Furthermore, to evaluate the potential of negative lamin A/C expression (negative vs. positive) as an independent predictor for overall survival of GC, multivariate Cox regression analyses were performed. While tumour invasion failed to demonstrate independency, only status of metastasis and negative lamin A/C expression may play a role to predict the overall survival in GC (p = 0.040 and p = 0.041, respectively; Table 3). Table 3 The overall survival univariate and multivariate Cox regression analysis Clinicopathological Variable Relative Risk (95% CI) p -Value Univariate Gender 0.948 (0.549–1.637) 0.038 Tumour Size 1.621 (0.974–2.697)
0.063 Metastasis Selleckchem VS-4718 Protein Tyrosine Kinase inhibitor 2.057 (1.110–3.810) 0.022a Invasion 2.012 (1.098–3.698) 0.024a Stage 0.915 (0.709–1.181) 0.497 Histological Differentiation 1.704 (0.969–2.997) 0.064 Lamin A/C 0.582 (0.349–0.969) 0.038a Multivariate Metastasis 1.905 (1.029–3.526) 0.040a Lamin A/C 0.585 (0.350–0.978) 0.041a Abbreviation: 95% CI, 95% confidence interval. a Statistically significant (p < 0.05).
Figure 5 Estimated overall survival according to the expression of lamin A/C in 126 cases of GCs (the Kaplan – Meier method). Based on the results of immunohistochemical staining, the expression of lamin A/C was classified as the negative expression (n = 56) and the positive (n = 70). Log-rank test shows that GC patients with the negative lamin A/C expression
showed significantly poorer prognosis than those with the positive expression. Discussion A-type lamins are essential components of the nuclear lamina . Aside from their structural role in the OICR-9429 datasheet formation of the nuclear lamina, buy Atezolizumab lamins A and C are found in the nucleoplasm adjacent to sites of DNA synthesis and RNA processing, suggesting that these proteins could influence both DNA replication and gene expression [2–4]. The A-type lamins, lamins A and C, are synthesized from alternatively spliced transcripts of lamin A gene (LMNA) [9, 10]. A-type lamins are absent in early embryonic development and in certain stem cell populations in adults [11–13] and are expressed only after commitment of cells to a particular differentiation pathway [12, 14]. Mutations in LMNA produce an intriguingly diverse spectrum of diseases including muscular dystrophies (Emery-Dreifuss muscular dystrophy, limb-girdle muscular dystrophy type 1B), neuropathy (Charcot-Marie-Tooth disease type 2), dilated cardiomyopathy with conduction system disease, familial partial lipodystrophy (s.c. fat loss and diabetes), mandibuloacral dysplasia (skeletal malformations and lipodystrophy), atypical Werner’s syndrome, and Hutchinson-Gilford progeria syndrome(precocious aging syndromes) [15–19]. To date, some 200 mutations have been identified in LMNA.