[omega-3 Fatty acid-containing diet (Racol) reduces toxicity of chemoradiation therapy for patients with esophageal cancer].

Recently, it is reported that a omega-3 fatty acid-containing diet (Racol) enhances innate immunity and reduces mucosal damage in the small intestine during chemotherapy. The aim of this study is to examine the effects of a omega-3 fatty acid-containing diet (Racol) on the toxicity of chemoradiation therapy (CRT) for patients with esophageal cancers. Toxicity of CRT was evaluated in 10 patients who took Rakol at a maximum dose of 600 mL/day during CRT, compared with 10 patients who did not take Rakol. Regarding blood toxicity, the decrease of platelets did not differ between the former and the latter. However, the incidence of grade 2~4 neutropenia was lower in the former than in the latter (p=0.0043). With regard to gastrointestinal toxicity, the incidence of grade 2~4 diarrhea was also lower in the former than in the latter (p=0.0118). Moreover, the incidence of grade 2~4 stomatitis/pharyngitis tended to decrease in patients who took Rakol compared with those who did not (p=0.0812). The current results indicated that a omega-3 fatty acid-containing diet (Racol) may be beneficial to patients with esophageal cancers who receive CRT by reducing CRT toxicity.

Per2 gene expressions in the suprachiasmatic nucleus and liver differentially respond to nutrition factors in rats.

BACKGROUND: We previously reported that parenteral nutrition (PN) altered the circadian rhythm of clock gene expression in the suprachiasmatic nucleus (SCN) and liver of rats. The present study was designed to investigate what factor(s) in the PN solution causes the alteration. METHODS: Male Wistar rats, kept under light and dark conditions, were divided into 4 groups after cannulation. The sham operation group received saline solution from 8 am to 8 pm at the rate of 36 mL/kg/12 hours. The glucose, amino acid, and saline groups received a glucose solution (20% wt/vol glucose, 261 kcal/kg/d, Na(+) 50 meq/L and Cl(-) 50 meq/L), an amino acid solution (4.3% wt/vol 1.78 gN/kg/d, Na +50 meq/L and Cl(-) 50 meq/L) and a saline solution from 8 am to 8 pm at a rate of 240 mL/kg/12 hours, respectively. Rats were killed every 4 hours (9 am = Zeitgeber Time (ZT) 02, 1 pm = ZT06, 5 pm = ZT10, 9 pm = ZT14, 1 am = ZT18, 5 am = ZT22, n = 3 at each point), and brain and liver samples were removed. rPer2 expression in the SCN and liver was analyzed by in situ hybridization and Northern blotting, respectively. RESULTS: Compared with the sham-operation rats, the peak time of rPer2 expression in the SCN was significantly affected by glucose, amino acid, and saline solutions. Among them, glucose-group rats showed the rPer2 expression most similar to that of diurnal PN. On the other hand, the rPer2 expression in the liver was shifted in the glucose and amino-acid-solution groups. The pattern of rPer2 expressions in the amino acid group was most similar to that of the diurnal PN group. CONCLUSIONS: These results indicate that the most potent entrainer for the SCN clock is glucose, whereas that for the liver is amino acid.

Reduced MLH1 expression after chemotherapy is an indicator for poor prognosis in esophageal cancers.

PURPOSE: Loss of function or expression of the mismatch repair gene MLH1 has been implicated in experimentally acquired resistance to cisplatin (CDDP) and other anticancer agents. The clinical significance of MLH1 expression was evaluated in advanced thoracic squamous cell carcinoma of the esophagus (ESCC) treated by neoadjuvant chemotherapy. EXPERIMENTAL DESIGN: We investigated MLH1 and P53 expression by immunohistochemistry in the surgical specimens of 107 patients who had undergone preoperative chemotherapy using CDDP along with 5-FU and ADM. These findings were correlated with the clinical outcome for this treatment. Biopsy samples before chemotherapy in 20 of these patients, and another 43 surgical specimens without chemotherapy, were also examined as control samples. RESULTS: In surgical specimens of ESCC, low MLH1 expression was not frequent without chemotherapy, whereas it was commonly observed after chemotherapy (14 versus 37%, P = 0.0057). Comparison between samples before and after chemotherapy revealed that MLH1 expression was unchanged during chemotherapy in 12 of 20 patients (60%) but was from high to low in 8 of 20 patients (40%). In the surgical specimen after neoadjuvant chemotherapy, MLH1 expression was not correlated with any clinicopathological factors, including the response to chemotherapy. However, low MLH1 showed poorer prognosis than high MLH1 (5-year survival 40.6 versus 19.3%, P = 0.0393), and in multivariate analysis, MLH1 was an independent prognostic factor for this multimodal treatment, following lymph node metastasis and clinical response to chemotherapy. Positive p53 expression, which was not affected by chemotherapy, was weakly associated with a poor response and clinical outcome, although this trend was not significant. CONCLUSIONS: In advanced ESCC, expression of MLH1 is reduced during CDDP-based chemotherapy, and this may partly account for poor postoperative survival.