Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Only a minority of all patients with CML can today be treated by allogeneic bone marrow transplantation (BMT) but the probability of cure for such patients is high. The complications of BMT are similar to those that occur following transplant for other diseases, notably GVHD, pneumonitis and infections. Of special interest is the demonstration that a graft-versus-leukaemia effect plays a role in the cure of CML. Studies using the polymerase chain reaction to detect minimal residual disease (BCR/ABL transcripts) may prove useful in predicting relapse and optimizing conditioning schedules. It is now important to test whether BMT can be equally successful in older patients (over 50 years) and in those lacking HLA-identical sibling donors. For other patients autografting may offer the possibility of achieving complete cytogenetic remission and perhaps prolonging life.
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PMID:Bone marrow transplantation for chronic myeloid leukaemia. 157 36

Chronic myelogenous leukemia is a clonal proliferative disorder of pluripotent hematopoietic stem cells. Cure may be achieved by myeloablative conditioning treatment and marrow transplantation. In addition, allogeneic marrow can exert a graft-versus-leukemia effect. The graft-versus-leukemia effect may be directed against leukemia-specific antigens or against antigens on all hematopoietic cells, or it can be part of a graft-versus-host reaction. We report an informative post-transplant course of a patient with yet another leukemia-specific effect. This patient was transplanted with marrow from his HLA-identical sister in an advanced phase of CML and developed acute and chronic GVHD. After a severe pneumonia a high proportion of his metaphases in the bone marrow were male and Philadelphia chromosome negative. Later all metaphases were again female and leukemic cells could not be detected by reverse transcriptase polymerase chain reaction analysis (RT-PCR) for BCR/ABL. This course indicates that normal hematopoietic stem cells may survive intensive chemotherapy, bone marrow transplantation and GVHD. They may be recruited from a dormant state into proliferation during severe infections. In contrast, CML may be eliminated by the graft-versus-host reaction that recognizes recruited cells and spares dormant cells.
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PMID:Graft-versus-host reaction spares normal stem cells in chronic myelogenous leukemia. 870 5

This report describes a precise molecular analysis of a rare case of Philadelphia chromosome (Ph) positive acute myeloid leukemia (AML) (FAB classification M2). Phenotypic markers were positive for cells of the myeloid lineage, but negative for B cell and T cell lineage. The leukemic cells carried a Philadelphia chromosome. Major breakpoint cluster region (M-BCR) rearrangement was detected by the Southern blot analysis. Reverse transcriptase polymerase chain reaction analysis revealed the presence of b3a2 BCR/ABL mRNA transcripts. The patient achieved complete remission by conventional remission induction therapy for acute myeloid leukemia. M-BCR rearrangement could not be detected during complete remission. After hematological remission of an 8-month duration, the patient relapsed and died of respiratory distress due to pneumonia. Our case indicate Ph-positive AML with M-BCR rearrangement actually exists. Ph-positive AML carries either M-BCR rearrangement expressing the P210 BCR-ABL or minor breakpoint cluster region (m-BCR) rearrangement producing the P190 BCR-ABL. Therefore, additional other factor (s) apart from the Ph chromosome must be responsible for the acute malignant transformation.
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PMID:Molecular analysis of a case of Philadelphia chromosome-positive acute myeloid leukemia. 906 90

21-year-old male was diagnosed as having acute lymphoblastic leukemia (ALL) in March 2001. Standard G-banding analysis revealed normal karyotype. He achieved complete remission after the first course of induction therapy and underwent allogeneic PBSCT in August 2001. However, leukemic cells appeared in the peripheral blood demonstrating complex chromosomal abnormalities with Philadelphia chromosome (Ph1) and expressing minor BCR/ABL transcripts. We thus retrospectively examined the bone marrow sample at presentation with both interphase FISH and RT-PCR methods. Surprisingly, almost all leukemic blasts at presentation turned out to possess the minor type of BCR/ABL fusion gene. In spite of the second allogeneic PBSCT, the patient died of pneumonia and graft-versus-host disease in the liver in September 2002. This case is rare in that cytogenetic analysis failed to detect Ph1 due to leukemic cells dormancy. The application of both FISH and RT-PCR studies would appear to be essential to avoid overlooking Ph1-positive ALL.
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PMID:[Philadelphia chromosome-positive acute lymphoblastic leukemia showing normal karyotype at presentation]. 1468 77

A 77-year-old man was referred to our hospital because of elevated LDH and leukoblastosis in the peripheral blood in June 2002. Physical examination revealed neither hepatosplenomegaly nor superficial lymphadenopathy. A bone marrow film showed dysmegakaryocytopoiesis with many micromegakaryocytes and MPO-positive blasts appearing in 20-30% of NCC. A diagnosis of MDS (RAEB-t) was made. Blastic cells were positive for CD13, 33, 34 and HLA-DR. Karyotypic analysis at diagnosis revealed 46XY, inv(3) (q21q26), t(9;22) (q34; q11) and minor-BCR/ABL chimeric m-RNA was detected by RT-PCR. Mild chemotherapy (low dose Ara-C etc) was given but the disease progressed to the AML stage with thrombocytosis in August. In September imatinib was given because of Ph positivity, but the effect was transient. In October massive leukocytosis with myeloblastosis was uncontrollable. In December 2002 the patient died of pneumonia, after a total course of 7.5 months. This rare case with Ph chromosome and 3q21q26 syndrome showed a poor prognosis as previously reported.
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PMID:[3q21q26 syndrome with minor-BCR/ABL type Ph chromosome]. 1497 33

A 78-year-old male, who had CKD and chronic heart failure, was referred to our hospital for evaluation of leukocytosis. His bone marrow contained 12% blast cells and chromosome analysis showed the Ph chromosome as well as other changes. The patient was diagnosed with the accelerated-phase CML because FISH and RT-PCR disclosed BCR/ABL fusion signals and minor BCR/ABL, respectively. Imatinib was administered, but the CML was resistant to this treatment. We gave him nilotinib employing a reduced and intermittent administration protocol because of the progression of anemia and heart failure. The patient achieved PCyR in 8 months, but, 12 months later, his WBC count increased and 83% of the cells were blasts. Because the probable diagnosis was the blast crisis of CML, we switched from nilotinib to dasatinib. However, leukocytosis worsened and he died of pneumonia. It was later revealed that he had a normal karyotype and both FISH and RT-PCR analysis of BCR/ABL were negative. His final diagnosis was Ph negative AML developing from Ph positive CML in PCyR. Since there were no dysplastic changes indicative of MDS, it was assumed that the AML was not secondary leukemia caused by the tyrosine kinase inhibitor but, rather, de novo AML.
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PMID:[Development of Ph negative acute myeloid leukemia in a patient with minor-BCR/ABL positive chronic myeloid leukemia achieving a partial cytogenetic response during tyrosine kinase inhibitor treatment]. 2625 79