Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of tuberculous pleurisy due to Mycobacterium fortuitum in a 47-year-old woman with chronic granulocytic leukemia is described. The mycobacterial aetiology of the pleurisy was confirmed by pleural biopsy and by positive culture of M. fortuitum in pleural fluid. Antituberculosis chemotherapy with INH, RMP and EMB, combined initially with prednisolone, was successful in spite of total resistance of the strain to the drugs used. A short review of mycobacterioses and of recent literature on the topic, especially on M. fortuitum, is also presented.
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PMID:Tuberculosis pleurisy due to Mycobacterium fortuitum in a patient with chronic granulocytic leukemia. 106 52

Eight patients with haematologic malignancies contracted fatal invasive aspergillosis during an outbreak. Five patients were neutropenic. Bronchofiberoscopic examination with microbiology specimen brush and bronchoalveolar lavage yielded Aspergillus fumigatus in only 2/5 patients examined. The specific diagnosis reached during lifetime in 5 patients was based on a combination of invasive procedures (lung biopsy in 2, percutaneous lung puncture in 1), the presence of a lung abscess (3 patients), seroconversion (1 patient), and purulent maxillary sinusitis caused by A. fumigatus together with repeated abundant growth of A. fumigatus in the sputum (1 patient). Six patients received amphotericin B. The infection was temporarily controlled only in 2 bone marrow transplant recipients whose granulocyte counts recovered. In 3/8 patients the pneumonia was of polymicrobial aetiology, Mycobacterium tuberculosis (2 patients), Pneumocystis carinii (1 patient), and Legionella pneumophila (1 patient) being the other microbes involved. 3/4 bone marrow transplant recipients with aspergillosis had been transplanted for chronic myeloid leukaemia, supporting the previously reported association of bone marrow transplantation for chronic myeloid leukaemia and the risk of invasive aspergillosis. Improved diagnostic methods for earlier definitive diagnosis of invasive aspergillosis as well as more efficacious and less toxic antifungal agents are needed to allow early treatment.
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PMID:Invasive pulmonary aspergillosis: a diagnostic and therapeutic problem. Clinical experience with eight haematologic patients. 332 14

Remarkable chromosome abnormalities were observed in bone marrow cells from a woman with chronic myelocytic leukemia and atypical tuberculosis due to Mycobacterium avium-intracellulare infection. Four chromosome breaks occurred at bands 1p13, 1q32, 11p15, and 22q11. These breaks resulted in a complex Philadelphia (Ph) translocation between chromosomes #1, #11, and #22 and in an inversion of chromosome #1. Oncogenes on these chromosomes include N-ras and c-sk on chromosome #1, c-H-ras on chromosome #11, and c-sis on chromosome #22. Complex chromosome rearrangements may facilitate multiple oncogene changes, thereby permitting several steps in cancer development to occur simultaneously.
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PMID:The Philadelphia (Ph) chromosome in leukemia. III. Complex Ph translocation plus inversion in chronic myelocytic leukemia. 385 75

Mycobacterium xenopi was isolated from bronchoscopic and resected lung specimens from a patient who had diabetes mellitus and chronic myelogenous leukemia. While in remission, the patient developed spreading pulmonary infiltrates and died. At postmortem examination, acid fast bacilli were found in enormous numbers in histologic preparations of pulmonary hilar and mesenteric lymph nodes. Concomitant pulmonary infection with Aspergillus, Pneumocystis carinii, and cytomegalovirus was also evident. The probable dissemination of M. xenopi to pulmonary hilar and mesenteric lymph nodes attests to its invasive potential in the immunocompromised host and reinforces its role as an agent of nontuberculous mycobacterial disease.
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PMID:Mycobacterium xenopi: infection in an immunocompromised host. 710 49

A patient with chronic myeloid leukaemia developed bone marrow granulomas during treatment with interferon alpha-2b. Some granulomas had necrotic centres and giant cells and there was marked eosinophilia surrounding them. The granulomas disappeared when the interferon treatment was discontinued. Mycobacteriosis was ruled out. The most likely explanation for the granuloma formation was drug hypersensitivity.
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PMID:Granulomatous bone marrow inflammation during treatment of chronic myeloid leukaemia with interferon alpha-2b. 749 Mar 29

The pathogenic mechanisms of immunosuppression leading to susceptibility of Mycobacterium tuberculosis (MT) infection in chronic myelocytic leukemia (CML) are not clear. To address this issue, we measured the proliferative response, variation of T cell subpopulations (CD4+, CD8+, TCR-V delta 2 and TCR-V beta 8 T cells) and the cytokine profile (IL-1 beta, IL-2, IL-4, IL-6, IL-10, TNF-alpha, IFN-gamma) after MT stimulation of peripheral blood mononuclear cells (PBMC) in a patient with concomitant CML and active pulmonary tuberculosis. The results were compared to four patients with active pulmonary tuberculosis and no other coexistent diseases. The immunologic response to phytohemagglutinin (PHA) was also evaluated. In contrast to controls, the CML PBMC failed to proliferate in response to MT antigens. Mycobacterium-reactive CD4+, V delta 2 and V beta 8 T cells did not expand after MT stimulation of the CML PBMC. In MT antigens-stimulated cultures from the CML patient, IL-2 was not produced and mild reduction of IL-1 beta and INF-gamma were observed. In contrast, IL-10 was markedly elevated in these cultures. Similarly, PHA-stimulated PBMC from the CML patient showed no expansion of CD4+ and CD8+. T cells. In these cell cultures, INF-gamma concentration in supernatants was decreased and IL-10 was significantly elevated. This study suggests that patients with CML may present a profound immunosuppression of essential cellular and molecular immune effectors, a scenario which might contribute to the development of active tuberculosis. These findings further support the need of establishing immunotherapeutic modalities with potential value for myeloproliferative disorders.
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PMID:Abnormal immunological response to Mycobacterium tuberculosis antigens in a patient with chronic myelocytic leukemia and active tuberculosis. 1002 42

Allogeneic bone marrow transplant recipients are prone to pulmonary infections caused by a wide spectrum of organisms. Since the first bone marrow transplatation (BMT) done in 1983 at the Tata Memorial Hospital, we have recently seen the first case of Mycobacterium Fortuitum Chelonae complex among 117 BMT (including 90 allogeneic and 27 autologous) patients. The patient was on immunosuppressants for chronic GVHD post allogeneic BMT done for CML-CP. He developed pulmonary mycobacterial infection 13 months post BMT. Diagnosis was difficult because of the atypical presentation, negative culture reports, and the presence of multiple pathogens due to immunosuppression. In our case the diagnosis was eventually established after examination of material obtained by bronchoscopy. Patient has shown response to antituberculosis drugs after 2 months. This shows the need to consider atypical mycobacterial infection in the differential diagnosis of pulmonary illness in the post allogeneic BMT setting.
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PMID:Mycobacterial pulmonary infection post allogeneic bone marrow transplantation. 1142 41

Forty isolates of rapidly growing Mycobacteria, Mycobacterium fortuitum group including M. fortuitum and M. peregrinum and M. chelonae group including M. chelonae subsp. chelonae and M. chelonae subsp. abscessus at Showa University Fujigaoka Hospital collected between February 1981 and December 1997 were investigated in this study. These isolates were from the patients who were not infected with HIV. The average age of fourteen patients, from whom M. fortuitum group was isolated, was 58 years, ranging from 17 to 80 years old. One patient (71-year-old) with chronic myelogenous leukemia and another (64-year-old) with chronic diabetes mellitus were diagnosed with skin abscesses of M. fortuitum group, which were located on the right site of the neck and in the scar after injecting insulin (injection abscess), respectively. The average age of twenty-six patients, from whom M. chelonae group was isolated, was 57 years, ranging from 32 to 84 years old. One patient (75-year-old) with articular rheumatism was diagnosed with a lung infection of mixed M. chelonae group and Pseudomonas aeruginosa, and another (74-year-old) with diabetes mellitus and kidney failure was strongly suspected of a lung infection. The isolates of the two mycobacteria from the remaining patients were due to colonization, while these patients had the following underlying diseases contributing to infections: pulmonary emphysema; diabetes mellitus; leukemia; collagen diseases; lung cancer; chronic kidney diseases; systemic lupus erythematosus; carcinomatous pleurisy; bronchiectasis; post-tuberculosis. Most isolates of the two mycobacteria were separated from the specimens of patients' respiratory tracts, but since M. chelonae group was a contaminant in the tap-water for diluting concentrated chlorhexidine, the organism happened to be isolated with the mucous membranes of the 6 patients' colons that were picked up while using the washed fiber-scope. These findings suggest that M. fortuitum and M. chelonae groups, in spite of the fact that they rarely cause infection, have a significant risk of infecting aged patients in general hospitals with various underlying diseases attributable to infections. As only a few colonies were isolated from patients' specimens in the majority of cases, it took time to carry out these clinical examinations, and to improve this "laboratory's delay", it is needed to make faster report to clinicians.
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PMID:[Evaluation of rapidly growing Mycobacteria isolates in a general hospital: reports from the hospital microbiology laboratory]. 1144 97

A 64-year-old woman with chronic myelogenous leukemia (CML) was admitted due to prolonged fever and lung infiltrates. An open lung biopsy was required to make the diagnosis of pulmonary alveolar proteinosis (PAP) and infection with Mycobacterium kansasii. She was treated successfully with combined antimycobacterial therapy for 14 months. However, the leukemia progressed and the patient developed recurrent bilateral lung infiltrates. Blood and bronchoalveolar fluid cultures yielded growth of Acinetobacter. She died shortly thereafter due to septic shock. The relationship between M. kansasii infection, PAP, and abnormal host defense in CML is discussed.
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PMID:Disseminated Mycobacterium kansasii infection with pulmonary alveolar proteinosis in a patient with chronic myelogenous leukemia. 1458 59

BXH-2 mice develop a fatal myeloid leukemia by a two-step mutagenic process. First, a BXH-2-specific recessive mutation causes a myeloproliferative syndrome. Second, retroviral insertions alter oncogenes or tumor suppressors, resulting in clonal expansion of leukemic cells. We have identified a recessive locus on chromosome 8 (Myls) that is responsible for myeloproliferation in BXH-2. This Myls interval has been narrowed down to 2 Mb and found to contain several positional candidates, including the interferon consensus sequence-binding protein 1 gene (Icsbp, also known as interferon regulatory factor 8 [IRF8]). We show that BXH-2 mice carry a mutation (915 C to T) resulting in an arginine-to-cysteine substitution at position 294 within the predicted IRF association domain of the protein. Although expression of Icsbp1 mRNA transcripts is normal in BXH-2 splenocytes, these cells are unable to produce interleukin 12 and interferon-gamma in response to activating stimuli, confirming that R294C behaves as a loss-of-function mutation. Myeloproliferation in BXH-2 mice is concomitant to increased susceptibility to Mycobacterium bovis (BCG) despite the presence of resistance alleles at the Nramp1 locus. These results suggest a two-step model for chronic myeloid leukemia in BXH-2, in which inactivation of Icsbp1 predisposes to myeloproliferation and immunodeficiency. This event is required for retroviral replication, and subsequent insertional mutagenesis that causes leukemia in BXH-2 mice.
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PMID:A mutation in the Icsbp1 gene causes susceptibility to infection and a chronic myeloid leukemia-like syndrome in BXH-2 mice. 1578 80


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