Table 1 summarizes the baseline characteristics of the 286 enrolled patients in this study. The participants had a mean age of 63.79 years, and 62.15% were male. Tumors were located in the pancreatic head for 165 cases (57.69%) and in the pancreas tail for 121 cases (42.31%). Most tumors progressed locally (183 cases of T4 and T3 tumors, 64.0%), and lymph node metastasis was common (n = 156, 54.5%). The cancer was staged as I in 48 patients (16.67%), II in 48 (16.67%), III in 57 (19.44%), and IV in 135 (47.22%). Pathological differentiation was detailed as follows: 42 cases (14.58%) were poorly differentiated, 104 cases (36.11%) were well differentiated, and 142 cases were moderately differentiated (49.31%). Additionally, 50 (17.36%) of the patients had a positive family history of pancreatic cancer. The baseline prevalence of smoking and drinking was 41.67% (120) and 33.33% (96), respectively. Table 2 presents information on lipid levels, fasting blood glucose, and body mass index (BMI). The lipid profile was distributed as follows: total cholesterol (TC) < 5.7mmol/L(251,87.76%) versus TC ≥ 5.7mmol/L (35, 12.24%); triglycerides (TG) < 1.7 mmol/L (203, 70.98%) versus TG ≥ 1.7mmol/L (83, 29.02%); low-density lipoprotein cholesterol (LDL-C) < 3.37 mmol/L (237,82.87%) versus LDL-C ≥ 3.37mmol/L (49, 17.13%); high-density lipoprotein cholesterol (HDL-C) < 1.15mmol/L (208, 72.73%) versus HDL-C ≥ 1.15mmol/L (78, 27.27%); ApoB/ApoA < 0.85(129, 45.10%) versus ApoB/ApoA ≥ 0.85 (157, 54.90%) .
The median OS for all patients was 19.5 ± 1.6 months, and the 1-year OS rates was 38.9%. The results of this study indicate that patients with higher ApoB/ApoA had an OS rate of 83.44%, compared to 79.07% for patients with lower ApoB/ApoA. Specifically, Kaplan-Meier analysis [Figure 1E] showed that patients with higher ApoB/ApoA (≥ 0.85) have a significantly higher probability of overall survival (OS) (log-rank test = 4.075; P = 0.044) compared to those with lower ApoB/ApoA (< 0.70). Furthermore, in a univariate Cox proportional hazards model of pancreatic cancer (PC) with OS, the T stage, N stage, M stage, CA199, CA125, CEA, and ApoB/ApoA were associated with OS (Table 3). In multivariate regression analyses, T stage (HR: 1.732, 95% CI: 1.339–2.215, P < 0.001), N stage (HR: 1.616, 95% CI: 1.270–2.057, P < 0.001), M stage (HR: 2.745, 95% CI: 1.692–4.454, P < 0.001) and ApoB/ApoA (HR:2.028, 95% CI: 1.174-2.504, P = 0.011) were related with OS (Table 3).
The median PFS for all patients was 11.7 ± 0.99 months, and the 1- year PFS rates was 23.9%. In a univariate Cox proportional hazards model of PC with PFS, the T stage, N stage, M stage, CA125 and ApoB/ApoA associated with the pancreatic cancer PFS (Table 4). In multivariate regression analyses, T stage (HR: 1.554, 95% CI: 1.223–1.975, P < 0.001), N stage (HR: 1.463, 95% CI: 1.169–1.847, P < 0.001), M stage (HR: 3.225, 95% CI: 2.025–5.134, P < 0.001) and ApoB/ApoA (HR:1.800, 95% CI: 1.076-3.009, P = 0.025) were related with PFS (Table 4).
Table 5 summarizes the association between ApoB/ApoA ratio level and clinicopathological characteristics. Notably, a significant correlation was found between ApoB/ApoA ratio level and tumor location (P=0.012). However, no significant relationships were observed between ApoB/ApoA ratio level and age, sex, T stage, TNM stage, differentiation, histological type, BMI, fasting blood sugar, family history, smoking, alcohol consumption, or levels of CA199, CA125, and CEA. These findings are important for understanding the potential role of ApoB/ApoA ratio level as a biomarker for tumor location in this population.