β-catenin accumulation and S33F mutation of CTNNB1 gene in co lorectal cancer in Saudi Arabia. Polish Journal of Pathology
, 18. Alomar SY, Mansour L, Abuderman A, Alkhuriji A, Arafah M, Alwasel S, Harrath AH, Almutairi M, Trayhyrn P, Dar JA. . 2016
Several risk factors associated with colorectal cancer (CRC) have been identified including β-catenin/CTNNB1 hotspot mutations. The levels of β-catenin within a cell are regulated via phosphorylation of the N terminus of β-catenin by GSK-3β. Thus far three serines (S33, 37, 45) and one threonine (T41) are considered to be the substrates for GSK-3β phosphorylation. In the present investigation an attempt was made to study the role of β-catenin mutations in exon-3 in 60 colorectal cancer patients from Kingdom of Saudi Arabia (KSA). The hot spot mutation region of β-catenin exon 3 was evaluated in matched tumor and normal tissues using PCR and direct sequencing. Sequencing of exon 3 of the CTNNB1 gene revealed an activating mutation (S33F) in one of the tumor samples as compared to the normal tissue from the same patient where there was no such mutation found. Immunohistochemical staining showed the accumulation of β-catenin protein both in cytoplasm and in the nuclei of cancer cells as compared to normal tissue
Frequencies of natural killer (NK) cells from patients with non-small cell lung cancer (NSCLC) or small cell lung cancer (SCLC) did not differ from healthy controls.
CD56+ T cells were studied in samples of peripheral blood from small-cell lung cancer (SCLC) and non-small-cell lung cancer (NSCLC) patients compared with healthy controls.
These experiments were designed to investigate the effects of IL-17 upon the phenotype and function of human Natural Killer (NK) cells.