Linda Wolff
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View article: C-terminal binding protein 2 interacts with JUNB to control macrophage inflammation
C-terminal binding protein 2 interacts with JUNB to control macrophage inflammation Open
Although acute inflammatory responses are critical for survival, chronic inflammation is a leading cause of disease and mortality worldwide. Nevertheless, our mechanistic understanding of pathogenesis is still limited and precise treatment…
View article: Unclassifiable renal carcinoma with medullary phenotype and SMARCB1 deficiency: case report
Unclassifiable renal carcinoma with medullary phenotype and SMARCB1 deficiency: case report Open
Background Renal medullary carcinoma (RMC) is an aggressive tumor representing less than 0.5% of renal cell carcinomas (RCC), and it is considered rare. When it occurs, patients typically have sickle cell trait, sickle cell disease, or an …
View article: Supplementary Data from Retroviral Insertional Mutagenesis Identifies Genes that Collaborate with <i>NUP98-HOXD13</i> during Leukemic Transformation
Supplementary Data from Retroviral Insertional Mutagenesis Identifies Genes that Collaborate with <i>NUP98-HOXD13</i> during Leukemic Transformation Open
Supplementary Figures and Tables
View article: Supplementary Data from Retroviral Insertional Mutagenesis Identifies Genes that Collaborate with <i>NUP98-HOXD13</i> during Leukemic Transformation
Supplementary Data from Retroviral Insertional Mutagenesis Identifies Genes that Collaborate with <i>NUP98-HOXD13</i> during Leukemic Transformation Open
Supplementary Figures and Tables
View article: Data from Retroviral Insertional Mutagenesis Identifies Genes that Collaborate with <i>NUP98-HOXD13</i> during Leukemic Transformation
Data from Retroviral Insertional Mutagenesis Identifies Genes that Collaborate with <i>NUP98-HOXD13</i> during Leukemic Transformation Open
The t(2;11)(q31;p15) chromosomal translocation results in a fusion between the NUP98 and HOXD13 genes and has been observed in patients with myelodysplastic syndrome (MDS) or acute myelogenous leukemia. We previously showed t…
View article: Data from Retroviral Insertional Mutagenesis Identifies Genes that Collaborate with <i>NUP98-HOXD13</i> during Leukemic Transformation
Data from Retroviral Insertional Mutagenesis Identifies Genes that Collaborate with <i>NUP98-HOXD13</i> during Leukemic Transformation Open
The t(2;11)(q31;p15) chromosomal translocation results in a fusion between the NUP98 and HOXD13 genes and has been observed in patients with myelodysplastic syndrome (MDS) or acute myelogenous leukemia. We previously showed t…
View article: Supplementary Figure 1 from Methylation-Independent Silencing of the Tumor Suppressor <i>INK4b</i> (p15) by CBFβ-SMMHC in Acute Myelogenous Leukemia with inv(16)
Supplementary Figure 1 from Methylation-Independent Silencing of the Tumor Suppressor <i>INK4b</i> (p15) by CBFβ-SMMHC in Acute Myelogenous Leukemia with inv(16) Open
Supplementary Figure 1 from Methylation-Independent Silencing of the Tumor Suppressor INK4b (p15) by CBFβ-SMMHC in Acute Myelogenous Leukemia with inv(16)
View article: Supplementary Tables 1-2 from Methylation-Independent Silencing of the Tumor Suppressor <i>INK4b</i> (p15) by CBFβ-SMMHC in Acute Myelogenous Leukemia with inv(16)
Supplementary Tables 1-2 from Methylation-Independent Silencing of the Tumor Suppressor <i>INK4b</i> (p15) by CBFβ-SMMHC in Acute Myelogenous Leukemia with inv(16) Open
Supplementary Tables 1-2 from Methylation-Independent Silencing of the Tumor Suppressor INK4b (p15) by CBFβ-SMMHC in Acute Myelogenous Leukemia with inv(16)
View article: Supplementary Figure 1 from Methylation-Independent Silencing of the Tumor Suppressor <i>INK4b</i> (p15) by CBFβ-SMMHC in Acute Myelogenous Leukemia with inv(16)
Supplementary Figure 1 from Methylation-Independent Silencing of the Tumor Suppressor <i>INK4b</i> (p15) by CBFβ-SMMHC in Acute Myelogenous Leukemia with inv(16) Open
Supplementary Figure 1 from Methylation-Independent Silencing of the Tumor Suppressor INK4b (p15) by CBFβ-SMMHC in Acute Myelogenous Leukemia with inv(16)
View article: Supplementary Tables 1-2 from Methylation-Independent Silencing of the Tumor Suppressor <i>INK4b</i> (p15) by CBFβ-SMMHC in Acute Myelogenous Leukemia with inv(16)
Supplementary Tables 1-2 from Methylation-Independent Silencing of the Tumor Suppressor <i>INK4b</i> (p15) by CBFβ-SMMHC in Acute Myelogenous Leukemia with inv(16) Open
Supplementary Tables 1-2 from Methylation-Independent Silencing of the Tumor Suppressor INK4b (p15) by CBFβ-SMMHC in Acute Myelogenous Leukemia with inv(16)
View article: Data from Methylation-Independent Silencing of the Tumor Suppressor <i>INK4b</i> (p15) by CBFβ-SMMHC in Acute Myelogenous Leukemia with inv(16)
Data from Methylation-Independent Silencing of the Tumor Suppressor <i>INK4b</i> (p15) by CBFβ-SMMHC in Acute Myelogenous Leukemia with inv(16) Open
The tumor suppressor gene INK4b (p15) is silenced by CpG island hypermethylation in most acute myelogenous leukemias (AML), and this epigenetic phenomenon can be reversed by treatment with hypomethylating agents. Thus far, it was no…
View article: Supplementary Figure 1 Legend from Methylation-Independent Silencing of the Tumor Suppressor <i>INK4b</i> (p15) by CBFβ-SMMHC in Acute Myelogenous Leukemia with inv(16)
Supplementary Figure 1 Legend from Methylation-Independent Silencing of the Tumor Suppressor <i>INK4b</i> (p15) by CBFβ-SMMHC in Acute Myelogenous Leukemia with inv(16) Open
Supplementary Figure 1 Legend from Methylation-Independent Silencing of the Tumor Suppressor INK4b (p15) by CBFβ-SMMHC in Acute Myelogenous Leukemia with inv(16)
View article: Supplementary Figure 1 Legend from Methylation-Independent Silencing of the Tumor Suppressor <i>INK4b</i> (p15) by CBFβ-SMMHC in Acute Myelogenous Leukemia with inv(16)
Supplementary Figure 1 Legend from Methylation-Independent Silencing of the Tumor Suppressor <i>INK4b</i> (p15) by CBFβ-SMMHC in Acute Myelogenous Leukemia with inv(16) Open
Supplementary Figure 1 Legend from Methylation-Independent Silencing of the Tumor Suppressor INK4b (p15) by CBFβ-SMMHC in Acute Myelogenous Leukemia with inv(16)
View article: Data from Methylation-Independent Silencing of the Tumor Suppressor <i>INK4b</i> (p15) by CBFβ-SMMHC in Acute Myelogenous Leukemia with inv(16)
Data from Methylation-Independent Silencing of the Tumor Suppressor <i>INK4b</i> (p15) by CBFβ-SMMHC in Acute Myelogenous Leukemia with inv(16) Open
The tumor suppressor gene INK4b (p15) is silenced by CpG island hypermethylation in most acute myelogenous leukemias (AML), and this epigenetic phenomenon can be reversed by treatment with hypomethylating agents. Thus far, it was no…
View article: UTX maintains the functional integrity of the murine hematopoietic system by globally regulating aging-associated genes
UTX maintains the functional integrity of the murine hematopoietic system by globally regulating aging-associated genes Open
Epigenetic regulation is essential for the maintenance of the hematopoietic system, and its deregulation is implicated in hematopoietic disorders. In this study, UTX, a demethylase for lysine 27 on histone H3 (H3K27) and a component of COM…
View article: Acquired expression of CblQ367P in mice induces dysplastic myelopoiesis mimicking chronic myelomonocytic leukemia
Acquired expression of CblQ367P in mice induces dysplastic myelopoiesis mimicking chronic myelomonocytic leukemia Open
Key Points Acquired expression of CblQ367P induces sustained proliferation of myelomonocytes, multilineage dysplasia, and splenomegaly resembling CMML. Combined inhibition of PI3K and JAK2 efficiently suppressed the growth of CblQ367P-indu…
View article: Distal regulation of c-myb expression during IL-6-induced differentiation in murine myeloid progenitor M1 cells
Distal regulation of c-myb expression during IL-6-induced differentiation in murine myeloid progenitor M1 cells Open
The c-Myb transcription factor is a major regulator that controls differentiation and proliferation of hematopoietic progenitor cells, which is frequently deregulated in hematological diseases, such as lymphoma and leukemia. Understanding …
View article: Propagation of trimethylated H3K27 regulated by polycomb protein EED is required for embryogenesis, hematopoietic maintenance, and tumor suppression
Propagation of trimethylated H3K27 regulated by polycomb protein EED is required for embryogenesis, hematopoietic maintenance, and tumor suppression Open
Significance Polycomb repressive complex 2 (PRC2) is a central regulator in all forms of histone H3 Lys27 (H3K27) methylation. Interaction of embryonic ectoderm development (EED) with trimethylated H3K27 (H3K27me3) is required for the allo…
View article: Maintenance of the functional integrity of mouse hematopoiesis by EED and promotion of leukemogenesis by EED haploinsufficiency
Maintenance of the functional integrity of mouse hematopoiesis by EED and promotion of leukemogenesis by EED haploinsufficiency Open
View article: Identification of cooperative genes for <i>E2A‐PBX1</i> to develop acute lymphoblastic leukemia
Identification of cooperative genes for <i>E2A‐PBX1</i> to develop acute lymphoblastic leukemia Open
E2A‐ PBX 1 is a chimeric gene product detected in t(1;19)‐bearing acute lymphoblastic leukemia ( ALL ) with B‐cell lineage. To investigate the leukemogenic process, we generated conditional knock‐in ( cKI ) mice for E2A‐ PBX 1 , in which E…
View article: Fbxl10 overexpression in murine hematopoietic stem cells induces leukemia involving metabolic activation and upregulation of Nsg2
Fbxl10 overexpression in murine hematopoietic stem cells induces leukemia involving metabolic activation and upregulation of Nsg2 Open
Key Points Fbxl10 is a bona fide oncogene in vivo. Fbxl10 overexpression in HSCs induces mitochondrial metabolic activation and enhanced expression of Nsg2.