M. Celeste Simon
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View article: HIF2α inhibits glutaminase clustering in mitochondria to sustain growth of clear cell renal cell carcinoma
HIF2α inhibits glutaminase clustering in mitochondria to sustain growth of clear cell renal cell carcinoma Open
Clear cell renal cell carcinomas (ccRCCs) are largely driven by HIF2α and are avid consumers of glutamine. However, inhibitors of glutaminase 1 (GLS1), the first step in glutaminolysis, have not shown benefit in phase III trials, and HIF2α…
View article: Chemoresistance of TP53 mutant acute myeloid leukemia requires the mevalonate byproduct, geranylgeranyl pyrophosphate, for induction of an adaptive stress response
Chemoresistance of TP53 mutant acute myeloid leukemia requires the mevalonate byproduct, geranylgeranyl pyrophosphate, for induction of an adaptive stress response Open
Acute myeloid leukemia with mutations in TP53 ( TP53 mut AML) is fatal with a median survival of 6 months. RNA sequencing on purified AML patient samples showed that TP53 mut AML had higher expression of mevalonate pathway genes. Using nov…
View article: BMAL1 and ARNT enable circadian HIF2α responses in clear cell renal cell carcinoma
BMAL1 and ARNT enable circadian HIF2α responses in clear cell renal cell carcinoma Open
Circadian disruption enhances cancer risk, and many tumors exhibit disordered circadian gene expression. We show rhythmic gene expression is unexpectedly robust in clear cell renal cell carcinoma (ccRCC). The core circadian transcription f…
View article: SWI/SNF ATPase silenced HLF potentiates lung metastasis in solid cancers
SWI/SNF ATPase silenced HLF potentiates lung metastasis in solid cancers Open
Metastasis is the main cause of cancer-related deaths, yet the underlying mechanisms remain elusive. Here, using clear cell renal cell carcinoma (ccRCC), a tumor type with frequent lung metastases, we conduct an in vivo genome-wide CRISPR-…
View article: Author Correction: FBP1 controls liver cancer evolution from senescent MASH hepatocytes
Author Correction: FBP1 controls liver cancer evolution from senescent MASH hepatocytes Open
View article: Osalmid sensitizes clear cell renal cell carcinoma to navitoclax through a STAT3/BCL-XL pathway
Osalmid sensitizes clear cell renal cell carcinoma to navitoclax through a STAT3/BCL-XL pathway Open
View article: Nuclear speckles regulate functional programs in cancer
Nuclear speckles regulate functional programs in cancer Open
View article: FBP1 controls liver cancer evolution from senescent MASH hepatocytes
FBP1 controls liver cancer evolution from senescent MASH hepatocytes Open
View article: 900 An iron-rich subset of macrophages promotes tumor growth through a Bach1-Ednrb axis
900 An iron-rich subset of macrophages promotes tumor growth through a Bach1-Ednrb axis Open
View article: Cancer-associated fibroblasts maintain critical pancreatic cancer cell lipid homeostasis in the tumor microenvironment
Cancer-associated fibroblasts maintain critical pancreatic cancer cell lipid homeostasis in the tumor microenvironment Open
View article: An iron-rich subset of macrophages promotes tumor growth through a Bach1-Ednrb axis
An iron-rich subset of macrophages promotes tumor growth through a Bach1-Ednrb axis Open
We define a subset of macrophages in the tumor microenvironment characterized by high intracellular iron and enrichment of heme and iron metabolism genes. These iron-rich tumor-associated macrophages (iTAMs) supported angiogenesis and immu…
View article: Glutamine availability regulates cDC subsets in tissue
Glutamine availability regulates cDC subsets in tissue Open
Proliferating tumor cells take up glutamine for anabolic processes engendering glutamine deficiency in the tumor microenvironment. How this might impact immune cells is not well understood. Using multiple mouse models of soft tissue sarcom…
View article: Author Correction: Targeting glutamine metabolism slows soft tissue sarcoma growth
Author Correction: Targeting glutamine metabolism slows soft tissue sarcoma growth Open
View article: BMAL1-HIF2α heterodimers contribute to ccRCC
BMAL1-HIF2α heterodimers contribute to ccRCC Open
View article: Chemoresistance of<i>TP53</i>mutant AML requires the mevalonate byproduct, GGPP, for regulation of ROS and induction of a mitochondria stress response
Chemoresistance of<i>TP53</i>mutant AML requires the mevalonate byproduct, GGPP, for regulation of ROS and induction of a mitochondria stress response Open
Acute myeloid leukemia (AML) with mutations in the tumor suppressor gene, TP53 ( TP53 mut AML), is fatal with a median survival of only 6 months. RNA sequencing on purified AML patient samples show TP53 mut AML has higher expression of mev…
View article: Data from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer
Data from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer Open
The tumor microenvironment in pancreatic ductal adenocarcinoma (PDAC) plays a key role in tumor progression and response to therapy. The dense PDAC stroma causes hypovascularity, which leads to hypoxia. Here, we showed that hypoxia drives …
View article: Supplementary Figure S13 from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer
Supplementary Figure S13 from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer Open
Supplementary Figure S13
View article: Supplementary Figure S2 from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer
Supplementary Figure S2 from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer Open
Supplementary Figure S2
View article: Supplementary Data from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer
Supplementary Data from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer Open
Supplementary Methods, Tables, References
View article: Supplementary Figure S11 from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer
Supplementary Figure S11 from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer Open
Supplementary Figure S11
View article: Supplementary Figure S1 from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer
Supplementary Figure S1 from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer Open
Supplementary Figure S1
View article: Supplementary Figure S6 from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer
Supplementary Figure S6 from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer Open
Supplementary Figure S6
View article: Supplementary Figure S3 from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer
Supplementary Figure S3 from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer Open
Supplementary Figure S3
View article: Supplementary Figure S4 from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer
Supplementary Figure S4 from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer Open
Supplementary Figure S4
View article: Supplementary Figure S5 from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer
Supplementary Figure S5 from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer Open
Supplementary Figure S5
View article: Supplementary Figure S3 from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer
Supplementary Figure S3 from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer Open
Supplementary Figure S3
View article: Supplementary Figure S13 from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer
Supplementary Figure S13 from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer Open
Supplementary Figure S13
View article: Supplementary Figure S7 from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer
Supplementary Figure S7 from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer Open
Supplementary Figure S7
View article: Supplementary Figure S10 from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer
Supplementary Figure S10 from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer Open
Supplementary Figure S10
View article: Supplementary Figure S9 from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer
Supplementary Figure S9 from A Histone Methylation–MAPK Signaling Axis Drives Durable Epithelial–Mesenchymal Transition in Hypoxic Pancreatic Cancer Open
Supplementary Figure S9