Survival in Limited Disease Small Cell Lung Cancer According to N3 Lymph Node Involvement.

BACKGROUND/AIM: There are several definitions of limited disease (LD) in small cell lung cancer (SCLC), differing with respect to N3 disease accepted. We analyzed patients from a randomized trial comparing two schedules of thoracic radiotherapy (TRT) in LD SCLC to investigate whether there were survival differences between N3 subcategories (n=144). PATIENTS AND METHODS: Patients with a baseline CT scan available were analysed. Patients received four courses of cisplatin/etoposide and TRT of 45 Gy/30 fractions (twice daily) or 42 Gy/15 fractions (once daily). RESULTS: Median overall survival (OS) was 23.3 months in the whole cohort. N3-patients (n=37) had shorter survival than those with N0-2 (16.7 vs. 33.0 months; p<0.001). There were no significant OS-differences between the N3 subcategories, but patients with metastases to two or more N3 regions had shorter survival than other N3 patients (13.4 vs. 19.9 months; p=0.011). CONCLUSION: There were no survival differences between the N3 subcategories, suggesting that all N3 disease should be considered as LD.

DHA alters expression of target proteins of cancer therapy in chemotherapy resistant SW620 colon cancer cells.

Diets rich in n-3 polyunsaturated fatty acids (PUFAs) have been associated with a reduced risk of several types of cancer. Recent reports have suggested that these PUFAs enhance the cytotoxic effect of cancer chemoradiotherapy. The effect of docosahexaenoic acid (DHA) on key cell cycle regulators and target proteins of cancer therapy was investigated in the human malign colon cancer cell line SW620. Cell cycle check point proteins such as p21 and stratifin (14-3-3 sigma) increased at mRNA and protein level, whereas cell cycle progression proteins such as cell division cycle 25 homolog and cyclin-dependent kinase 1 decreased after DHA treatment. Protein levels of inhibitors of apoptosis family members associated with chemotherapy resistance and cancer malignancy, survivin and livin, decreased after the same treatment: likewise the expression of NF-kappaB. Levels of the proapoptotic proteins phosphorylated p38 MAPK and growth arrest-inducible and DNA damage-inducible gene 153/C/EBP-homologous protein (CHOP) increased. The results indicate that DHA treatment causes simultaneous cell cycle arrest in both the G1 and G2 phase. In conclusion, DHA affects several target proteins of chemotherapy in a favorable way. This may explain the observed enhanced chemosensitivity in cancer cells supplemented with n-3 PUFAs and encourage further studies investigating the role of n-3 PUFAs as adjuvant to chemotherapy and radiotherapy in vivo.