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- Karapanagioti, A., et al.
(författare)
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Aberrant expression pattern of circadian clock genes in type 1 gastric neuroendocrine neoplasms compared to ECL-cell hyperplasia
- 2021
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Ingår i: Journal of neuroendocrinology (Print). - : European Neuroendocrine Association. - 0953-8194 .- 1365-2826. ; 33:S1, s. 37-37
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Introduction: There is a continuity of changes from ECL-cell hyperplasia to type 1 gastric neuroendocrine neoplasms (GNEN1) development with important clinical implications. Aim(s): Although the effect of the circadian clock system on neuroendocrine tumorigenesis has been addressed, the role of the peripheral clock system in the transition from ECL-cell hyperplasia to GNEN1 remains to be explored.Materials and methods: Six GNEN1 patients and 10 patients with ECL-cell hyperplasia were included. Blood samples were collected at 8 am, 3pm and 10pm for peripheral blood mononuclear ells (PBMCs) isolation. The mRNA expression of clock-related genes (CLOCK, BMAL1, CRY-1, PER2, ROR-α and REV-ERBβ) were evaluated by real-time quantitative PCR from PBMCs. Results: In GNEN1 patients, BMAL genes where lower expressed at night than early in the morning (p=0.02), whereas patients with ECL-cell hyperplasia expressed lower levels of PER2 and REV-ERBβ (p=0.03 and p=0.05,respectively). In addition, GNEN1 patients expressed lower levels of CLOCK, PER2 and REV-ERBβ in the early evening than in the morning (p=0.04; p=0.03; p=0.05, respectively). When comparing the two groups (GNEN1 vs. ECL-cell hyperplasia) at the three different time points, a marginal increase in CLOCK, PER2 and REV-ERBβ expression early in the morning (p=0.06, 0.02 and 0.07, respectively) along with a marginal increase in REV-ERBβ and BMAL expression in the early evening (p=0.09 and p=0.08, respectively) and a marginal increase in BMAL at night (p=0.09) in GNEN1 patients was observed.Conclusion: Our findings point towards an upregulated expression of clock-related genes in patients with GNEN1 as compared to ECL-cell hyperplasia, suggesting a possible involvement in GNEN1 tumorigenesis that needs to be confirmed in a larger patients group.
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