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S Iravani

Publications and source records attributed to S Iravani.

8 recordsLinked to original sources
PubMed1999

Precursor B lymphoblastic lymphoma presenting as lytic bone lesions.

Precursor B lymphoblastic lymphoma is an aggressive but potentially curable disease. This lymphoma most often manifests in the skin and lymph nodes and, less commonly, as lytic bone lesions. In the bone, this lymphoma must be differentiated from small round blue cell tumors, diffuse large B-cell lymphoma, and acute myelogenous leukemia. We describe the morphologic and immunophenotypic features in 4 patients, 2 children, 1 teenager, and 1 adult, who initially presented with bone pain and osteolytic lesions but without peripheral blood or iliac bone marrow involvement. Positive immunohistochemical staining of the neoplastic cells was observed for anti-CD10 (3/4), CD20 (3/4), CD34 (1/4), CD43 (4/4), CD45/CD45RB (2/4), CD79a (4/4), CD99 (MIC2) (2/4), and terminal deoxynucleotidyl transferase (4/4). CD3 was absent in all cases. Immunophenotyping these neoplasms is essential to establish the correct diagnosis of precursor B lymphoblastic lymphoma, and a panel of antibodies is required because of the immunophenotypic heterogeneity.

Adolescent↗
PubMed1998

Altered expression of c-erbB-2, DF3, b72.3, p53 and Ki-67 with progression and differentiation to two distinct histologic types of invasive carcinoma in the MCF10AT human xenograft model of proliferative breast disease.

Human breast epithelial MCF10AT cells form simple ducts in nude/beige mice which eventually become hyperplastic and sporadically progress to carcinomas. Altered immunohistochemical detection of c-erbB-2, DF3, B72.3, p53 and Ki-67 was observed with progression and differentiation to two distinct histologic types of invasive carcinoma. c-erbB-2 and DF3 were detected in 50% and 18% of lesions at the stage of atypical hyperplasia and expression increased to 78% and 54% in invasive adenocarcinomas. In contrast, a group of six unusual undifferentiated tumors with squamoid features did not express c-erbB-2 or DF3, but both B72.3 (4/6) and p53 (6/6) were detected.

Adenocarcinoma↗
PubMed1998

Elevated c-Src protein expression is an early event in colonic neoplasia.

The molecular events regulating the development and progression of colonic neoplasia are currently being delineated. Recent studies have implicated c-Src protein kinase activation as an early event in the malignant transformation of colonic epithelial cells. However, increased c-Src activity has also been reported in colon carcinomas as well as in metastatic hepatic and extrahepatic colon carcinomas. To further investigate the potential role of c-Src in the progression of colonic neoplasia, we analyzed c-Src levels by immunohistochemistry in 27 colorectal resection specimens. Mouse monoclonal antibody to c-Src protein was applied to 3-micron sections from formalin-fixed, paraffin-embedded tissues using the avidin-biotin-peroxidase method. The combination of adenomatous (AD) and adjacent carcinomatous mucosa (CA) specimens were present in 20 of 27 patients. In 15 cases, synchronous metastatic (MT) lesions were available for evaluation. Strong c-Src expression was evident in 95% of AD (n = 20), in contradistinction to 32% of MT (n = 19) and 14% of CA (n = 22). Weak-to-moderate c-Src expression was seen in adjacent normal colonic mucosa (NM) in 96% of cases. Signed rank test univariate analysis revealed a statistically significant difference in c-Src expression between NM/AD (p = 0.0001), NM/CA (p = 0.0001), NM/MT (p = 0.0006), AD/CA (p = 0.0001), and AD/MT (p = 0.0002). No significant correlation between levels of c-Src expression and patient survival, tumor size, histologic grade, or tumor configuration was observed using the Cox's Regression Model. Similar results were obtained by analysis of c-Src protein levels and c-Src kinase activity as measured by Western blot and in vitro kinase assays of representative cases. Our results indicate that: (a) elevated c-Src expression is an important early event during colorectal carcinogenesis; (b) its activation may be involved in tumor progression in a subset of colonic carcinomas; and (c) additional molecular events are necessary for invasion to occur.

Adult↗