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)

A high seropositivity rate of human T cell lymphotropic virus type 1 (HTLV-1) infection was found in Jamaican patients with chronic diseases. However, except for tropical spastic paraparesis, polymyositis, adult T cell leukaemia/lymphoma and polyneuropathies of undetermined cause, HTLV-1 seropositivity rates in chronic disease patients were not significantly different from that found in healthy Jamaicans. These results indicate that there is no increased risk of HTLV-1 infection or HTLV-1 associated disease in patients with chronic diseases compared to the general Jamaican population. The association of unclassified polyneuropathies with HTLV-1 reported herein is a novel one which requires further studies to elucidate its nature.
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PMID:Seroprevalence of HTLV-1 in chronic disease patients in Jamaica. 757 Aug 19

Between October 1988 and December 1992, 167 patients with leukemia receiving marrow transplants from HLA-identical donors and conditioned with cyclophosphamide (120 mg/kg) were randomized to additional treatment with either busulfan (16 mg/kg, n = 88) or total body irradiation (TBI; n = 79). The busulfan-treated patients had an increased cumulative incidence of veno-occlusive disease of the liver, ie, 12% compared with 1% in the TBI group (P = .009). Furthermore, hemorrhagic cystitis occurred in 24% of the busulfan patients versus 8% in the TBI patients (P = .003). In patients with advanced disease beyond first remission or first chronic phase, transplantation-related mortality was 62% among the busulfan-treated patients compared with 12% among the TBI recipients (P = .002). These differences between the two groups were statistically significant in multivariate analysis. Seizures were seen in 6% of the busulfan-treated patients and were absent in the TBI group (P = .03). Grade II-IV of acute graft-versus-host disease (GVHD) was similar in the two groups, but grade III-IV and chronic disease was more common in the busulfan-treated group (P = .04). Death associated with GVHD occurred in 17% of the busulfan-treated group and 2% of the TBI group (P = .003). Patients treated with busulfan had a 3-year actuarial survival of 62%, which was worse than the 76% among those treated with TBI (P < .03). In multivariate analysis, poor survival was associated with advanced disease (P < .0001), no posttransplant septicemia (P = .0006), grade II-IV GVHD (P = .006), and busulfan treatment (P < .02). The incidence of relapse did not differ between the two groups. Relapse-free survival was also similar in the two treatment groups on analysis of data from all patients, children, patients with early disease, and those with acute myeloid leukemia, acute lymphoblastic leukemia, and chronic myeloid leukemia. However, in adults (P = .05) and patients with advanced disease (P = .005), leukemia-free survival was significantly better in those treated with TBI. We conclude that patients treated with busulfan have more early toxicity and an increased transplant-related mortality in patients with advanced disease. TBI is therefore the treatment of choice, especially in adults and patients with advanced disease. However, busulfan is an acceptable alternative for patients with early disease and for those in whom TBI is not feasible.
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PMID:A randomized trial comparing busulfan with total body irradiation as conditioning in allogeneic marrow transplant recipients with leukemia: a report from the Nordic Bone Marrow Transplantation Group. 816 51

Cluster outbreaks of lymphoma and leukemia have been associated with viral infections in many species including humans, cattle, and cats. This study describes epidemiological, clinical, and pathological features of cluster outbreaks of lymphoma in multiferret households and examines and compares the Aleutian disease virus (ADV) and feline leukemia virus (FeLV) status of cases, ferrets at risk, and controls. Three ferret groups with 21 cases of histologically diagnosed lymphoma (12.6% cumulative incidence) and their cohabitants (n = 35) were examined and compared with three control groups (n = 52) of cohabitating ferrets without lymphoma. A familial distribution was observed in one group but most cases were not consanguinous. Ferrets greater than 3 years of age developed chronic disease in two of the groups and 2-year-old adults had acute disease in the remaining group. Lymphocytosis, splenomegaly, and lymphadenopathy were prominent features. Histologically, predominantly small noncleaved cell and polymorphous lymphoid lesions were observed. All of the ferrets with lymphoma that were tested for ADV and FeLV using serology or PCR were negative. The rate of ADV antibody among cases or ferrets at risk was not significantly different from controls. None of the cluster ferrets were seropositive for FeLV p27 antigen using a monoclonal ELISA. Infection with a novel ferret virus is suspected, but an etiological agent has not yet been identified.
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PMID:Clusters of lymphoma in ferrets. 863 Jun 83

Since human lymphotropic virus, type 1(HTLV-1) associated adult T-cell leukemia (ATL) has various clinical appearances and courses, it is difficult for the clinician to differentiate acute disease which needs immediate treatment from chronic disease which can be observed with no specific treatment. The Lymphoma Study Group of Japan (1984-87) proposed four clinical subtypes: (1) smoldering type; more than 5% of abnormal T-lymphocytes with less than 4000/microliters of lymphocytes in peripheral blood and few abnormal blood chemistry profiles and ATL infiltration, (2) chronic type; absolute lymphocytosis with T-lymphocytosis of more than 4000/microliters, LDH < 2 times the normal upper limit and no hypercalcemia with possible lymph-node, liver, spleen, skin and lung involvement, (3) lymphoma type; no lymphocytosis with less than 1% of abnormal T-lymphocytes, and histologically-proven lymph-node enlargement, and (4) acute type; the patients not classified into any of the above 3 types. The median survival time (MST) was 6.2 months for acute type, 10.2 months for lymphoma type, and 24.3 months for chronic type; 62.8% of smoldering type was still alive up to 4 years. ATL has a poor prognosis because of life-threatening complications including infections and hypercalcemia. Among infectious complications, cytomegalovirus (CMV) is frequently encountered in autopsy patients. It is important to make an early diagnosis since an anti-CMV agent, ganciclovir is now available for clinical use. It takes 10-14 days to culture CMV in vitro, but now rapid diagnosis can be made by direct immunoperoxidase staining with human monoclonal antibodies against an immediate-early antigen. Another major complication is hypercalcemia. The patients' serum and tumor tissues are found to have parathyroid hormone related protein (PTHrP) associated with hypercalcemia. Serum PTHrP (1-34) is determined by radioimmunoassay and its values seem to be correlated with hypercalcemia and the disease activity. There are still many problems to solve for ATL, but recent advances have been made in clinical subtypes and the above 2 complications.
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PMID:[Clinical classification of adult T-cell leukemia and its complications]. 869 35

In the majority of clonal expansions of CD3+ large granular lymphocytes (LGL), referred to as T-LGL leukemia, patients have a chronic disease, often manifested by severe neutropenia, rheumatoid arthritis, and mild to moderate splenomegaly. The characteristic leukemic phenotype is CD3+, CD8+, CD16+, CD57+ and CD56-. Here we report an unusual case of T-LGL (CD3cyt+, CD3surface-, CD16+, CD56-) with clinicopathological features (acute presentation, large tumor mass, and systemic illness with highLGL counts at diagnosis) similar to those described for patients with CD3-natural killer (NK)-LGL leukemia. Two distinct stages of maturation arrest were observed: in the lymph node abnormal cells were CD4+, CD8+ whereas the majority of circulating leukemic cells expressed only CD8. TCR gamma (TCR gamma) gene configuration demonstrated that these originated from the same T cell clone, suggesting a maturation process between the two populations, or preferential passage of CD8 single positive cells into the blood.
Leukemia 1996 Sep
PMID:Aggressive acute CD3+, CD56- T cell large granular lymphocyte leukemia with two stages of maturation arrest. 875 72

The most frequently discussed ethical issue on the subject of cancer is whether patients should be told their diagnosis. Cancer patients' knowledge of their diagnosis and the relationship between patient characteristics and that knowledge were evaluated in a cross-sectional study. From July 1992 to December 1993 at Tri-Service General Hospital, Taipei, a total of 964 patients with cytologically- or pathologically-proven cancer were studied. Of those studied, 359 patients (37.2%) knew their diagnosis. The proportion of patients who believed that they had a benign tumor was 25.1%; 12.6% believed they had nonneoplastic disease (inflammation or other chronic disease); 7.5% believed they had precancerous changes; and 17.6% knew nothing about their diagnosis. Multivariate analyses showed that patients with the following characteristics were inclined to know their diagnosis: younger age (20-59 yr), higher levels of education (> 9 yr) with relatives of a high socioeconomic status, cancer of a genital organ, cancer requiring disfiguring treatment (osteosarcoma, leukemia), cancer in obvious sites (head and neck), cancer of more than one type (multiple primary lesions), cancer of good prognosis (excluding lung, liver, gall bladder or pancreatic cancers), aggressive anticancer treatment and longer duration of pathologic proof (> 14 d). The results showed that concealing the diagnosis from cancer patients is still very common in Taiwan. Patient's sociodemographic background and disease-related factors were the most important patient characteristics related to their knowledge of the diagnosis.
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PMID:Cancer patients' knowledge of their diagnoses. 887 Apr 30

T cell chronic lymphocytic/prolymphocytic leukemia (T-CLL/T-PLL) and large granular lymphocyte leukemia of T or NK cell type (T-LGL or NK-LGL leukemia) are chronic lymphoproliferative diseases derived from post-thymic immunocompetent lymphoid cells. T-PLL is morphologically characterized by a prominent central nucleolus in a medium-sized cell expressing a mature T cell immunophenotype. Clonal genetic changes involving chromosome 14 and T cell receptor gene rearrangements are characteristics of these diseases. They are usually progressive and there is no efficient treatment available. The classification of some cases presenting with a morphological picture similar to B-CLL, but with immunophenotypic and clinical features resembling T-PLL, as T-CLL is still controversial. The phenotypic profiles and the establishment of clonality are the hallmarks of defining T-LGL leukemia and NK-LGL leukemia. The CD3+/CD57+/CD56- immunophenotype and the clonal rearrangement of the T cell receptor genes characterize T-LGL leukemia, which presents clinically with a rather indolent course of disease, complicated by frequent infections secondary to neutropenia. NK-LGL leukemia cells express CD3-/CD56+/CD57-, but in most cases clonality cannot easily be established. Clinically the patient may either present with constitutional symptoms and suffer a short and aggressive course of disease or may have a more chronic disease similar to T-LGL leukemia. Therefore, it may be reasonable to subdivide NK-LGL proliferation into the more aggressive 'NK-LGL leukemia/lymphoma' and 'chronic NK cell lymphocytosis'.
Leukemia 1997 Apr
PMID:Chronic lymphatic leukemias of T and NK cell type. 917 39

Large granular lymphocyte leukaemia (LGL leukaemia) is a rare, chronic lymphoproliferative bone marrow disease which can be considered a subtype of chronic T-cell lymphocytic leukaemia (T-CLL). We describe three patients with large granular lymphocyte leukaemia. They all suffered from chronic disease with neutropenia and relative lymphocytosis. An expansion of mature lymphocytes with the CD3+, CD8+, CD57+ immunophenotype was demonstrated in all three patients. Two patients had a history of recurring infections. Serological findings compatible with rheumatic disease were present in all three patients, and two suffered from rheumatoid arthritis. We have made a brief survey of this disease, which is characterized by relative or absolute lymphocytosis, neutropenia, and an increased risk of infection. Rheumatoid arthritis and other associated autoimmune manifestations occur frequently. Large granular lymphocyte leukaemia should be considered a possible diagnosis in patients with chronic neutropenia and relative lymphocytosis, in particular if rheumatic manifestations are also present. Flow cytometric immunophenotyping is a sensitive method in diagnosing this disease.
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PMID:[Large granular lymphocytic leukemia]. 953 26

CD95 (Fas)-induced apoptosis plays a critical role in the elimination of activated lymphocytes and induction of peripheral tolerance. Defects in CD95/CD95L (Fas-Ligand)-apoptotic pathway have been recognized in autoimmune lymphoproliferative diseases (ALPS) and lpr or gld mice and attributed to CD95 and CD95L gene mutations, respectively. Large granular lymphocyte (LGL) leukemia is a chronic disease characterized by a proliferation of antigen-activated cytotoxic T lymphocytes. Autoimmune features such as hypergammaglobulinemia, rheumatoid factor, and circulating immune complexes are common features in LGL leukemia and ALPS. Therefore, we hypothesize that expansion of leukemic LGL may be secondary to a defective CD95 apoptotic pathway. In this study, we investigated expression of CD95 and CD95L in 11 patients with CD3(+) LGL leukemia and explored the apoptotic response to agonistic CD95 monoclonal antibody (MoAb). We found that leukemic LGL from each patient expressed constitutively high levels of CD95/CD95L, similar to those seen in normal activated T cells. However, cells from 9 of these 11 patients were totally resistant to anti-CD95-induced apoptosis. Similarly, cells were resistant to anti-CD3-MoAb-triggered cell death. Lack of anti-CD95-induced apoptosis was not due to mutations in the CD95 antigen. Leukemic LGL were not intrinsically resistant to CD95-dependent death, because LGL from all but 1 patient underwent apoptosis after phytohemagglutinin/interleukin-2 activation. The patient whose leukemic LGL were intrinsically resistant to CD95 had an aggressive form of LGL leukemia that was resistant to combination chemotherapy. These findings that leukemic LGL are resistant to CD95-dependent apoptosis despite expressing high levels of CD95 are similar to observations made in CD95L transgenic mice. These data suggest that LGL leukemia may be a useful model of dysregulated apoptosis causing human malignancy and autoimmune disease.
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PMID:Dysregulation of CD95/CD95 ligand-apoptotic pathway in CD3(+) large granular lymphocyte leukemia. 984 44

In two female patients aged 44 and 86 years, a chronic lymphocytosis was observed caused by a proliferation of large granular lymphocytes (LGL). The first one had been successfully treated for Hodgkin lymphoma long before, the second had diabetes mellitus type 2. Immunophenotyping showed the proliferating lymphocytes to be natural killer (NK) cells. In contrast to the proliferation of B- and T-lymphocytes, data on the prognosis and treatment of NK-lymphocytosis are very scarce. A literature search revealed three major clinical entities in which LGL proliferate: at one end of the spectrum we see the very aggressive NK-LGL leukaemia, at the other, NK-lymphocytosis, a benign chronic disorder, in between is the relatively indolent chronic T-LGL leukaemia. Both patients suffered from chronic NK-lymphocytosis with a favourable course; there were no further symptoms 4 and 2 years, respectively, after the diagnosis. In cases of prolonged lymphocytosis of unknown origin, immunophenotyping of the lymphocytes is essential. Only in this way can one arrive at the proper diagnosis and reach conclusions as to the prognosis and the possible methods of treatment.
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PMID:[Two patients with chronic lymphocytosis of large granular lymphocytes; benign or premalignant?]. 1091 13


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