Tony Kaoma
YOU?
Author Swipe
View article: Hub genes in a pan-cancer co-expression network show potential for predicting drug responses
Hub genes in a pan-cancer co-expression network show potential for predicting drug responses Open
Dataset 1. Gene co-expression network data. It contains network nodes, weighted network and list of hubs. Dataset 2. qPCR data from independent validation, including MIQE and additional information.
View article: PARK7/DJ-1 deficiency impairs microglial activation in response to LPS-induced inflammation
PARK7/DJ-1 deficiency impairs microglial activation in response to LPS-induced inflammation Open
Background Specific microglia responses are thought to contribute to the development and progression of neurodegenerative diseases, including Parkinson’s disease (PD). However, the phenotypic acquisition of microglial cells and their role …
View article: Glioblastoma-instructed microglia transition to heterogeneous phenotypic states with phagocytic and dendritic cell-like features in patient tumors and patient-derived orthotopic xenografts
Glioblastoma-instructed microglia transition to heterogeneous phenotypic states with phagocytic and dendritic cell-like features in patient tumors and patient-derived orthotopic xenografts Open
View article: Early-life influenza A (H1N1) infection independently programs brain connectivity, HPA AXIS and tissue-specific gene expression profiles
Early-life influenza A (H1N1) infection independently programs brain connectivity, HPA AXIS and tissue-specific gene expression profiles Open
View article: PARK7/DJ-1 deficiency impairs microglial activation in response to LPS-induced inflammation
PARK7/DJ-1 deficiency impairs microglial activation in response to LPS-induced inflammation Open
Background Specific microglia responses are thought to contribute to the development and progression of neurodegenerative diseases, including Parkinson’s disease (PD). However, the phenotypic acquisition of microglial cells and their role …
View article: consICA: an R package for robust reference-free deconvolution of multi-omics data
consICA: an R package for robust reference-free deconvolution of multi-omics data Open
Motivation Deciphering molecular signals from omics data helps understanding cellular processes and disease progression. Effective algorithms for extracting these signals are essential, with a strong emphasis on robustness and reproducibil…
View article: Cross‐Talk between miRNAs from the <i>Dlk1‐Dio3</i> Locus and Histone Methylation to Protect Male Cerebellum from Methyl Donor Deficiency
Cross‐Talk between miRNAs from the <i>Dlk1‐Dio3</i> Locus and Histone Methylation to Protect Male Cerebellum from Methyl Donor Deficiency Open
Scope Disruption of the one carbon metabolism during development, i.e., following a gestational vitamin B9 and B12 deficiencies, is involved in birth defects and brain development delay. Using a rat nutritional model, consisting of pups bo…
View article: P02.18.B INTEGRATIVE OMICS ANALYSIS OF IDH1 MUTANT GLIOMA PATIENTS REVEALS ALTERATIONS IN BUTYRATE METABOLISM
P02.18.B INTEGRATIVE OMICS ANALYSIS OF IDH1 MUTANT GLIOMA PATIENTS REVEALS ALTERATIONS IN BUTYRATE METABOLISM Open
BACKGROUND Mutations in isocitrate dehydrogenase (IDH) 1 or 2 define glioma classification and determine the biology of these tumors. Although IDH is an essential enzyme in the cellular metabolism, powerful genome-wide analyses focus mostl…
View article: DeSUMOylation of chromatin-bound proteins limits the rapid transcriptional reprogramming induced by daunorubicin in acute myeloid leukemias
DeSUMOylation of chromatin-bound proteins limits the rapid transcriptional reprogramming induced by daunorubicin in acute myeloid leukemias Open
Genotoxicants have been used for decades as front-line therapies against cancer on the basis of their DNA-damaging actions. However, some of their non-DNA-damaging effects are also instrumental for killing dividing cells. We report here th…
View article: Impact of IDH Mutations, the 1p/19q Co-Deletion and the G-CIMP Status on Alternative Splicing in Diffuse Gliomas
Impact of IDH Mutations, the 1p/19q Co-Deletion and the G-CIMP Status on Alternative Splicing in Diffuse Gliomas Open
By generating protein diversity, alternative splicing provides an important oncogenic pathway. Isocitrate dehydrogenase (IDH) 1 and 2 mutations and 1p/19q co-deletion have become crucial for the novel molecular classification of diffuse gl…
View article: Actin cytoskeleton depolymerization increases matrix metalloproteinase gene expression in breast cancer cells by promoting translocation of cysteine-rich protein 2 to the nucleus
Actin cytoskeleton depolymerization increases matrix metalloproteinase gene expression in breast cancer cells by promoting translocation of cysteine-rich protein 2 to the nucleus Open
The actin cytoskeleton plays a critical role in cancer cell invasion and metastasis; however, the coordination of its multiple functions remains unclear. Actin dynamics in the cytoplasm control the formation of invadopodia, which are membr…
View article: Supplementary Table S4 from Extracellular ATP and CD39 Activate cAMP-Mediated Mitochondrial Stress Response to Promote Cytarabine Resistance in Acute Myeloid Leukemia
Supplementary Table S4 from Extracellular ATP and CD39 Activate cAMP-Mediated Mitochondrial Stress Response to Promote Cytarabine Resistance in Acute Myeloid Leukemia Open
Table S4
View article: Supplementary Table S7 from Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism
Supplementary Table S7 from Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism Open
Summary of all GSEA data identified in AraC- versus PBS-treated AML cells in PDX and LOW versus HIGH Responder to AraC in PDX.
View article: Supplementary Table S3 from Extracellular ATP and CD39 Activate cAMP-Mediated Mitochondrial Stress Response to Promote Cytarabine Resistance in Acute Myeloid Leukemia
Supplementary Table S3 from Extracellular ATP and CD39 Activate cAMP-Mediated Mitochondrial Stress Response to Promote Cytarabine Resistance in Acute Myeloid Leukemia Open
Table S3
View article: Supplementary Table S5 from Extracellular ATP and CD39 Activate cAMP-Mediated Mitochondrial Stress Response to Promote Cytarabine Resistance in Acute Myeloid Leukemia
Supplementary Table S5 from Extracellular ATP and CD39 Activate cAMP-Mediated Mitochondrial Stress Response to Promote Cytarabine Resistance in Acute Myeloid Leukemia Open
Table S5
View article: Data from Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism
Data from Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism Open
Chemotherapy-resistant human acute myeloid leukemia (AML) cells are thought to be enriched in quiescent immature leukemic stem cells (LSC). To validate this hypothesis in vivo, we developed a clinically relevant chemotherapeutic app…
View article: Data from Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism
Data from Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism Open
Chemotherapy-resistant human acute myeloid leukemia (AML) cells are thought to be enriched in quiescent immature leukemic stem cells (LSC). To validate this hypothesis in vivo, we developed a clinically relevant chemotherapeutic app…
View article: Supplementary Table S6 from Extracellular ATP and CD39 Activate cAMP-Mediated Mitochondrial Stress Response to Promote Cytarabine Resistance in Acute Myeloid Leukemia
Supplementary Table S6 from Extracellular ATP and CD39 Activate cAMP-Mediated Mitochondrial Stress Response to Promote Cytarabine Resistance in Acute Myeloid Leukemia Open
Table S6
View article: Supplementary Table S6 from Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism
Supplementary Table S6 from Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism Open
HIGH CD36 gene signature generated from upregulated genes in AML patients that express the most CD36 mRNA compared to that of the lowest expression of CD36 in TCGA cohort.
View article: Supplementary Table S2 from Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism
Supplementary Table S2 from Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism Open
Determination of LICs frequency in bone marrow and spleen from AraC- or PBS-treated AML-xenografted NSG mice using in vivo limiting dilution assay.
View article: Supplementary Table S2 from Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism
Supplementary Table S2 from Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism Open
Determination of LICs frequency in bone marrow and spleen from AraC- or PBS-treated AML-xenografted NSG mice using in vivo limiting dilution assay.
View article: Supplementary Table S6 from Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism
Supplementary Table S6 from Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism Open
HIGH CD36 gene signature generated from upregulated genes in AML patients that express the most CD36 mRNA compared to that of the lowest expression of CD36 in TCGA cohort.
View article: Supplementary Table S1 from Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism
Supplementary Table S1 from Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism Open
(1) Clinical characteristics of 27 AML patients used in this study for engraftment in NSG mice, including the 25 ones treated in vivo with 60 mg/kg/d cytarabine (AraC) for 5 days. (2) Clinical and mutational characteristics of AML cell lin…
View article: Supplementary Table S7 from Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism
Supplementary Table S7 from Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism Open
Summary of all GSEA data identified in AraC- versus PBS-treated AML cells in PDX and LOW versus HIGH Responder to AraC in PDX.
View article: Supplementary Methods and Supplementary Figures 1 through 18 from Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism
Supplementary Methods and Supplementary Figures 1 through 18 from Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism Open
Supplementary Methods. Supplementary Figure S1. Clinical distributions of AML patients from TUH and 3 independent patient cohorts. Supplementary Figure S2. In vivo treatment with 60 mg/kg/d of cytarabine (AraC) given daily for 5 days induc…
View article: Supplementary Table S3 from Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism
Supplementary Table S3 from Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism Open
(1) Gene signatures of AraC residual AML blasts in vivo from three AML patients xenografted and treated with AraC. (2) Functional analyses of up-regulated genes of AraC residual AML blasts in vivo. (3) Functional analyses of down-regulated…
View article: Supplementary Table S4 from Extracellular ATP and CD39 Activate cAMP-Mediated Mitochondrial Stress Response to Promote Cytarabine Resistance in Acute Myeloid Leukemia
Supplementary Table S4 from Extracellular ATP and CD39 Activate cAMP-Mediated Mitochondrial Stress Response to Promote Cytarabine Resistance in Acute Myeloid Leukemia Open
Table S4
View article: Supplementary Table S5 from Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism
Supplementary Table S5 from Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism Open
Up- and down-regulated genes in AML patients that have the lower response (LowR) to AraC in vivo in NSG mice compared to high responder (HighR) to AraC in vivo using PDX assay.
View article: Supplementary Table S1 from Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism
Supplementary Table S1 from Chemotherapy-Resistant Human Acute Myeloid Leukemia Cells Are Not Enriched for Leukemic Stem Cells but Require Oxidative Metabolism Open
(1) Clinical characteristics of 27 AML patients used in this study for engraftment in NSG mice, including the 25 ones treated in vivo with 60 mg/kg/d cytarabine (AraC) for 5 days. (2) Clinical and mutational characteristics of AML cell lin…
View article: Supplementary Table S5 from Extracellular ATP and CD39 Activate cAMP-Mediated Mitochondrial Stress Response to Promote Cytarabine Resistance in Acute Myeloid Leukemia
Supplementary Table S5 from Extracellular ATP and CD39 Activate cAMP-Mediated Mitochondrial Stress Response to Promote Cytarabine Resistance in Acute Myeloid Leukemia Open
Table S5