Adam Chatoff
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View article: Phosphoserine aminotransferase 1 promotes serine synthesis pathway and cardiac repair after myocardial infarction
Phosphoserine aminotransferase 1 promotes serine synthesis pathway and cardiac repair after myocardial infarction Open
Background and Purpose: The permanent loss of cardiomyocytes (CMs) following myocardial infarction (MI), coupled with the heart's limited regenerative capacity, often leads to heart failure. Phosphoserine aminotransferase 1 (PSAT1) is a pr…
View article: Opposing effects of systemic and pancreas-specific inhibition of BCKDK on pancreatic carcinogenesis
Opposing effects of systemic and pancreas-specific inhibition of BCKDK on pancreatic carcinogenesis Open
Branched-chain amino acid (BCAA) metabolism is perturbed in patients with pancreatic cancer, but the contribution of systemic or pancreas-intrinsic BCAA catabolism to pancreatic carcinogenesis is unclear. We show here that pancreas-specifi…
View article: A nuclear branched-chain amino acid catabolism pathway controls histone propionylation in pancreatic cancer
A nuclear branched-chain amino acid catabolism pathway controls histone propionylation in pancreatic cancer Open
Branched-chain amino acid (BCAA) catabolism contributes prominently to the TCA cycle in the healthy pancreas but is suppressed in pancreatic ductal adenocarcinoma (PDA). The impact of this metabolic remodeling on cancer phenotypes remains …
View article: KRAS G12V mutation-selective requirement for ACSS2 in colorectal adenoma formation
KRAS G12V mutation-selective requirement for ACSS2 in colorectal adenoma formation Open
Oncogenic KRAS mutations are prevalent in colorectal cancer (CRC) and linked to poor prognosis and therapeutic resistance. Emerging evidence suggests that specific KRAS mutations differentially influence treatment responses. In this study,…
View article: Selective and brain-penetrant ACSS2 inhibitors target breast cancer brain metastatic cells
Selective and brain-penetrant ACSS2 inhibitors target breast cancer brain metastatic cells Open
Breast cancer brain metastasis (BCBM) typically results in an end-stage diagnosis and is hindered by a lack of brain-penetrant drugs. Tumors in the brain rely on the conversion of acetate to acetyl-CoA by the enzyme acetyl-CoA synthetase 2…
View article: The Glucose Transporter 5 Enhances CAR-T Cell Metabolic Function and Anti-tumour Durability
The Glucose Transporter 5 Enhances CAR-T Cell Metabolic Function and Anti-tumour Durability Open
Activated T cells undergo a metabolic shift to aerobic glycolysis to support the energetic demands of proliferation, differentiation, and cytolytic function. Transmembrane glucose flux is facilitated by glucose transporters (GLUT) that pla…
View article: Table S8 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression
Table S8 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression Open
TCGA melanoma patient data
View article: Table S1 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression
Table S1 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression Open
CRISPR KO library containing 128 genes comprising the nucleotide metabolism signature
View article: Data from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression
Data from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression Open
p16 is a tumor suppressor encoded by the CDKN2A gene whose expression is lost in approximately 50% of all human cancers. In its canonical role, p16 inhibits the G1–S-phase cell cycle progression through suppression of cyclin-dependent kina…
View article: Table S2 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression
Table S2 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression Open
Primers used in this study
View article: Table S1 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression
Table S1 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression Open
CRISPR KO library containing 128 genes comprising the nucleotide metabolism signature
View article: FIGURE 2 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression
FIGURE 2 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression Open
p16/CDKN2A negatively correlates with multiple nucleotide metabolism genes, proteins, and metabolites. A–D, SKMEL28 human melanoma cells were infected with lentivirus expressing a shRNA targeting p16 (shp16). shGFP was used as a control (s…
View article: FIGURE 1 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression
FIGURE 1 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression Open
Multiple CRISPR KO screens identify nucleotide metabolism genes that are selectively depleted in p16/CDKN2Alow cells. A, Schematic of our CRISPR screens. p16/Cdkn2a wildtype cells were infected with lentiviruses expressing shGFP control (s…
View article: Data from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression
Data from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression Open
p16 is a tumor suppressor encoded by the CDKN2A gene whose expression is lost in approximately 50% of all human cancers. In its canonical role, p16 inhibits the G1–S-phase cell cycle progression through suppression of cyclin-dependent kina…
View article: Table S6 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression
Table S6 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression Open
mRNA expression of nucleotide metabolism genes
View article: FIGURE 5 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression
FIGURE 5 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression Open
shp16 tumors are more sensitive to the antifolate methotrexate. A and B, SKMEL28 human melanoma cells were infected with lentivirus expressing a shRNA targeting GFP (shCont) or p16 (shp16). A total of 107 cells were subcutaneously implante…
View article: Figure S4 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression
Figure S4 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression Open
shp16 tumor bearing mice treated with methotrexate have a trend towards a survival advantage; and methotrexate does not affect body weight or blood cell counts. Related to Figure 5.
View article: FIGURE 4 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression
FIGURE 4 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression Open
Multiple antifolates induce apoptosis in p16 knockdown cells. A–D, SKMEL28 human melanoma cells were infected with lentivirus expressing a shRNA targeting p16 (shp16). shGFP was used as a control (shCont). A, Cells were treated with the in…
View article: Figure S2 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression
Figure S2 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression Open
Knockdown or knockout of Cdkn2a in mouse melanoma cell lines increases sensitivity to multiple anti-folates but not to de novo pyrimidine synthesis; Knockdown of RB1 does not recapitulate the anti-folate response exhibited by shp16 cells. …
View article: Table S6 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression
Table S6 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression Open
mRNA expression of nucleotide metabolism genes
View article: FIGURE 3 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression
FIGURE 3 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression Open
p16/CDKN2Alow cells are more sensitive to inhibitors of nucleotide metabolism. A, Table of inhibitors used in in vitro cell line studies. 1C metabolism = one carbon metabolism. B, SKMEL28 human melanoma cells were infected with lentivirus …
View article: FIGURE 1 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression
FIGURE 1 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression Open
Multiple CRISPR KO screens identify nucleotide metabolism genes that are selectively depleted in p16/CDKN2Alow cells. A, Schematic of our CRISPR screens. p16/Cdkn2a wildtype cells were infected with lentiviruses expressing shGFP control (s…
View article: Figure S4 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression
Figure S4 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression Open
shp16 tumor bearing mice treated with methotrexate have a trend towards a survival advantage; and methotrexate does not affect body weight or blood cell counts. Related to Figure 5.
View article: Table S4 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression
Table S4 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression Open
CRISPR screen results for mouse Yumm5.2 cells
View article: Table S3 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression
Table S3 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression Open
CRISPR screen results for human SKMEL28 cells
View article: Table S4 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression
Table S4 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression Open
CRISPR screen results for mouse Yumm5.2 cells
View article: Figure S1 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression
Figure S1 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression Open
Knockdown of p16 or Cdkn2a in human and mouse melanoma cell lines, respectively, and DepMap dependency score data based on CDKN2A expression. Related to Figure 1.
View article: FIGURE 5 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression
FIGURE 5 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression Open
shp16 tumors are more sensitive to the antifolate methotrexate. A and B, SKMEL28 human melanoma cells were infected with lentivirus expressing a shRNA targeting GFP (shCont) or p16 (shp16). A total of 107 cells were subcutaneously implante…
View article: Table S5 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression
Table S5 from <i>De Novo</i> Purine Metabolism is a Metabolic Vulnerability of Cancers with Low p16 Expression Open
31 common genes identified in screens and publicly available data