Nishant Gandhi
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View article: TET2-mutant clonal hematopoiesis enhances macrophage antigen presentation and improves immune checkpoint therapy in solid tumors
TET2-mutant clonal hematopoiesis enhances macrophage antigen presentation and improves immune checkpoint therapy in solid tumors Open
Clonal hematopoiesis (CH) is detectable in upwards of 20% of patients with solid tumors and is associated with worsened prognosis; however, its role in tumor immunology and immune checkpoint therapy (ICT) is unknown. Using a bone marrow ch…
View article: Figure S1 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Figure S1 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
Expression of key ferroptosis evasion genes SCD1 and SLC7A11 is higher in KRAS/STK11/KEAP1 co-mutant LUADs which causes poor clinical outcomes.
View article: Figure S3 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Figure S3 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
SCD1 inhibition modulate several kinases in LUAD and SCD1 knockdown induces ferroptotic cell death in DKO.
View article: Figure S4 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Figure S4 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
Survival analysis of different treatment group of mice harboring Isogenic H358 NTC and H358 STK11/KEAP1 KO cells and de novo A549 and H460 cells induced tumors.
View article: Supplementary Table S7 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Supplementary Table S7 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
Shows the lung cancer clinical samples with high SCD1 expression.
View article: Supplementary Table S5 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Supplementary Table S5 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
Shows the list of primers used in the study.
View article: Supplementary Table S2 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Supplementary Table S2 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
Shows details of the drugs used in the study.
View article: Supplementary Table S6 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Supplementary Table S6 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
Shows the list of antibodies used in the study.
View article: Figure S2 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Figure S2 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
SCD1 inhibition augments the cytotoxic response of SLC7A11 inhibitor, erastin, in KRAS/STK11/KEAP1 co-mutant LUADs.
View article: Supplementary Table S3 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Supplementary Table S3 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
Shows the details of the cell lines used in the study.
View article: Data from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Data from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
Concurrent inactivating mutations in STK11 and KEAP1 drive primary resistance to therapies, leading to worse outcomes in KRAS-mutated lung adenocarcinoma (KRASmut LUAD), and are associated with metabo…
View article: Supplementary Table S1 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Supplementary Table S1 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
Shows the details and number of the clinical samples used in the study.
View article: Supplementary Table S8 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Supplementary Table S8 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
Shows the percentage of the SCD1 high population in KRAS mutant LUADs.
View article: Supplementary Table S9 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Supplementary Table S9 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
Shows the percentage of LUAD cases with SCD1 and SLC7A11 expression.
View article: Supplementary Table S4 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma
Supplementary Table S4 from SCD1 Inhibition Blocks the AKT–NRF2–SLC7A11 Pathway to Induce Lipid Metabolism Remodeling and Ferroptosis Priming in Lung Adenocarcinoma Open
Shows details of the kits, assays used in the study.
View article: Angiotensin Receptor Blockade Does Not Decrease Synthetic Angiotensin II (Giapreza®) Effectiveness in Perioperative Hypotension Surrounding Kidney Transplant
Angiotensin Receptor Blockade Does Not Decrease Synthetic Angiotensin II (Giapreza®) Effectiveness in Perioperative Hypotension Surrounding Kidney Transplant Open
Background/Objectives: The use of angiotensin II (AT2S) as a vasopressor in patients receiving angiotensin receptor blockers (ARBs) prior to kidney transplant (KT) raises theoretical concerns. At our center, AT2S is the first-line vasopres…
View article: 96 The Effect of Individualized Intravenous Heparin Dosing on Activated Partial Thromboplastin Time Values in Neurocritical Care Patients
96 The Effect of Individualized Intravenous Heparin Dosing on Activated Partial Thromboplastin Time Values in Neurocritical Care Patients Open
View article: Identifying distinct prognostic and predictive contributions of tumor epithelium versus tumor microenvironment in colorectal cancer
Identifying distinct prognostic and predictive contributions of tumor epithelium versus tumor microenvironment in colorectal cancer Open
Here we identified a pair of new, distinct 10-gene signatures (the EPIS vs. the TMES) capable of distinguishing the cellular contribution of the tumor EPI vs. the TME in determining CRC prognosis and therapeutic outco…
View article: Data from Structurally Oriented Classification of <i>FOXA1</i> Alterations Identifies Prostate Cancers with Opposing Clinical Outcomes and Distinct Molecular and Immunologic Subtypes
Data from Structurally Oriented Classification of <i>FOXA1</i> Alterations Identifies Prostate Cancers with Opposing Clinical Outcomes and Distinct Molecular and Immunologic Subtypes Open
Purpose:Around 10% to 15% of prostate cancers harbor recurrent aberrations in the Forkhead Box A1 gene, FOXA1, whereby the alteration type and the effect on the forkhead (FKH) domain affect protein function. We developed a FOXA1<…
View article: Figure 4 from Structurally Oriented Classification of <i>FOXA1</i> Alterations Identifies Prostate Cancers with Opposing Clinical Outcomes and Distinct Molecular and Immunologic Subtypes
Figure 4 from Structurally Oriented Classification of <i>FOXA1</i> Alterations Identifies Prostate Cancers with Opposing Clinical Outcomes and Distinct Molecular and Immunologic Subtypes Open
Treatment-associated outcomes by FOXA1 alteration class. The survival analysis is conducted on patients who received (A) first-line ADT, including goserelin, leuprolide, triptorelin, degarelix, and relugolix. B, Second…
View article: Supplementary Figure 1-10 from Structurally Oriented Classification of <i>FOXA1</i> Alterations Identifies Prostate Cancers with Opposing Clinical Outcomes and Distinct Molecular and Immunologic Subtypes
Supplementary Figure 1-10 from Structurally Oriented Classification of <i>FOXA1</i> Alterations Identifies Prostate Cancers with Opposing Clinical Outcomes and Distinct Molecular and Immunologic Subtypes Open
Supplementary Figures 1-10
View article: Figure 5 from Structurally Oriented Classification of <i>FOXA1</i> Alterations Identifies Prostate Cancers with Opposing Clinical Outcomes and Distinct Molecular and Immunologic Subtypes
Figure 5 from Structurally Oriented Classification of <i>FOXA1</i> Alterations Identifies Prostate Cancers with Opposing Clinical Outcomes and Distinct Molecular and Immunologic Subtypes Open
Molecular associations by FOXA1 alteration class. Percentages of (A) TMPRSS2–ERG fusions, (B) TP53 mutations, (C) MSI-high status, and (D) TMB-high status based on FOXA1 alteration cl…
View article: Figure 1 from Structurally Oriented Classification of <i>FOXA1</i> Alterations Identifies Prostate Cancers with Opposing Clinical Outcomes and Distinct Molecular and Immunologic Subtypes
Figure 1 from Structurally Oriented Classification of <i>FOXA1</i> Alterations Identifies Prostate Cancers with Opposing Clinical Outcomes and Distinct Molecular and Immunologic Subtypes Open
FOXA1 alterations in prostate cancer. A, Bar graphs showing percentages of amplifications and mutations found in the top 20 cancers with FOXA1 alterations from the Caris Life Sciences POA database. CUP, carcinoma of un…
View article: Figure 2 from Structurally Oriented Classification of <i>FOXA1</i> Alterations Identifies Prostate Cancers with Opposing Clinical Outcomes and Distinct Molecular and Immunologic Subtypes
Figure 2 from Structurally Oriented Classification of <i>FOXA1</i> Alterations Identifies Prostate Cancers with Opposing Clinical Outcomes and Distinct Molecular and Immunologic Subtypes Open
FOXA1 alterations and implications on protein structure. A, Distinctions between our classification scheme and two seminal studies are shown through an alluvial plot. B, MTR of each AA position of FOXA1. Horizontal lin…
View article: Figure 6 from Structurally Oriented Classification of <i>FOXA1</i> Alterations Identifies Prostate Cancers with Opposing Clinical Outcomes and Distinct Molecular and Immunologic Subtypes
Figure 6 from Structurally Oriented Classification of <i>FOXA1</i> Alterations Identifies Prostate Cancers with Opposing Clinical Outcomes and Distinct Molecular and Immunologic Subtypes Open
FOXA1 alteration classes by race. A, FOXA1 alteration classes are examined by race. B, The distribution of FOXA1 alteration classes by race. *q value <0.05, **q value <0.01, ***q value < 0.001, ****q valu…
View article: Figure 3 from Structurally Oriented Classification of <i>FOXA1</i> Alterations Identifies Prostate Cancers with Opposing Clinical Outcomes and Distinct Molecular and Immunologic Subtypes
Figure 3 from Structurally Oriented Classification of <i>FOXA1</i> Alterations Identifies Prostate Cancers with Opposing Clinical Outcomes and Distinct Molecular and Immunologic Subtypes Open
OS based on FOXA1 alteration class. OS is depicted based on forest plots as organized by each FOXA1 alteration class for (A) all prostate tumors, (B) prostate samples, and (C) metastatic samples. D,
View article: Supplementary Table 1-11 from Structurally Oriented Classification of <i>FOXA1</i> Alterations Identifies Prostate Cancers with Opposing Clinical Outcomes and Distinct Molecular and Immunologic Subtypes
Supplementary Table 1-11 from Structurally Oriented Classification of <i>FOXA1</i> Alterations Identifies Prostate Cancers with Opposing Clinical Outcomes and Distinct Molecular and Immunologic Subtypes Open
Supplementary Tables 1-11
View article: Table 1 from Structurally Oriented Classification of <i>FOXA1</i> Alterations Identifies Prostate Cancers with Opposing Clinical Outcomes and Distinct Molecular and Immunologic Subtypes
Table 1 from Structurally Oriented Classification of <i>FOXA1</i> Alterations Identifies Prostate Cancers with Opposing Clinical Outcomes and Distinct Molecular and Immunologic Subtypes Open
Patient demographics.
View article: Molecular Characterization and Clinical Outcomes of Pancreatic Neuroendocrine Neoplasms Harboring PAK4-NAMPT Alterations
Molecular Characterization and Clinical Outcomes of Pancreatic Neuroendocrine Neoplasms Harboring PAK4-NAMPT Alterations Open
PURPOSE The mammalian target of rapamycin (mTOR) inhibitor everolimus is US Food and Drug Administration-approved for advanced pancreatic neuroendocrine neoplasms (pNENs), yet resistance is common, necessitating the identification of resis…
View article: Structurally Oriented Classification of <i>FOXA1</i> Alterations Identifies Prostate Cancers with Opposing Clinical Outcomes and Distinct Molecular and Immunologic Subtypes
Structurally Oriented Classification of <i>FOXA1</i> Alterations Identifies Prostate Cancers with Opposing Clinical Outcomes and Distinct Molecular and Immunologic Subtypes Open
Purpose: Around 10% to 15% of prostate cancers harbor recurrent aberrations in the Forkhead Box A1 gene, FOXA1, whereby the alteration type and the effect on the forkhead (FKH) domain affect protein function. We developed a FOXA1 classific…