Quantitative Methylation Profiles for Multiple Tumor Suppressor Gene Promoters in Salivary Gland Tumors

Methylation profiling of tumor suppressor gene (TSGs) promoters is quickly becoming a powerful diagnostic tool for the early detection, prognosis, and even prediction of clinical response to treatment. Few studies address this in salivary gland tumors (SGTs); hence the promoter methylation profile of various TSGs was quantitatively assessed in primary SGT tissue to determine if tumor-specific alterations could be detected.DNA isolated from 78 tumor and 17 normal parotid gland specimens was assayed for promoter methylation status of 19 TSGs by fluorescence-based, quantitative methylation-specific PCR (qMSP). The data were utilized in a binary fashion as well as quantitatively (using a methylation quotient) allowing for better profiling and interpretation of results..Screening promoter methylation profiles in SGTs showed considerable heterogeneity. The methylation status of certain markers was surprisingly high in even normal salivary tissue, confirming the need for such controls. Several TSGs were found to be associated with malignant SGTs, especially SDC. Further study is needed to evaluate the potential use of these associations in the detection, prognosis, and therapeutic outcome of these rare tumors

Role of DNA methylation in head and neck cancer

Head and neck cancer (HNC) is a heterogenous and complex entity including diverse anatomical sites and a variety of tumor types displaying unique characteristics and different etilogies. Both environmental and genetic factors play a role in the development of the disease, but the underlying mechanism is still far from clear. Previous studies suggest that alterations in the genes acting in cellular signal pathways may contribute to head and neck carcinogenesis. In cancer, DNA methylation patterns display specific aberrations even in the early and precancerous stages and may confer susceptibility to further genetic or epigenetic changes. Silencing of the genes by hypermethylation or induction of oncogenes by promoter hypomethylation are frequent mechanisms in different types of cancer and achieve increasing diagnostic and therapeutic importance since the changes are reversible. Therefore, methylation analysis may provide promising clinical applications, including the development of new biomarkers and prediction of the therapeutic response or prognosis. In this review, we aimed to analyze the available information indicating a role for the epigenetic changes in HNC

The natural history of parallel transjugular intrahepatic portosystemic stent shunts using uncovered stent: the role of host-related factors

Objectives: Parallel shunts (PS) are used in the management of transjugular intrahepatic portosystemic stent‐shunt (TIPS) insufficiency, a major limitation of the technique. This study describes the natural history of PS, and uses them as a model to assess the role of host factors in the development of primary shunt insufficiency. Methods: Out of 338 patients with TIPS, 40 (11.8%) patients required insertion of a PS. Baseline and follow‐up data of these patients were collected. Regular shunt surveillance involved biannual clinic visits and transjugular portography. Results: The non‐PS group (group 1; n=298) and the PS group (group 2; n=40) had similar baseline demographic and disease characteristics. Index shunts of both groups and the PS produced a significant portal pressure gradient drop (P<0.001), which was less in the index shunts of Group 2 (P<0.02 for both). PS had similar cumulative shunt patency rates to those of the index shunts of Group 1, and both were greater than those of index shunts in Group 2 (P<0.001 for both). The intervention rate (number of interventions/number of check portograms × 100) was similar for PS and the index shunts of Group 1 (38.7% and 43% respectively), but was significantly higher in the index shunts of Group 2 (85.6%; P<0.01 for both). In Group 1 and Group 2, 144 patients (48.3%) and 21 patients (52.5%) died during follow‐up after a median period of 23.4 and 8.9 months respectively. Conclusions: These findings do not support the hypothesis that shunt insufficiency is related to host factors