Adipocytokines are adipocyte-secreted hormones associated with some malignancies such as colorectal, breast, and prostate cancer. We hypothesized that changes in the levels of adipocytokines may indicate the carcinogenesis and progression of colorectal cancer and adenoma, and investigated the association of the blood levels of several adipocytokines through a case-control study. Blood levels of adiponectin, leptin, resistin, visfatin, and C-peptide at diagnosis were measured in 115 colorectal cancer patients and 115 age-, sex-, and body mass index-matched controls. The same analysis was performed in 72 colorectal adenoma patients and 72 controls. Logistic regression models were used for estimating odds ratios and 95% confidence intervals, and one-way ANOVA was performed to determine the prevalence of each variable between two or more groups. Resistin and visfatin levels in cancer patients were significantly higher than those of controls on multivariate analysis (P = 0.03 and P < 0.01, respectively). Stage progression significantly correlated with resistin and visfatin levels (P < 0.01 for both). The adiponectin level in adenoma patients was significantly lower than that of controls on multivariate analysis (P = 0.04). Its level was inversely correlated with the number of adenoma (P = 0.02), but not correlated with the size of adenoma. Resistin and visfatin may be good biomarkers of colorectal malignant potential and stage progression. Adiponectin level may be a good biomarker of colorectal adenoma. (Cancer Sci 2010; 101: 1286-1291 A dipocytokines, such as adiponectin, leptin, resistin, visfatin, tumour necrosis factor (TNF)-a, and interleukin (IL)-6 are cytokines secreted by visceral adipose tissue, and they have recently been suggested to be associated with obesityrelated diseases.(1,2) Many epidemiologic studies have shown a positive correlation between obesity and increased risk of colorectal cancer and adenoma as well as other cancers at various sites (e.g. breast, prostate gland, and endometrium). (3)(4)(5) In obesity mouse models, severe macrophage invasion was observed in the vascular ⁄ stromal compartment of adipose tissue, suggesting that excess adiposity is associated with chronic inflammation.(6,7) Other reports have shown that prostaglandin E2 stimulates leptin secretion from cultured human adipose tissue cells and that cyclooxygenase 2 inhibitors prevent an increase in leptin production.(8) In inflammation-associated colorectal cancers, such as those associated with inflammatory bowel diseases, non-genetic stimuli such as overexpression of IL-6 also enhance the survival and proliferation of preneoplastic cells. (9) Leptin was also reported to induce IL-6 production by Apc Min ⁄ + colon epithelial cells which leads to autocrine ⁄ paracrine trans IL-6 receptor signaling.(10) This results in the promotion and survival proliferation of preneoplastic cells. On the other hand, adiponectin reportedly inhibits inflammation and angiogenesis while leptin induces tumor angiogenesis. (11,12) These findings in e...

Resistin and visfatin may be good biomarkers of gastric cancer.

No abstract

No significant survival benefit was found for CPT-P. Both regimens were well tolerated, but the toxicity profiles differed significantly. Treatment with existing anticancer agents has limitations to improving the prognosis of CCC.

Endoscopic biopsy prior to chemotherapy provides an opportunity for studying biomarkers to predict the overall survival in gastric cancer patients. This prospective study was performed to identify prognostic biomarkers in patients with unresected gastric cancer. Fifty-nine cases of chemotherapy-naive metastatic gastric cancer were enrolled in this study. A microarray analysis was performed using 40 biopsy samples to identify candidate genes whose expressions might be correlated with the overall survival. After adjusting for clinical covariates based on a multivariate analysis, the identified genes were validated using real-time reverse transcription polymerase chain reaction (RT-PCR) analysis in 19 independent validation samples. Ninety-eight candidate genes whose expression levels were significantly correlated with the overall survival were identified using a microarray analysis based on a proportional hazards model (P < 0.005). Multivariate analysis was performed to assess 10 of these genes, and the results yielded a statistical significance level for DACH1 and PDCD6. We further evaluated these two genes in independent samples using real-time RT-PCR and found that lower mRNA expression levels of PDCD6 were correlated significantly with a poor overall survival. We identified PDCD6 as a prognostic biomarker in patients with unresected gastric cancer using endoscopic biopsy samples. O ver the past two decades, various anticancer agents have been examined for their efficacy against gastric cancer, including 5-fluorouracil (5-FU) and 5-FU-based drugs, taxanes, CPT-11 and cisplatin, all administered either as monotherapy or in combination regimens;(1) however, the median survival time (MST) of these patients remains at only approximately 7 months.(2,3) In a recent randomized phase III trial examining oral S-1 monotherapy and cisplatin plus irinotecan combination therapy, the response rates to both S-1 and to the cisplatin plus irinotecan combination therapy were approximately 50%, indicating that around half of the patients did not respond to chemotherapy, (4)(5)(6)(7) and the MST in both the arms was less than 1 year.(8) Thus, the prognosis of patients with gastric cancer remains poor.The commonly recognized prognostic factors in cases of unresectable gastric cancer are the performance status, presence/ absence of liver metastases, presence/absence of peritoneal metastases and the serum levels of alkaline phosphatase.(9) Many molecular biomarkers have been also investigated for their potential to predict the outcome in hypothesis-based studies. Several studies have shown that the mRNA levels and immunohistochemical staining intensity of thymidylate synthase (TS) in gastric cancers treated with fluorouracil are associated with the response and survival; in addition, the excision repair crosscomplementing (ERCC)1 gene expression level has been shown to be associated with the clinical outcome in patients treated with cisplatin.(10,11) HER2 expression has also been reported to be a prognostic marker in cases of differe...

Addition of carboplatin to neoadjuvant chemotherapy in HER2-negative breast cancer may improve pathological complete response (pCR) rates. We evaluated the efficacy and safety of carboplatin and weekly paclitaxel (wPTX) followed by cyclophosphamide, epirubicin, and 5-fluorouracil (CEF) as neoadjuvant chemotherapy for HER2-negative breast cancer. Patients with stage II/IIIA HER2-negative breast cancer were randomly assigned to preoperatively receive CP-CEF (four 3-week cycles of carboplatin [area under the curve 5 mg/mL/min, day 1] and wPTX [80 mg/m(2), day 1, 8, 15] followed by four 3-week cycles of CEF [500/100/500 mg/m(2)] or P-CEF (four cycles of wPTX followed by four cycles of CEF). The primary objective was pCR rate. Of 181 eligible patients, 89 were randomly assigned to the CP-CEF and 92 to the P-CEF. Two patients in each arm refused to receive neoadjuvant chemotherapy. Overall 88 patients in the CP-CEF and 91 patients in the P-CEF were assessable for efficacy and safety. The pCR rate in the CP-CEF was significantly higher than that in the P-CEF (31.8 vs. 17.6 %, one-sided P = 0.01). Among patients with triple-negative breast cancer, the pCR rate in the CP-CEF was significantly higher than that in the P-CEF [61.2 (23/37) vs. 26.3 % (10/38), P = 0.003]. Grade 3-4 neutropenia was observed in the CP-CEF more frequently than in the P-CEF (65.9 vs. 38.5 %). Adding carboplatin to neoadjuvant wPTX followed by CEF for HER2-negative breast cancer improved the pCR rate and exacerbated hematotoxicity.

Resistin may be a biomarker for the progression of SCCE. In addition, the impaired responses to body weight loss of adiponectin and leptin in the patients with SCCE were suggested.

No abstract