Somatostatin receptor type 5 (SSTR5) P335L is a hypofunctional, single nucleotide polymorphism of SSTR5 with implications in the diagnostics and therapy of pancreatic neuroendocrine neoplasms.
For the British population we found association to B</span>PAD with missense mutation Leu48Met (P = 0.003) and missense mutation Pro335Leu (P = 0.004).
These data suggest that SSTR5 P335L is a hypofunctional protein with a potentially harmful effect on function, as well as potential latent effect, and therefore it could affect the clinical response to somatostatin analog therapy for patients with pancreatic cancer.
For the British population we found association to B</span>PAD with missense mutation Leu48Met (P = 0.003) and missense mutation Pro335Leu (P = 0.004).
For the British population we found association to B</span>PAD with missense mutation Leu48Met (P = 0.003) and missense mutation Pro335Leu (P = 0.004).
For the British population we found association to B</span>PAD with missense mutation Leu48Met (P = 0.003) and missense mutation Pro335Leu (P = 0.004).
These data suggest that SSTR5 P335L is a hypofunctional protein with a potentially harmful effect on function, as well as potential latent effect, and therefore it could affect the clinical response to somatostatin analog therapy for patients with pancreatic cancer.
For the British population we found association to B</span>PAD with missense mutation Leu48Met (P = 0.003) and missense mutation Pro335Leu (P = 0.004).
After adjusting for multiple testing, the SNP-prostate cancer associations did not differ by intakes of protein, although two interactions by intake of plant protein were of marginal statistical significance [SSTR5 (somatostatin receptor 5)-rs197056 (uncorrected p for interaction, 0.001); SSTR5-rs197057 (uncorrected p for interaction, 0.002)].
After adjusting for multiple testing, the SNP-prostate cancer associations did not differ by intakes of protein, although two interactions by intake of plant protein were of marginal statistical significance [SSTR5 (somatostatin receptor 5)-rs197056 (uncorrected p for interaction, 0.001); SSTR5-rs197057 (uncorrected p for interaction, 0.002)].
The allele frequencies were significantly (P<0.01) different between the acromegaly patients and the additional large control group. rs34037914 and rs642249 remained significantly associated with acromegaly after Bonferroni correction and permutation tests (odds ratio (OR)=3.38; 95% confidence interval (CI), 1.78-6.42; P=0.00016 and OR=2.41; 95% CI, 1.41-4.13; P=0.0014 respectively).
For the British population we found association to BPAD with missense mutation Leu48Met</span> (P = 0.003) and missense mutation Pro335Leu (P = 0.004).
For the British population we found association to BPAD with missense mutation Leu48Met</span> (P = 0.003) and missense mutation Pro335Leu (P = 0.004).
Analysis of the entire SSTR5 gene disclosed the variant c.142C>A (p.L48M, rs4988483) in the heterozygous state in both blood and tumor, while no pathogenic mutations were noted in the MEN1, AIP, p27Kip1 and SSTR2 genes.
Our results suggest that genetic variation in the SSTR5 gene and, particularly, the rs4988483 single nucleotide polymorphism influence circulating IGFI and IGFBP3 hormone levels with no measurable effect on prostate cancer risk.