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C Assaf

Publications and source records attributed to C Assaf.

21 records · Page 2Linked to original sources
PubMed1999

Origin of primary gastric T-cell lymphomas from intraepithelial T-lymphocytes: report of two cases.

AIMS: The classification of primary gastric T-cell lymphomas is uncertain due to the exceeding rarity of these tumours; many of the reported cases were felt to be similar to node-based lymphomas. We describe two cases of primary gastric T-cell lymphoma with evidence of origination from intraepithelial T-lymphocytes. METHODS AND RESULTS: Both tumours were restricted to the stomach; one displaying a large ulcerated mass, the other a widespread superficial tumour manifestation. Histologically the first tumour was composed of sheets of medium-sized lymphoid cells showing marked epitheliotropism at the edge of the ulcer, and a CD3+, CD4-, CD8-, CD20-, CD56-, CD103+, beta F1+ phenotype. The second case differed histologically and immunophenotypically from the first case. In addition to lamina propria and submucosal infiltration, the lymphoma contained an extensive intraepithelial component even in large areas without other evidence of tumour. The neoplastic cells ranged in size from small to medium and large. Immunohistology disclosed a CD3+, CD4+, CD8-, CD20-, CD56-, beta F1+ phenotype. Staining for CD103 could not be performed in this case since frozen material was not available. CONCLUSIONS: The prominent epitheliotropism, the marked intraepithelial growth and the expression of CD103 strongly imply a derivation of these primary gastric lymphomas from intraepithelial T-lymphocytes. Additional studies of larger series will clarify whether the findings described here are typical of primary gastric T-cell lymphomas.

Adult↗
PubMed1996

Anaplastic large-cell lymphomas of T-cell and null-cell phenotype express cytotoxic molecules.

To further specify the cellular origin and nature of anaplastic large-cell lymphoma (ALCL) and its relationship to other lymphoid neoplasms, particularly Hodgkin's disease (HD), we investigated the presence of cytotoxic molecules in a large well-characterized series of these tumors. For expression of the cytotoxic molecules perforin and granzyme B, in situ hybridization (ISH) and immunohistology were used, respectively. Overall, 23 of 25 ALCLs of T/null phenotype and five (three mixed cellularity and two nodular sclerosis) of 57 HD cases showed the presence of perforin transcripts and/or granzyme B molecules in neoplastic cells. Polymerase chain reaction (PCR) analysis of ALCLs showed that most (10 of 11) cases of null-cell ALCL (null-ALCL) contained a clonal rearrangement of T-cell receptor beta-chain genes, as did T-cell ALCL (T-ALCL; 9 of 10 cases). However, both cytotoxic molecules and clonally rearranged T-cell receptor beta-chain genes were absent in seven of seven and eight of nine cases of B-cell ALCL (B-ALCL), respectively. These data show that all or nearly all T-ALCLs, irrespective of the clinical subform or the lack of T-cell-associated molecules, are derived from activated cytotoxic T cells. The same appears to be true for the neoplastic cells of rare HD cases. These findings indicate that T-ALCLs are different from B-ALCLs and the majority of HD cases, and suggest that some HD cases, especially those with T-cell antigen-positive tumor cells, may be closely related to T-ALCL, at least in terms of cellular origin.

Biomarkers↗