A5076152468- Melanoma and MAPK Pathways
- Synthesis and biological activity
- Cancer Cells and Metastasis
- Cancer-related Molecular Pathways
- Click Chemistry and Applications
- Chemical Synthesis and Analysis
- Cancer Mechanisms and Therapy
- PI3K/AKT/mTOR signaling in cancer
- Advanced Breast Cancer Therapies
- Photochromic and Fluorescence Chemistry
- Multicomponent Synthesis of Heterocycles
- Glycosylation and Glycoproteins Research
- Cancer Research and Treatments
- Asymmetric Hydrogenation and Catalysis
- Advanced Proteomics Techniques and Applications
- Monoclonal and Polyclonal Antibodies Research
- Microwave-Assisted Synthesis and Applications
- Metastasis and carcinoma case studies
- Peptidase Inhibition and Analysis
- FOXO transcription factor regulation
- HER2/EGFR in Cancer Research
- Photoreceptor and optogenetics research
- Nanoplatforms for cancer theranostics
- Morinda citrifolia extract uses
- Protein Tyrosine Phosphatases
Duquesne University
2013-2021
KU Leuven
2018-2020
Mylan (United States)
2014
Jawaharlal Nehru Centre for Advanced Scientific Research
2011
Bristol-Myers Squibb (United States)
1992
Abstract Isonitriles are delicately poised chemical entities capable of being coaxed to react as nucleophiles or electrophiles. Directing this tunable reactivity with metal and non‐metal catalysts provides rapid access a large array complex nitrogenous structures ideally functionalized for medicinal applications. Isonitrile insertion into transition complexes has featured in numerous synthetic mechanistic studies, leading deployment isonitriles catalytic processes, including multicomponent...
Triple-negative breast cancers (TNBCs) represent 15% to 20% of all and are often associated with poor prognosis. The lack targeted therapies for TNBCs contributes higher mortality rates. Aberrations in the phosphoinositide-3-kinase (PI3K) mitogen-activated protein kinase pathways have been linked increased cancer proliferation survival. It has proposed that these survival characteristics enhanced through compensatory signaling crosstalk mechanisms. While between PI3K extracellular...
Epithelial to mesenchymal transition (EMT) is a cellular program that converts non-motile epithelial cells into invasive cells. EMT implicated in cancer metastasis, chemo-resistance, progression, and generation of stem (CSCs). Inducing (MET), the reverse phenomenon EMT, proposed as novel strategy target triple negative tamoxifen-resistant breast cancer. Triple (TNBC) characterized by loss hormone receptors, highly phenotype, lack targeted therapy. Estrogen receptor-positive can be tamoxifen,...
Sirtuin (Sir2) proteins being key regulators of numerous cellular processes have been, over the recent past, subject intense study. Sirs been implicated in diverse physiological ranging from aging and cancer to neurological dysfunctions. Studies on Sir2s using tools genetics, molecular biology, biochemistry structural biology provided significant insight into functions this class deacetylases. This apart, medicinal chemistry approaches enabled discovery modulators (both activators...
The epithelial to mesenchymal transition (EMT) is characterized by a loss of cell polarity, decrease in the marker E-cadherin, and an increase markers including zinc-finger E-box binding homeobox (ZEB1). EMT also associated with migration anchorage-independent growth. Induction reversal EMT, (MET), emerging strategy being explored attenuate metastatic potential aggressive cancer types, such as triple-negative breast cancers (TNBCs) tamoxifen-resistant (TAMR) ER-positive cancers, which have...
Chemical probes that covalently interact with proteases have found increasing use for the study of protease function and localization. The design synthesis such is still a bottleneck, as strategies to target different families are highly diverse. We set out synthesize chemical based on substrate specificity inclusion an uncleavable peptide bond mimic photocrosslinker covalent modification target. With caspase-3 model protease, we designed reduced amide triazolo peptides mimetics, whose...
Abstract The mitogen-activated protein kinase (MAPK) pathway has well-established roles in cellular processes including proliferation, differentiation, and regulation of cell fate, namely survival apoptosis. In breast cancer, constitutive activation the MAPK/extracellular signal-regulated kinases (ERK) pathways have been linked to chemoresistance metastatic progression through distinct mechanisms epithelial-to-mesenchymal transition (EMT). Our previous studies shown that overexpression MEK5...
Abstract Mitogen Activated Protein Kinase (MAPK) pathways initiate with external signaling, proceed through a sequence of protein kinases, and alter cell proliferation, growth, survival. MAPK well-ordered but are interconnected modified by the cell's internal needs. The MEK-catalyzed phosphorylation its target ERK represents most selective interaction signaling cascades. type III MEK1/2 inhibitor, Mekinist, was recently approved FDA for treatment unresectable or metastatic melanoma BRAF...
Abstract Triple-negative breast cancer (TNBC) presents a clinical challenge due to the aggressive nature of disease and lack targeted therapies. Constitutive activation MAPK/extracellular signal-regulated kinases (MEK) pathways has been linked chemoresistance metastatic progression through distinct mechanisms, including epithelial-to-mesenchymal transition (EMT). Here we proposed investigate dual inhibition MEK1/2 MEK5 as more efficacious method for intervention target mesenchymal highly...
Abstract Review: [180 refs.
Abstract The purpose of the current study is to examine how structural variation on methyl anthranilates can differentially affect specific branches MAPK signaling cascade. goal correlate role MEK1/2 versus MEK5 in breast cancer proliferation and migration modeled by profile pERK isoforms treated BT-474 (ER+/PR+/HER2high) MDA-MB-231 (ER−/PR−/HER2low) human cell lines. pathway a complex interconnected cascade activated extracellular stimuli, including growth factors, cytokines, mechanical...
Abstract Triple negative breast cancers (TNBCs) represent 15-20% of all and are often associated with a poor prognosis. The lack targeted therapies for TNBCs contributes to higher mortality rates. Therefore, there is need identify survival pathways that may be in TNBCs. Aberrations the Phosphoinositide-3-kinase (PI3K) Mitogen Activated Protein Kinase (MAPK) have been linked increased cancer proliferation survival. It has proposed these characteristics enhanced through compensatory signaling...
Epithelial to mesenchymal transition is an important cellular adaptation that helps cancer cells acquire a spindle-like phenotype from cuboidal phenotype, degrade the extracellular matrix, invade neighboring tissues, and metastasize other organs form secondary tumor. Cellular plasticity governed by growth factors act in paracrine manner activate downstream oncogenes regulate activity of epigenetic factors, which facilitate phenotypic switch epithelial mesenchymal, ultimately leading...
Abstract Triple negative breast cancer is characterized by the loss of hormone receptors and lack targeted therapy. Most invasive cancers, including triple (TNBC) have a mesenchymal phenotype, which associated with increased chemoresistance. Activation MEK1/2 MEK5 pathways plays crucial role in activation epithelial to transition program increases survival, proliferation, migration cells. Disruption actin skeleton via ras src mediated extracellular regulated kinase 1/2 (ERK1/2) ERK5...
Abstract Epithelial to mesenchymal transition is an important cellular adaptation that helps cancer cells acquire a spindle-like phenotype from cuboidal phenotype, degrade the extracellular matrix, invade neighboring tissues, and metastasize other organs form secondary tumor. Cellular plasticity governed by growth factors act in paracrine manner activate downstream oncogenes regulate activity of epigenetic factors, which facilitate phenotypic switch epithelial mesenchymal, ultimately leading...
Abstract Extracellular signal-regulated kinase (ERK) 5, a member of mitogen activated protein (MAPK) family, is an emerging target in cancer therapeutics. Activation ERK5 via overexpression induces EMT and hormone-independent growth breast cancer. leads to the loss cell polarity, downregulation E-cadherin, upregulation mesenchymal markers snail, zinc-finger E-box binding homeobox (ZEB1), vimentin. also associated with drug resistance. Although ERK1/2 activation known mediate EMT, effect...