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Akram Thabet Nasher

Researcher at Sana'a University

Publications -  11
Citations -  339

Akram Thabet Nasher is an academic researcher from Sana'a University. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 4, co-authored 7 publications receiving 240 citations.

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Inflammatory bacteriome featuring Fusobacterium nucleatum and Pseudomonas aeruginosa identified in association with oral squamous cell carcinoma.

TL;DR: Functional prediction showed that genes involved in bacterial mobility, flagellar assembly, bacterial chemotaxis and LPS synthesis were enriched in the tumors while those responsible for DNA repair and combination, purine metabolism, phenylalanine, tyrosine and tryptophan biosynthesis, ribosome biogenesis and glycolysis/gluconeogenesis were significantly associated with the controls.
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Robust species taxonomy assignment algorithm for 16S rRNA NGS reads: application to oral carcinoma samples.

TL;DR: A robust algorithm for species-level classification of NGS reads from oral samples is developed and pilot test it for profiling bacteria within OSCC tissues, ensuring reliable classification by giving priority to the human, oral reference set.
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Exome sequencing of oral squamous cell carcinoma in users of Arabian snuff reveals novel candidates for driver genes.

TL;DR: There was a trend for higher number of mutations, amplifications and driver events in samples with history of shammah exposure particularly those that tested EBV positive, suggesting an interaction between tobacco exposure and EBV.
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Viral infection and oral habits as risk factors for oral squamous cell carcinoma in Yemen: a case-control study.

TL;DR: Shammh use is a major risk factor for oral cancer in Yemen and the association of shammah use alone with OSCC exceeded that of shamsah use in combination with qat chewing, smoking, or both.
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Possible interaction between tobacco use and EBV in oral squamous cell carcinoma

TL;DR: The EBV latent membrane protein 1 (LMP1), an active transmembrane receptor, appears to mediate malignant transformation by activating the nuclear-factor-kappa B (NF-ᴋB), c-Jun N-terminal kinase (JNK) and phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathways as mentioned in this paper.