Vascular epidermis growth factor as a surrogate to evaluate the therapeutic efficacy of pancreatic cancer treated by gamma rays / 中华胰腺病杂志

Objective To analyze the relationship between the change of serum vascular epidermis growth factor(VEGF) level and curative effect of pancreatic cancer treated by gamma rays, and evaluate it clinical significance. Methods The serum VEGF level of thirty patients with pancreatic cancer treated by gamma rays were determined before and one month after treatment. The relationship between curative effect,survival, life quality and the serum VEGF level was analyzed. Results The serum VEGF level of 30 cases before treatment was (624.1 ± 144.3) pg/ml, whereas one month after treatment it was (279.3 ± 83.4) pg/ml(P ＜0.01 ). In the 19 patient whose serum VEGF level decreased by more than 50%, CR + PR was gained in 18 patients, improved quality of life in 7 patients, and in the 11 patient whose serum VEGF level decreased by less than 50%, CR + PR in 7 patients, improved quality of life in 1 patient( P = 0.012, P = 0. 028). In 24patients who completed 2 years follow-up, 11 of 15 patients whose serum VEGF level decreased by more than 50% survived more than 1 year, which was higher than that of the patients whose serum VEGF level decreased by less than 50%. Conclusions The serum VEGF level decreased significantly after gamma rays treatment and the extent of decrease could be used as a surrogate to evaluate the therapeutic efficacy.

The effect of folic acid on the development of stomach and other gastrointestinal cancers / 中华医学杂志(英文版)

<p><b>OBJECTIVE</b>To evaluate the roles of folic acid and beta-carotene in the chemoprevention of gastric and other gastrointestinal (GI) cancers.</p><p><b>METHODS</b>In a randomized, double-blind, placebo-controlled trial, a total of 216 patients with atrophic gastritis were randomly assigned to one of the four groups: (1) folate (FA, 20 mg per day plus vitamin B(12) 1 mg, intramuscularly, per month for one year, then 20 mg two times a week plus 1 mg per three months for the next year); (2) natural beta-carotene (N-betaC, 30 mg per day for first year, then 30 mg two times a week for the next); (3) synthetic beta-carotene (S-betaC, administered as in N-betaC); and (4) placebo. Follow-ups continued from 1994 to 2001.</p><p><b>RESULTS</b>A total of 7 new cases of gastrointestinal cancers were diagnosed with 3 stomach, 1 colon and 1 esophageal cancers occurring in the placebo group; 1 stomach cancer in both of the N-betaC and S-betaC groups, and no cancer occurring in FA group. In terms of GI cancers, there was a significant reduction in the FA group, compared with the placebo group (P = 0.04). A similar trend was observed in both N-betaC and S-betaC groups (P = 0.07 - 0.08). Taken together, the three intervention groups displayed a highly significant decrease in occurrence (P = 0.004, vs placebo), and a lower risk for GI cancers (OR = 0.12; 95% confidence interval, 0.03 - 0.51). For development of gastric cancer, any one of the three active-treated groups did not reach statistically significant reduction. The FA group showed obvious improvement of the gastric mucosal lesions with more patients displaying lesions reversed or stable atrophy and inflammation (P = 0.04), reversed intestinal metaplasia (P = 0.06) at the end of follow-up, and reversed displasia (P = 0.017) at 12 months. Two cases of false jaundice were found in beta-carotene groups with no influence on administration, and no side-effects were reported in FA group.</p><p><b>CONCLUSIONS</b>This trial revealed the interventional effect of folic acid on the development of GI cancers, a similar effect of beta-carotene was also detected. Also, folic acid may be of use to treat atrophic gastritis by preventing or reversing the precancerous lesions.</p>

Effects of endostatin transfected bifidobacterium on experimental liver cancer / 中华消化杂志

0.05), respectively. Conclusions Above data indicated that the ETB 2 could significantly restrain the development of mice liver cancer, and the effects depended on the time of administration. The mechanism may be due to its' effects of antiangiogensis, increasing necrosis and decreasing proliferation. Bifidobacterium has no significant antitumor function but could improve the immune function. Bifidobacterium may cooperate with endostatin in antitumor process.