Sateja Paradkar

ORCID: 0000-0002-0630-9792
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Renal cell carcinoma treatment
  • CAR-T cell therapy research
  • Cancer, Hypoxia, and Metabolism
  • interferon and immune responses
  • PARP inhibition in cancer therapy
  • Biochemical and Molecular Research
  • Melanoma and MAPK Pathways
  • Nanoparticle-Based Drug Delivery
  • Cutaneous Melanoma Detection and Management
  • DNA Repair Mechanisms
  • Sirtuins and Resveratrol in Medicine
  • Cancer Immunotherapy and Biomarkers
  • RNA modifications and cancer
  • Protein Degradation and Inhibitors
  • Ferroptosis and cancer prognosis
  • Autophagy in Disease and Therapy
  • Endoplasmic Reticulum Stress and Disease
  • Immunotherapy and Immune Responses
  • T-cell and B-cell Immunology
  • Diet and metabolism studies
  • Computational Drug Discovery Methods
  • Cancer, Lipids, and Metabolism
  • Cancer-related Molecular Pathways
  • Cancer therapeutics and mechanisms
  • Pancreatic and Hepatic Oncology Research

Yale University
2021-2024

University of New Haven
2022-2024

Whitehead Institute for Biomedical Research
2020

Birla Institute of Technology and Science - Hyderabad Campus
2018

Birla Institute of Technology and Science, Pilani
2018

<div>Abstract<p>Despite recent advances in the treatment of melanoma, many patients with metastatic disease still succumb to their disease. To identify tumor-intrinsic modulators immunity we performed a whole-genome CRISPR screen melanoma and identified <i>Setdb1</i> as well all components human silencing hub complex. We found that loss leads increased immunogenicity complete tumor clearance CD8<sup>+</sup> T cell–dependent manner. Mechanistically, causes...

10.1158/2326-6066.c.7655000 preprint EN 2025-02-03

Solid lipid nanoparticles (SLNs) represent an affordable, easily scalable, stable and biocompatible drug delivery system with a high to ratio which also improves solubility of poorly soluble drugs.SLNs were developed by using glyceryl monostearate as the single in presence surfactant Poloxamer 188 evaluated efficiency SLNs load therapeutic cargo, curcumin (CUR).The nano-formulation was optimized Quality Design approach understand effect various process parameters on quality attributes,...

10.2174/1567201815666180503120113 article EN Current Drug Delivery 2018-05-07

Abstract The treatment of primary central nervous system tumors is challenging due to the blood–brain barrier and complex mutational profiles, which associated with low survival rates. However, recent studies have identified common mutations in gliomas [isocitrate dehydrogenase (IDH)-wild-type mutant, WHO grades II–IV; grade IV referred as glioblastomas (GBM)]. These drive epigenetic changes, leading promoter methylation at nicotinic acid phosphoribosyl transferase (NAPRT) gene locus,...

10.1158/1535-7163.mct-24-0012 article EN cc-by-nc-nd Molecular Cancer Therapeutics 2024-05-01

Abstract Despite recent advances in the treatment of melanoma, many patients with metastatic disease still succumb to their disease. To identify tumor-intrinsic modulators immunity we performed a whole-genome CRISPR screen melanoma and identified Setdb1 as well all components HUSH complex. We found that loss leads increased immunogenicity complete tumor clearance CD8+ T-cell dependent manner. Mechanistically, causes de-repression endogenous retroviruses (ERVs) cells triggers tumor-cell...

10.1158/2326-6066.cir-23-0514 article EN Cancer Immunology Research 2024-11-26

Abstract Cancer associated mutations in citric acid cycle enzymes cause overproduction of 2-hydroxyglutarate (2HG), fumarate, or succinate, commonly referred to as oncometabolites. These oncometabolite-producing are prevalent 70% gliomas, >76% hereditary leiomyomatosis and renal cell carcinoma, >25% paraganglioma pheochromocytomas, respectively contribute their progression. cancers harbor vulnerabilities multiple cellular pathways because competitive inhibition alpha...

10.1158/1538-7445.am2024-3086 article EN Cancer Research 2024-03-22

Hereditary leiomyomatosis and renal cell carcinoma (HLRCC) is caused by loss of function mutations in fumarate hydratase (FH) results an aggressive subtype with limited treatment options. Loss FH leads to accumulation fumarate, oncometabolite that disrupts multiple cellular processes drives tumor progression. High levels inhibit alpha ketoglutarate-dependent dioxygenases, including the ten-eleven translocation (TET) enzymes, can lead global DNA hypermethylation. Here, we report patterns...

10.1158/1541-7786.mcr-23-1003 article EN cc-by-nc-nd Molecular Cancer Research 2024-07-01

<div>Abstract<p>The treatment of primary central nervous system tumors is challenging due to the blood–brain barrier and complex mutational profiles, which associated with low survival rates. However, recent studies have identified common mutations in gliomas [isocitrate dehydrogenase (IDH)-wild-type mutant, WHO grades II–IV; grade IV referred as glioblastomas (GBM)]. These drive epigenetic changes, leading promoter methylation at nicotinic acid phosphoribosyl transferase...

10.1158/1535-7163.c.7380232 preprint EN 2024-08-01

<div>Abstract<p>The treatment of primary central nervous system tumors is challenging due to the blood–brain barrier and complex mutational profiles, which associated with low survival rates. However, recent studies have identified common mutations in gliomas [isocitrate dehydrogenase (IDH)-wild-type mutant, WHO grades II–IV; grade IV referred as glioblastomas (GBM)]. These drive epigenetic changes, leading promoter methylation at nicotinic acid phosphoribosyl transferase...

10.1158/1535-7163.c.7380232.v1 preprint EN 2024-08-01
Coming Soon ...