Subject(s)
Antineoplastic Agents/administration & dosage , Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy , Piperazines/administration & dosage , Pyrimidines/administration & dosage , Adult , Benzamides , Cytogenetic Analysis , Female , Humans , Imatinib Mesylate , Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics , Remission InductionSubject(s)
Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Lymphoma, B-Cell/drug therapy , Neutrophils/drug effects , Receptors, IgG/biosynthesis , Antibodies, Monoclonal/administration & dosage , Antibodies, Monoclonal, Murine-Derived , Drug Synergism , Flow Cytometry , Granulocyte Colony-Stimulating Factor/administration & dosage , Humans , Immunophenotyping , RituximabABSTRACT
A 31-year-old woman was given a diagnosis of aplastic anemia (AA) in 2000 and was treated with anti-thymocyte globulin (ATG) (horse serum), cyclosporine and granulocyte-colony stimulating factor (G-CSF). In 2002, she came to our hospital. The laboratory data revealed severe cytopenia according to the criteria by Camitta. A cytogenetic study revealed a normal female karyotype. We demonstrated CD55-negative and CD59-negative clones in her erythrocytes and granulocytes. HLA-DR 1501 was negative. After corticosteroid pulse therapy, the del(13q) (7/21 cells) was noted in her marrow cells. She was re-treated with ATG (rabbit serum), cyclosporine and G-CSF without particular cytogenetic changes after the therapy. Deletion of the 13q anomaly is rarely detected in patients with AA and its clinical significance in this disease is not well known. In the literature, AA patients with the del(13q) responded well to immunosuppressive therapy, irrespective of the timing of the appearance of the del(13q) anomaly. Further investigation will be needed to clarify the significance of del(13q) in AA.
Subject(s)
Anemia, Aplastic/genetics , Anemia, Aplastic/therapy , Antilymphocyte Serum/therapeutic use , Chromosome Deletion , Chromosomes, Human, Pair 13/genetics , Adult , Female , HumansSubject(s)
Heart Neoplasms/pathology , Leiomyoma/pathology , Uterine Neoplasms/pathology , Vascular Neoplasms/pathology , Female , Heart Atria , Heart Failure/etiology , Heart Neoplasms/complications , Humans , Leiomyoma/complications , Middle Aged , Neoplasm Invasiveness , Neoplastic Cells, Circulating , Urinary Tract Infections/complications , Uterine Neoplasms/complications , Vascular Neoplasms/complications , Vena Cava, InferiorABSTRACT
A 53-year-old woman with refractory acute myeloid leukemia had a cough and chest pain. Chest X-ray and computed tomography demonstrated a cavity for which antibiotics, antituberculosis and antifungal agents were not effective. A diagnosis of pulmonary aspergillosis and pulmonary alveolar proteinosis (PAP) was made on the basis of the detection of aspergillus using transbronchial lung biopsy and PAS-positive materials in the sputum. Even though some cases with PAP in hematological malignancy have been reported, the diagnosis of PAP was obtained in most of them at autopsy. In our experience three of seven cases of hematological malignancy had concomitant occurrence of aspergillosis and PAP. We should therefore pay particular attention to the possibility of PAP in patients with hematological neoplasia exhibiting pulmonary fungal infection, especially aspergillosis.
Subject(s)
Aspergillosis/complications , Leukemia, Myeloid/complications , Lung Diseases, Fungal/complications , Pulmonary Alveolar Proteinosis/complications , Acute Disease , Aspergillosis/diagnosis , Female , Humans , Leukemia, Myeloid/diagnosis , Lung Diseases, Fungal/diagnosis , Middle Aged , Pulmonary Alveolar Proteinosis/diagnosisABSTRACT
We encountered a patient with Philadelphia-negative chronic myeloid leukaemia, with t(7;11)(p15;p15), in whom acute leukaemia phase (acute myeloid leukaemia-M2 morphology) developed within a short period. We detected a novel gene fusion between NUP98 and HOXA11 both in the chronic phase and in the acute leukaemia phase in this case. Although it is well known that a fusion of NUP98-HOXA9 in myeloid malignancies is created by the t(7;11)(p15;p15), this case suggests the possibility that HOXA11 might be another partner gene for NUP98 in t(7;11)(p15;p15) leukaemia.
