Philip L. Lorenzi
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View article: Publisher Correction: Systemic Metabolic Alterations After Aneurysmal Subarachnoid Hemorrhage: A Plasma Metabolomics Approach
Publisher Correction: Systemic Metabolic Alterations After Aneurysmal Subarachnoid Hemorrhage: A Plasma Metabolomics Approach Open
View article: Supplementary Figure 6 from Vincristine Enhances the Efficacy of MEK Inhibitors in Preclinical Models of KRAS-mutant Colorectal Cancer
Supplementary Figure 6 from Vincristine Enhances the Efficacy of MEK Inhibitors in Preclinical Models of KRAS-mutant Colorectal Cancer Open
Supplementary Figure 6 shows that vinorelbine is also synergistic with trametinib in KRAS-mutant CRC 3D spheroids
View article: Supplementary Figure 1 from Vincristine Enhances the Efficacy of MEK Inhibitors in Preclinical Models of KRAS-mutant Colorectal Cancer
Supplementary Figure 1 from Vincristine Enhances the Efficacy of MEK Inhibitors in Preclinical Models of KRAS-mutant Colorectal Cancer Open
Supplementary Figure 1 shows that the combination of trametinib and vincristine is synergistic in multiple KRAS-mutant CRC cell lines and enhances apoptotic cell death.
View article: Supplementary File 2 from Vincristine Enhances the Efficacy of MEK Inhibitors in Preclinical Models of KRAS-mutant Colorectal Cancer
Supplementary File 2 from Vincristine Enhances the Efficacy of MEK Inhibitors in Preclinical Models of KRAS-mutant Colorectal Cancer Open
HTS data using 3D CRC spheroids showing growth curves and heat maps to demonstrate efficacy of different compounds when combined with trametinib.
View article: Supplementary Figure 2 from Vincristine Enhances the Efficacy of MEK Inhibitors in Preclinical Models of KRAS-mutant Colorectal Cancer
Supplementary Figure 2 from Vincristine Enhances the Efficacy of MEK Inhibitors in Preclinical Models of KRAS-mutant Colorectal Cancer Open
Supplementary Figure 2 shows that the combination of trametinib and vincristine reduces weight of CRC PDXs.
View article: Supplementary Figure 5 from Vincristine Enhances the Efficacy of MEK Inhibitors in Preclinical Models of KRAS-mutant Colorectal Cancer
Supplementary Figure 5 from Vincristine Enhances the Efficacy of MEK Inhibitors in Preclinical Models of KRAS-mutant Colorectal Cancer Open
Supplementary Figure 5 shows that trametinib increases the intracellular accumulation of daunorubicin in KRAS-mutant CRC cells.
View article: Supplementary File 1 from Vincristine Enhances the Efficacy of MEK Inhibitors in Preclinical Models of KRAS-mutant Colorectal Cancer
Supplementary File 1 from Vincristine Enhances the Efficacy of MEK Inhibitors in Preclinical Models of KRAS-mutant Colorectal Cancer Open
HTS data showing efficacy of different compounds as single agents.
View article: The asns inhibitor asx-173 potentiates l-asparaginase anticancer activity
The asns inhibitor asx-173 potentiates l-asparaginase anticancer activity Open
Background Cancer cells reprogram metabolic pathways to meet increased energy and biosynthetic demands. Among those pathways, elevated asparagine metabolism regulated by asparagine synthetase (ASNS) has been linked to progression of variou…
View article: CNSC-14. CARBOPLATIN IMPAIRS OPTIC NERVE MYELINATION IN NEUROFIBROMATOSIS TYPE 1 (NF1) BY REDUCING CHOLESTEROL LEVELS AND INDUCING OLIGODENDROCYTE LOSS
CNSC-14. CARBOPLATIN IMPAIRS OPTIC NERVE MYELINATION IN NEUROFIBROMATOSIS TYPE 1 (NF1) BY REDUCING CHOLESTEROL LEVELS AND INDUCING OLIGODENDROCYTE LOSS Open
BACKGROUND Vision impairment is a major concern for patients with Neurofibromatosis type 1 (NF1)-associated optic pathway glioma (OPG). Carboplatin-based chemotherapy is commonly used to treat NF1-OPG, but it does not consistently improve …
View article: Fructose and glucose from sugary drinks enhance colorectal cancer metastasis via SORD
Fructose and glucose from sugary drinks enhance colorectal cancer metastasis via SORD Open
View article: Figure S4 from Selective Alanine Transporter Utilization Is a Therapeutic Vulnerability in ARID1A-Mutant Ovarian Cancer
Figure S4 from Selective Alanine Transporter Utilization Is a Therapeutic Vulnerability in ARID1A-Mutant Ovarian Cancer Open
ARID1A does not create a dependence on GPTs.
View article: Figure S3 from Selective Alanine Transporter Utilization Is a Therapeutic Vulnerability in ARID1A-Mutant Ovarian Cancer
Figure S3 from Selective Alanine Transporter Utilization Is a Therapeutic Vulnerability in ARID1A-Mutant Ovarian Cancer Open
SLC38A2 and SLC7A8 are direct target genes of the SWI/SNF complex.
View article: Figure S8 from Selective Alanine Transporter Utilization Is a Therapeutic Vulnerability in ARID1A-Mutant Ovarian Cancer
Figure S8 from Selective Alanine Transporter Utilization Is a Therapeutic Vulnerability in ARID1A-Mutant Ovarian Cancer Open
The effects of SLC38A2 inhibition alone or in combination with anti-PD-L1 on tumor microenvironment.
View article: Figure S6 from Selective Alanine Transporter Utilization Is a Therapeutic Vulnerability in ARID1A-Mutant Ovarian Cancer
Figure S6 from Selective Alanine Transporter Utilization Is a Therapeutic Vulnerability in ARID1A-Mutant Ovarian Cancer Open
SLC38A2 inhibition reduces the marker of cell proliferation in ARID1A-inactivated OCCCs.
View article: Figure S2 from Selective Alanine Transporter Utilization Is a Therapeutic Vulnerability in ARID1A-Mutant Ovarian Cancer
Figure S2 from Selective Alanine Transporter Utilization Is a Therapeutic Vulnerability in ARID1A-Mutant Ovarian Cancer Open
Inactivation of the SWI/SNF complex sensitizes cells to SLC38A2 inhibition and SLC7A8 overexpression.
View article: Data from Selective Alanine Transporter Utilization Is a Therapeutic Vulnerability in ARID1A-Mutant Ovarian Cancer
Data from Selective Alanine Transporter Utilization Is a Therapeutic Vulnerability in ARID1A-Mutant Ovarian Cancer Open
Subunits of the SWI/SNF chromatin remodeling complex are altered in ∼20% of human cancers. Exemplifying the alterations is the ARID1A mutation that occurs in ∼50% of ovarian clear-cell carcinoma (OCCC), a disease with limited therap…
View article: Figure S1 from Selective Alanine Transporter Utilization Is a Therapeutic Vulnerability in ARID1A-Mutant Ovarian Cancer
Figure S1 from Selective Alanine Transporter Utilization Is a Therapeutic Vulnerability in ARID1A-Mutant Ovarian Cancer Open
ARID1A knockout increases intracellular alanine in OVCAR429 cells.
View article: Figure S7 from Selective Alanine Transporter Utilization Is a Therapeutic Vulnerability in ARID1A-Mutant Ovarian Cancer
Figure S7 from Selective Alanine Transporter Utilization Is a Therapeutic Vulnerability in ARID1A-Mutant Ovarian Cancer Open
SLC38A2 regulates CAR T cell-based assault.
View article: Figure S5 from Selective Alanine Transporter Utilization Is a Therapeutic Vulnerability in ARID1A-Mutant Ovarian Cancer
Figure S5 from Selective Alanine Transporter Utilization Is a Therapeutic Vulnerability in ARID1A-Mutant Ovarian Cancer Open
ARID1A regulates alanine metabolism in OCCC cells.
View article: The glutaminase activity of ASNS fuels glutamine metabolism in leukemia
The glutaminase activity of ASNS fuels glutamine metabolism in leukemia Open
Not available.
View article: TCA cycle mode switch determines the fate of pirtobrutinib-tolerant persister cells in mantle cell lymphoma
TCA cycle mode switch determines the fate of pirtobrutinib-tolerant persister cells in mantle cell lymphoma Open
Bruton tyrosine kinase inhibitors (BTKis) and cell therapy have successfully been used to treat mantle cell lymphoma (MCL). However, therapy resistance inevitably emerges. Cancer cells can progressively develop stable resistance by travers…
View article: N-acetylaspartate from fat cells regulates postprandial body temperature
N-acetylaspartate from fat cells regulates postprandial body temperature Open
N-acetylaspartate (NAA), the brain's second most abundant metabolite, provides essential substrates for myelination through its hydrolysis1. However, the physiological roles of NAA in other tissues remain unknown. Here, we show …
View article: Selective Alanine Transporter Utilization Is a Therapeutic Vulnerability in ARID1A-Mutant Ovarian Cancer
Selective Alanine Transporter Utilization Is a Therapeutic Vulnerability in ARID1A-Mutant Ovarian Cancer Open
Subunits of the SWI/SNF chromatin remodeling complex are altered in ∼20% of human cancers. Exemplifying the alterations is the ARID1A mutation that occurs in ∼50% of ovarian clear-cell carcinoma (OCCC), a disease with limited therapeutic o…
View article: The ASNS inhibitor ASX-173 potentiates L-asparaginase anticancer activity
The ASNS inhibitor ASX-173 potentiates L-asparaginase anticancer activity Open
Cancer cells reprogram metabolic pathways to meet increased energy and biosynthetic demands. Among those pathways, elevated asparagine metabolism regulated by asparagine synthetase (ASNS) has been linked to tumor progression in various can…
View article: Immature Acta2R179C/+ smooth muscle cells cause moyamoya-like cerebrovascular lesions in mice prevented by boosting OXPHOS
Immature Acta2R179C/+ smooth muscle cells cause moyamoya-like cerebrovascular lesions in mice prevented by boosting OXPHOS Open
View article: Downregulation of LATS1/2 Drives Endothelial Senescence-Associated Stemness (SAS) and Atherothrombotic Lesion Formation
Downregulation of LATS1/2 Drives Endothelial Senescence-Associated Stemness (SAS) and Atherothrombotic Lesion Formation Open
Background Atherothrombosis, the main event leading to acute coronary syndrome (ACS), is strongly linked to disturbed blood flow (d-flow) regions. Although the involvement of the Hippo pathway and its kinases Large Tumor Suppressor Kinase …
View article: Isocitrate dehydrogenase 1 regulates cardiac metabolic adaptation during oncometabolic stress
Isocitrate dehydrogenase 1 regulates cardiac metabolic adaptation during oncometabolic stress Open
View article: Autophagic signaling promotes systems-wide remodeling in skeletal muscle upon oncometabolic stress by D2-HG.
Autophagic signaling promotes systems-wide remodeling in skeletal muscle upon oncometabolic stress by D2-HG. Open
View article: CHD1 loss reprograms SREBP2-driven cholesterol synthesis to fuel androgen-responsive growth and castration resistance in SPOP-mutated prostate tumors
CHD1 loss reprograms SREBP2-driven cholesterol synthesis to fuel androgen-responsive growth and castration resistance in SPOP-mutated prostate tumors Open
View article: Blood-based proteomic profiling identifies OSMR as a novel biomarker of AML outcomes
Blood-based proteomic profiling identifies OSMR as a novel biomarker of AML outcomes Open
Inflammation is increasingly recognized as a critical factor in acute myeloid leukemia (AML) pathogenesis. We performed blood-based proteomic profiling of 251 inflammatory proteins in 543 patients with newly diagnosed AML. Using a machine …