Public articles linked to the same research event.
bioRxiv Using GISTIC copy number from the TCGA PanCancer Atlas to classify tumors as PTEN intact, hemizygous, or homozygous deletion, this study scored a five-gene glutaminolysis signature (GLS, SLC1A5, GOT1, GLUD1, GPT2) against loss severity across fourteen tumor types and found that the signature decreased with PTEN loss in all fourteen (significantly in twelve) but was not MYC-mediated; instead the decline tracked chromosomal position, since GLUD1 and GOT1 flank PTEN on 10q and thirty-seven neighboring genes carrying no glutaminolysis annotation tracked PTEN copy number just as closely (mean rho 0.843 versus 0.842), with co-deletion fidelity falling monotonically with distance from PTEN (rho = -0.
Using GISTIC copy number from the TCGA PanCancer Atlas to classify tumors as PTEN intact, hemizygous, or homozygous deletion, this study scored a five-gene glutaminolysis signature (GLS, SLC1A5, GOT1, GLUD1, GPT2) against loss severity across fourteen tumor types and found that the signature decreased with PTEN loss in all fourteen (significantly in twelve) but was not MYC-mediated; instead the decline tracked chromosomal position, since GLUD1 and GOT1 flank PTEN on 10q and thirty-seven neighboring genes carrying no glutaminolysis annotation tracked PTEN copy number just as closely (mean rho 0.843 versus 0.842), with co-deletion fidelity falling monotonically with distance from PTEN (rho = -0.
Using GISTIC copy number from the TCGA PanCancer Atlas to classify tumors as PTEN intact, hemizygous, or homozygous deletion, this study scored a five-gene glutaminolysis signature (GLS, SLC1A5, GOT1, GLUD1, GPT2) against loss severity across fourteen tumor types and found that the signature decreased with PTEN loss in all fourteen (significantly in twelve) but was not MYC-mediated; instead the decline tracked chromosomal position, since GLUD1 and GOT1 flank PTEN on 10q and thirty-seven neighboring genes carrying no glutaminolysis annotation tracked PTEN copy number just as closely (mean rho 0.843 versus 0.842), with co-deletion fidelity falling monotonically with distance from PTEN (rho = -0.
Using GISTIC copy number from the TCGA PanCancer Atlas to classify tumors as PTEN intact, hemizygous, or homozygous deletion, this study scored a five-gene glutaminolysis signature (GLS, SLC1A5, GOT1, GLUD1, GPT2) against loss severity across fourteen tumor types and found that the signature decreased with PTEN loss in all fourteen (significantly in twelve) but was not MYC-mediated; instead the decline tracked chromosomal position, since GLUD1 and GOT1 flank PTEN on 10q and thirty-seven neighboring genes carrying no glutaminolysis annotation tracked PTEN copy number just as closely (mean rho 0.843 versus 0.842), with co-deletion fidelity falling monotonically with distance from PTEN (rho = -0.