A5031703799- Melanoma and MAPK Pathways
- Synthesis and biological activity
- Cancer Mechanisms and Therapy
- Protein Degradation and Inhibitors
- Skin Protection and Aging
- Synthesis of Tetrazole Derivatives
- Computational Drug Discovery Methods
- Ocular Oncology and Treatments
- Dermatologic Treatments and Research
- Cancer-related Molecular Pathways
- melanin and skin pigmentation
- Nanoplatforms for cancer theranostics
- Photodynamic Therapy Research Studies
- Ubiquitin and proteasome pathways
- Antioxidant Activity and Oxidative Stress
- Cancer Genomics and Diagnostics
- Protein Interaction Studies and Fluorescence Analysis
- RNA Research and Splicing
- Wnt/β-catenin signaling in development and cancer
- HER2/EGFR in Cancer Research
- Cancer Immunotherapy and Biomarkers
- Glutathione Transferases and Polymorphisms
- Hair Growth and Disorders
- RNA Interference and Gene Delivery
- Dermatological and Skeletal Disorders
Harvard University
2006-2024
Massachusetts General Hospital
2005-2024
Lund University
2013
Abstract During surface‐enhanced Raman scattering (SERS), molecules exhibit a significant increase in their signals when attached, or very close vicinity, to gold silver nanostructures. This effect is exploited as the basis of new class optical labels. Here we demonstrate robust and sensitive SERS labels probes for imaging live cells. These hybrid consist nanoparticles with Rose Bengal Crystal Violet attached reporter molecules. are stable nontoxic, do not suffer from photobleaching, can be...
For patients with advanced melanoma, primary and secondary resistance to selective BRAF inhibition remains one of the most critically compelling challenges. One rationale argues that novel biologically informed strategies are needed maximally cripple melanoma cells up front before compensatory mechanisms emerge. As p53 is uncommonly mutated in restoration its function represents an attractive adjunct inhibition.Thirty-seven BRAF(V600E)-mutated lines were subjected synergy studies vitro using...
Uveal malignant melanoma (UMM), the most common primary adult intraocular tumor with a marked metastatic potential, is genetically unique and has unfortunately had few treatment breakthroughs. In this study, we subjected UMM cell line to high‑throughput library screening 1,018 FDA‑approved compounds identify potential UMM‑selective cytotoxic agents. Amlodipine, dihydropyridine calcium channel blocker (CCB), ranked no. 2 8 of compounds. Thus, further characterized differential effects...
The underlying forces that shape mutational patterns within any type of cancer have been poorly characterized. One the best preserved exclusionary relationships is between BRAF(V600E) and NRAS(Q61) in melanomas. To explore possible mechanisms which could explain this phenomenon, we overexpressed a set melanoma lines vice versa. Controlled expression second activating oncogene led to growth arrest ("synthetic suppression") subset cells, was accompanied by cell cycle senescence several along...
Keloids are characterized by excessive extracellular collagen and exaggerated scarring. Large-volume lesions can be functionally debilitating, therapeutically intractable, psychologically devastating. A key barrier to translational momentum for novel anti-keloid agents is the lack of a faithful high-content screen (HCS). We devised phenotype-based assay that measures secreted keloidal fibroblasts (KF) in tissue hypoxic conditions (1% oxygen). Four KFs one normal dermal fibroblast line were...
Abstract Mutual exclusiveness of oncogenes is a general phenomenon in cancer. Specifically melanoma BRAF and NRAS mutations do not co-exist except few (0.7%) cases. Here, we are looking for critical exclusive common target(s) meant synthetic lethality therapy. To specifically evaluate mutation dependent gene regulation melanoma, mRNA microarray expression analysis was performed cell lines where growth suppressive non-suppressive properties depend on mutual targets BRAFV600E NRASQ61R/K...
Abstract In the US alone, 44,250 men and 32,000 women are expected to be diagnosed with melanoma in 2012. Metastatic is leading cause of skin cancer-related deaths worldwide. metastatic cutaneous (CM), anti-BRAF anti-MEK agents have recently been shown attenuate progression disease, though durable responses still rare (NEJM articles). For ocular (OM), there currently no established treatment strategy. Thus, one major unmet need field identification novel “driver” physiologies which underpin...
<p>PDF file, 74K, Mean survival fraction upon exposure to 10uM vemurafenib among p53 mutated and p53WT cell lines.</p>
<p>PDF file, 86K, Overexpression of survivin leads to a decrease in percentage FITC-annexin V positive cells.</p>
<p>PDF file, 75K, Survival curves for A375 and A375(PLX-R) which have been induced into resistance.</p>
<p>PDF file, 88K, Nutlin-3 induces p53 and Hdm2 but not Mdm4 even though the basal levels of is higher than Hdm2.</p>
<p>PDF file, 136K, Synergistic cytotoxicity between vemurafenib and Nt3. Green cells are live while dead red in this assay.</p>
<p>PDF file, 57K, Suppression of survivin levels by Nt3 (6 uM) in 4 melanoma lines.</p>
<div>Abstract<p><b>Purpose:</b> For patients with advanced melanoma, primary and secondary resistance to selective BRAF inhibition remains one of the most critically compelling challenges. One rationale argues that novel biologically informed strategies are needed maximally cripple melanoma cells up front before compensatory mechanisms emerge. As p53 is uncommonly mutated in restoration its function represents an attractive adjunct...