Predictors of 1-year postoperative mortality in radical colon cancer surgery.

AIM: The aim of this study was to determine the impact of patient, tumor and surgery-related parameters on 1-year postoperative mortality in a cohort of patients operated in a single tertiary center. MATERIALS AND METHODS: The study included 605 patients diagnosed with colon cancer between January 2013 and December 2015 that underwent radical surgery in a tertiary center. Patient demographics, comorbidities, preoperative biological parameters alongside with tumor and surgery-related factors were prospectively recorded and then analyzed in relation 1-year postoperative mortality. RESULTS: One-year mortality rate in the study group was 10.9%. Independent risk factors in relation to 1-year mortality were advanced TNM stage (OR 3.10, 1.10 - 8.75 95% CI ), emergency surgery (OR 1.91, 1.11 - 3.74 95% CI ), location of the tumor in the ascending colon (OR 2.17, 1.32 - 3.57 95% CI ), multiorgan resections (OR 2.07, 1.15 - 3.74 95% CI), age over 63 years (OR 2.05, 1.16 - 3.62 95% CI) and the history of alcohol consumption (OR 2.058, 1.17 - 3.61 95% CI ). DISCUSSION: Postoperative complications are still being reported in colon cancer surgery, despite technological progress and constant research in the field. So far, factors that influence postoperative mortality have been mostly studied up to 30 days postoperatively. According to some recent papers, reporting 30-day mortality data can underestimate accurate communication of postoperative adverse events. Thus, 1-year mortality in colon cancer surgery could be a better indicator of the impact on surgery on postoperative period of this patients and factors that influence it should be well known. KEY WORDS: Surveillance, Colon cancer, 1-year mortality.

A Rare Association between Left Lobe Secondary Biliary Cirrhosis and Budd-Chiari Syndrome Secondary to Hepatocellular Carcinoma in the Non-Cirrhotic Right Liver Lobe.

Liver cirrhosis is a diffuse chronic liver disease affecting the entire liver. The fibrosis accumulation and distribution in the liver are known to be heterogeneous. "Localized" or "focal" cirrhosis is only anecdotically reported. Acute hepatitis E virus (HEV) infection is uncommon in western countries, especially in temperate climate areas and is very often missed or underdiagnosed. However, it may be responsible of up to 15% of acute-on-chronic liver failure cases. We present the case of a 35-year-old patient with a very uncommon association of Budd-Chiari syndrome secondary to hepatocellular carcinoma (HCC) developed on a non-cirrhotic right liver lobe and secondary biliary cirrhosis of the left liver lobe, that further complicated with acute HEV infection leading to acute-on-chronic liver failure and death.

Crosstalk between EGFR and p53 in hepatocellular carcinoma.

BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most frequent cancers worldwide, with a high mortality. Most patients present with late stage disease, when the treatment options are limited to systemic chemotherapy. The purpose of our study was to evaluate the significance of p53 and EGFR expression in HCC, and to determine whether these two markers correlate with conventional parameters of prognosis. MATERIALS AND METHODS: Our study included a total of 45 patients, diagnosed histopathologically with HCC. Clinicopathological data including sex, age, tumor necrosis, tumor size, histologic grading, tumor stage, the presence of cirrhosis and chronic hepatitis, were recorded from the Institute database. Three independent microscopic fields were selected for each sample and all the tumor cells within each microscopic field were counted, and then the positive percent of p53 cells were calculated. Three staining patterns were recognized: diffuse, heterogenous and focal. The intensity of EGFR staining was scored on a scale of 0-3+: 0 no staining; 1+ when a weak membrane staining was observed; 2+ when membrane staining is more intense than in 1+, but less than 3+, and 3+ when intense dark brown staining delineated the membrane. To determine the relationship between EGFR expression and p53, we performed double staining in the same HCC specimens. RESULTS: By immunohistochemical staining, p53 protein was detected in tumor cell nuclei in 20 HCCs (44%). We found a significant correlation between the intensity of p53 expression and the histological grade (p=0.008). EGFR expression was detected in 17 (38%) cases, linked to histological grade (p=0.039). Moreover, the intensity of p53 expression was significantly correlated with EGFR intensity (p=0.014). CONCLUSIONS: Our results suggest that overexpression of p53 and EGFR plays an important role in hepatocarcinogenesis and contributes to more advanced disease. These markers are not only valuable predictors of prognosis in HCC, but they are also rational targets for new anti-tumor strategies.

Detection of early lymphangiogenesis by lymphatic microvascular density and endothelial proliferation status in preneoplastic and neoplastic lesions of the uterine cervix.

The characteristics of lymphangiogenesis in preneoplastic and neoplastic lesions of the uterine cervix are not well known and the role of this process in tumor progression and metastasis is not well understood. The aim of the present study was to characterize the morphology and distribution of lymphatic vessels and lymphatic proliferative status and to evaluate the value of lymphatic microvascular density (LMVD) in premalignant and malignant lesions of the uterine cervix. One hundred and twenty-eight paraffin-embedded cervical specimens were immunostained with D2-40 antibody specific for lymphatic endothelial cells. Colocalization of D2-40 and Ki67 for the proliferative characterization of lymphatic vessels was obtained by performing double immunostaining. A low density of lymphatic vessels was detected in normal cervix and squamous metaplasia. Intense and particular lymphangiogenic response was found in low and high grade squamous intraepithelial lesions and microinvasive carcinoma. Lymphatic proliferation occurred early in cervical lesions, being more active in premalignant lesions and microinvasive carcinomas than in invasive lesions. Our results suggest an early initiation of an active lymphangiogenesis in cervical lesions. These findings support the hypothesis that cervical preneoplastic lesions represent a critical point in the development of the lymphatic network vasculature. Early lymphangiogenesis could explain lymph node metastasis associated with cervical invasive carcinomas at preliminary diagnosis.