摘要:

AbstractHuman T cell leukemia virus type I (HTLV‐I) is associated with adult T cell leukemia/lymphoma (ATLL), which is well known as a T cell malignancy. In order to clarify whether HTLV‐I plays a role as a virus‐encoded superantigen in the neoplastic process, we examined the TCR Vβ families in the peripheral blood at four different clinical stages: carrier, smoldering leukemia, chronic leukemia, and acute leukemia. An increased number of CD4 T cells was found in each of the four clinical stages. However, we found neither uniform specific losses nor uniform clonal expansion of particular TCR Vβ gene families in any case from the four clinical stages. However, a suppression of the random TCR Vβ families was found. Our data did not therefore directly suggest the existence of a common superantigen model of HTLV‐I which induces an increase in CD4 T cells. The random suppression in the TCR Vβ repertoire is most likely caused by the influence of HTLV‐I neoplastic pathogenesis rather than by virus‐encoded superantigens. In the patients with acute leukemia, one or two families of the Vβ repertoires were very strongly expressed, while in chronic leukemia, no such repertoire of strong expression was observed. The immunological reaction of the hosts might thus be different between the above described groups. © 199

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199605)52:1<1::AID-AJH1>3.0.CO;2-Z

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1996

数据来源: WILEY

摘要:

AbstractThe erythropoietin receptor (EpoR) is a type I transmembrane protein that is a member of the family of hemopoietin receptors. Several members of this family have soluble receptor forms that are secreted by the cells rather than expressed on the cell surface. An alternatively spliced EpoR transcript has been described in human erythroid precursors that, if translated, would produce a truncated, soluble EpoR lacking the transmembrane domain. To determine if the human EpoR is expressed in a soluble form, we developed a sensitive enzyme‐linked immunosorbent assay (ELISA) for the EpoR, and we analyzed human serum and plasma. Sheep were immunized with a fusion protein (EREx) consisting of glutathione‐S‐transferase (GST) and the human EpoR extracellular domain. The sheep antiserum was affinity‐purified on immobilized EREx, and then used in a two‐stage antigen capture ELISA. The plasma from 20 normal subjects was studied with this assay. There was wide variability in the levels of soluble EpoR in these subjects (range,<10–2,200 ng/ml). An average value of 550 ± 735 ng/ml for soluble EpoR was obtained in these normals. Protein A adsorption of the test plasma prior to the assay had no effect on the values obtained. Assay of serum from the same normal subjects showed an average decrease of 88% in soluble EpoR levels compared to plasma. There was no correlation between hematocrit and soluble EpoR level. This assay may have utility in the further elucidation of erythropoietin physiology. © 1996 Wi

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199605)52:1<8::AID-AJH2>3.0.CO;2-Z

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1996

数据来源: WILEY

摘要:

AbstractPatients with polycythemia vera (PV) or essential thrombocythemia (ET) show a high frequency of thrombosis. The reduction of hematocrit after phlebotomy and normalization of platelet counts do not completely eliminate thrombotic risk. Some preliminary studies reported a reduction in the concentration of natural anticoagulants (NA) in this group of patients. For this reason we evaluated protein S (PS) total antigen, antithrombin III (AT III), and protein C (PC) activity in 81 patients with chronic myeloproliferative disorders (33 with PV and 48 with ET). Data were compared with those obtained in 70 healthy sex‐ and age‐matched subjects. Fifty‐seven percent of patients (46 out of 81) showed one or more thrombotic episodes at diagnosis or during follow‐up. Interestingly, we found a NA deficit in 43.5% of patients with thrombosis versus only 5.7% in the group of patients without thrombosis. These results may suggest new interpretations about the pathogenesis of thrombosis in PV or ET patients. © 1996 Wiley

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199605)52:1<14::AID-AJH3>3.0.CO;2-9

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1996

数据来源: WILEY

摘要:

AbstractSixty cases of B‐cell nodal non‐Hodgkin's malignant lymphoma (B‐ML), and 46 cases of T‐cell nodal lymphoma (T‐ML) were surveyed for Epstein‐Barr virus (EBV) genomes, RNA, and associated proteins. We used a Southern blot analysis, polymerase chain reaction (PCR), and EBV‐encoded small RNA‐1 (EBER‐1) in situ hybridization to investigate the presence of EBV. We performed an immunohistochemical study on EBV‐related oncoproteins, such as EBV‐determined nuclear antigen‐2 (EBNA‐2), latent membrane protein (LMP), and viral interleukin‐10 (vIL‐10). In addition, we also analyzed the terminal repetitive sequence of EBV (EBV‐TR) to investigate the EBV‐infected cell clonality. Non‐Hodgkin's lymphomas were grouped into three types by number of EBV‐infected cells: I) almost all lymphoma cells showed an EBV presence; II) some scattered lymphoma cells showed an EBV presence; and III) only a few cells showed such a presence, which was probably due to a latent EBV infection. In 25 of 60 B‐MLs, EBV‐infected cells were found; 7 were type I, 1 was type II, and 17 were type III. In 27 of 46 T‐MLs, EBV‐infected cells were found; no cases were type I, 5 cases were type II, and 22 cases were type III. Seven B‐MLs and 3 T cell lymphomas showed clonal TR bands. Expression of EBNA‐2 was found in only three B‐MLs, whereas LMP was seen in four B‐MLs and six T‐MLs. All EBNA‐2/LMP‐positive cases showed an EBV presence. In B‐MLs, expression of EBNA‐2 and LMP was detected in almost all lymphoma cells; In T‐MLs, however, LMP was found in only a small portion of the lymphoma cells. Expression of IL‐10 was closely associated with LMP. In summary, it was thus speculated that EBV infection was associated

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199605)52:1<21::AID-AJH4>3.0.CO;2-8

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1996

数据来源: WILEY

摘要:

AbstractImmunophenotyping of peripheral blood lymphocytes from six patients with B‐cell chronic lymphocytic leukemia (B‐CLL) and five normal volunteers was done and their T and Tn epitopes analyzed using specific monoclonal antibodies and flow cytometry. Lymphocytes from all patients showed strong Tn expression as compared to normal control lymphocytes. By contrast, T antigen was not expressed. The Tn expression may be a useful diagnostic and prognostic marker for B‐CLL. © 1996 Wiley‐L

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199605)52:1<29::AID-AJH5>3.0.CO;2-8

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1996

数据来源: WILEY

摘要:

AbstractDuring a physical checkup, a 42‐year‐old Japanese man with liver dysfunction was diagnosed as having β‐thalassemia. Using molecular biological techniques including PCR, we investigated the chemical basis of the hematological disorder. We found that a frameshift attributable to the insertion of a thymidine into or following the TTT sequence of codon 42 transformed codon 43 (GAG) into a stop codon (TGA). We believe that this mutation has not been previously reported. © 1996 Wiley‐

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199605)52:1<39::AID-AJH6>3.0.CO;2-7

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1996

数据来源: WILEY

摘要:

AbstractIn polycythemia vera (PV), treatment with chlorambucil and radioactive phosphorus (p32) increases the risk of leukemic transformation from 1% to 13–14%. This risk has been estimated to be 1–5.9% with hydroxyurea (HU) therapy. When compared with historical controls, the risk with use of HU does not appear to be statistically significant. The leukemogenic risk of HU therapy in essential thrombocytosis (ET) and in myelofibrosis with myeloid metaplasia (MMM) is unknown. HU remains the main myelotoxic agent in the treatment of PV, ET, and MMM. We studied 64 patients with these three disorders, seen at our institution during 1993–1995. The patients were studied for their clinical characteristics at diagnosis, therapies received, and development of myelodysplasia or acute leukemia (MDS/AL). Forty‐two had PV, 15 ET, and 6 MMM, and 1 had an unclassified myeloproliferative disorder. Of the 42 patients with PV, 18 were treated with phlebotomy alone, 16 with HU alone, 2 with p32, 2 with multiple myelotoxic agents, and 2 with interferon‐α(IFN‐α). Two patients from the phlebotomy‐treated group, one from the HU‐treated group, and 1 from the multiple myelotoxic agent‐treated group developed MDS/AL in the larger group, 11 received no treatment or aspirin alone, 18 were treated with phlebotomy alone, 25 with HU, 5 with multiple myelotoxic agents, 2 with p32, 2 with IFN‐α, and 1 with melphalan. Study of the entire group of 64 patients showed that only one additional patient (total of 5 out of 64) developed MDS/AL. This patient had been treated with HU alone. Statistical analysis did not show any association between clinical characteristics at diagnosis, or HU therapy, and development of MDS/AL (P= 0.5). Thus, our data provide no evidence suggestive of increased risk of transformation to MDS/AL with HU therapy in PV, ET, and MMM. Larger, prospective studies are needed to study this issue further.

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199605)52:1<42::AID-AJH7>3.0.CO;2-6

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1996

数据来源: WILEY

摘要:

AbstractA small number of patients seropositive for the human immunodeficiency virus (HIV) have been reported as developing acute non‐lymphoblastic leukemia (ANLL). In the cases previously published, the authors never reported a study of the link joining HIV infection and leukemia. We describe here the case of a 41‐year‐old HIV positive patient who developed ANLL (FAB classification M5). Using molecular techniques, we looked for a direct link between these two co‐existing diseases. We showed the absence of HIV expression in the malignant clone, suggesting that the association of ANLL and Acquired Immune Deficiency Syndrome is not a direct consequence of the myeloid precursors infection. Nevertheless a relationship may exist through a disorganization of the bone marrow micro‐environment. © 1996 Wiley

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199605)52:1<47::AID-AJH8>3.0.CO;2-6

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1996

数据来源: WILEY

摘要:

AbstractWe report a case of human T‐cell lymphotropic virus type 1 (HTLV‐1)‐infected adult T‐cell lymphoma that has multiple chromosomal abnormalities, including the presence of an additional 7q22‐36, which contains the locus of the T‐cell receptor (TCR) beta chain gene. Specific TCR Jβ1/Jβ2 gene rearrangements were detected in both marrow and peripheral blood DNA, with evidence of further evolution of the transformed clonal population within the peripheral lymphocytes. To our knowledge, this is the first case in which gene rearrangements have been associated with additional TCR loci. Consequently, it is advised that every effort should be made to correlate chromosomal abnormalities with gene rearrangement by molecular methods. © 1996 W

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199605)52:1<53::AID-AJH9>3.0.CO;2-5

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1996

数据来源: WILEY

摘要:

AbstractParaneoplastic pemphigus (PNP) is an autoimmune disorder occurring in the setting of an underlying neoplasm in which patients have polymorphous skin and mucous membrane lesions.We describe a patient with non‐Hodgkin's lymphoma who developed bullous, ulcerating lesions in an area being treated with radiation therapy. The diagnosis of PNP was confirmed by indirect immunofluorescence of the patient's serum on rat bladder. The disorder was refractory to therapy, and ultimately the patient expired. © 1996 Wiley‐Liss,

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199605)52:1<58::AID-AJH10>3.0.CO;2-3

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1996

数据来源: WILEY