Benjamin Kroger
YOU?
Author Swipe
View article: CD99 promotes self-renewal in hematopoietic stem cells and leukemia stem cells by regulating protein synthesis
CD99 promotes self-renewal in hematopoietic stem cells and leukemia stem cells by regulating protein synthesis Open
Blood production is sustained by hematopoietic stem cells (HSCs), which are typically the only blood cells capable of long-term self-renewal. HSCs exhibit and depend on low levels of protein synthesis to self-renew. However, the mechanisms…
View article: A germline <i>ETV6</i> mutation disrupts hematopoiesis via de novo creation of a nuclear export signal
A germline <i>ETV6</i> mutation disrupts hematopoiesis via de novo creation of a nuclear export signal Open
Germline mutations in the transcriptional regulator ETV6 are a root cause of familial inherited thrombocytopenia and predispose carriers to myelodysplastic syndromes and acute leukemias. Here, we report that the ETV6 P214L mutation creates…
View article: RAS-mutant leukaemia stem cells drive clinical resistance to venetoclax
RAS-mutant leukaemia stem cells drive clinical resistance to venetoclax Open
View article: Accelerated Clonal Hematopoiesis in Pediatric and Young Adult Survivors of Childhood Cancer
Accelerated Clonal Hematopoiesis in Pediatric and Young Adult Survivors of Childhood Cancer Open
Clonal hematopoiesis of indeterminate potential(CHIP) is a recognized consequence of aging and a precursor to myelodysplastic syndrome and acute myeloid leukemia which independently increases all-cause mortality in adults. Childhood cancer…
View article: Data from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Data from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
Immune checkpoint blockade (ICB) therapy revolutionized cancer treatment, but many patients with impaired MHC-I expression remain refractory. Here, we combined FACS-based genome-wide CRISPR screens with a data-mining approach to identify d…
View article: Supplemental Figures 1-3 and Table 1 from Foxo-dependent Par-4 Upregulation Prevents Long-term Survival of Residual Cells Following PI3K–Akt Inhibition
Supplemental Figures 1-3 and Table 1 from Foxo-dependent Par-4 Upregulation Prevents Long-term Survival of Residual Cells Following PI3K–Akt Inhibition Open
Figures S1-3 show regulation of Par-4 by PI3K-Akt-Foxo pathway. Table 1 shows primer sequences.
View article: Table S3 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S3 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
Traf3-knockout signature derived from RNA-seq
View article: Table S1 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S1 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
MAGeCK analysis of CRISPR screen results to identify the regulators of MHC-I/PD-L1
View article: Table S1 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S1 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
MAGeCK analysis of CRISPR screen results to identify the regulators of MHC-I/PD-L1
View article: Data from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Data from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
Immune checkpoint blockade (ICB) therapy revolutionized cancer treatment, but many patients with impaired MHC-I expression remain refractory. Here, we combined FACS-based genome-wide CRISPR screens with a data-mining approach to identify d…
View article: Table S4 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S4 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
RNA-seq and H3K27ac ChIP-seq of MHC-I-high and MHC-I-low primary melanoma samples
View article: Table S5 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S5 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
Information on the ICB treatment clinical cohorts used in this study
View article: Data from Foxo-dependent Par-4 Upregulation Prevents Long-term Survival of Residual Cells Following PI3K–Akt Inhibition
Data from Foxo-dependent Par-4 Upregulation Prevents Long-term Survival of Residual Cells Following PI3K–Akt Inhibition Open
Tumor recurrence is a leading cause of death and is thought to arise from a population of residual cells that survive treatment. These residual cancer cells can persist, locally or at distant sites, for years or decades. Therefore, underst…
View article: Table S6 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S6 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
Effect of different drug treatment on the expression of genes encoding MHC-I, TAP1, PD-L1, and PD-L2
View article: Table S5 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S5 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
Information on the ICB treatment clinical cohorts used in this study
View article: Table S7 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S7 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
RNA-seq of bulk B16F10 tumors that underwent different treatments
View article: Table S7 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S7 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
RNA-seq of bulk B16F10 tumors that underwent different treatments
View article: Supplemental Figures 1-3 and Table 1 from Foxo-dependent Par-4 Upregulation Prevents Long-term Survival of Residual Cells Following PI3K–Akt Inhibition
Supplemental Figures 1-3 and Table 1 from Foxo-dependent Par-4 Upregulation Prevents Long-term Survival of Residual Cells Following PI3K–Akt Inhibition Open
Figures S1-3 show regulation of Par-4 by PI3K-Akt-Foxo pathway. Table 1 shows primer sequences.
View article: Table S2 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S2 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
RNA-seq and ATAC-seq of TRAF3-normal and -deficient B16F10 cells treated with vehicle control or IFNγ
View article: Table S4 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S4 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
RNA-seq and H3K27ac ChIP-seq of MHC-I-high and MHC-I-low primary melanoma samples
View article: Table S2 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S2 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
RNA-seq and ATAC-seq of TRAF3-normal and -deficient B16F10 cells treated with vehicle control or IFNγ
View article: Table S3 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S3 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
Traf3-knockout signature derived from RNA-seq
View article: Data from Foxo-dependent Par-4 Upregulation Prevents Long-term Survival of Residual Cells Following PI3K–Akt Inhibition
Data from Foxo-dependent Par-4 Upregulation Prevents Long-term Survival of Residual Cells Following PI3K–Akt Inhibition Open
Tumor recurrence is a leading cause of death and is thought to arise from a population of residual cells that survive treatment. These residual cancer cells can persist, locally or at distant sites, for years or decades. Therefore, underst…
View article: Table S6 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Table S6 from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
Effect of different drug treatment on the expression of genes encoding MHC-I, TAP1, PD-L1, and PD-L2
View article: Supplementary Figures from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Supplementary Figures from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
Supplementary Figures S1-S8
View article: Supplementary Figures from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Supplementary Figures from Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
Supplementary Figures S1-S8
View article: 700 Increasing MHC-I expression to potentiate immune checkpoint blockade therapy
700 Increasing MHC-I expression to potentiate immune checkpoint blockade therapy Open
Background Cancer immunotherapy, especially immune checkpoint blockade (ICB) therapy, is leading to a paradigm shift in cancer treatment, as a small percentage of cancer patients have obtained durable remission following ICB treatment. Suc…
View article: Abstract 65: Therapeutically increasing MHC-I expression potentiates immune checkpoint blockade
Abstract 65: Therapeutically increasing MHC-I expression potentiates immune checkpoint blockade Open
Immune checkpoint blockade (ICB) therapy revolutionized cancer treatment, but many patients with impaired MHC-I expression remain refractory. Here, we combined FACS-based genome-wide CRISPR screens with a data-mining approach to identify d…
View article: Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade
Therapeutically Increasing MHC-I Expression Potentiates Immune Checkpoint Blockade Open
Immune checkpoint blockade (ICB) therapy revolutionized cancer treatment, but many patients with impaired MHC-I expression remain refractory. Here, we combined FACS-based genome-wide CRISPR screens with a data-mining approach to identify d…
View article: Mapping the Relative Biological Effectiveness of Proton, Helium and Carbon Ions with High-Throughput Techniques
Mapping the Relative Biological Effectiveness of Proton, Helium and Carbon Ions with High-Throughput Techniques Open
Large amounts of high quality biophysical data are needed to improve current biological effects models but such data are lacking and difficult to obtain. The present study aimed to more efficiently measure the spatial distribution of relat…