Search

Objective: To study the profile and outcome of therapy for hepatocellular carcinoma (HCC) in India. Methods: Data analysis of HCC patients enrolled in liver clinic between 1990 and 2005. Results: We registered 324 HCC patients [males 284 (88%), mean age 52.4 ± 13.1 years]. The etiology of HCC was: hepatitis B virus 165 (51%), hepatitis C virus 38 (12%), alcohol 20 (6%), combined 31 (10%) and unknown 70 (21%). Serum α-fetoprotein was >400 ng in 36%, portal vein invasion was seen in 40% and distant metastases in 13%. Therapy was offered to 141 (43.5%) patients, but survival data was available in only 130 (93%) of them. Treatment given and median survival time was as follows: surgical resection, 19 months (n = 14); transarterial chemoembolization, 11 months (n = 23); transarterial rhenium therapy, 26 months (n = 7); radiofrequency ablation, 24 months (n = 4); acetic acid ablation, 13 months (n = 17); oral chemotherapy, 26 months (n = 33), and combination therapy, 26 months (n = 32). Vascular invasion, Okuda staging and therapy were independent factors associated with survival. Treated patients had longer median survival compared to untreated ones (16 months vs. 7 months, p < 0.05). Conclusions: Hepatitis B infection is the predominant cause of HCC in India. Serum α-fetoprotein was diagnostic in only one third of our patients. Most patients present late, when curative therapies are not possible. Treated patients had better survival than untreated ones. Copyright © 2009 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Objective: The Wnt/β-catenin signaling cascade is an important signal transduction pathway in human cancers. Overexpression of β-catenin and its downstream effector, cyclin D1, is implicated in malignant transformation and acquisition of an invasive tumor phenotype. This study aimed to determine the clinical significance of Wnt/β-catenin canonical pathway components in breast cancer. Methods: Expression of β-catenin, disheveled (Dvl) and cyclin D1 was examined in invasive ductal carcinomas (IDCs) of the breast by immunohistochemical analysis. Results: Of the 98 IDCs analyzed, 30% of tumors displayed both nuclear and cytoplasmic staining of Dvl protein, while 52% showed nuclear localization. Loss of cell surface β-catenin was observed in 66% of breast carcinomas, whereas nuclear expression was observed in 48% IDCs. Cyclin D1 overexpression was observed in 60% IDCs; 31/59 (53%) of these tumors showed nuclear expression of β-catenin, suggesting upregulation of the canonical Wnt/β-catenin pathway. Our study demonstrates a significant association between nuclear localization of Dvl and β-catenin (p < 0.01, OR = 15.8). Conclusion: To our knowledge, this is the first study showing an association between nuclear localization of Dvl and β-catenin in IDCs and suggests the upregulation of Wnt/β-catenin pathway components, β-catenin, Dvl and cyclin D1 in IDCs of the breast. Copyright © 2008 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Objective: TheMEMD gene was reported to be overexpressed in human esophageal squamous cell carcinoma (ESCC), using differential display. The aim of this study was to determine the clinical significance of MEMD/ALCAM in esophageal tumorigenesis. Methods: Analysis of MEMD/ALCAM expression in esophageal tissues was carried out at protein and RNA level using immunohistochemistry and semiquantitative RT-PCR, respectively. Results: Increased MEMD/ALCAM expression was observed in 42/65 (65%) ESCCs (p = 0.000, odds ratio, OR = 3.665) and in 17/25 (68%) dysplasias (p = 0.000, OR = 4.248) compared to paired distant histologically normal esophageal tissues. Increased MEMD mRNAlevels were observed in ESCCs and dysplasias showing overexpression of MEMD/ALCAM protein. Interestingly, increased membranous MEMD/ALCAM expression was observed in dysplasias in comparison with ESCCs (p = 0.002, OR = 3.177). MEMD/ALCAM overexpression in ESCCs was associated with late clinical stage (p = 0.002, OR = 3.619), enhanced tumor invasiveness (p = 0.002, OR = 3.619), and nodal metastasis (p = 0.000, OR = 4.206). Conclusion: To our knowledge, this is the first report showing MEMD expression at pre-malignant stage (dysplasia), suggesting that MEMD/ALCAM expression is an early event in the development of esophageal cancer. Furthermore, in ESCCs its correlation with late clinical stage, enhanced tumor invasiveness and nodal metastasis suggests an association with aggressive tumor behavior. Our data suggest that MEMD/ALCAM may serve as a potential marker for early diagnosis, tumor invasion and nodal metastasis in ESCCs. Copyright © 2005 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]