Md. Rafikul Islam
Postdoctoral Fellow
Also affiliated: American International University-Bangladesh (2016–2018); Kyushu University (2025); International Islamic University Chittagong (2011–2021); Bangladesh Agricultural University (2020); German Institute of Food Technologies (2021); Eastern Medical College and Hospital (2014); Cardiovascular Institute Hospital (2018–2021); Noakhali Science and Technology University (2024); University of Florida (2016); Southeast University (2014); Winthrop Rockefeller Foundation (2023–2024); Dhaka University of Engineering & Technology (2022–2025); Shaheed Suhrawardy Medical College (2019); Jahangirnagar University (2024); BRAC University (2014); Islamic University of Technology (2024–2025); University of Chittagong (1997–2015); Yokohama City University (2018–2021); University of Rajshahi (2011–2016)
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Md. Rafikul Islam's current research focuses on investigating how mutations in RNA sequences and RNA splicing factors contribute to cancer progression through Nonsense-mediated mRNA decay (NMD). This work aims to identify potential therapeutic targets by examining the role of NMD in both normal biological processes and pathological conditions, including the collection of tumor samples from cancer patients.
His doctoral research involved evaluating the anticancer effects and mechanisms of novel therapeutic agents using in vitro and in vivo models. These studies utilized techniques such as in vivo imaging, hematological analysis, and immunohistochemical analysis in various animal models, including B16-FO-Lu mouse melanoma and nude mice, to assess tumor growth and treatment efficacy. Islam has published 77 papers with 925 citations and an h-index of 16.
Islam collaborates with researchers at the University of Arkansas for Medical Sciences, including Mohammad Alinoor Rahman (8 shared publications), Preeti Nagar (6 shared publications), Mojnu Miah (2 shared publications), and Allen Gies (2 shared publications).
Metrics
- h-index: 16
- Publications: 77
- Citations: 925
Positions
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Postdoctoral Fellow 2022–presentUniversity of Arkansas for Medical Sciences Bichemistry and Molecular Biology ORCID
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Assistant professor 2022International Islamic University Chittagong Department of Pharmacy ORCID
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Lecturer 2010–2013International Islamic University Chittagong Department of Pharmacy ORCID
Selected Publications
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Targeting EZH2 oncogenic splicing: decoding the regulatory network and antisense correction (2026)
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CRISPR-mediated Correction of Oncogenic AS-NMD in Splicing Factor Mutant Cancer (2026)
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Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation (2026)
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Mitochondrial antioxidant enzyme (SOD2) at the crossroads of redox signaling and cancer progression (2026)
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SUMOylation Protects Endothelial Cell-Expressed Leukocyte-Specific Protein 1 from Ubiquitination-Mediated Proteasomal Degradation and Facilitates Its Nuclear Export (2026)
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Targeting EZH2 Oncogenic Splicing: Decoding the Regulatory Network and Antisense Correction (2026)
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SRSF6 and SRSF1 coordinately enhance the inclusion of human MUSK exon 10 to generate a Wnt-sensitive MuSK isoform (2025)
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Alternative magnetic field exposure suppresses tumor growth via metabolic reprogramming (2024)
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Abstract 395: An alternating magnetic field suppresses tumor growth (2024)
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Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing (2024)
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RNA Splicing in Cancer and Targeted Therapies (2023)
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Nonsense-Mediated mRNA Decay as a Mediator of Tumorigenesis (2023)
Collaboration Network
Top Collaborators
- Nonsense-Mediated mRNA Decay as a Mediator of Tumorigenesis
- SRSF6 and SRSF1 coordinately enhance the inclusion of human MUSK exon 10 to generate a Wnt-sensitive MuSK isoform
- RNA Splicing in Cancer and Targeted Therapies
- Targeting EZH2 Oncogenic Splicing: Decoding the Regulatory Network and Antisense Correction
- Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing
Showing 5 of 7 shared publications
- Nonsense-Mediated mRNA Decay as a Mediator of Tumorigenesis
- SRSF6 and SRSF1 coordinately enhance the inclusion of human MUSK exon 10 to generate a Wnt-sensitive MuSK isoform
- Mitochondrial antioxidant enzyme (SOD2) at the crossroads of redox signaling and cancer progression
- RNA Splicing in Cancer and Targeted Therapies
- Targeting EZH2 Oncogenic Splicing: Decoding the Regulatory Network and Antisense Correction
Showing 5 of 7 shared publications
- SRSF6 and SRSF1 coordinately enhance the inclusion of human MUSK exon 10 to generate a Wnt-sensitive MuSK isoform
- Targeting EZH2 Oncogenic Splicing: Decoding the Regulatory Network and Antisense Correction
- CRISPR-mediated Correction of Oncogenic AS-NMD in Splicing Factor Mutant Cancer
- Targeting EZH2 oncogenic splicing: decoding the regulatory network and antisense correction
- Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
- Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
- Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
- Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
- Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
- Alternative magnetic field exposure suppresses tumor growth via metabolic reprogramming
- Abstract 395: An alternating magnetic field suppresses tumor growth
- Alternative magnetic field exposure suppresses tumor growth via metabolic reprogramming
- Abstract 395: An alternating magnetic field suppresses tumor growth
- Alternative magnetic field exposure suppresses tumor growth via metabolic reprogramming
- Abstract 395: An alternating magnetic field suppresses tumor growth
- Alternative magnetic field exposure suppresses tumor growth via metabolic reprogramming
- Abstract 395: An alternating magnetic field suppresses tumor growth
- Alternative magnetic field exposure suppresses tumor growth via metabolic reprogramming
- Abstract 395: An alternating magnetic field suppresses tumor growth
- Alternative magnetic field exposure suppresses tumor growth via metabolic reprogramming
- Abstract 395: An alternating magnetic field suppresses tumor growth
- Alternative magnetic field exposure suppresses tumor growth via metabolic reprogramming
- Abstract 395: An alternating magnetic field suppresses tumor growth
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