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    Prognostic Significance of Preoperative Bowel Obstruction in Stage III Colorectal Cancer.

    Ann Surg Oncol. 2011 Mar 3;

    Authors: Katoh H, Yamashita K, Wang G, Sato T, Nakamura T, Watanabe M

    BACKGROUND: Previous studies have suggested a detrimental prognostic effect of preoperative obstruction proximal to colorectal cancer (CRC). If such a detrimental effect is preserved in each stage of advanced (stage II or III) CRC, we can identify high-risk patients. METHODS: We enrolled 641 patients with pathologically confirmed advanced CRC (stage II, n = 207; stage III, n = 434) who had undergone curative resection of the primary lesion. The association of preoperative obstruction with clinicopathologic parameters was evaluated. Kaplan-Meier analysis and Cox proportional hazard models were used to estimate the effect of preoperative obstruction on disease-free survival in each stage. RESULTS: Preoperative obstruction was seen in 63 patients (9.8%) (stage II, n = 16; stage III, n = 47). Multivariable analysis showed that preoperative obstruction was significantly associated with preoperative elevation of carcinoembryonic antigen level in patients with colon cancer (odds ratio = 3.59; P < 0.001), while it was correlated with poor differentiation in patients with rectal cancer (odds ratio = 3.99; P = 0.016). Preoperative obstruction was a significant prognostic factor in stage III CRC (P < 0.001), but not in stage II disease. Multivariable prognostic analysis showed that preoperative obstruction was a remnant independent prognostic factor in stage III CRC. This finding was confirmed by separate analyses of colon and rectal cancer. Preoperative obstruction was associated with systemic recurrence (P = 0.003) rather than peritoneal or local recurrence. CONCLUSIONS: These findings suggest that preoperative obstruction may predict worse long-term prognosis in patients with stage III CRC and may be a potential clinical marker to identify patients with high-risk stage III CRC.

    PMID: 21369738 [PubMed - as supplied by publisher]

    www.ncbi.nlm.nih.gov


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    BACKGROUND:The effect of body mass index (BMI) on treatment outcomes for patients with locally advanced cervical carcinoma who receive definitive chemoradiation is unclear.METHODS:The cohort in this study included all patients with cervical carcinoma (n = 404) who had stage IB1 disease and positive lymph nodes or stage ?IB2 disease and received treatment at the authors' facility between January 1998 and January 2008. The mean follow-up was 47.2 months. BMI was calculated using the National Institute of Health online calculator. BMI categories were created according to the World Health Organization classification system. Primary outcomes were overall survival, disease-free survival, and complication rate. Univariate and multivariate analyses were performed. Kaplan-Meier survival curves were generated and compared using Cox proportional hazard models.RESULTS:On multivariate analysis, compared with normal weight (BMI 18.5-24.9 kg/m2), a BMI <18.5 kg/m2 was associated with decreased overall survival (hazard ratio, 2.37; 95% confidence interval, 1.28-4.38; P < .01). The 5-year overall survival rate was 33%, 60%, and 68% for a of BMI <18.5 kg/m2, a BMI from 18.5 kg/m2 to 24.9 kg/m2, and a BMI >24.9 kg/m2, respectively. A BMI <18.5 kg/m2 was associated with increased risk of grade 3 or 4 complications compared with a BMI >24.9 kg/m2 (radiation enteritis: 16.7% vs 13.6%, respectively; P = .03; fistula: 11.1% vs 8.8%, respectively; P = .05; bowel obstruction: 33.3% vs 4.4%, respectively; P < .001; lymphedema: 5.6% vs 1.2%, respectively; P = .02).CONCLUSIONS:Underweight patients (BMI <18.5 kg/m2) with locally advanced cervical cancer had diminished overall survival and more complications than normal weight and obese patients. Cancer 2010. © 2010 American Cancer Society. dx.doi.org


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    BACKGROUND:The objective of this study was to determine whether lower expression levels of DICER1 are associated with disease recurrence in patients with endometrioid endometrial cancer. The authors also explored DNA methylation and haploinsufficiency as potential mechanisms related to altered DICER1 expression in these tumors.METHODS:DICER1 expression was assessed by quantitative polymerase chain reaction in a selected cohort of endometrioid endometrial tumors (N = 169). Loss of heterozygosity analyses were conducted using 2 single nucleotide polymorphisms, and combined bisulfate restriction analysis was used to assess methylation in the 5?-untranslated region of DICER1 in representative tumors. The correlations between DICER1 expression and clinicopathologic variables, including overall survival (OS) and disease-free survival (DFS), were assessed using nonparametric rank-sum tests and Cox proportional hazard models as appropriate. Survival distributions were described using the Kaplan-Meier method. A nested case-control analysis was conducted to confirm the association between transcript levels and disease recurrence.RESULTS:Lower DICER1 expression (hazard ratio [HR], 1.36; 95% confidence interval [CI], 1.05-1.75; P = .02) and advanced disease stage (HR, 2.79; 95%CI, 1.59-4.90; P < .001) were associated with worse DFS. Three variables were associated significantly with reduced OS: age (HR, 1.04; 95%CI, 1.02-1.06; P < .0001), advanced disease stage (HR, 6.41; 95%CI, 3.57-11.52; P < .0001), and high tumor grade (HR, 2.96; 95%CI, 1.46-5.99; P = .003). Nested case-control analyses confirmed that there were lower DICER1 transcript levels in patients who had recurrent disease (P = .01). Deletion of DICER1 sequences was an infrequent event (5% of analyzed patients), and no methylation was observed in the 5? DICER1 regulatory region.CONCLUSIONS:Lower DICER1 transcript levels were correlated with disease recurrence and worse DFS survival in patients with endometrioid endometrial cancer. The factors that influence DICER1 transcript levels in primary endometrial cancers remain unknown. Cancer 2010. © 2010 American Cancer Society. dx.doi.org


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    BACKGROUND:In a cohort including 5112 prostate cancer (pCa) patients, the authors investigated associations among triglycerides (TG), total cholesterol (TC), and pCa while taking into account glucose.METHODS:A cohort (n = 200,660) based on 4 groups of men, according to age at cohort entry, with TG, TC, and glucose measurements was selected from the Apolipoprotein MOrtality RISk (AMORIS) database. Of these, 5112 men developed pCa. Multivariate Cox proportional hazard models were used to analyze associations among TG, TC, and pCa. Competing risks were assessed graphically.RESULTS:Age-stratified analyses for quartiles of TG, TC, and glucose showed a negative association between glucose and pCa risk (HR, 0.93; 95% CI, 0.86-1.01), 0.93 (0.86-1.01), 0.87 (0.81-0.94) for the second, third, and fourth quartiles compared with the first (Ptrend = .001). Stratified analysis by glucose levels (<6.11 or ?6.11 mmol/L) showed a positive association between hypertriglyceridemia (TG?1.71 mmol/L) and pCa risk, when there were high glucose levels (HR, 1.23; 95% CI, 1.01-1.48). No association was found for hypercholesterolemia (TC?6.50 mmol/L). Competing risk analysis showed that protective effects of glucose were overestimated in conventional Cox proportional hazard models and strengthened positive findings between TG and pCa risk.CONCLUSIONS:The authors'; findings supported the hypothesis that factors of the glucose and lipid metabolism influence pCa risk. Competing risk assessment showed that it is important to take into account the long natural history and age distribution of pCa when interpreting results. The authors'; findings indicate another reason to fight the increasing prevalence of obesity and dyslipidemia. Cancer 2010. © 2010 American Cancer Society. dx.doi.org


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    BACKGROUND:Somatostatin (SST) inhibited cell proliferation and negatively regulated the release of growth hormones by means of specific receptors (SSTR). Genetic variation in SSTR had been associated with risk of human cancers but had never been investigated in pancreatic cancer.METHODS:In this retrospective study the SSTR5 gene in paired tumor and blood samples from 33 pancreatic adenocarcinoma patients using the Sanger method were sequenced. Three single nucleotide polymorphisms (SNPs) in samples from 863 patients with pancreatic ductal adenocarcinoma and 876 healthy controls using the TaqMan method were analyzed. The associations between gene polymorphisms and pancreatic cancer risk and survival were analyzed by multivariate logistic regression and Cox proportional hazard models, respectively.RESULTS:No somatic mutations were identified, but 3 nonsynonymous SSTR5 SNPs (P109S, L48M, and P335L) in pancreatic tumors were identified. The SSTR5 P109S variant allele was associated with a 1.62-fold increased risk of pancreatic cancer (95% confidence interval [CI]: 1.08-2.43, P = 0.019). Furthermore, the SSTR5 L48M AC variant and smoking had a joint effect on pancreatic cancer risk (pinteraction = 0.035). The odds ratios (95% confidence intervals) were 0.58 (0.34-0.97), 1.49 (1.18-1.89), and 2.27 (1.35-3.83) for the variant genotype alone, smoking alone, and both factors, respectively, compared with no factors. Finally, SSTR5 P335L CC and P109S CC combined were associated with lower overall survival durations in patients with resectable disease.CONCLUSIONS:These data suggest that SSTR5 genetic variants play a role in pancreatic cancer development and progression. Cancer 2011. © 2011 American Cancer Society. dx.doi.org


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