Ki-1 (CD30)-positive, large-cell anaplastic lymphoma (LCAL) is a distinctive subset of non-Hodgkin's lymphoma; morphologically, the neoplastic cells of LCAL may closely resemble Reed-Sternberg cell variants of Hodgkin's disease.
A novel association, Epstein-Barr virus-positive Ki-1+/CD30+ anaplastic large cell non-Hodgkin's lymphoma of B-cell phenotype in immunosuppressed renal transplant recipients is reported.
A further heterogeneity in the relative proportion of naive and memory TIL-T was also observed within lymphoma (range: 11 to 68% in B-cell NHL, 5 to 69% in HD).
A 56-year-old man with refractory B-cell lymphocytic non-Hodgkin's lymphoma was treated in a Phase II study with interleukin-2 (IL-2) (Roussel-Uclaf, Romainville, France).
Molecular genetic analysis showed that bcl-2 was rearranged in only 2 of 77 patients: one was affected by hairy cell leukemia and one by diffuse small cleaved cell lymphoma with peripheral blood invasion.
Fourteen patients with FSCCL and 1 patient with DSCCL had a phenotype of follicular center cells (FCC) (CALLA+, SIgD-, Leu-1-, Leu-8- and negative ALPase), and 11 patients with FSCCL had bcl-2 gene rearrangements.
Fourteen patients with FSCCL and 1 patient with DSCCL had a phenotype of follicular center cells (FCC) (CALLA+, SIgD-, Leu-1-, Leu-8- and negative ALPase), and 11 patients with FSCCL had bcl-2 gene rearrangements.
Fourteen patients with FSCCL and 1 patient with DSCCL had a phenotype of follicular center cells (FCC) (CALLA+, SIgD-, Leu-1-, Leu-8- and negative ALPase), and 11 patients with FSCCL had bcl-2 gene rearrangements.
Fourteen patients with FSCCL and 1 patient with DSCCL had a phenotype of follicular center cells (FCC) (CALLA+, SIgD-, Leu-1-, Leu-8- and negative ALPase), and 11 patients with FSCCL had bcl-2 gene rearrangements.
Fourteen patients with FSCCL and 1 patient with DSCCL had a phenotype of follicular center cells (FCC) (CALLA+, SIgD-, Leu-1-, Leu-8- and negative ALPase), and 11 patients with FSCCL had bcl-2 gene rearrangements.
Recent data, particularly in haematological malignancies such as acute non-lymphocytic leukaemia, myeloma and non-Hodgkin's lymphoma, indicate that P-glycoprotein may be involved in the development of clinical drug resistance.
Twenty cases of Japanese non-Hodgkin's lymphoma with B cell markers were studied with respect to their immunoglobulin heavy (IgH) chain gene loci on chromosome 14 and BCL2 loci on chromosome 18.
Twenty-nine cases of non-Hodgkin's lymphoma of low-grade malignancy in a European population were investigated for the presence of bcl-2 and bcl-1 gene rearrangement.
Twenty-nine cases of non-Hodgkin's lymphoma of low-grade malignancy in a European population were investigated for the presence of bcl-2 and bcl-1 gene rearrangement.
These studies suggest that acquisition of changes in the short arm of chromosome 17, which may be interrelated with the p53 gene, may carry a poor prognosis in patients with non-Hodgkin's lymphoma.
No geographic incidence variation was detected for -7 and +21 in ANLL; +8 in MDS; 6q- and +8 in ALL; +12 in chronic lymphocytic leukemia; 6q- in non-Hodgkin's lymphoma (NHL); t(8;14) in Burkitt's lymphoma; t(11;22) in Ewing's sarcoma; i(12p) in germ cell tumors; 1p- in neuroblastoma; structural abnormalities of 3q, 8q, and 9p in PAS; or 3p- in renal cell carcinoma.
Thus, bcl-1 rearrangement occurred at MTC or p94PS in 12 of 23 centrocytic lymphomas (52%), confirming a nonrandom association and suggesting a pathogenetic role for the bcl-1 locus in this immunohistologic subtype of NHL.
The BCL1 locus was rearranged in 9 out of 25 (36%) cases of intermediate lymphocytic cell lymphomas (ILL), in 1 out of 8 cases of diffuse small cleaved cell lymphoma, in 1 out of 12 cases of diffuse mixed cell lymphoma, and in 1 out of 21 cases of diffuse large cell lymphoma.
Morphology in Ki-1(CD30)-positive non-Hodgkin's lymphoma is correlated with clinical features and the presence of a unique chromosomal abnormality, t(2;5)(p23;q35).