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Mohammad Burhan Uddin

Researcher at University of Louisiana at Monroe

Publications -  21
Citations -  403

Mohammad Burhan Uddin is an academic researcher from University of Louisiana at Monroe. The author has contributed to research in topics: Medicine & Biology. The author has an hindex of 7, co-authored 15 publications receiving 212 citations. Previous affiliations of Mohammad Burhan Uddin include Primeasia University & Case Western Reserve University.

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Role and Therapeutic Targeting of the PI3K/Akt/mTOR Signaling Pathway in Skin Cancer: A Review of Current Status and Future Trends on Natural and Synthetic Agents Therapy.

TL;DR: This review summarizes recent advances in the roles of PI3K/Akt/mTOR and their targets in the development and progression of a broad spectrum of cutaneous cancers and discusses the current progress in preclinical and clinical studies for the development of PI-Akt-based targeted therapies with nutraceuticals and synthetic small molecule inhibitors.
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An N6-methyladenosine at the transited codon 273 of p53 pre-mRNA promotes the expression of R273H mutant protein and drug resistance of cancer cells.

TL;DR: A novel function of pre‐mRNA m6A is uncovered as a determinant of mutant protein expression in cancer cells heterozygously carrying the TP53 R273H mutation, thus sensitizing cells carrying R 273H to anticancer drugs.
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The m 6 A RNA methylation regulates oncogenic signaling pathways driving cell malignant transformation and carcinogenesis

TL;DR: The m6A RNA methylation is the most prevalent internal modification in mammalian mRNAs which plays critical biological roles by regulating vital cellular processes Dysregulations due to aberrant expression of its regulatory proteins are frequently observed in many pathological conditions, particularly in cancer Normal cells undergo malignant transformation via activation or modulation of different oncogenic signaling pathways through complex mechanisms as discussed by the authors.
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Inhibition of glucosylceramide synthase eliminates the oncogenic function of p53 R273H mutant in the epithelial-mesenchymal transition and induced pluripotency of colon cancer cells.

TL;DR: It is demonstrated that p53-R273H promotes EMT and induced pluripotency of CSCs in cancer cells exposed to doxorubicin, mainly through Zeb1 and β-catenin transcription factors and indicates that restoration of p53 through inhibition of ceramide glycosylation might be an effective treatment approach for targeting cancers heterozygously harboring TP53 missense mutations.
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Dysregulations of Functional RNA Modifications in Cancer, Cancer Stemness and Cancer Therapeutics.

TL;DR: It is concluded that, while advanced technologies have uncovered the contributions of many of RNA modifications in cancer, the underlying mechanisms are still poorly understood and further studies are needed to elucidate the mechanism of how RNA modifications promote cell malignant transformation and generation of cancer stem cells, which will lead to the development of new strategies for cancer prevention and treatment.