Relationship between Chinese medicine dietary patterns and the incidence of breast cancer in Chinese women in Hong Kong: a retrospective cross-sectional survey.

BACKGROUND: This retrospective cross-sectional study aimed to investigate the relationship between Chinese medicine (CM) dietary patterns (hot, neutral, and cold) and the incidence of breast cancer among Chinese women in Hong Kong. METHODS: Breast cancer cases (n = 202) and healthy controls (n = 202) were matched according to demographics. Chinese women residing in Hong Kong for the past 7 years were recruited by media advertisements (e.g., via newspapers, radio, and posters). The control participants were recruited by convenience sampling from health workshops held in clinics and communities of 15 districts of Hong Kong. After completing test-retest reliability, all participants were asked to complete diet pattern questionnaires about their food preferences and dietary patterns. The Student's unpaired t test, Chi square test, and logistic regression were conducted using SPSS software. RESULTS: Three major CM dietary patterns were identified: hot, neutral, and cold. The participants with breast cancer exhibited a stronger preference for hot food than the control group (Chi square test, P < 0.001). A higher frequency of breast cancer was associated with a higher frequency of dining out for breakfast (4-5 times per week, Chi square test, P = 0.015; 6-7 times per week, Chi square test, P < 0.001) and lunch (4-5 times per week, Chi square test, P < 0.001; 6-7 times per week, Chi square test, P = 0.006). The participants with no history of breast cancer consumed CM supplements and Guangdong soups (1-2 times per week, Chi square test, P = 0.05; >3 times per week, Chi square test, P < 0.001) more frequently than those with breast cancer. CONCLUSIONS: Non-breast cancer participants adopted a neutral (healthy and balanced) dietary pattern, and consumed CM supplements and Guangdong soups more frequently.

Suppression of C6 gliomas via application of rat hyperplasia gene.

BACKGROUND: Among all neurological tumors, tumor incidence of the neuroepithelial tissue is the highest, where 50% are gliomas. Treatment for gliomas has traditionally included surgery and adjuvant therapy. With advancements in medicine, gene therapy has entered the clinical setting, in which control of tumor growth, tumor volume and decrease of supply of blood to the tumor have been observed. Rat hyperplasia suppressor gene (rHSG) has been proven to inhibit the injury-mediated proliferation of vascular smooth muscle cells. METHODS: A recombinant adenovirus, Adv-rHSG-GFP, was constructed and characterized by in vitro and in vivo studies. The function of rHSG on cell proliferation was determined in vitro by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) exclusion assay and plate clone formation, while a C6/Sprague Dawley rat glioma model was established to observe the effect of rHSG in vivo. RESULTS: Overexpression of rHSG displayed a strong effect on suppressing C6 cells proliferation in vitro and growth of glioma in vivo, which suggests the use of rHSG as a possible treatment strategy for glioma. p21Cip1, p27Kip1 and proliferating cell nuclear antigen were found to be involved in the tumor suppression mechanism of rHSG. CONCLUSIONS: rHSG can markedly inhibit of the growth of rat glioma cells. The suppression mechanism of rHSG may be related to cell cycle regulation, which shows that rHSG is a potential therapeutic target of glioma tumor. This preclinical study supports a further in-depth study on the effect of rHSG on cell proliferation, migration and change in the extracellular matrix component of glioma cells.

Celecoxib anti-aromatase neoadjuvant (CAAN) trial for locally advanced breast cancer.

OBJECTIVES: To evaluate the efficacy and safety of combing aromatase inhibitor (AI) and cyclooxygenase-2 (COX-2) inhibitor neoadjuvantly in postmenopausal patients with invasive hormone-sensitive breast cancer. METHODS: Eighty-two patients were randomly assigned to receive exemestane 25mg daily and celecoxib 400mg twice daily (group A, n=30), exemestane 25mg daily (group B, n=24) and letrozole 2.5mg daily (group C, n=28). RESULTS: All groups showed clinical responses (58.6% for group A, 54.5% for group B and 62.0% for group C) and decrease in tumor area (61.8% for group A, 58.1% for group B and 55.7% for group C). 3 out of 5 patients with complete clinical response were observed from group A and 2 out of 69 patients operated with pathologic complete response were observed in group C. The mean microscopic tumor size was 2.53 cm for group A, 3.05 cm for group B and 2.10 cm for group C. The differences were only statistically significant when group C was compared with group B (P=0.025). The toxicity profiles among groups were satisfactory. CONCLUSION: AI is effective in treating breast cancer and may be safely used preoperatively. The addition of COX-2 inhibitor may provide additional benefit.

Evaluation of neoadjuvant inhibition of aromatase activity and signal transduction in breast cancer.

PURPOSE: To evaluate the efficacy and safety of combing aromatase inhibitor (AI) and signal transduction inhibitor neoadjuvantly in postmenopausal patients with invasive hormone-sensitive breast cancer. PATIENTS AND METHODS: Postmenopausal women with hormone-sensitive breast cancer were given three months of letrozole 2.5mg daily and imatinib 400mg twice daily preoperatively. End-points of this study included clinical and pathologic responses, toxicities, and change in [(18)F]fluorodeoxyglucose (FDG) uptake in tumor. Expression of c-Kit was also evaluated in breast cancer tissue by immunostaining. RESULTS: Thirteen patients, aged 52--78, were accrued. Five patients (38.5%) experienced grade 3 toxicity including neutropenia, skin rash, dermatitis, hypokalemia, shortness of breath, acute coronary syndrome, and acute chronic gastritis. Three patients were withdrawn after two months of treatment due to hematoma in tumor and toxicity. Of the ten evaluable patients, nine patients (90%) achieved clinical partial response and one patient (10%) had stable disease. One patient (10%) achieved pathologic complete response. Average relative changes of FDG uptake was -69.5% among responders. Eight out of 13 tissue samples were tested for c-Kit expression and the expression was detected in all. CONCLUSIONS: In this pilot study, the dramatic response to this neoadjuvant combination treatment warrants further clinical trials. Further investigation on the involvement of c-Kit pathway in the treatment response is also suggested. However, dosage reduction of imatinib may be required to avoid its potential toxicity.