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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinicopathologic features of 14 patients with angioimmunoblastic lymphadenopathy (AIL)-related lesions were analyzed. Lymph node biopsy specimens from all the patients showed a diffuse obliteration of lymph node architecture, prominent vascular proliferation, a polymorphous cellular infiltrate, including immunoblasts, and varying degrees of clear cell proliferation. The patients were eight males and six females, with a median age of 58.5 years. All but one were in an advanced stage at the time of diagnosis. Bone marrow involvement was observed in eight patients. Thirteen patients had a negative serologic reaction for antibody to human T-cell leukemia virus type I (HTLV-I), and one patient was considered to be a HTLV-I carrier. Polyclonal hypergamma-globulinemia was observed in 6 patients, and 6 of the 12 patients showed elevated IgE levels. Immunophenotyping of the involved lymph nodes revealed a preponderance of T-cells in all the patients. Eleven of these patients showed a predominance of CD4+ over CD8+ T-cells, and only one patient showed a predominance of CD8+ over CD4+ T-cells. Two of five patients whose gene analysis was carried out showed clonal rearrangement of the T-cell receptor beta chain gene without rearrangement of the immunoglobulin heavy chain genes. Twelve patients received doxorubicin-containing combination chemotherapy; of these, 7 patients achieved complete response, and the other 5 had partial response. Nine patients are still alive with a median follow-up period of 21 months, and five patients died during the follow-up period. Progression to high-grade T-cell lymphoma with systemic infiltration was ascertained in two of three cases for which autopsy was performed. From our experience, we recommend doxorubicin-containing combination chemotherapy as initial therapy for AIL-related lesions.
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PMID:Clinicopathologic and therapeutic aspects of angioimmunoblastic lymphadenopathy-related lesions. 173 25

A series of T-cell proliferations in peripheral blood, bone marrow, or tissue samples were analyzed for clonality. The technique used employs the polymerase chain reaction to amplify portions of the rearranged T-cell receptor beta chain genes, using primers recognizing conserved sequences of the variable, diversity, and joining region segments. We examined 17 cases of T-cell lymphoma or leukemia; a clone was identified in 13 cases (76%) overall and in 7 of 8 cases (87.5%) in which both beta-chain alleles were known to be rearranged, as shown by restriction enzyme analysis. No clonal rearrangements were detected in samples from 13 non-T-cell disorders, including B-cell lymphomas, reactive lymphoid proliferations, and nonlymphoid tumors. This method is useful for detecting clones in thymic and post-thymic T-cell malignancies and has the advantages of being extremely rapid (a result is obtained within hours of the biopsy procedure), requiring no radiolabeling, using only a small amount of tissue, and being applicable to formalin-fixed, paraffin-embedded tissue.
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PMID:The rapid detection of clonal T-cell proliferations in patients with lymphoid disorders. 201 72

In a previous paper (Proc. Natl. Acad. Sci. USA 84: 4264, 1987) we reported an unusual DNA rearrangement in T-cell receptor beta chain gene loci in cells from a patient with human T-cell leukemia. A D beta 1-J beta 2.3 junction was found on one chromosome, while the other chromosome kept the germline configuration. Although the DNA fragment located between the D beta 1 and J beta 2.3 loci should have disappeared from the cells, it was found on chromosome 6 as an inserted segment. We have now determined the nucleotide sequences bordering both sides of the inserted segment. The signal sequence for D beta-J beta rearrangement at the 5' side of J beta 1.2 gene seems to have been used for the insertion. The 3' end of the inserted segment corresponded to the edge of the signal heptamer at the 5' side of J beta 2.3 which was used for the initial D beta 1-J beta 2.3 joining. This indicates that, during D beta-J beta rearrangement, the intervening sequence was excised as a linear molecule.
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PMID:Evidence that the intervening sequence was excised as a linear molecule during D beta-J beta rearrangement in T-cell receptor beta chain gene loci. 283 88

Thy 1.2+ cells of L8313 leukemia bearing mice were previously shown to produce granulocyte macrophage colony stimulating activity (GM-CSA) and interleukin-3 (IL-3). Cell lines with the Thy 1.2+ phenotype were established from spleen cells of the leukemic mice, and were designated STIL-3 C5 and STIL-3 D10. They produced and released GM-CSA and IL-3 activities in culture supernatant. C5 cells were phenotypically Thy 1.2+ and Lyt 2.1+ with rearrangement of the T-cell receptor beta chain gene also being identified. D10 was Thy 1.2+ and L3T4+ with T-cell receptor beta chain gene rearrangement not detectable. Since the same sized rearranged bands were observed between C5 and L8313 leukemic mouse spleen cells, it is indicated that C5 cells are derived from the leukemic cells. Inoculation of these cells into mice induced granulocytosis. These results indicated that L8313, which was thought to be a "granulocytic leukemia", is actually a T-cell leukemia, whose granulocytosis is a leukemoid reaction induced by normal hemopoietic cells responding to the hemopoietic stimulating factors, GM-CSA and IL-3, produced by the leukemic T cells. Thus, L8313 should be known as a T-cell leukemia associated with granulocytosis.
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PMID:Establishment of a hemopoietic stimulating factor producing murine leukemia cell lines: pathogenesis of granulocytosis in L8313 bearing mice. 290 47

A T-cell line, ATN-1, was established by culturing peripheral blood mononuclear cells derived from a patient with adult T-cell leukemia/lymphoma (ATL/L). Identities of the patterns of chromosomal abnormalities, cell surface phenotypes, morphologic findings, rearrangement patterns of T-cell receptor beta chain gene, and an integration site of human T-cell leukemia virus I proviral genome indicated that ATN-1 was derived from original leukemic cells. Both ATN-1 and the original leukemic cells showed a variety of patterns of chromosomal abnormalities that include 3q-, 6q-, rearrangements involving 2q31, 7q11.2, 8q11, 8q24, 19p13.3, and also 14q11 and 14q32, where genes for the T-cell receptor alpha chain and the immunoglobulin heavy chain are located. Availability of a genuine ATL/L cell line with these chromosomal abnormalities may greatly facilitate the biologic analysis of ATL/L.
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PMID:Cytogenetic characterization of a T-cell line, ATN-1, derived from adult T-cell leukemia cells. 326 Aug 13

We describe a human acute unclassified leukemia with a unique t(4;17) translocation that coexpresses T-lymphoid and myeloid surface antigens after in vitro culture in the presence of the tumor promoter, TPA. Under these conditions, the joining regions of the immunoglobulin heavy chain and T-cell receptor gamma and beta chain complexes remained in germ line configuration. A T-cell receptor beta chain variable gene probe, however, revealed the presence of rearrangements in the V beta M3-2 gene region after bilineage differentiation. These results may be pertinent to the interrelationship of T-cell receptor gene rearrangements and the control of T-cell antigen surface expression.
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PMID:In vitro differentiation of a null-acute leukemia: T-lymphoid surface antigen expression associated with rearrangement in T-cell receptor beta chain variable genes. 349 9

A cDNA clone representing the gene encoding the beta chain of the human T-cell antigen receptor has been isolated recently. By using fragments of this cDNA as hybridization probes in Southern blot analysis of restriction endonuclease-digested genomic DNA, we have now examined the structure of the gene in DNA from 26 patients with acute leukemia and from 23 normal individuals. We have found that the T-cell antigen receptor gene has undergone somatic rearrangement in 14 of 14 patients with the phenotypic diagnosis of T-cell acute lymphoblastic leukemia. In this group of patients, similar patterns of rearrangement appear to occur in different patients. This finding suggests that there is either a limited repertoire of possible rearrangements or an association between the development of leukemia and specific patterns of rearrangement. DNA from 6 patients with acute myeloblastic leukemia, 6 patients with non-B, non-T acute lymphoblastic leukemia, and 23 nonleukemic individuals showed no rearrangement or polymorphism. One case of T-cell acute lymphoblastic leukemia, however, showed rearrangement of both the T-cell receptor beta chain and the constant region of the immunoglobulin gene. Studies with mixtures of DNAs from leukemic bone marrow cells and cultured skin fibroblasts, as well as with remission and relapse marrow DNAs from the same patients, indicate that this technique can detect 1% leukemic cells in a mixed population. In addition, DNA from the marrow of a patient in relapse contains a similar rearrangement to that found in the marrow sample taken at the time of diagnosis, which suggests that the original clone of leukemic cells was responsible for relapse. Our results indicate that assessment of rearrangement of the T-cell antigen receptor gene will be valuable in the diagnosis and management of leukemia and can be used to evaluate clonality in T-cell neoplasia.
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PMID:Somatic rearrangement of T-cell antigen receptor gene in human T-cell malignancies. 385 57

The differentiative capacity of a unique haematopoietic cell type has been investigated. These cells have been found to be a common target in vitro to infection and immortalization by radiation leukemia viruses (RadLVs). Many continuous lines of these cells have been generated. Since RadLV retroviruses are known to be strictly T-cell-tropic in vivo, we have questioned whether these cells are precursors of T cells. To this end, the RadLV-induced C1-V13D cell line has been inoculated into thymus of sublethally irradiated syngeneic CBA/H mice and tested for capacity to proliferate and differentiate, i.e. express T-cell markers. When inoculated in high number, C1-V13D cells can induce a thymic tumour within 14 to 21 days. Expression of T-cell markers on these cells was determined by fluorescence-activated cell sorting (FACS) analysis, after gating out C1-V13D cells on the basis of their high 90 degree scatter and their high forward scatter. They can also be distinguished by their unique expression of RadLVgp70 envelope (env) protein, B220, CD44, and aberrant expression of a class I epitope. Explanted primary thymomas from many animals showed no evidence of T-cell marker expression on C1-V13D cells upon reisolation. However, when C1-V13D was further passaged intrathymically, there was clear expression of Thy-1, CD4, CD8, and TCR-alpha beta on C1-V13D cells reisolated from these tumours. Two-colour FACS analysis and fluorescent antibody staining have confirmed the acquisition of T-cell surface markers by C1-V13D cells growing in this environment. Northern analysis confirmed endogenous expression of T-cell receptor beta chain genes in C1-V13D cells isolated after the third passage. All data indicate that RadLV preferentially infects a unique haematopoietic precursor cell in spleen which can differentiate along the T lineage once located within the thymic environment. The cell lines described here represent valuable models for studying T-cell differentiation from lymphoid stem cells, and for dissecting the early events in leukemogenesis.
Leukemia 1993 Aug
PMID:T-cell differentiative capacity of haematopoietic stem cells immortalized in vitro with radiation leukemia virus. 810 19

We describe a patient with Philadelphia-chromosome-positive (Ph' +) chronic myelogenous leukemia (CML), who developed an anaplastic large cell lymphoma (ALCL) with T-phenotype, after 43 months successful treatment with alpha-interferon (IFN). Characterization studies of lymphoma cells showed positivity for Ki-1 monoclonal antibody, T-cell surface markers, T-cell receptor beta chain rearrangement, and germline configuration of the BCR gene. At the time of lymphoma diagnosis, the patient had achieved complete hematologic remission from CML with partial karyotypic conversion (50% Ph' + cells). After twelve weekly courses of polychemotherapy, he obtained complete remission from lymphoma. At present, five years from CML diagnosis, the patient has a remarkably stable disease, being in remission from lymphoma and in well controlled CML chronic phase. Our case thus represents the first well documented description of a T-cell non-Hodgkin's lymphoma developed during the course of CML.
Leukemia 1993 Nov
PMID:Occurrence of a Ki-1-positive anaplastic large-cell lymphoma in a patient with Ph' positive chronic myelogenous leukemia successfully treated by alpha-interferon. 823 Dec 59

Two patients with chronic myelocytic leukemia (CML) mixed crisis and one with Philadelphia-chromosome-positive (Ph1 +) acute lymphoblastic leukemia (ALL) with cross-lineage nature had a considerable number of granulocytes with monoclonally rearranged immunogenotype. The gene configurations of immunoglobulin heavy chain (IgH), T-cell receptor beta chain (TCR beta), and gamma chain (TCR gamma) in the granulocytic cells were identical to those in the blasts, indicating that both the blasts and the granulocytes were derived from common leukemic progenitors with the IgH gene rearrangements. In a colony assay of cells from in the Ph1 + ALL patient, the leukemic cells showed the potential to differentiate into granulocytes in the presence of either granulocyte-macrophage colony-stimulating factor (GM-CSF) or granulocyte-CSF (G-CSF). Interleukin 7 (IL-7) exerted synergistic effects on colony and cluster formation in cultures with these cytokines. Further, IL-3, GM-CSF, and G-CSF receptor gene expression was found in the leukemic cells. Our findings indicate that the Ph1 + common progenitors in these three patients preserved the potential for granulocytic differentiation even after the occurrence of the Ig (and TCR) gene rearrangements as the first genomic event in lymphocyte differentiation. The phenomenon of cross-lineage in leukemic cells, at least in Ph1 + leukemia, can be considered to demonstrate the potential of leukemic progenitors to differentiate in multiple directions.
Leukemia 1993 Feb
PMID:A granulocytic population with rearranged immunogenotype in chronic myelocytic leukemia blast crisis and Philadelphia-chromosome-positive acute leukemia with cross-lineage nature. 838 Nov 95


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