Vikash P. Chauhan
YOU?
Author Swipe
View article: Engineered prime editors with minimal genomic errors
Engineered prime editors with minimal genomic errors Open
View article: Mutant p53 exploits enhancers to elevate immunosuppressive chemokine expression and impair immune checkpoint inhibitors in pancreatic cancer
Mutant p53 exploits enhancers to elevate immunosuppressive chemokine expression and impair immune checkpoint inhibitors in pancreatic cancer Open
View article: Synthetic Approaches of Benzimidazole Derivatives on Anti-Diabetic Activity: A Review
Synthetic Approaches of Benzimidazole Derivatives on Anti-Diabetic Activity: A Review Open
Background: Thiazolidine-2,4-dione (2,4-TZD) is a versatile and valuable chemical structure that features a five-membered ring with an oxygen atom at the 2-position, a double bond at the 4-position, and contains both a nitrogen and a sulph…
View article: Fixation alters the physical properties of tumor tissue that regulate nanomedicine transport
Fixation alters the physical properties of tumor tissue that regulate nanomedicine transport Open
To have the desired therapeutic effect, nanomedicines and macromolecular medications must move from the site of injection to the site of action, without having adverse effects. Transvascular transport is a critical step of this navigation,…
View article: Mutant p53 Exploits Enhancers to Elevate Immunosuppressive Chemokine Expression and Impair Immune Checkpoint Inhibitors in Pancreatic Cancer
Mutant p53 Exploits Enhancers to Elevate Immunosuppressive Chemokine Expression and Impair Immune Checkpoint Inhibitors in Pancreatic Cancer Open
Summary Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer without effective treatments. It is characterized by activating KRAS mutations and p53 alterations. However, how these mutations dysregulate cancer-cell-intrinsic gene…
View article: Engineered prime editors with minimal genomic errors
Engineered prime editors with minimal genomic errors Open
Prime editors make programmed genome modifications by writing new sequences into extensions of nicked DNA 3’ ends. These edited 3’ new strands must displace competing 5’ strands to install edits, yet a bias toward retaining the competing 5…
View article: 1517 Mutant-p53 amplifies Cxcl1 expression from distal enhancers blunting immune checkpoint inhibition efficacy in pancreatic cancer
1517 Mutant-p53 amplifies Cxcl1 expression from distal enhancers blunting immune checkpoint inhibition efficacy in pancreatic cancer Open
Background Myeloid cells, unlike other immune cells such as T cells or NK cells, are known residents in the solid tumor microenvironment (TME). In the absence of checkpoints and in proinflammatory conditions, M1 macrophages are known to be…
View article: Supplementary Methods from Obesity-Induced Inflammation and Desmoplasia Promote Pancreatic Cancer Progression and Resistance to Chemotherapy
Supplementary Methods from Obesity-Induced Inflammation and Desmoplasia Promote Pancreatic Cancer Progression and Resistance to Chemotherapy Open
Supplementary Methods
View article: Data from Obesity-Induced Inflammation and Desmoplasia Promote Pancreatic Cancer Progression and Resistance to Chemotherapy
Data from Obesity-Induced Inflammation and Desmoplasia Promote Pancreatic Cancer Progression and Resistance to Chemotherapy Open
It remains unclear how obesity worsens treatment outcomes in patients with pancreatic ductal adenocarcinoma (PDAC). In normal pancreas, obesity promotes inflammation and fibrosis. We found in mouse models of PDAC that obesity also promotes…
View article: Supplementary Tables S1 - S6 from Obesity-Induced Inflammation and Desmoplasia Promote Pancreatic Cancer Progression and Resistance to Chemotherapy
Supplementary Tables S1 - S6 from Obesity-Induced Inflammation and Desmoplasia Promote Pancreatic Cancer Progression and Resistance to Chemotherapy Open
Supplementary Tables S1 - S6. Supplementary Table S1. CT values for demosplasia-related genes in PAN02 tumors. Data obtained from PCR array. Supplementary Table S2. CT values for demosplasia-related genes in AK4.4 tumors. Data obtained fro…
View article: Data from Obesity-Induced Inflammation and Desmoplasia Promote Pancreatic Cancer Progression and Resistance to Chemotherapy
Data from Obesity-Induced Inflammation and Desmoplasia Promote Pancreatic Cancer Progression and Resistance to Chemotherapy Open
It remains unclear how obesity worsens treatment outcomes in patients with pancreatic ductal adenocarcinoma (PDAC). In normal pancreas, obesity promotes inflammation and fibrosis. We found in mouse models of PDAC that obesity also promotes…
View article: Supplementary Tables S1 - S6 from Obesity-Induced Inflammation and Desmoplasia Promote Pancreatic Cancer Progression and Resistance to Chemotherapy
Supplementary Tables S1 - S6 from Obesity-Induced Inflammation and Desmoplasia Promote Pancreatic Cancer Progression and Resistance to Chemotherapy Open
Supplementary Tables S1 - S6. Supplementary Table S1. CT values for demosplasia-related genes in PAN02 tumors. Data obtained from PCR array. Supplementary Table S2. CT values for demosplasia-related genes in AK4.4 tumors. Data obtained fro…
View article: Supplementary Figures S1 - S15 from Obesity-Induced Inflammation and Desmoplasia Promote Pancreatic Cancer Progression and Resistance to Chemotherapy
Supplementary Figures S1 - S15 from Obesity-Induced Inflammation and Desmoplasia Promote Pancreatic Cancer Progression and Resistance to Chemotherapy Open
Supplementary Figures S1 - S15. Supplementary Figure S1. Effect of obesity on tumor initiation. Supplementary Figure S2. Adipose tissue - tumor interaction. Supplementary Figure S3. Correlation of collagen-I levels with tumor size, co-expr…
View article: Supplementary Figures S1 - S15 from Obesity-Induced Inflammation and Desmoplasia Promote Pancreatic Cancer Progression and Resistance to Chemotherapy
Supplementary Figures S1 - S15 from Obesity-Induced Inflammation and Desmoplasia Promote Pancreatic Cancer Progression and Resistance to Chemotherapy Open
Supplementary Figures S1 - S15. Supplementary Figure S1. Effect of obesity on tumor initiation. Supplementary Figure S2. Adipose tissue - tumor interaction. Supplementary Figure S3. Correlation of collagen-I levels with tumor size, co-expr…
View article: Supplementary Methods from Obesity-Induced Inflammation and Desmoplasia Promote Pancreatic Cancer Progression and Resistance to Chemotherapy
Supplementary Methods from Obesity-Induced Inflammation and Desmoplasia Promote Pancreatic Cancer Progression and Resistance to Chemotherapy Open
Supplementary Methods
View article: Data from Multiphoton Phosphorescence Quenching Microscopy Reveals Kinetics of Tumor Oxygenation during Antiangiogenesis and Angiotensin Signaling Inhibition
Data from Multiphoton Phosphorescence Quenching Microscopy Reveals Kinetics of Tumor Oxygenation during Antiangiogenesis and Angiotensin Signaling Inhibition Open
Purpose:The abnormal function of tumor blood vessels causes tissue hypoxia, promoting disease progression and treatment resistance. Although tumor microenvironment normalization strategies can alleviate hypoxia globally, how local oxygen l…
View article: Supplementary Data from Multiphoton Phosphorescence Quenching Microscopy Reveals Kinetics of Tumor Oxygenation during Antiangiogenesis and Angiotensin Signaling Inhibition
Supplementary Data from Multiphoton Phosphorescence Quenching Microscopy Reveals Kinetics of Tumor Oxygenation during Antiangiogenesis and Angiotensin Signaling Inhibition Open
Supplementary Data from Multiphoton Phosphorescence Quenching Microscopy Reveals Kinetics of Tumor Oxygenation during Antiangiogenesis and Angiotensin Signaling Inhibition
View article: Data from Multiphoton Phosphorescence Quenching Microscopy Reveals Kinetics of Tumor Oxygenation during Antiangiogenesis and Angiotensin Signaling Inhibition
Data from Multiphoton Phosphorescence Quenching Microscopy Reveals Kinetics of Tumor Oxygenation during Antiangiogenesis and Angiotensin Signaling Inhibition Open
Purpose:The abnormal function of tumor blood vessels causes tissue hypoxia, promoting disease progression and treatment resistance. Although tumor microenvironment normalization strategies can alleviate hypoxia globally, how local oxygen l…
View article: Supplementary Data from Multiphoton Phosphorescence Quenching Microscopy Reveals Kinetics of Tumor Oxygenation during Antiangiogenesis and Angiotensin Signaling Inhibition
Supplementary Data from Multiphoton Phosphorescence Quenching Microscopy Reveals Kinetics of Tumor Oxygenation during Antiangiogenesis and Angiotensin Signaling Inhibition Open
Supplementary Data from Multiphoton Phosphorescence Quenching Microscopy Reveals Kinetics of Tumor Oxygenation during Antiangiogenesis and Angiotensin Signaling Inhibition
View article: Altered DNA repair pathway engagement by engineered CRISPR-Cas9 nucleases
Altered DNA repair pathway engagement by engineered CRISPR-Cas9 nucleases Open
CRISPR-Cas9 introduces targeted DNA breaks that engage competing DNA repair pathways, producing a spectrum of imprecise insertion/deletion mutations (indels) and precise templated mutations (precise edits). The relative frequencies of thes…
View article: Multiphoton Phosphorescence Quenching Microscopy Reveals Kinetics of Tumor Oxygenation during Antiangiogenesis and Angiotensin Signaling Inhibition
Multiphoton Phosphorescence Quenching Microscopy Reveals Kinetics of Tumor Oxygenation during Antiangiogenesis and Angiotensin Signaling Inhibition Open
Purpose: The abnormal function of tumor blood vessels causes tissue hypoxia, promoting disease progression and treatment resistance. Although tumor microenvironment normalization strategies can alleviate hypoxia globally, how local oxygen …
View article: Altered DNA repair pathway engagement by engineered CRISPR-Cas9 nucleases
Altered DNA repair pathway engagement by engineered CRISPR-Cas9 nucleases Open
CRISPR-Cas9 introduces targeted DNA breaks that engage competing DNA repair pathways, producing a spectrum of imprecise insertion/deletion mutations (indels) and precise templated mutations (precise edits). The relative frequencies of thes…
View article: Dendritic cell paucity in mismatch repair–proficient colorectal cancer liver metastases limits immune checkpoint blockade efficacy
Dendritic cell paucity in mismatch repair–proficient colorectal cancer liver metastases limits immune checkpoint blockade efficacy Open
Significance Immune checkpoint blockade (ICB) has been efficacious in several cancer types. However, mismatch repair–proficient (pMMR) metastatic colorectal cancer (CRC), ∼95% of total metastatic CRC cases, typically does not respond to IC…
View article: Identification of a long non-coding RNA regulator of liver carcinoma cell survival
Identification of a long non-coding RNA regulator of liver carcinoma cell survival Open
Genomic studies have significantly improved our understanding of hepatocellular carcinoma (HCC) biology and have led to the discovery of multiple protein-coding genes driving hepatocarcinogenesis. In addition, these studies have identified…
View article: Identification of a long non-coding RNA regulator of liver carcinoma cell survival
Identification of a long non-coding RNA regulator of liver carcinoma cell survival Open
Genomic studies have significantly improved our understanding of hepatocellular carcinoma (HCC) biology and have led to the discovery of multiple protein-coding genes driving hepatocarcinogenesis. In addition, these studies have identified…
View article: Abstract 2744: Blocking CXCR4 alleviates desmoplasia, increases T-lymphocyte infiltration, and improves immunotherapy in metastatic breast cancer
Abstract 2744: Blocking CXCR4 alleviates desmoplasia, increases T-lymphocyte infiltration, and improves immunotherapy in metastatic breast cancer Open
Metastatic breast cancers (mBCs) are largely resistant to immune checkpoint blockade, but the mechanisms remain unclear. Primary breast cancers are characterized by a dense fibrotic stroma, which is considered immunosuppressive in multiple…
View article: Reprogramming the microenvironment with tumor-selective angiotensin blockers enhances cancer immunotherapy
Reprogramming the microenvironment with tumor-selective angiotensin blockers enhances cancer immunotherapy Open
Cancer-associated fibroblasts (CAFs) can either suppress or support T lymphocyte activity, suggesting that CAFs may be reprogrammable to an immunosupportive state. Angiotensin receptor blockers (ARBs) convert myofibroblast CAFs to a quiesc…
View article: Pattern of Emergent Head Computed Tomography Findings in a Tertiary Care Hospital during off Working Hours: Retrospective Analysis
Pattern of Emergent Head Computed Tomography Findings in a Tertiary Care Hospital during off Working Hours: Retrospective Analysis Open
Introduction: Emergency head computed tomography (CT) is rising exponentially during off working hours due to evidence-based medicine, patient’s expectation and desires, easy availability and apprehension of medico-legal cases, thereby rai…
View article: Blocking CXCR4 alleviates desmoplasia, increases T-lymphocyte infiltration, and improves immunotherapy in metastatic breast cancer
Blocking CXCR4 alleviates desmoplasia, increases T-lymphocyte infiltration, and improves immunotherapy in metastatic breast cancer Open
Significance Although immune checkpoint blockade (ICB) along with nab-paclitaxel has increased progression-free survival in triple-negative breast cancer patients, a large fraction of metastatic breast cancer (mBC) patients do not benefit …
View article: Solid stress and elastic energy as measures of tumour mechanopathology
Solid stress and elastic energy as measures of tumour mechanopathology Open