1/19. The inv(11)(p15q22) chromosome translocation of therapy-related myelodysplasia with NUP98-DDX10 and DDX10-NUP98 fusion transcripts.Chromosomal abnormalities involving the 11p15 or 11q22-23 bands have been reported in several types of human neoplasms including hematopoietic malignancies. The abnormalities are observed in therapy-related malignancies and less frequently in de novo myeloid malignancies. Abnormality of the MLL gene located on chromosome 11q23 has been well known in therapy-related myeloid malignancies, but it has been reported only recently that the inv(11)(p15q22) in de novo or therapy-related myeloid malignancies results in the fusion of NUP98 on chromosome 11p15 and DDX10 on chromosome 11q22. NUP98 is a nucleoporin that composes the nuclear pore complex and is the target gene in leukemia with the t(7;11)(p15;p15). The DDX10 gene encodes a putative adenosine triphosphate-dependent DEAD box rna helicase. Here we present another patient with acute myelocytic leukemia (M4) transformed from chronic myelomonocytic leukemia with the inv(11) chromosome who had been treated with etoposide for a germ cell tumor. By reverse transcription polymerase chain reaction (RT-PCR) of the rna from the leukemic cells of the patient, DDX10-NUP98 and NUP98-DDX10 fusion transcripts were detected. Our case confirms that the inv(11) is a rare chromosomal translocation that is associated with therapy-related or de novo myeloid malignancy and involves NUP98 and DDX10 but not MLL. RT-PCR of the fusion transcripts might be applied to the detection of a small number of leukemic cells in the bone marrow or blood of patients in remission or in the cells harvested for autologous transplantation.- - - - - - - - - - ranking = 1keywords = leukemia (Clic here for more details about this article) |
2/19. Radiation-induced brain calcification: paradoxical high signal intensity in T1-weighted MR images.BACKGROUND: Irradiation to the central nervous system (CNS) in childhood is known to induce cerebral calcification after a latent period. Calcification has been generally found to show nil or a reduction in signal intensity in magnetic resonance (MR) images. However, we have studied three patients with radiation-induced brain calcification, who manifested increased signal intensity on T1-weighted MR images. METHOD: Three girls had each been diagnosed as having a suprasellar germ cell tumour and were treated with conventional fractionated radiotherapy in their childhood. In one case, chemotherapy was given prior to the CNS irradiation. FINDINGS: All three patients survived their disease, and a follow-up CT scan revealed calcification in the brain, which has shown an increased signal intensity in the T1-weighted images of MR. INTERPRETATION: Cerebral calcification may be presented as a high signal intensity in the T1-weighted MR images. This may be explained by a surface-relaxation effect by the calcium salt particle, precipitated in the brain due to radiation-induced mineralising microangiopathy.- - - - - - - - - - ranking = 20.77374046171keywords = radiation-induced (Clic here for more details about this article) |
3/19. Primitive neuroectodermal tumors after prophylactic central nervous system irradiation in children. association with an activated K-ras gene.Three patients had supratentorial malignant brain tumors 7 to 9 years after prophylactic central nervous system (CNS) treatment for acute lymphocytic leukemia or malignant T-cell lymphoma. Therapy was administered at the age of 3 to 8 years and included cranial irradiation (total dose, 1800 to 2400 cGy) and intrathecal methotrexate. The brain tumors had histologic and immunohistochemical features of primitive neuroectodermal tumors (PNET), including neuroblastic rosettes, rhythmic arrangement of tumor cells, and immunohistochemical expression of glial, and in one patient neuronal, marker proteins. Using polymerase chain reaction-mediated dna amplification from paraffin-embedded tissues and subsequent dna sequence analysis, an activating point mutation was detected in the K-ras protooncogene in one tumor. This mutation was a G to A transition in position 2 of codon 12, substituting aspartate (GAT) for glycine (GGT). This type of mutation has not been observed before in human brain tumors, but it is frequent in radiation-induced murine lymphomas. These observations suggest that PNET can be induced after completion of the embryonal and fetal development of the human CNS. Oncogene-activating point mutations may represent a pathogenetic mechanism involved in the genesis of radiation-induced brain tumors.- - - - - - - - - - ranking = 21.107073795043keywords = radiation-induced, leukemia (Clic here for more details about this article) |
4/19. Epipodophyllotoxin-related leukemia. Identification of a new subset of secondary leukemia.Thirty-seven children and adults who developed acute nonlymphocytic leukemia after the administration of chemotherapy that included etoposide or teniposide for a variety of hematologic and solid malignancies were identified. The secondary leukemia that occurred in these patients could be distinguished from the secondary leukemia that occurs after treatment with alkylating agents by the following: a shorter latency period; a predominance of monocytic or myelomonocytic features; and frequent cytogenetic abnormalities involving 11q23. patients receiving an epipodophyllotoxin are at risk for developing secondary leukemia that has features distinct from the syndrome of secondary leukemia associated with alkylating agents.- - - - - - - - - - ranking = 4.3333333333333keywords = leukemia (Clic here for more details about this article) |
5/19. Embryonal carcinoma of the testis after acute myelomonocytic leukemia: a case report.A case of embryonal carcinoma of the testis after acute myelomonocytic leukemia is reported. The interval between the initial diagnosis of leukemia and the appearance of embryonal carcinoma was almost three years. Although the patient had received neither irradiation nor alkylating agents, the case is regarded as one of secondary malignancy. Possible contributing factors are discussed.- - - - - - - - - - ranking = 2keywords = leukemia (Clic here for more details about this article) |
6/19. Associated leukemia and mixed germ cell tumor in a patient with gonadal dysgenesis.A 16-year-old phenotypic female developed acute myeloblastic leukemia with a fulminant course very shortly after surgery and chemotherapy for a mixed germ cell tumor of the ovary. The karyotype (46, XY, 47, XY 8) suggested de novo rather than therapy-associated leukemia. The relationship between germ cell tumors and leukemia, their common yolk sac derivation and the role of the y chromosome are discussed. The idea that XY gonadal dysgenesis may be familial also is discussed.- - - - - - - - - - ranking = 2.3333333333333keywords = leukemia (Clic here for more details about this article) |
7/19. True malignant histiocytosis with trisomy 9 following primary mediastinal germ cell tumor.A 24-year-old Japanese man was admitted due to bloody phlegm in May 2002. A diagnosis of mediastinal germ cell tumor, mixed type involving seminoma, immature teratoma and embryonal carcinoma, was made by transthoracic needle biopsy. Three months later, his complete blood counts revealed pancytopenia with high fever. Examination of bone marrow revealed increased atypical large histiocytes (5.6%) with hemophagocytosis, and thus, hemophagocytic syndrome related to germ cell tumor was diagnosed. In addition, chromosomal analysis of the bone marrow cells revealed a 47, XY, 9 genotype. Chemotherapies for germ cell tumor and hemophagocytic syndrome were performed without any improvement, and he died of diffuse alveolar damage. autopsy revealed diffuse infiltration of immature histiocytes with hemophagocytosis in the liver, spleen and bone marrow. The atypical histiocytes were positive for CD68 and lysozyme and negative for lymphoid markers, and the diagnosis of true malignant histiocytosis associated with mediastinal germ cell tumor was made. The rare chromosomal abnormality of trisomy 9, a marker for benzene-related leukemia, was seen in the present case without apparent benzene exposure.- - - - - - - - - - ranking = 0.33333333333333keywords = leukemia (Clic here for more details about this article) |
8/19. Coexistence of testicular carcinoma and hairy cell leukemia.The coexistence of two relatively rare disorders in 1 patient often induces speculation about possible cause and effect of these disorders. The suitable therapeutic regimen for both diseases and roentgenologic manifestations are described.- - - - - - - - - - ranking = 1.3333333333333keywords = leukemia (Clic here for more details about this article) |
9/19. Cutaneous toxicity of autologous bone marrow transplantation in nonseminomatous germ cell tumors.High doses of carboplatin or cisplatin combined with cyclophosphamide and etoposide followed by autologous bone marrow transplantation (ABMT) rescue have been used in the treatment of testicular tumors that have had a bad prognosis. Unusual cutaneous complications, evoking radiation-induced dermatitis, have been seen in two of eight patients with the same regimen. This new type of toxicity seems to be related to high-dose combination chemotherapies. Good results in the treatment of patients with testicular tumors on relapse who continue to respond to chemotherapy lead to the extension of this type of schedule and cutaneous toxicity will probably develop.- - - - - - - - - - ranking = 10.386870230855keywords = radiation-induced (Clic here for more details about this article) |
10/19. Disseminated primitive neuroectodermal tumor: diagnosis using immunocytochemistry, electron microscopy, and molecular probes.A patient with a disseminated small cell tumor presented with hyperuricemia, gingival hypertrophy, lymphadenopathy, and bone marrow replacement with tumor cells. Initial histologic examination and clinical presentation were consistent with presumed marker silent lymphoma/leukemia. Despite initial treatment with and response to lymphoma/leukemia therapy the patient relapsed in the testis, bone marrow, pancreas, and skin whereupon subsequent and retrospective immunocytochemical, ultrastructural, cytogenetic, and molecular analysis led to the diagnosis of primitive neuroectodermal tumor (PNET). Despite extensive investigation and autopsy no primary site of tumor could be found demonstrating that PNET should be considered in the differential diagnosis of disseminated small cell tumors without an apparent primary.- - - - - - - - - - ranking = 0.66666666666667keywords = leukemia (Clic here for more details about this article) |
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