Krishan Kumar

ORCID: 0000-0003-4406-2644
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Protein Degradation and Inhibitors
  • Pancreatic and Hepatic Oncology Research
  • Multiple Myeloma Research and Treatments
  • Ubiquitin and proteasome pathways
  • Cancer Cells and Metastasis
  • Cancer Genomics and Diagnostics
  • Cancer-related gene regulation
  • Cancer Research and Treatments
  • Epigenetics and DNA Methylation
  • Cancer, Hypoxia, and Metabolism
  • PI3K/AKT/mTOR signaling in cancer
  • Melanoma and MAPK Pathways
  • Pancreatic function and diabetes
  • Histone Deacetylase Inhibitors Research
  • Cancer-related molecular mechanisms research
  • RNA modifications and cancer
  • Peptidase Inhibition and Analysis
  • Prostate Cancer Treatment and Research
  • Polyamine Metabolism and Applications
  • Cholangiocarcinoma and Gallbladder Cancer Studies
  • Occupational and environmental lung diseases
  • Advanced Breast Cancer Therapies
  • Quality and Safety in Healthcare
  • Chronic Lymphocytic Leukemia Research
  • Galectins and Cancer Biology

Northwestern University
2013-2023

The Ohio State University
2017-2023

Banaras Hindu University
2022

Rajendra Institute of Medical Sciences
2021

Ranchi University
2020

Indo-American Center
2018-2019

Robert H. Lurie Comprehensive Cancer Center of Northwestern University
2013-2019

Jesse Brown VA Medical Center
2013-2016

Chang Gung University
2014

Linkou Chang Gung Memorial Hospital
2014

Journal Article Somatic mutations in the PTCH, SMOH, SUFUH and TP53 genes sporadic basal cell carcinomas Get access J. Reifenberger, Reifenberger Departments of Dermatology Neuropathology, Heinrich‐Heine‐University, Moorenstraße 5, D‐40225 Düsseldorf, Germany Julia Reifenberger. E‐mail: reifenbergerj@med.uni‐duesseldorf.de Search for other works by this author on: Oxford Academic Google Scholar M. Wolter, Wolter C. B. Knobbe, Knobbe Köhler, Köhler A. Schönicke, Schönicke Scharwächter,...

10.1111/j.1365-2133.2005.06353.x article EN British Journal of Dermatology 2005-01-01

Abstract Pancreatic ductal adenocarcinoma (PDAC) is associated with pronounced fibrosis that contributes to chemoresistance, in part, through increased histone acetylation. Because bromodomain (BRD) and extra terminal domain (BET) proteins are “readers” of acetylation marks, we targeted BET PDAC cells grown three-dimensional collagen. We show treatment inhibitors decreases growth (AsPC1, CD18, Panc1) Transfection siRNA against BRD4, which human tumors, also cells. additionally decrease...

10.1158/1535-7163.mct-13-0925 article EN Molecular Cancer Therapeutics 2014-05-08

Abstract JQ1 and I-BET151 are selective inhibitors of BET bromodomain proteins that have efficacy against a number different cancers. Since the effectiveness targeted therapies is often limited by development resistance, we examined whether it was possible for cancer cells to develop resistance inhibitor JQ1. Here show pancreatic developing demonstrate cross-resistance insensitivity BRD4 downregulation. The resistant maintain expression c-MYC, increase JQ1-target genes FOSL1 HMGA2 evidence...

10.1038/srep09489 article EN cc-by Scientific Reports 2015-03-25

Cancer stem cells (CSCs) represent a unique sub-population of tumor with the ability to initiate growth and sustain self-renewal. Although CSC biomarkers have been described for various tumors, only few markers identified nasopharyngeal carcinoma (NPC). In this study, we show that CD24+ isolated from human NPC cell lines express genes (Sox2, Oct4, Nanog, Bmi-1, Rex-1), activation Wnt/β-catenin signaling pathway. possess typical characteristics include enhanced proliferation, increased colony...

10.1371/journal.pone.0099412 article EN cc-by PLoS ONE 2014-06-23

Pancreatic ductal adenocarcinoma (PDAC) is associated with a pronounced collagen-rich stromal reaction that has been shown to contribute chemo-resistance. We have previously PDAC cells are resistant gemcitabine chemotherapy in the collagen microenvironment because of increased expression chromatin remodeling protein high mobility group A2 (HMGA2). now found human tumors display higher levels histone H3K9 and H3K27 acetylation fibrotic regions. show relative grown on tissue culture plastic,...

10.1371/journal.pone.0064566 article EN cc-by PLoS ONE 2013-05-16

The fibrotic reaction, which can account for over 70%-80% of the tumor mass, is a characteristic feature human pancreatic ductal adenocarcinoma (PDAC) tumors. It associated with activation and proliferation stellate cells (PSCs), are key regulators collagen I production fibrosis in vivo. In this report, we show that members bromodomain extraterminal (BET) family proteins expressed primary PSCs isolated from PDAC tumors, BRD4 positively regulating, BRD2 BRD3 negatively expression...

10.1172/jci.insight.88032 article EN JCI Insight 2017-02-08

Bromodomain and extraterminal domain (BET) proteins, which are important epigenetic readers, often dysregulated in cancer. While a number of BET inhibitors currently early phase clinical trials, show limited single-agent activity. The purpose this study is to determine if Quercetin, naturally occurring polyphenolic flavonoid found abundant fruits vegetables, can enhance the anti-tumor effects inhibitors. efficacy combination was evaluated vitro xenograft model pancreatic Co-treatment with...

10.3390/ijms20174293 article EN International Journal of Molecular Sciences 2019-09-02

Patients with pancreatic cancer, which is characterized by an extensive collagen-rich fibrotic reaction, often present metastases. A critical step in cancer metastasis epithelial-to-mesenchymal transition (EMT), can be orchestrated the Snail family of transcription factors. To understand role (SNAI1) development, we generated transgenic mice expressing pancreas. Because chronic pancreatitis contribute to Snail-expressing were treated cerulein induce pancreatitis. Although significant tissue...

10.1158/1541-7786.mcr-12-0637 article EN Molecular Cancer Research 2013-06-13

Eighteen congenital melanocytic naevi (CMN) from 17 patients and 18 dysplastic (DMN) were screened for mutations in the BRAF oncogene (present study) N-ras (in course of two foregoing studies) by single-strand conformational polymorphism (SSCP)/sequencing analysis. demonstrated both types lesion. As a whole, CMN (94.4%) five DMN (27.7%) harboured either or mutations. is frequently found to be mutated human cutaneous melanomas, it may constitute risk factor melanoma formation within DMN.

10.1097/00008390-200510000-00008 article EN Melanoma Research 2005-09-22

Human pancreatic ductal adenocarcinoma (PDAC) tumors are associated with dysregulation of mRNA translation. In this report, it is demonstrated that PDAC cells grown in collagen exhibit increased activation the MAPK-interacting protein kinases (MNK) mediate eIF4E phosphorylation. Pharmacologic and genetic targeting MNKs reverse epithelial-mesenchymal transition (EMT), decrease cell migration, reduce expression EMT-regulator ZEB1 without affecting levels. Paradoxically, eIF4E,...

10.1158/1541-7786.mcr-15-0285 article EN Molecular Cancer Research 2015-11-26

The fibrotic reaction is a characteristic feature of human pancreatic ductal adenocarcinoma (PDAC) tumors. It associated with activation and proliferation stellate cells (PSCs), which are key regulators fibrosis in vivo. While there increasing interest the regulation PD-L1 expression cancer immune cells, other stromal such as PSCs, has not been fully evaluated. Here we show that PSCs vitro express higher mRNA protein levels compared to present PDAC cells. We inhibitors targeting bromodomain...

10.1038/s41598-018-31658-1 article EN cc-by Scientific Reports 2018-08-30

BET inhibitors (BETi), which target transcription of key oncogenic genes, are currently being evaluated in early-phase clinical trials. However, because BETis show limited single-agent activity, there is increasing interest identifying signaling pathways to enhance the efficacy BETis. Here, we demonstrate increased MNK kinase-dependent eIF4E phosphorylation following treatment with BETis, indicating activation a prosurvival feedback mechanism response PROTACs, promote degradation proteins,...

10.1158/1535-7163.mct-18-0768 article EN Molecular Cancer Therapeutics 2018-11-16

Pancreatic ductal adenocarcinoma (PDAC) is associated with a pronounced fibro-inflammatory stromal reaction that contributes to tumor progression. A critical step in invasion and metastasis the epithelial-to-mesenchymal transition (EMT), which can be regulated by Snail family of transcription factors. Overexpression (Snai1) mutant Kras(G12D) pancreas transgenic mice, using an elastase (EL) promoter, resulted fibrosis. To identify how modulates inflammation pancreas, we examined effect...

10.1158/1541-7786.mcr-14-0111 article EN Molecular Cancer Research 2014-06-19

Cancer cells can invade in three-dimensional collagen as single or a cohesive group of that require coordination cell-cell junctions and the actin cytoskeleton. To examine role Gα13, G12 family heterotrimeric G protein, regulating cellular invasion collagen, we established novel method to track cell by membrane type 1 matrix metalloproteinase-expressing cancer cells. We show knockdown Gα13 decreased metalloproteinase-driven proteolytic enhanced E-cadherin-mediated adhesion. E-cadherin...

10.1074/jbc.m115.669606 article EN cc-by Journal of Biological Chemistry 2015-11-21

Background: Pancreatic ductal adenocarcinoma (PDAC) is characterized by the presence of dense stroma that enriched in hyaluronan (HA), with increased HA levels associated more aggressive disease. Increased HA-degrading enzymes hyaluronidases (HYALs) are also tumor progression. In this study, we evaluate regulation HYALs PDAC. Methods: Using siRNA and small molecule inhibitors, evaluated using quantitative real-time PCR (qRT-PCR), Western blot analysis, ELISA. The binding BRD2 protein on...

10.3390/cells12111490 article EN cc-by Cells 2023-05-27

Overactivation of immune responses is a hallmark autoimmune disease pathogenesis. This includes the heightened production inflammatory cytokines such as Tumor Necrosis Factor α (TNFα), and secretion autoantibodies isotypes rheumatoid factor (RF) anticitrullinated protein antibody (ACPA). Fcγ receptors (FcγR) expressed on surface myeloid cells bind Immunoglobulin G (IgG) complexes. Recognition autoantigen-antibody complexes by FcγR induces an phenotype that results in tissue damage further...

10.3390/ijms24087623 article EN International Journal of Molecular Sciences 2023-04-21

Abstract Cells in the pancreas that have undergone acinar-ductal metaplasia (ADM) can transform into premalignant cells eventually become cancerous. Although epithelial-mesenchymal transition regulator Snail (Snai1) cooperate with Kras acinar to enhance ADM development, contribution of Snail-related protein Slug (Snai2) development is not known. Thus, transgenic mice expressing and were generated. Surprisingly, attenuated Kras-induced ERK1/2 phosphorylation proliferation. Co-expression also...

10.1038/srep29133 article EN cc-by Scientific Reports 2016-07-01

event.Documents or records provide evidence that the products are manufactured according to pre-developed processes and predefined specifications.Good Documentation Practice (GDP GDocP), a term used in pharmaceutical industry, is essential for integrity of data collection reporting supporting development, registrations, commercialization, life-cycle management products. 1Adhering GDPs assures preventing errors within manufacturing environment during analysis which could otherwise impact...

10.15406/japlr.2017.04.00100 article EN cc-by-nc Journal of Analytical & Pharmaceutical Research 2017-03-08
Coming Soon ...