Biomedical subjects

Ahmed S Sultan

Publications and source records attributed to Ahmed S Sultan.

3 recordsLinked to original sources

PubMed2006

Molecular markers of hepatitis C virus-related hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is triggered by many factors including infection with hepatitis C virus (HCV). However, the molecular basis of the development of HCV-related HCC remains unknown. The present study was designed to reveal the interference of the HCV infection in HCC patients with a set of anti-apoptotic factors, and expression levels of some molecular markers between HCV-related HCC and non-HCV-related HCC. We have determined the plasma circulating levels of Bcl-2, TGF-betaI, VEGF, beta2-MG and immunohistochemistry staining of p53 in HCV-related HCC patients (n = 40) and compared them in relation to both HCV-free HCC patients (n = 37) and normal control group (n = 20). The present data do not distinctly predict a significant role of HCV infection on the circulating Bcl-2 protein since in both HCC and HCC/HCV groups a limited number of patients have high levels of Bcl-2. However, TGF-betaI expression is markedly decreased in all patients, particularly in HCC associated with HCV. Moreover, serum VEGF is significantly higher in HCC patients with or without HCV infection than in normal control. No significant difference, however, was found between HCV-infected and HCV-free groups. Presence of HCV is associated with a high incidence of Loss of Heterozygosity (LOH) at M6P/IGFIIr site compared to HCV-free patients. Although beta2-MG is markedly elevated in all patients, a significant increase was observed in the presence of HCV. Immunohistochemical positive total staining for p53 protein was detected in 32/77 (41.5%); HCC-positive HCV was 21/40 (52.2%), and HCC-negative HCV was 11/37 (29.73%). Collectively, in HCC patients, HCV infection does not affect the levels of Bcl-2 and VEGF. beta2-MG and LOH levels at the M6P/IGFIIr site were higher in the presence of HCV concomitant with a decrease in TGF-beta1. There was no significant correlation between p53 and stage of the disease or between p53 protein expression and clinicopathological manifestations.

Adult↗

PubMed2005

Stat5 promotes homotypic adhesion and inhibits invasive characteristics of human breast cancer cells.

Signal transducer and activator of transcription-5 (Stat5) mediates prolactin (PRL)-induced differentiation and growth of breast epithelial cells. We have recently identified active Stat5 as a tumor marker of favorable prognosis in human breast cancer, and determined that Stat5 activation is lost during metastatic progression. Here we provide novel evidence for an invasion-suppressive role of Stat5 in human breast cancer. Activation of Stat5 by PRL in human breast cancer lines was associated with increased surface levels of the invasion-suppressive adhesion molecule E-cadherin in vitro and in xenotransplant tumors in vivo. Inducible E-cadherin was blocked by dominant-negative (Dn) Stat5 or Dn-Jak2, but not by Dn-Stat3. Further experimental data indicated a role of Stat5 as a coordinate regulator of additional invasion-related characteristics of human breast cancer cells, including cell surface association of beta-catenin, homotypic cell clustering, invasion through Matrigel, cell migration, and matrix metalloproteinase activity. A role of Stat5 as a suppressor of breast cancer invasion and metastatic progression provides a biological mechanism to explain the favorable prognosis associated with active Stat5 in human breast cancer.

Animals↗

PubMed2005

Ultrahigh density microarrays of solid samples.

We present a sectioning and bonding technology to make ultrahigh density microarrays of solid samples, cutting edge matrix assembly (CEMA). Maximized array density is achieved by a scaffold-free, self-supporting construction with rectangular array features that are incrementally scalable. This platform technology facilitates arrays of >10,000 tissue features on a standard glass slide, inclusion of unique sample identifiers for improved manual or automated tracking, and oriented arraying of stratified or polarized samples.

Equipment Design↗