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Acute Biphenotypic Leukemia
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Keiko Mizuno – One of the best experts on this subject based on the ideXlab platform.
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bridging necrosis and reticulin bridging fibrosis induced by intrahepatic involvement of Acute Biphenotypic Leukemia
Apmis, 2006Co-Authors: Naoto Kuroda, M Mizobuchi, Y Shimamura, Masanori Daibata, Isao Miyoshi, Masahiko Ohara, Takashi Hirouchi, Keiko MizunoAbstract:A 47-year-old Japanese woman was diagnosed as having Acute Biphenotypic Leukemia with association of t(9;22)(q34;qll). Cholestatic liver dysfunction arose, and she died of cachexia and intracranial hemorrhage. Autopsy showed unusual hepatic fibrosis. In the liver, bridging infiltration, bridging necrosis and bridging fibrosis by leukemic cells were seen. It seemed that the degree of fibrosis was associated with the number of aggregates of infiltrating leukemic cells. The fibrotic foci were predominantly composed of reticulin and collagen fibers, and distortion of the lobules was observed. Immuno-histochemically, dense bundles of alpha-smooth muscle actin (ASMA)-positive stromal cells, namely activated hepatic stellate cells (HSCs), were observed in the immature fibrotic foci as well as along the sinusoids densely infiltrated by leukemic cells. No cells positive for TGF-β1 or PDGF-BB were identified. In conclusion, extensive intrahepatic involvement by neoplastic cells in adult Acute Biphenotypic Leukemia may cause the unusual “disorganized” hepatic fibrosis.
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Bridging necrosis and reticulin bridging fibrosis induced by intrahepatic involvement of Acute Biphenotypic Leukemia.
APMIS, 2006Co-Authors: Naoto Kuroda, Keiko Mizuno, M Mizobuchi, Y Shimamura, Masanori Daibata, Isao Miyoshi, Masahiko Ohara, Takashi Hirouchi, Gang-hong LeeAbstract:A 47-year-old Japanese woman was diagnosed as having Acute Biphenotypic Leukemia with association of t(9;22)(q34;q11). Cholestatic liver dysfunction arose, and she died of cachexia and intracranial hemorrhage. Autopsy showed unusual hepatic fibrosis. In the liver, bridging infiltration, bridging necrosis and bridging fibrosis by leukemic cells were seen. It seemed that the degree of fibrosis was associated with the number of aggregates of infiltrating leukemic cells. The fibrotic foci were predominantly composed of reticulin and collagen fibers, and distortion of the lobules was observed. Immunohistochemically, dense bundles of alpha-smooth muscle actin (ASMA)-positive stromal cells, namely activated hepatic stellate cells (HSCs), were observed in the immature fibrotic foci as well as along the sinusoids densely infiltrated by leukemic cells. No cells positive for TGF-beta1 or PDGF-BB were identified. In conclusion, extensive intrahepatic involvement by neoplastic cells in adult Acute Biphenotypic Leukemia may cause the unusual “disorganized” hepatic fibrosis.
Naoto Kuroda – One of the best experts on this subject based on the ideXlab platform.
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bridging necrosis and reticulin bridging fibrosis induced by intrahepatic involvement of Acute Biphenotypic Leukemia
Apmis, 2006Co-Authors: Naoto Kuroda, M Mizobuchi, Y Shimamura, Masanori Daibata, Isao Miyoshi, Masahiko Ohara, Takashi Hirouchi, Keiko MizunoAbstract:A 47-year-old Japanese woman was diagnosed as having Acute Biphenotypic Leukemia with association of t(9;22)(q34;qll). Cholestatic liver dysfunction arose, and she died of cachexia and intracranial hemorrhage. Autopsy showed unusual hepatic fibrosis. In the liver, bridging infiltration, bridging necrosis and bridging fibrosis by leukemic cells were seen. It seemed that the degree of fibrosis was associated with the number of aggregates of infiltrating leukemic cells. The fibrotic foci were predominantly composed of reticulin and collagen fibers, and distortion of the lobules was observed. Immuno-histochemically, dense bundles of alpha-smooth muscle actin (ASMA)-positive stromal cells, namely activated hepatic stellate cells (HSCs), were observed in the immature fibrotic foci as well as along the sinusoids densely infiltrated by leukemic cells. No cells positive for TGF-β1 or PDGF-BB were identified. In conclusion, extensive intrahepatic involvement by neoplastic cells in adult Acute Biphenotypic Leukemia may cause the unusual “disorganized” hepatic fibrosis.
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Bridging necrosis and reticulin bridging fibrosis induced by intrahepatic involvement of Acute Biphenotypic Leukemia.
APMIS, 2006Co-Authors: Naoto Kuroda, Keiko Mizuno, M Mizobuchi, Y Shimamura, Masanori Daibata, Isao Miyoshi, Masahiko Ohara, Takashi Hirouchi, Gang-hong LeeAbstract:A 47-year-old Japanese woman was diagnosed as having Acute Biphenotypic Leukemia with association of t(9;22)(q34;q11). Cholestatic liver dysfunction arose, and she died of cachexia and intracranial hemorrhage. Autopsy showed unusual hepatic fibrosis. In the liver, bridging infiltration, bridging necrosis and bridging fibrosis by leukemic cells were seen. It seemed that the degree of fibrosis was associated with the number of aggregates of infiltrating leukemic cells. The fibrotic foci were predominantly composed of reticulin and collagen fibers, and distortion of the lobules was observed. Immunohistochemically, dense bundles of alpha-smooth muscle actin (ASMA)-positive stromal cells, namely activated hepatic stellate cells (HSCs), were observed in the immature fibrotic foci as well as along the sinusoids densely infiltrated by leukemic cells. No cells positive for TGF-beta1 or PDGF-BB were identified. In conclusion, extensive intrahepatic involvement by neoplastic cells in adult Acute Biphenotypic Leukemia may cause the unusual “disorganized” hepatic fibrosis.
Kazuo Dan – One of the best experts on this subject based on the ideXlab platform.
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establishment of a cell line with variant bcr abl breakpoint expressing p180bcr abl from late appearing philadelphia positive Acute Biphenotypic Leukemia
Genes Chromosomes and Cancer, 1998Co-Authors: Koiti Inokuchi, Tamiko Shinohara, Makoto Futaki, Hideki Hanawa, Sakae Tanosaki, Hiroki Yamaguchi, Takeo Nomura, Kazuo DanAbstract:In Acute Leukemia (AL) with a late-appearing Philadelphia (la-Ph) translocation, it is unclear whether these translocations arise from the same molecular event as classical Ph translocations. In order to elucidate the molecular events of la-Ph and subsequent translocations of la-Ph Leukemia, we performed molecular analysis on the complex rearrangements, in a cell line, MY, which was established from bone marrow mononuclear cells of a patient with a la-Ph Acute Biphenotypic Leukemia. This la-Ph, expressing an Acute lymphoblastic Leukemia (ALL)-type BCR/ABL transcript, produces a novel P180BCR/ABL fusion protein reflecting deletion of 174 bases (58 amino acids) encoded by the a2 exon of the ABL gene. An immune complex kinase assay showed that this protein had autophosphorylation activity. Fluorescence in situ hybridization (FISH) in conjunction with G-banding analysis revealed that the initial der(9)t(9;22)(q34;q11) progressed to a der(9)(9pter–>9q34::22q11–>22q13::5q11.2 –>5q15:: 10q23–>10qter) by, first, a three-way translocation among the der(9)t(9;22)(q34;q11), chromosome 5, and the normal chromosome 22, and then a subsequent translocation with chromosome 10. Moreover, both the end-stage leukemic cells of the patient and the MY cell line had another translocation, t(X;12)(p11.2;p13). The 12p breakpoint was located near the ETV6 gene by analysis of pulsed-field gel electrophoresis, but transcription of ETV6 was unaffected. Tumorigenicity analysis indicated that an additional translocation, t(2;3)(p16;q29), may have caused a more malignant clone, because only MY cells with the t(2;3)(p16;q29) were capable of growing subcutaneously in nude mice within 40 days. The molecular events of leukemogenesis and leukemic progression in the present la-Ph AL occurred by accumulation of unique translocations. This cell line, MY, expressing a novel variant P180BCR/ABL protein with a deletion of the a2 exon of the ABL gene, may be useful for elucidating the pathophysiology of this fusion protein and for studying ETV6-related leukemogenesis and t(2;3), as well as the molecular mechanisms of the complex translocations.
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Establishment of a cell line with variant BCR/ABL breakpoint expressing P180BCR/ABL from late-appearing Philadelphia-positive Acute Biphenotypic Leukemia.
Genes Chromosomes and Cancer, 1998Co-Authors: Koiti Inokuchi, Tamiko Shinohara, Makoto Futaki, Hideki Hanawa, Sakae Tanosaki, Hiroki Yamaguchi, Takeo Nomura, Kazuo DanAbstract:In Acute Leukemia (AL) with a late-appearing Philadelphia (la-Ph) translocation, it is unclear whether these translocations arise from the same molecular event as classical Ph translocations. In order to elucidate the molecular events of la-Ph and subsequent translocations of la-Ph Leukemia, we performed molecular analysis on the complex rearrangements, in a cell line, MY, which was established from bone marrow mononuclear cells of a patient with a la-Ph Acute Biphenotypic Leukemia. This la-Ph, expressing an Acute lymphoblastic Leukemia (ALL)-type BCR/ABL transcript, produces a novel P180BCR/ABL fusion protein reflecting deletion of 174 bases (58 amino acids) encoded by the a2 exon of the ABL gene. An immune complex kinase assay showed that this protein had autophosphorylation activity. Fluorescence in situ hybridization (FISH) in conjunction with G-banding analysis revealed that the initial der(9)t(9;22)(q34;q11) progressed to a der(9)(9pter–>9q34::22q11–>22q13::5q11.2 –>5q15:: 10q23–>10qter) by, first, a three-way translocation among the der(9)t(9;22)(q34;q11), chromosome 5, and the normal chromosome 22, and then a subsequent translocation with chromosome 10. Moreover, both the end-stage leukemic cells of the patient and the MY cell line had another translocation, t(X;12)(p11.2;p13). The 12p breakpoint was located near the ETV6 gene by analysis of pulsed-field gel electrophoresis, but transcription of ETV6 was unaffected. Tumorigenicity analysis indicated that an additional translocation, t(2;3)(p16;q29), may have caused a more malignant clone, because only MY cells with the t(2;3)(p16;q29) were capable of growing subcutaneously in nude mice within 40 days. The molecular events of leukemogenesis and leukemic progression in the present la-Ph AL occurred by accumulation of unique translocations. This cell line, MY, expressing a novel variant P180BCR/ABL protein with a deletion of the a2 exon of the ABL gene, may be useful for elucidating the pathophysiology of this fusion protein and for studying ETV6-related leukemogenesis and t(2;3), as well as the molecular mechanisms of the complex translocations.