Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Much progress has been made in allogeneic bone marrow transplantation for severe aplastic anemia (SAA) and acute leukemia (AL). In SAA it was shown that hemopoietic chimerism and apparently permanent cures can be achieved in the majority of patients by conditioning with cyclophosphamide followed by bone marrow transplantation (BMT) from an HLA-identical sibling. The previous transfusion history is crucial for failure or success: untransfused patients do very well while graft rejection is an enormous problem in most polytransfused ones. We have shown that most patients without HLA-identical sibling donors can be adequately helped as well. After conditioning with ALG followed by transfusion of haploidentical marrow and low dose androgens there is partial to complete autologous hemopoietic reconstitution in virtually all patients. This points to the fact that most of these patients have pluripotent hemopoietic stem cells that are intact, but apparently unable to differentiate to mature cells, because they are inhibited by autoimmune mechanisms. The results of BMT in patients with endstage leukemia are modest. New pilotstudies with early marrow grafts, i.e. for ANLL in first remission and for ALL in second remission indicate that with this type of approach potentially over 50% of all patients with HLA-identical siblings can be cured. We recommend that HLA-typing should be performed early in families with SAA and AL and that the possibility of a marrow graft should be seriously considered before the patients have endstage disease. Marrow grafts are technically simple but they may pose enormous problems such as graft versus host reaction (GvH), interstitial pneumonia, graft rejection and leukemic recurrence. Therefore, the procedure should only be performed in highly specialized centers with much knowledge and experience in the immunobiology of bone marrow transplantation.
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PMID:[Bone marrow transplantation in severe aplastic anemia and acute leukemia]. 4 65

We have reported 100 consecutive patients with refractory acute leukemia treated with chemotherapy, total body irradiation (TBI) and marrow from an HLA identical sibling. At the time of the report 17 patients were alive after 11-53 months. All patients have now been followed more than 3 years. At the time of the last report 4 of the 17 patients had relapsed: two in the marrow, one in the central nervous system and one in the testicle. Three of these four patients have died of their disease 27, 34 and 50 months following transplant. The patient with a solitary testicular relapse remains in complete remission 49 months after local irradiation without concomitant systemic therapy. One other patient died 26 months following transplantation from cardiopulmonary complications following multiple respiratory infections. Of the 13 surviving patients, three suffer from chronic graft-versus-host disease. Summaries of the problems encountered in these patients after the first 100 days are presented. Ten of the original 100 patients are living productive lives 36-80 months after transplantation. The data clearly demonstrate that long-term unmaintained remissions are possible in a small fraction of patients with terminal leukemia treated with various chemotherapy regimens and TBI followed by marrow transplantation.
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PMID:Allogeneic marrow grafting for acute leukemia: a follow-up of long-term survivors. 4 72

F(ab')2 fragments of rabbit antibodies specific for human B lymphocytes will block human anti-B lymphocyte alloantibodies. F(ab')2 of anti-beta2m will block HLA alloantibodies. The F(ab')2 fragments can be used to improve the typing of B cell lines and certain leukemia cells which express both HLA and B lymphocyte alloantigens. Pretreatment of these cells with anti-beta2m F(ab')2 preparations allows the observation of B cell alloantigen reactions independently of HLA reactions. Similar use of rabbit anti-B cell F (ab')2 allows HLA reactions to be observed free from the "extra reactions" caused by B alloantibodies that are present in many HLA typing sera.
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PMID:Blocking of HLA and B lymphocyte alloantigens with F (ab')2 fragments of rabbit antibodies. 6 5

The majority of human lymphocytic and myelocytic leukemia cells express a polymorphic antigen that is found on peripheral blood B-lymphocytes and cultured lymphoblastoid B-cell lines. These B-lymphocyte antigens were detected by 34 human alloantisera that were repeatedly absorbed with pooled platelets to remove all activity against HLA antigens and T-lymphocytes. Absorption studies indicated that a common antigen was present on both B-lymphocytes and positive leukemia cells. Leukemia cells could be subdivided into two groups based on the presence of the B-lymphocyte antigen. Fourteen of 18 acute myelocytic leukemia cells, 10 of 13 acute lymphoblastic leukemia cells, 4 of 6 chronic myelocytic leukemia cells, and 2 of 2 chronic lymphocytic leukemia cells were positive. This group of leukemia cells also reacted with rabbit anti-B-cell sera raised to papain digests of spleen cell membranes. F(ab')2 fragments of the rabbit antsera were shown to specifically block the reactions of the human antisera against B-cells and leukemia cells. These results suggested that the rabbit and human anti-B-cell sera were reacting with identical molecules. This conclusion was supported by immunoprecipitation data.
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PMID:Human B-lymphocyte antigens expressed by lymphocytic and myelocytic leukemia cells. II. Detection by human anti-B-cell alloantisera. 6 14

Eight human sera from healthy individuals with no history of immunization with human transplantation antigens have demonstrated complement dependent cytotoxicity to cells of some patients with active acute leukemia. The antigen(s) detected by these sera are absent from normal and remission lymphocytes and appear most often in ALL patients with a high peripheral lymphoblast count. Some B and T lymphoblastoid cell lines carry the antigen(s) as evidenced by their ability to react with and absorb the antileukemia activity. The data support the existence of at least two overlapping specificities detected by these antileukemia sera. The leukemia antigen(s) show no strong correlation with any known HLA antigen. These observations provide evidence for a human leukemia blast associated antigen or set of antigens which may be immunogenic in man. Their relationship to normal HLA antigens of loci other than A, B or C is unknown.
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PMID:Normal human sera cytotoxic to cells of human acute leukemia. 6 21

Leukemia cells from 13 of 27 patients stimulated lymphocytes of their HLA-identical siblings in mixed leukocyte cultures (MLC). Stimulation correlated with high background uptake of tritiated thymidine and high percentages of cells that stained with fluorescein-conjugated polyvalent goat antiserum against human immunoglobulin. Results were similar to those reported with fractionated autologous lymphocyte subpopulations in normal individuals. Investigation of leukemia-specific stimulation in MLC is therefore problematic.
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PMID:Relationship between leukemia antigens and stimulation in mixed leukocyte culture. 6 37

A human serum (obtained from a multiparous and multiple-transfused patient with chronic myelogenous leukemia) and a rabbit antiserum (obtained by immunization with papain extracts from a B-lymphoblastoid cell line) showed reactivity against antigenic specificities (different from HLA) expressed on peripheral blood B-lymphocytes, unmarked lymphocytes, and monocytes. These antigenic determinants were expressed on myeloblasts and lymphoblasts from patients with acute leukemia (during the active phase of their disease) and on B-lymphoblastoid cell lines and lymphocytes from patients with chronic lymphocytic leukemia. Purified peripheral blood T-lymphocytes, mitogen (phytohemagglutinin)-activated T-lymphocytes, and lymphoblasts (with T-cell characteristics) obtained from patients with acute lymphoblastic leukemia or established lymphoblastoid cell lines lacked these antigenic specificities. Absorption experiments indicate that the antigen(s) detected on normal mononuclear cell populations, leukemia cells, and B-lymphoblastoid cell lines were either identical or highly cross-reactive.
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PMID:Recognition by human and rabbit sera of common antigens to leukemia blast cells, peripheral blood B-lymphocytes, and monocytes. 7 Nov 97

Normal human granulocyte alloantigens were found on chronic myelogenous, acute myeloblastic leukemia cells, and a cell line of chronic myeloblastic origin (K562). Antigens were detected by human antisera positive for normal peripheral blood granulocytes but devoid of HLA activity. Very few acute lymphoblastic leukemia cells reacted positively, and none of the chronic lymphocytic leukemia cells seemed to bear granulocyte surface antigens. The recognition of these normal tissue isoantigens on myeloblastic leukemia cells is a necessary prerequisite for the identification of "leukemia-specific" of "leukemia-associated" antigens.
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PMID:Human granulocyte antigens detected on leukemia cells and a chronic myelogenous cell line. 7 3

Acute lymphoblastic leukaemic in two boys relapsed after engraftment of marrow from siblings identical at HLA A, B, and D loci but went into remission during subsequent graft-versus-host reactions without specific anti-leukaemia therapy. Later leukaemic relapse was primarily in extramedullary sites, with little or no involvement of bone-marrow, liver, or spleen. Cytogenetic studies in both cases showed that the relapsed leukaemic blasts were those of the recipients while marrow cells and blood lymphocytes detected during marrow remission originated from the female donors. Blood lymphocytes from one of the recepients kiled. 51Cr-labelled autologous lymphoblast. The prolonged bone-marrow remission in the face of active and even massive extramedullary leukaemia suggests a graft-versus-leukaemia reaction in these two patients.
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PMID:Remission of relapsed leukaemia during a graft-versus-host reaction. A "graft-versus-leukaemia reaction" in man? 7 13

Mixed lymphocyte culture (MLC) studies of families with several leukemia patients, all potential bone marrow transplant recipients, demonstrated that cells from acute myelogenous leukemia patients (5 of 5) and acute undifferentiated leukemia patients (1 of 4) in relapse stimulated autologous lymphocytes as well as lymphocytes from siblings known to be identical at the major histocompatibility linkage group. In the patients studied, the blast transformation induced by leukemia cells was not detectable when the patient was in remission. Stimulation by leukemia cells also elicited increased responses of the lymphocytes from normal haploidentical siblings, parents, and unrelated individuals as compared to stimulation by normal allogeneic cells or leukemia cells of patients with leukemia in remission. The primed lymphocyte test (PLT) was used successfully to establish HLA-D identity of the leukemia patients and their respective HLA-identical siblings, despite high percentages of circulatory blasts. Utilizing lymphocytes from normal siblings primed against the leukocytes from an HLA-identical sibling with leukemia, we also presented results of PLT's which suggested that the stimulation induced by leukemia cells in MLC was produced by leukemia-associated antigens.
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PMID:Antigens associated with acute leukemia detected in the primed lymphocyte test. 14 47


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