Biomedical subjects

Amany Abd El-Hameed

Publications and source records attributed to Amany Abd El-Hameed.

3 recordsLinked to original sources

PubMed2005

De novo nodal diffuse large B-cell lymphoma: identification of biologic prognostic factors.

BACKGROUND: Diffuse large B-cell Lymphoma (DLBCL) represents the most frequent type of non-Hodgkin lymphoma (NHL). Although combination chemotherapy has improved the outcome, long-term cure is now possible for approximately 50% of all patients, making the search for parameters identifying patients at high risk particularly needed. The presence of bcl-2 gene rearrangement in de novo DLBCL suggests a possible follicle center cell origin and perhaps a distinct clinical behavior. This study investigated the frequency and prognostic significance of t(14;18) translocation and bcl-2 protein overexpression in a cohort of patients with de novo nodal DLBCL who where uniformly evaluated and treated. MATERIAL AND METHODS: A total of 40 patients with de novo nodal DLBCL treated at National Cancer Institute (NCI), Cairo University were investigated. Formalin? fixed, paraffin-embedded sections were analyzed for: 1) bcl-2 gene rearrangement including major break point region (mbr) and minor cluster region (mcr) by polymerase chain reaction (PCR), and 2) bcl-2 protein expression by immunohistochemistry using Dako 124 clone. Results were correlated with the clinical features and subsequent clinical course. RESULTS: Bcl-2 gene rearrangement was detected in 8 cases (20%), 2 cases at mbr, and 6 cases at mcr. Bcl-2 protein (>10%) was expressed in 24 cases (60%), irrespective of the presence of t(14;18) translocation. The t(14;18), and bcl-2 protein overexpression were more frequently associated with failure to achieve a complete response to therapy (p=0.008, and 0.04, respectively). DLBCL patients with t(14;18), and bcl-2 protein expression had a significantly reduced 5-year disease free survival (p=0.04, and 0.01, respectively). CONCLUSION: The t(14;18) translocation, and bcl-2 protein expression define a group of DLBCL patients with a poor prognosis, and could be used to tailor treatment, and to identify candidates for therapeutic approaches. Geographic differences in t(14;18) may be related to the difference in distribution of bcl-2 breakpoints.

Adult↗

PubMed2005

Survivin expression in colorectal adenocarcinoma using tissue microarray.

BACKGROUND: The additional prognostic information closely related to tumor cell biology is essential for the identification of patients with poor prognosis. Survivin, an identified inhibitor of apoptosis, is unique for its expression in human malignancies but not in normal adult cells. This study examined the expression, and potential prognostic value of survivin in colorectal adenocarcinoma (CRC) on tissue microarray (TMA) sections. Analysis of large numbers of tissue samples, improved tissue salvage, cost reduction, ease of interpretation, and significant time saving were realized by using the arrays. MATERIAL AND METHODS: Two-hundred and eighty cases of colorectal adenocarcinoma were arrayed. Immunohistochemical stains of TMA sections were performed for survivin, bcl-2, and p53. Cases were followed up for 5 years. RESULTS: Survivin was detected in 147 of 230 cases (63.9%). No expression of survivin was observed in normal tissues. There was no correlation between survivin immunoreactivity and age, sex, tumor site, tumor size, histopathologic subtype, tumor grade and clinical stage (p >0.05). Prevalence of survivin expression was significantly higher in bcl-2 positive than in bcl-2 negative cases (88.1% versus 42.1%, p <0.0001), but was not associated with p53 (p=0.09). The 5-year disease free survival (DFS) for patients with survivin positive colorectal adenocarcinoma was significantly lower than that for patients with survivin negative tumors (46% versus 68.7%, p=0.001). CONCLUSION: Survivin expression in colorectal adenocarcinoma provides an important prognostic parameter and targeted antagonists of survivin may be beneficial as apoptosis-based therapy for colon cancer.

Adenocarcinoma↗

PubMed2004

Contribution of hepatitis C virus and Helicobacter Pylori co-infection as possible predisposing factors in the occurrence of gastric mucosal dysplasia.

BACKGROUND AND PURPOSE: Current views on B-cell lymphoma genesis suggest that several exogenous factors, acting in a multistep fashion upon a predisposing condition, may be involved in B-cell clonal expansion, a potentially prelymphomatous stage. This study was done to investigate the extrahepatic localization of Hepatitis C virus (HCV)in the gastric mucosa and the possibility of its involvement besides Helicobacter pylori (H. pylori) as possible predisposing factors that might play a role in the occurrence of gastric dysplasia or lymphoproliferation following gastritis and may end in carcinogenesis. PATIENTS AND METHODS: A well characterized series of 45 patients with chronic liver disease complaining of gastric dyspepsia were subjected to Upper Gastrointestinal Endoscopy and histological examination of gastric biopsy with studying the prevalence of serologic and molecular markers of HCV and H. pylori in the patients' serum and their gastric tissue. HCV-RNA detection in gastric tissue was done only for those who showed gastric dysplasia. RESULTS: Histopathological examination of the gastric biopsies revealed that 20 patients (44.4%) had chronic active gastritis, 15 patients (33.4%) had chronic gastritis and 10 patients (22.2%) had gastric dysplasia with chronic gastritis. As for hepatitis C virus, 38 patients (84.4%) were reactive for serum antibodies (HCV-Abs) and 18 patients (40%) showed Polymerase Chain Reaction (PCR) positivity. Helicobacter pylori antibody reactivity was detected in 37 patients (82.2%) while PCR positivity was detected in 24 patients (53.3%) both in their serum as well as in gastric tissues. Seventeen out of twenty cases showing chronic active gastritis were serologically positive for both H. pylori and HCV. Patients who showed dysplasia on pathological examination (n=10) were all HCV-Abs positive (p-value = 0.32), seven patients were serum HCV-RNA positive (p-value = 0.083) and 3 of them showed HCV-RNA positivity in their gastric tissue. Nine out of the patients with gastric dysplastic changes proved positive for H. pylori DNA both in serum (p-value= 0.027) and tissue (p-value= 0.029). CONCLUSIONS: We suggest that Hepatitis C virus may be considered, in addition to Helicobacter pylori, as another potential infectious co-factor in the occurrence of gastric mucosal dysplasia and thus might be associated in the multistep hypothesis of carcinogenesis.

Journal Article↗