Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.5.1.19 (NOS)
 7,285 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epstein-Barr virus (EBV)-positive T non-Hodgkin lymphomas (T-NHLs) have been described, but it is at present unknown how EBV infects T lymphocytes. It has been postulated that cytotoxic T cells (CTLs) or natural killer (NK) cells can be infected by EBV during the killing of an EBV-infected target cell. The objective of this study was therefore to determine whether the neoplastic cells in EBV-positive T-NHLs (n=221) of various locations have a cytotoxic phenotype. To identify EBV-harbouring cells, combinations were used of EBV-encoded RNA (EBER) in situ hybridization (RISH) and immunohistochemistry for T- and B-cell markers and the cytotoxic proteins TIA-1 and granzyme B. EBV was detected in the neoplastic cells of all nasal T-NHLs (n=9), 5/34 gastrointestinal (GI) T-NHLs, and 2/6 lung T-NHLs, but not in primary cutaneous T-NHLs (n=103). Moreover, EBV was found in the neoplastic cells of 2/48 nodal anaplastic large cell lymphomas (ALCLs), but not in neoplastic T cells of other nodal T-NHLs. However, 5/17 nodal peripheral T-NHLs not otherwise specified (PTCLs NOS) and 1/4 T-prolymphocytic leukaemias did contain EBV-positive non-T cells. Double staining revealed that in EBV-positive extranodal T-NHLs (n=16), the EBER-positive cells had a cytotoxic phenotype (TIA-1- and/or granzyme B-positive). In nodal non-ALCL T-NHLs, the EBER-positive cells were not positive for TIA-1 or granzyme B, nor did they express CD3, CD21 or HECA452. Instead, most of these cells expressed the B-cell marker CD20. These PTCLs NOS with EBER-positive cells showed features of AILD-like T-NHL. It is concluded that neoplastic cells of EBV-positive extranodal T-NHLs always have a cytotoxic phenotype, supporting the view that EBV can infect CTLs. In nodal non-ALCL T-NHL, EBV is only found in T-NHL with AILD-like features and is present in B cells, where it may contribute to the outgrowth of a malignant B-cell clone.
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PMID:Epstein-Barr virus is present in neoplastic cytotoxic T cells in extranodal, and predominantly in B cells in nodal T non-Hodgkin lymphomas. 1091 15

Although recurrent primary biliary cirrhosis (PBC) after liver transplantation (LT) has been reported, the full spectrum of changes and progression to fibrosis and cirrhosis is not yet established. We performed a detailed retrospective clinicopathologic analysis of 43 patients who underwent LT for PBC. Eight patients (18.6%) had definite recurrent PBC with florid duct lesions, 5 patients (11.6%) had recurrence with features of autoimmune liver disease, not otherwise specified (AILD-NOS), 7 patients (16.3%) had plasmacytosis only, 4 patients (9.3%) had chronic rejection, 18 patients (41.9%) have no recurrence at present, and 1 patient (2.3%) had acquired hepatitis C. Although definite diagnoses of PBC and AILD-NOS recurrences (n = 13) were made 1 month to 14 years (median, 4 years) post-LT, all patients had plasmacytosis in their earlier biopsy specimens. Also, these patients showed similar pre-LT and post-LT clinical features, with progressive fibrosis in 4 of 8 and 2 of 5 patients, respectively. Four of 13 patients with definite recurrence and 14 of 18 patients with no recurrence were administered azathioprine (AZA) as part of their post-LT therapy (P =.01). Six of 13 and 16 of 18 patients currently are alive, with median follow-ups of 11 and 5 years, respectively. No significant differences were seen with donor-recipient group A, group B, group O blood type, sex, or HLA mismatches; native liver histological characteristics; or tacrolimus-based therapy. In conclusion, recurrent autoimmune liver disease was seen in 30% of patients after LT for PBC and had features of PBC and/or AILD-NOS. Progression seen in 46% of patients was associated with late graft failure. Patients with no recurrent disease had shorter follow-up periods and more frequent immunosuppression, including AZA; some may still develop recurrence with longer follow-up.
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PMID:Liver transplantation for primary biliary cirrhosis: a long-term pathologic study. 1251 78