[A phase I study of subcutaneous envafolimab (KN035) monotherapy in Chinese patients with advanced solid tumors].

Objective: To evaluate the safety and antitumor activity of envafolimab monotherapy in Chinese patients with advanced solid tumors. Methods: This open-label, multicenter phase I trial included dose escalation and dose expansion phases. In the dose escalation phase, patients received subcutaneous 0.1, 0.3, 1.0, 2.5, 5.0 or 10.0 mg/kg envafolimab once weekly (QW) following a modified "3+ 3" design. The dose expansion phase was performed in the 2.5 mg/kg and 5.0 mg/kg (QW) dose cohorts. Results: At November 25, 2019, a total of 287 patients received envafolimab treatment. During the dose escalation phase, no dose-limiting toxicities (DLT) was observed. In all dose cohorts, drug-related treatment-emergent adverse events (TEAEs) for all grades occurred in 75.3% of patients, and grade 3 or 4 occurred in 20.6% of patients. The incidence of immune-related adverse reactions (irAE) was 24.0% for all grades, the most common irAEs (≥2%) included hypothyroidism, hyperthyroidism, immune-associated hepatitis and rash. The incidence of injection site reactions was low (3.8%), all of which were grades 1-2. Among the 216 efficacy evaluable patients, the objective response rate (ORR) and disease control rate (DCR) were 11.6% and 43.1%, respectively. Median duration of response was 49.1 weeks (95% CI: 24.0, 49.3). Pharmacokinetic (PK) exposure to envafolimab is proportional to dose and median time to maximum plasma concentration is 72-120 hours based on the PK results from the dose escalation phase of the study. Conclusion: Subcutaneous envafolimab has a favorable safety and promising preliminary anti-tumor activity in Chinese patients with advanced solid tumors.

[Carcinoembryonic antigen and immunoglobin in gastric juice in the diagnosis of gastric cancer].

Levels of carcinoembryonic antigen (CEA) and immunoglobin (Ig) in gastric juice of 93 patients with benign and malignant gastric diseases were assayed. The CEA level in gastric cancer patients (55.73 +/- 38.26 ng/ml) was obviously higher than that in peptic ulcer (15.51 +/- 12.09 ng/ml) and superficial gastritis (26.96 +/- 20.17 ng/ml). But no significant difference was found between the CEA levels of gastric cancer and chronic atrophic gastritis (48.66 +/- 31.87 ng/ml). Also, elevated CEA was closely correlated to intestinal metaplasia. The positive rate of Ig was significantly higher in gastric cancer (IgG greater than or equal to 185 ug/ml, IgA greater than or equal to 100 ug/ml) than in benign gastric diseases. Although no correlation is present in the CEA and Ig in gastric juice, the combination of these two methods could improve the diagnostic accuracy. We believe that the two assays are worthy for screening gastric cancer from patients with high risk, and for identifying precancerous lesions.