HDAC2 and the checkpoint kinase ATM in determining the responses of microsatellite instable colorectal cancer cells to 5-fluorouracil, as well as the molecular modes of action of Nerium oleander extract in cancer cells. His research also covers epigenetic anti-cancer treatment using stabilized carbocyclic decitabine analogs.

Metrics

h-index: 35
Publications: 120
Citations: 8,786

Selected Publications

Replication-associated base excision repair/single-strand break repair regulates PARG inhibitor response via the PRMT1/PRMT5/ATR axis (2025) DOI
TRIP12’s role in the governance of DNA polymerase β involvement in DNA damage response and repair (2025) DOI
DNA polymerase beta expression in head & neck cancer modulates the poly(ADP-ribose)-mediated replication checkpoint (2025) DOI
Overexpression of the WWE domain of RNF146 modulates poly-(ADP)-ribose dynamics at sites of DNA damage (2025) DOI
Abstract B005: Regulation of replication-induced PARP1/PARP2 activation by base excision repair: Implications for PARP and PARG inhibitor resistance (2024) DOI
Oncometabolite 2-hydroxyglutarate suppresses basal protein levels of DNA polymerase beta that enhances alkylating agent and PARG inhibition induced cytotoxicity (2024) DOI
Supplementary Table 3 from Contribution of ATM and ATR to the Resistance of Glioblastoma and Malignant Melanoma Cells to the Methylating Anticancer Drug Temozolomide (2023) DOI
Supplementary Table 2 from Contribution of ATM and ATR to the Resistance of Glioblastoma and Malignant Melanoma Cells to the Methylating Anticancer Drug Temozolomide (2023) DOI
Supplementary Table 1 from Contribution of ATM and ATR to the Resistance of Glioblastoma and Malignant Melanoma Cells to the Methylating Anticancer Drug Temozolomide (2023) DOI
Supplementary Table 3 from Contribution of ATM and ATR to the Resistance of Glioblastoma and Malignant Melanoma Cells to the Methylating Anticancer Drug Temozolomide (2023) DOI
Data from Contribution of ATM and ATR to the Resistance of Glioblastoma and Malignant Melanoma Cells to the Methylating Anticancer Drug Temozolomide (2023) DOI
Supplementary Data, Figure S1 - S3 from The SIAH1–HIPK2–p53ser46 Damage Response Pathway is Involved in Temozolomide-Induced Glioblastoma Cell Death (2023) DOI
Supplementary Data, Figure S1 - S3 from The SIAH1–HIPK2–p53ser46 Damage Response Pathway is Involved in Temozolomide-Induced Glioblastoma Cell Death (2023) DOI
Supplementary Figure S3 from Enhanced Histone Deacetylase Activity in Malignant Melanoma Provokes RAD51 and FANCD2-Triggered Drug Resistance (2023) DOI
Supplementary Table S1 from Enhanced Histone Deacetylase Activity in Malignant Melanoma Provokes RAD51 and FANCD2-Triggered Drug Resistance (2023) DOI