Ioachim 1 1 #

Ioachim 1 1 FK228 mouse Department of E7080 mw Pathology, Columbia University and Lenox Hill Hospital, New York, NY, USA The interaction with carcinoma (Ca) of lymphocytes (Ly) and intercellular matrix (Ma) were investigated comparatively in 22 gastric, 26 pulmonary and 28 breast Ca. Ly are constant companions of tumor cells which they may infiltrate and/or destroy.Their amounts vary with

the types of tumors.In the lung B-and T-cell Ly are abundant in non-small cell Ca and plasma cells in squamous cell Ca but are almost absent in carcinoids and small cell Ca.In the breast Ly are more abundant in e-cadherin + duct Ca than in the e-cadherin- lobular Ca.In the stomach B-and T-cells are numerous in intestinal type and rare in diffuse type. In all these Ca,well differentiated tumors are accompanied by more Ly than poorly differentiated The Ma appears normally loose in the former and collagenized, desmoplastic in the latter.The kinds, amounts and distribution of Ly also vary with the stage of Ca being more abundant in early stages and rare, replaced by desmoplasia in late stages.In the breast,aggregates of Ly are next to the precancerous lesions and Ca in CP673451 supplier situ far more than in late stages of infiltrating

Ca.FAS receptor was >than FAS-L ligand in mammary tumors and in their infiltrating Ly while their ratios were reversed in their lymph node metastases. In bronchi,Ly accumulate next to dysplastic changes. In the stomach, B-cells form barrier bands and reactive follicles in the mucosa around.atypical cells while T-cells,mainly CD8+ infiltrate the Ca cells. These observations indicate that the Ly and Ma reactions to Ca are not uniform but correlated

with the tumor type, grade and stage. O94 Role of the Tumor Suppressor p16 Protein in Tumor-Stromal Interactions in Breast Cancer Maysoon Al-Ansari1, Siti-Faujiah Hendrayani1, Abdelilah Aboussekhra 1 1 Department of Biological and Medical research, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia Carcinoma-associated fibroblasts (CAFs) play important roles in the genesis and thrive of various types of epithelial cancers, including breast carcinomas. Indeed, various genetic and epigenetic variations have been identified in stromal fibroblasts, Ketotifen and we have recently shown that CAFs as well as their corresponding counterparts (TCF) display neoplastic-specific changes (Hawsawi et al., 2008). In the present study we have shown that the level of p16 protein is lower in 80% of CAFs as compared to their corresponding TCFs. This decrease resulted from lower stability of the p16 mRNA owing to an increase in the level of the mRNA binding and destabilizing protein AUF1 in CAF cells. Furthermore, using specific p16-siRNA we have shown that p16 negatively controls the expression of various proteins involved in the stromal-epithelial interactions. These include the stromal cell-derived factor 1 (SDF1), the vascular endothelial growth factor (VEGF) and the matrix metalloproteinase-2 (MMP2).

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