Krishnendu Roy

ORCID: 0000-0003-0541-0714
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About
Contact & Profiles
Research Areas
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Immune cells in cancer
  • Nitric Oxide and Endothelin Effects
  • Immune Response and Inflammation
  • Cell Adhesion Molecules Research
  • Inflammatory mediators and NSAID effects
  • interferon and immune responses
  • Nanoplatforms for cancer theranostics
  • Inflammasome and immune disorders
  • Cancer Research and Treatments
  • Advanced Nanomaterials in Catalysis
  • Viral Infectious Diseases and Gene Expression in Insects
  • Neuroinflammation and Neurodegeneration Mechanisms
  • PI3K/AKT/mTOR signaling in cancer
  • Research on Leishmaniasis Studies
  • IL-33, ST2, and ILC Pathways
  • Advanced biosensing and bioanalysis techniques
  • Trypanosoma species research and implications
  • Blood disorders and treatments
  • Cancer, Hypoxia, and Metabolism
  • Atherosclerosis and Cardiovascular Diseases
  • Biochemical and Molecular Research
  • Advancements in Semiconductor Devices and Circuit Design
  • Lung Cancer Treatments and Mutations
  • Cancer-related Molecular Pathways

National Cancer Institute
2014-2024

National Institutes of Health
2006-2021

COPD Foundation
2011-2017

Burdwan Medical College & Hospital
2012

ORCID
2010

Center for Cancer Research
2009

Indian Institute of Chemical Biology
1990

AbstractThe family of NADPH oxidase (NOX) genes produces reactive oxygen species (ROS) pivotal for both cell signalling and host defense. To investigate whether NOX accessory gene expression might be a factor common to specific human tumour types, this study measured the levels 1–5, dual 1 2, as well those NoxO1, NoxA1, p47phox, p67phox p22phox in cancer lines adjacent normal tissue pairs by quantitative, real-time RT-PCR. The results demonstrate tumour-specific patterns that will inform...

10.1080/10715760902918683 article EN Free Radical Research 2009-01-01

Dual oxidase 2 is a member of the NADPH (Nox) gene family that plays critical role in biosynthesis thyroid hormone as well inflammatory response upper airway mucosa and wound healing, presumably through its ability to generate reactive oxygen species, including H2O2. The recently discovered overexpression Duox2 gastrointestinal malignancies, our limited understanding regulation expression, led us examine effect cytokines growth factors on human tumor cells. We found exposure pancreatic...

10.1074/jbc.m110.191031 article EN cc-by Journal of Biological Chemistry 2011-02-15

Pancreatitis is associated with release of proinflammatory cytokines and reactive oxygen species plays an important role in the development pancreatic cancer. We recently demonstrated that dual oxidase (Duox)2, NADPH essential for species-related, gastrointestinal host defense, regulated by IFN-γ-mediated Stat1 binding to Duox2 promoter tumor lines. Because LPS enhances invasiveness cancer vivo following TLR4-related activation NF-κB, we examined whether LPS, alone or combined IFN-γ, Duox2....

10.4049/jimmunol.1201725 article EN The Journal of Immunology 2013-01-08

NADPH oxidase 4 (NOX4) is a redox active, membrane-associated protein that contributes to genomic instability, signaling, and radiation sensitivity in human cancers based on its capacity generate H

10.1016/j.redox.2017.05.016 article EN cc-by Redox Biology 2017-05-29

Human colon cancers express higher levels of NADPH oxidase 1 [NOX1] than adjacent normal epithelium. It has been suggested that reactive oxygen species [ROS] derived from NOX1 contribute to DNA damage and neoplastic transformation in the colon, particularly during chronic inflammatory stress. However, mechanism(s) underlying increased expression malignant tumors or states involving intestine are poorly characterized. We examined effects two pro-inflammatory cytokines, IL-4 IL-13, on...

10.18632/oncotarget.17494 article EN Oncotarget 2017-04-27

Dual oxidase 2 (Duox2), one of the seven members NADPH gene family, plays a critical role in generating H2O2 for thyroid hormone biosynthesis and as an integral part host defense system respiratory epithelium gastrointestinal tract. Recent evidence suggests that regulation Duox2 expression is under control pro-inflammatory cytokines Duox2-induced reactive oxygen species (ROS) contribute to inflammation-related tissue injury occurs two pre-malignant, inflammatory conditions: chronic...

10.3892/ijo.2013.1821 article EN International Journal of Oncology 2013-02-11

// Yongzhong Wu 1 , Jennifer L. Meitzler Smitha Antony Agnes Juhasz Jiamo Lu Guojian Jiang Han Liu 2 Melinda Hollingshead Diana C. Haines 3 Donna Butcher Michaela S. Panter Krishnendu Roy James H. Doroshow 1, Center for Cancer Research, National Institute, Bethesda, MD, USA Division of Treatment and Diagnosis, Pathology/Histotechnology Laboratory, Leidos, Inc./Frederick Laboratory Frederick, Correspondence to: Doroshow, email: doroshoj@mail.nih.gov Keywords: dual oxidase, NADPH pancreatic...

10.18632/oncotarget.12032 article EN Oncotarget 2016-09-15

NADPH oxidase 5 (NOX5) generated reactive oxygen species (ROS) have been implicated in signaling cascades that regulate cancer cell proliferation. To evaluate and validate NOX5 expression human tumors, we screened a broad range of tissue microarrays (TMAs), report substantial overexpression malignant melanoma cancers the prostate, breast, ovary. In UACC‐257 cells possesses high levels functional endogenous NOX5, resulted enhanced growth, increased numbers BrdU positive cells, γ‐H2AX levels....

10.1002/mc.22708 article EN cc-by-nc Molecular Carcinogenesis 2017-08-01

Dual oxidase 2 (DUOX2) generates H2O2 that plays a critical role in both host defense and chronic inflammation. Previously, we demonstrated the proinflammatory mediators IFN-γ LPS enhance expression of DUOX2 its maturation factor DUOXA2 through STAT1- NF-κB‒mediated signaling human pancreatic cancer cells. Using panel colon cell lines, now report induction DUOX2/DUOXA2 mRNA protein by TH2 cytokine IL-4. IL-4 activated STAT6 that, when silenced, significantly decreased DUOX2. Furthermore,...

10.4049/jimmunol.1800469 article EN The Journal of Immunology 2019-09-23

The NADPH oxidases (NOXs) play a recognized role in the development and progression of inflammation-associated disorders, as well cancer. To date, several NOX inhibitors have been developed, through either high throughput screening or targeted disruption interaction partners, although only few reached clinical trials. improve efficacy bioavailability iodonium class inhibitor diphenylene (DPI), we synthesized 36 analogs DPI, focusing on improved solubility functionalization. inhibitory...

10.1016/j.bcp.2017.07.007 article EN cc-by Biochemical Pharmacology 2017-07-11

To facilitate functional investigation of the role NADPH oxidase 1 (NOX1) and associated reactive oxygen species in cancer cell signaling, we report herein development characterization a novel mouse monoclonal antibody that specifically recognizes C-terminal region NOX1 protein. The was validated stable overexpression knockout systems, demonstrates wide applicability for Western blot analysis, confocal microscopy, flow cytometry, immunohistochemistry. We employed our to characterize...

10.1371/journal.pone.0233208 article EN public-domain PLoS ONE 2020-05-19

10.1016/0006-291x(90)92109-d article EN Biochemical and Biophysical Research Communications 1990-07-01

Abstract Chronic pancreatitis increases the risk of developing pancreatic ductal adenocarcinoma (PDAC) and is associated with enhanced expression NADPH oxidase (NOX) isoform dual 2 (DUOX2). Interleukin-1 (IL-1) a major upstream pro-inflammatory cytokine secreted by malignant or microenvironmental cells that supports inflammation, tumorigenesis, invasiveness, tumor heterogeneity. Previously, our laboratory demonstrated DUOX2, one seven family members, significantly wide variety cytokines,...

10.1158/1538-7445.am2024-5327 article EN Cancer Research 2024-03-22

Abstract Chronic pancreatic inflammation is strongly associated with cancer. We previously demonstrated that inflammatory cytokines interact to produce a Duox2 (one of 7 members the NADPH Oxidase family)-dependent, reactive oxygen species (ROS)-related, pro-oxidant milieu could increase pathologic potential inflammation, enhancing malignant transformation. Furthermore, we have shown expression upregulated in patients chronic pancreatitis as well ductal adenocarcinoma (PDAC). Dexamethasone...

10.1158/1538-7445.am2016-1456 article EN Cancer Research 2016-07-15

Abstract NADPH oxidase (Nox)-dependent reactive oxygen species (ROS) play a critical role in cell signaling, proliferation, and mitogenesis. We have previously shown that silencing NOX1 gene expression with siRNA decreases growth angiogenesis human HT-29 colon cancer xenografts. To investigate the mechanism of inhibition, we studied cycle signaling pathways. found using RT-PCR Western analysis INK4 inhibitors (p15, p18, p19), as well CDK6, phospho-Cyclin E, Cyclin D1 were all decreased when...

10.1158/1538-7445.am2012-3066 article EN Cancer Research 2012-04-01

Recent studies suggest that of the molecules postulated to function as inhibitors NADPH oxidase family enzymes iodonium analogs known broadly interfere with flavin dehydrogenase demonstrate mechanistic validity poisons. In recent work, we have produced a series novel compounds putative these oxidases. To evaluate potential utility two favorable chemical properties, NSC 740104 and 751140, compared effects standard this class, diphenyleneiodonium di-2-thienyliodonium, respect...

10.3390/antiox10111757 article EN cc-by Antioxidants 2021-11-03

Abstract Normal ovarian surface epithelium (OSE) has been widely studied as the origin of cancer. Repetitive ovulation implicated in cancer initiation based on damage and inflammation incurred to OSE upon continuous cycles tear repair. Transforming growth factor-beta (TGF-β) plays a role this normal ovulatory cycle, having shown inhibit human proliferation induce apoptosis, which may prevent over-proliferation cells. NADPH oxidase 4 (NOX4), membrane-associated hydrogen peroxide-producing...

10.1158/1538-7445.am2020-3571 article EN Cancer Research 2020-08-15
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