1/42. Rituximab (anti-CD20 monoclonal antibody) administration in a young patient with resistant B-prolymphocytic leukemia.Following the administration of the human anti-CD20 monoclonal antibody IDEC-C2B8 (rituximab), a 31-year-old woman with B-prolymphocytic leukemia, who had been resistant to CHOP, fludarabine, pentostatin and 2-CdA, achieved complete remission. Rituximab was administered intravenously once a week for 4 weeks. The patient only had mild but tolerable side effects during the first cycle of therapy. She remains in complete remission 8 months following the discontinuation of treatment.- - - - - - - - - - ranking = 1keywords = leukemia (Clic here for more details about this article) |
2/42. Co-existence of cutaneous T-cell lymphoma and B hairy cell leukemia.A primary cutaneous form of peripheral T-cell lymphoma (PTCL) and a low grade B-cell non-Hodgkin's lymphoma that was classified as a variant of hairy cell leukemia (HCL) were simultaneously diagnosed in a 79-year-old woman by both phenotypic and genotypic analyses. The coexistence of a T- and B-cell lymphoma in the same patient is rare, and, to our knowledge, this particular association has not been previously described. The patient was referred to our Department for evaluation of multiple cutaneous itchy, reddish plaques; laboratory analyses disclosed a lymphocytosis, that presented 6 years earlier. A bone marrow aspirate showed a 50% B-cell interstitial infiltrate, while a skin biopsy surprisingly revealed a PTCL. Clonality of both neoplastic processes was assessed by Southern blot analysis. The indolent clinical course of the cutaneous disease, and the low and stable number of circulating neoplastic T cells supported the diagnosis of a mycosis fungoides (MF)-like PTCL. Possible oncogenic events and/or putative underlying viral infections which could have played a role in the occurrence of B- and T-cell non-Hodgkin's lymphomas in the same patient are discussed.- - - - - - - - - - ranking = 1keywords = leukemia (Clic here for more details about this article) |
3/42. polymyositis--an unusual manifestation of chronic graft-versus-host disease.polymyositis is a rare autoimmune manifestation of chronic graft-versus-host disease (GVHD) characterized by muscle pain, weakness, and an increase in muscle-related enzymes that responds well to treatment with immunosuppressive agents such as steroids and cyclosporine. We describe a case in which polymyositis was the main manifestation of chronic GVHD that occurred 12 months after allogeneic bone marrow transplantation in a patient with acute lymphocytic leukemia (ALL). The polymyositis responded well to treatment with steroids and cyclosporine, with no relapse of symptoms on tapering of the medication.- - - - - - - - - - ranking = 0.2keywords = leukemia (Clic here for more details about this article) |
4/42. Common germinal-center B-cell origin of the malignant cells in two composite lymphomas, involving classical Hodgkin's disease and either follicular lymphoma or B-CLL.BACKGROUND: Classical Hodgkin's disease (HD) and B-cell non-Hodgkin lymphoma (NHL) occasionally occur in the same patient. Such composite lymphomas represent interesting models to study the pathogenesis of B-cell lymphomas and the relationship between HD and B-cell NHL. MATERIALS AND methods: We analyzed two composite lymphomas (a combination of classical HD with follicular lymphoma [FL] and a combination of classical HD with B-cell chronic lymphocytic leukemia [B-CLL]) by micromanipulation of single cells from tissue sections and amplification of immunoglobulin V region genes for the clonal relationship of the tumor cells. RESULTS: In both cases, clonally related variable (V) genes with both shared as well as distinct somatic mutations were obtained from the two lymphomas, showing that in each of the cases the distinct tumor cells were members of a common germinal center (GC) B-cell clone. FL cells from two different lymph nodes of patient 1 showed a similar mutation pattern, suggesting that infiltration of these lymph nodes by tumor cells was not restricted to a particular FL cell or subclone. In the FL, a single cell was identified with a mutation signature indicating that premalignant cells can persist in the tissue. CONCLUSIONS: The cases presented here further underline the close relationship between HD and B-cell NHL and the role of the GC in lymphomagenesis. Whereas the latter was already suggested for FL and HD, the present study indicates that also in the B-CLL subset characterized by mutated Ig genes, important steps in malignant transformation happen in the GC, and that HRS cells can derive from CD5-positive B cells.- - - - - - - - - - ranking = 0.2keywords = leukemia (Clic here for more details about this article) |
5/42. Reactivation of latently infected hepatitis b virus in a leukemia patient with antibodies to hepatitis B core antigen.A 66-year-old man with chronic B-cell leukemia who had antibody to hepatitis B core antigen (anti-HBc) but not hepatitis B surface antigen (HBsAg) suffered from lethal hepatitis caused by hepatitis b virus (HBV) reactivation. He initially lacked circulating viral genomes in his sera and did not have a past history of liver dysfunction. In this patient, the immunosuppressive condition introduced by disease progression of leukemia induced reactivation of dormant HBV, and the withdrawal of chemotherapy resulted in fatal liver failure. Mutation-specific assay based on competitive polymerase chain reaction (PCR) and sequencing analyses revealed the predominant reactivation of an HBV strain with missence mutation (point mutation G-to-A at nucleotide 1896) in the precore regions, as well as point mutations in the core promoter regions. Therefore, it is important to note the risk of HBV reactivation, with resulting lethal hepatic failure, in anti-HBc-positive healthy individuals, even when they lack HBsAg. who receive immunomodulating therapy.- - - - - - - - - - ranking = 1.2keywords = leukemia (Clic here for more details about this article) |
6/42. skin and gingival lesions in a young woman with B-prolymphocytic leukemia (B-PLL).B-PLL has not been often associated with diffuse skin involvement or oral lesions. We present a 32 year-old woman in whom skin and gingival manifestations were the prominent clinical signs of disease relapse.- - - - - - - - - - ranking = 0.8keywords = leukemia (Clic here for more details about this article) |
7/42. Langerhans cell histiocytosis following childhood acute lymphoblastic leukemia.Langerhans cell histiocytosis (LCH) is a clonal proliferation of langerhans cells of unknown etiology that results in a range of clinical manifestations. LCH has been known to be associated with a variety of malignant diseases. A 7-year-old boy was treated for standard-risk acute lymphoblastic leukemia (ALL) at age 2 years, on a Children's Cancer Group chemotherapy protocol for 3 years and developed LCH 2 years after completion of chemotherapy. The case and a review of literature on the association of LCH and ALL are presented.- - - - - - - - - - ranking = 1keywords = leukemia (Clic here for more details about this article) |
8/42. B-Prolymphocytic leukemia: a case study.The case study reported is of a patient initially misdiagnosed as chronic lymphocytic leukemia. immunophenotyping studies ultimately identified the nature of the disease as B-cell prolymphocytic leukemia with concomitant warm autoimmune hemolytic anemia. The leukemia and hemolytic anemia were refractory to all conventional treatments administered. The patient survived a significantly shorter period of time than the median time of three years reported in the literature. The patient expired from complications resulting from B-cell PLL, warm autoimmune hemolytic anemia, and combination chemotherapy.- - - - - - - - - - ranking = 1.4keywords = leukemia (Clic here for more details about this article) |
9/42. Rheumatoid arthritis and B-cell chronic lymphocytic leukemia.The association between lymphoproliferate malignancies, especially lymphoma, and rheumatoid arthritis (RA) has been confirmed by several studies. However; there are few reports of RA patients who developed B-cell chronic lymphocytic leukemia (B-CLL) and vice versa. We report a patient with B-CLL who developed RA and another with RA who presented with B-CLL during follow-up. We discuss the incidence of B-CLL among the RA population and the possible interaction of the pathogenetic mechanisms of these two entities.- - - - - - - - - - ranking = 1keywords = leukemia (Clic here for more details about this article) |
10/42. B lineage acute lymphoblastic leukemia transformation in a child with juvenile myelomonocytic leukemia, type 1 neurofibromatosis and monosomy of chromosome 7. Possible implications in the leukemogenesis.This report describes the case of an 8-month-old infant with a diagnosis of juvenile myelomonocytic leukemia (JMML) and type 1 neurofibromatosis that presented progression to B lineage acute lymphoid leukemia (ALL). The same rearrangement of gene T-cell receptor gamma (TCR gamma) was detected upon diagnosis of JMML and ALL, suggesting that both neoplasias may have evolved from the same clone. Our results support the theory that JMML may derive from pluripotential cells and that the occurrence of monosomy of chromosome 7 within a clone of cells having an aberrant neurofibromatosis type 1 (NF1) gene may be the cause of JMML and acute leukemia.- - - - - - - - - - ranking = 2.2keywords = leukemia (Clic here for more details about this article) |
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