mortality/aging
• following pI-pC treatment, gamma-irradiated or ENU treated mutants progress to fatal myeloid disease unlike controls
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neoplasm
• within 7 months after pI-pC treated mutants were subjected to a sublethal dose of gamma-irradiation or an injection of ENU, 60% of gamma-irradiated and 73% of ENU-treated mutants succumbed to a spectrum of myeloproliferative diseases compared to none of the controls
• pI-pC treated gamma-irradiated mutants had leukemic infiltrates in the liver, lung, and lymph nodes
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hematopoietic system
• following pI-pC treatment, saw an increase in Mac-1+/Gr-1+ myeloid cells in bone marrow, indicating myeloid hyperplasia
• 3 weeks following pI-pC treatment, mutants had an average three-fold increase in granulocyte/macrophage progenitors (GMPs) and a three-fold reduction in the number of common lymphoid progenitors (CLPs) in the bone marrow
• enhanced self-renewal/proliferation of myeloid progenitors (hematopoietic stem cells (HSCs), GMPs and common myeloid progenitors (CMPs)) as indicated by their ability to generate colonies upon serial replating
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• following pI-pC treatment, gamma-irradiated or ENU treated mutants developed anemia
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• following pI-pC treatment, gamma-irradiated mutant bone marrow contained pseudo-Gaucher cells, indicating high cell turnover
• following pI-pC treatment, gamma-irradiated and ENU treated mice had a significant increase in either Mac-1+/Gr-1-lo mature monocytes or Mac-1+/Gr-1+ immature myeloid cells and mature neutrophils and decreased B and T cells in the bone marrow
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• following pI-pC treatment, gamma-irradiated or ENU treated mutants developed thrombocytopenia
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• following pI-pC treatment, gamma-irradiated or ENU treated mutants had increased cell counts of mature monocytes and neutrophils
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• following pI-pC treatment, spleens from gamma-irradiated mutants showed extensive disruption of the splenic architecture by poorly differentiated myeloid cells
• following pI-pC treatment, gamma-irradiated and ENU treated mice had a significant increase in either Mac-1+/Gr-1-lo mature monocytes or Mac-1+/Gr-1+ immature myeloid cells and mature neutrophils and decreased B and T cells in the spleen
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• following pI-pC treatment, gamma-irradiated or ENU treated mutants developed splenomegaly
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• following pI-pC treatment, spleens from ENU treated mutants demonstrated marked expansion of red-pulp with megakaryoctyes, prominent erythropoiesis, and well-differentiated myelopoiesis
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immune system
• following pI-pC treatment, saw an increase in Mac-1+/Gr-1+ myeloid cells in bone marrow, indicating myeloid hyperplasia
• 3 weeks following pI-pC treatment, mutants had an average three-fold increase in granulocyte/macrophage progenitors (GMPs) and a three-fold reduction in the number of common lymphoid progenitors (CLPs) in the bone marrow
• enhanced self-renewal/proliferation of myeloid progenitors (hematopoietic stem cells (HSCs), GMPs and common myeloid progenitors (CMPs)) as indicated by their ability to generate colonies upon serial replating
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• following pI-pC treatment, gamma-irradiated or ENU treated mutants had increased cell counts of mature monocytes and neutrophils
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• following pI-pC treatment, spleens from gamma-irradiated mutants showed extensive disruption of the splenic architecture by poorly differentiated myeloid cells
• following pI-pC treatment, gamma-irradiated and ENU treated mice had a significant increase in either Mac-1+/Gr-1-lo mature monocytes or Mac-1+/Gr-1+ immature myeloid cells and mature neutrophils and decreased B and T cells in the spleen
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• following pI-pC treatment, gamma-irradiated or ENU treated mutants developed splenomegaly
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• following pI-pC treatment, spleens from ENU treated mutants demonstrated marked expansion of red-pulp with megakaryoctyes, prominent erythropoiesis, and well-differentiated myelopoiesis
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homeostasis/metabolism
• following pI-pC treatment, gamma-irradiated or ENU treated mutants progress to fatal myeloid disease unlike controls
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growth/size/body
• following pI-pC treatment, gamma-irradiated or ENU treated mutants developed splenomegaly
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