Marwa Tantawy
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Marwa Tantawy has a total of 11 co-authors. Here are the top co-authors by number of shared publications:
- Daniel J. Lenihan
Cape Cardiology Group, Saint Francis Medical Center, Cape Girardeau, MO 63703, USA
1 shared publication - Eric Farber-Eger
Vanderbilt Translational and Clinical Cardiovascular Research Center, Vanderbilt University School of Medicine, Nashville, USA
1 shared publication - Kenneth H. Shain
Moffitt Cancer Center, Tampa, Florida, United States
1 shared publication - Lauren Lee Shaffer
Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA
1 shared publication - Mohammed E. Alomar
Cardio-Oncology Program, H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL 33216, USA
1 shared publication - Quinn Stanton Wells
Vanderbilt Translational and Clinical Cardiovascular Research Center, Cadiovacsular Medicine Division, Vanderbilt University School of Medicine, Nashville, TN (B.E.-S., A.S.P., K.A., E.F.-E., Q.S.W., J.G.T., J.J.C., R.V.S.).
1 shared publication
Latest Publications
- Open Access
Epigenome-Wide Association Studies of Proteasome Inhibitor-Related Cardiotoxicity in Patients with Multiple Myeloma
Background/Objectives: Carfilzomib (CFZ) and bortezomib (BTZ) are proteasome inhibitors used as the first-line therapy for relapsed or refractory multiple myeloma (MM) but are associated with cardiovascular adverse events (CVAEs). This study aims to identify differentially methylated positions (DMPs) and regions (DMRs), and enriched pathways associated with CVAEs related to CFZ or BTZ-based treatment. Methods: Baseline germline DNA methylation profiles from 79 MM patients (49 on CFZ and 30 on BTZ) in the Prospective Study of Cardiac Events During Proteasome Inhibitor Therapy (PROTECT) were analyzed. Epigenome-wide analyses were performed within each group, followed by meta-analyses to identify signals common to CVAEs associated with both medicines. Results: Four DMPs were significantly associated with CFZ-CVAEs, including cg15144237 within ENSG00000224400 (p = 9.45 × 10−10), cg00927646 within TBX3 (p = 9.78 × 10−8), and cg10965131 within WDR86 (p = 1.00 × 10−7). One DMR was identified in the FAM166B region (p = 5.46 × 10−7). There was no evidence of any DMPs in BTZ-treated patients, however two DMPs and one DMR reached a suggestive level of significance (p < 1.00 × 10−5): cg09666417 in DNAJC18 (p = 3.41 × 10−7) and cg12987761 in USP18 (p = 5.00 × 10−7), and a DMR mapped to the WDR86/WDR86-AS1 region (p = 8.11 × 10−8). Meta-analysis did not find any significant DMPs, with the top CpG being cg17933807 in GNL2 (p = 7.38 × 10−5). Pathway enrichment analyses identified peroxisome, MAPK, Rap1, adherens junction, phospholipase D, autophagy, and aldosterone-related pathways to be implicated in CVAEs. Conclusions: Our study identified distinct DMPs, DMRs, and pathways enrichment associated with CVAE, suggesting epigenetic contributors to CVAEs and supporting the need for larger validation studies.
Open AccessEpigenome-Wide Association Studies of Proteasome Inhibitor-Related Cardiotoxicity in Patients with Multiple Myeloma
Background/Objectives: Carfilzomib (CFZ) and bortezomib (BTZ) are proteasome inhibitors used as the first-line therapy for relapsed or refractory multiple myeloma (MM) but are associated with cardiovascular adverse events (CVAEs). This study aims to identify differentially methylated positions (DMPs) and regions (DMRs), and enriched pathways associated with CVAEs related to CFZ or BTZ-based treatment. Methods: Baseline germline DNA methylation profiles from 79 MM patients (49 on CFZ and 30 on BTZ) in the Prospective Study of Cardiac Events During Proteasome Inhibitor Therapy (PROTECT) were analyzed. Epigenome-wide analyses were performed within each group, followed by meta-analyses to identify signals common to CVAEs associated with both medicines. Results: Four DMPs were significantly associated with CFZ-CVAEs, including cg15144237 within ENSG00000224400 (p = 9.45 × 10−10), cg00927646 within TBX3 (p = 9.78 × 10−8), and cg10965131 within WDR86 (p = 1.00 × 10−7). One DMR was identified in the FAM166B region (p = 5.46 × 10−7). There was no evidence of any DMPs in BTZ-treated patients, however two DMPs and one DMR reached a suggestive level of significance (p < 1.00 × 10−5): cg09666417 in DNAJC18 (p = 3.41 × 10−7) and cg12987761 in USP18 (p = 5.00 × 10−7), and a DMR mapped to the WDR86/WDR86-AS1 region (p = 8.11 × 10−8). Meta-analysis did not find any significant DMPs, with the top CpG being cg17933807 in GNL2 (p = 7.38 × 10−5). Pathway enrichment analyses identified peroxisome, MAPK, Rap1, adherens junction, phospholipase D, autophagy, and aldosterone-related pathways to be implicated in CVAEs. Conclusions: Our study identified distinct DMPs, DMRs, and pathways enrichment associated with CVAE, suggesting epigenetic contributors to CVAEs and supporting the need for larger validation studies.