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); 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)
Postdoc Researcher
Research Areas
Biomedical Subjects
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Biography and Research Information
OverviewAI-generated summary
Md. Rafikul Islam is a postdoctoral fellow at the University of Arkansas for Medical Sciences, where his research focuses on the role of Nonsense-mediated mRNA decay (NMD) in cancer progression. He investigates how mutations in RNA sequences and splicing factors influence cancer development through NMD. His work also involves collecting tumor samples from cancer patients to understand the function of NMD in both normal and disease states. This research aims to provide new insights into NMD regulation by mutations and identify potential therapeutic targets for NMD-mediated cancers.
Islam completed his Ph.D. in Cancer Pharmacology at Yokohama City University Graduate School of Medicine in Japan. During his doctoral studies, he evaluated the anticancer effects and mechanisms of novel therapeutic agents using various in vitro and in vivo techniques. His Ph.D. research utilized a B16-FO-Lu mouse melanoma cell-induced tumor model in C57BL wild mice, assessing tumor growth through manual measurement and in vivo imaging systems (IVIS), alongside hematological and immunohistochemical analyses. He also employed nude mice and rabbit tumor models in his Ph.D. work.
His scholarly contributions include a h-index of 15, with a total of 76 publications and 895 citations. Islam has established collaborations with several researchers at the University of Arkansas for Medical Sciences, including Mohammad Alinoor Rahman, Preeti Nagar, Mojnu Miah, and Allen Gies, with whom he shares multiple publications.
Metrics
- h-index: 16
- Publications: 77
- Citations: 924
Selected Publications
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Targeting <i>EZH2</i> 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 <i>EZH2</i> Oncogenic Splicing: Decoding the Regulatory Network and Antisense Correction (2026)
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SRSF6 and SRSF1 coordinately enhance the inclusion of human <i>MUSK</i> 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 <i>MUSK</i> exon 10 to generate a Wnt-sensitive MuSK isoform
- RNA Splicing in Cancer and Targeted Therapies
- Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing
- Targeting <i>EZH2</i> Oncogenic Splicing: Decoding the Regulatory Network and Antisense Correction
Showing 5 of 7 shared publications
- Nonsense-Mediated mRNA Decay as a Mediator of Tumorigenesis
- SRSF6 and SRSF1 coordinately enhance the inclusion of human <i>MUSK</i> exon 10 to generate a Wnt-sensitive MuSK isoform
- RNA Splicing in Cancer and Targeted Therapies
- Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing
- Targeting <i>EZH2</i> 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
- 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
- Alternative magnetic field exposure suppresses tumor growth via metabolic reprogramming
- Abstract 395: An alternating magnetic field suppresses tumor growth
- SRSF6 and SRSF1 coordinately enhance the inclusion of human <i>MUSK</i> exon 10 to generate a Wnt-sensitive MuSK isoform
- Targeting <i>EZH2</i> Oncogenic Splicing: Decoding the Regulatory Network and Antisense Correction
- SRSF6 and SRSF1 coordinately enhance the inclusion of human <i>MUSK</i> exon 10 to generate a Wnt-sensitive MuSK isoform
- Targeting <i>EZH2</i> Oncogenic Splicing: Decoding the Regulatory Network and Antisense Correction
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