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1. Full Text Managing leptomeningeal melanoma metastases in the era of immune and targeted therapy
: Leptomeningeal melanoma metastases
by Smalley, Keiran S.M and Fedorenko, Inna V and Kenchappa, Rajappa S and Sahebjam, Solmaz and Forsyth, Peter A
International Journal of Cancer, ISSN 0020-7136, 09/2016, Volume 139, Issue 6, pp. 1195 - 1201
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2. Full Text Abstract IA04: Using comprehensive proteomic approaches to map signaling adaptations to BRAF and BRAF/MEK inhibition
by Fedorenko, Inna V and Paraiso, Kim H.T and Fang, Bin and Koomen, John M and Smalley, Keiran S.M
Clinical Cancer Research, ISSN 1078-0432, 02/2015, Volume 21, Issue 4 Supplement, pp. IA04 - IA04
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3. Full Text The complexity of microenvironment-mediated drug resistance
by Fedorenko, Inna V and Smalley, Keiran S. M
Genes and Cancer, ISSN 1947-6019, 2015, Volume 6, Issue 9-10, pp. 367 - 368
Fibroblasts | Host | Microenvironment | Drug resistance | Melanoma | microenvironment | host | melanoma | fibroblasts | drug resistance
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4. Full Text PTEN loss confers BRAF inhibitor resistance to melanoma cells through the suppression of BIM expression
by Paraiso, Kim H. T and Xiang, Yun and Rebecca, Vito W and Abel, Ethan V and Chen, Y. Ann and Munko, A. Cecilia and Wood, Elizabeth and Fedorenko, Inna V and Sondak, Vernon K and Anderson, Alexander R. A and Ribas, Antoni and Palma, Maurizia Dalla and Nathanson, Katherine L and Koomen, John M and Messina, Jane L and Smalley, Keiran S. M
Cancer Research, ISSN 0008-5472, 04/2011, Volume 71, Issue 7, pp. 2750 - 2760
This study addresses the role of PTEN loss in intrinsic resistance to the BRAF inhibitor PLX4720. Immunohistochemical staining of a tissue array covering all... 
METASTATIC MELANOMA | APOPTOSIS | PROTEIN | ONCOLOGY | PHOSPHORYLATION | CUTANEOUS MELANOMA | RAF KINASE | CANCER | MEDIATES RESISTANCE | LINES | ERK | RNA, Small Interfering - genetics | Up-Regulation | Humans | Drug Resistance, Neoplasm | Phosphatidylinositol 3-Kinases - metabolism | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Proto-Oncogene Proteins - biosynthesis | Bcl-2-Like Protein 11 | Melanoma - genetics | Apoptosis Regulatory Proteins - genetics | Indoles - pharmacology | Proto-Oncogene Proteins c-akt - metabolism | Proto-Oncogene Proteins B-raf - metabolism | Apoptosis Regulatory Proteins - biosynthesis | Melanoma - metabolism | Proto-Oncogene Proteins - antagonists & inhibitors | PTEN Phosphohydrolase - deficiency | Membrane Proteins - genetics | PTEN Phosphohydrolase - biosynthesis | Proto-Oncogene Proteins - genetics | Melanoma - pathology | Sulfonamides - pharmacology | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Membrane Proteins - biosynthesis | Membrane Proteins - antagonists & inhibitors | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Apoptosis Regulatory Proteins - antagonists & inhibitors | Cell Line, Tumor | Protein Kinase Inhibitors - pharmacology | Apoptosis - physiology | Mutation | RNA, Small Interfering - administration & dosage | Index Medicus | PTEN | melanoma | BRAF | PLX4032 | therapy | resistance
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5. Full Text BRAF Inhibition Generates a Host–Tumor Niche that Mediates Therapeutic Escape
by Fedorenko, Inna V and Wargo, Jennifer A and Flaherty, Keith T and Messina, Jane L and Smalley, Keiran S.M
Journal of Investigative Dermatology, ISSN 0022-202X, 12/2015, Volume 135, Issue 12, pp. 3115 - 3124
The current study defines a fibroblast-derived niche that facilitates the therapeutic escape of melanoma cells from BRAF inhibition. Vemurafenib treatment led... 
SURVIVAL | BINDING DOMAINS | CELLS | RESISTANCE CAM-DR | MELANOMA | GROWTH | FIBRONECTIN | RAF INHIBITORS | STROMAL FIBROBLASTS | FOCAL ADHESION KINASE | DERMATOLOGY | Fibronectins - analysis | Humans | Proto-Oncogene Proteins c-akt - physiology | Melanoma - pathology | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Transforming Growth Factor beta - pharmacology | Sulfonamides - therapeutic use | Melanoma - drug therapy | Cell Line, Tumor | Phosphatidylinositol 3-Kinases - physiology | Indoles - therapeutic use | Protein Kinase Inhibitors - pharmacology | Index Medicus | melanoma | fibroblasts | BRAF | resistance
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6. Full Text Inhibition of BRAF and BRAF+MEK drives a metastatic switch in melanoma
by Smalley, Keiran SM and Fedorenko, Inna V
Molecular & Cellular Oncology, ISSN 2372-3556, 10/2015, Volume 2, Issue 4, pp. e1008291 - e1008291
Recent analyses by our group and others showed that the majority of melanoma patients who fail BRAF inhibitor therapy do so at new disease sites. Using... 
melanoma | BRAF | metastasis | ephrin | resistance
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7. Full Text Abstract 5370: PTEN loss confers BRAF inhibitor resistance to melanoma cells through the suppression of BIM expression
by Paraiso, Kim H and Rebecca, Vito and Fedorenko, Inna V and Xiang, Yun and Wood, Elizabeth and Anderson, Alexander R and Sondak, Vernon K and Abel, Ethan V and Koomen, John M and Messina, Jane L and Smalley, Keiran S.M
Cancer Research, ISSN 0008-5472, 04/2011, Volume 71, Issue 8 Supplement, pp. 5370 - 5370
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8. Full Text Abstract A66: Integrative phosphoproteomic analysis of signaling pathways in MMS-mutated melanoma
by Joseph, Beulah D and Fedorenko, Inna V and Paraiso, Kim H.T and Fang, Bin and Koomen, John M and Smalley, Keiran S.M
Cancer Epidemiology Biomarkers & Prevention, ISSN 1055-9965, 10/2010, Volume 19, Issue 10 Supplement, pp. A66 - A66
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9. Full Text Phosphoproteomic analysis of basal and therapy‐induced adaptive signaling networks in BRAF and NRAS mutant melanoma
by Fedorenko, Inna V and Fang, Bin and Munko, Ana Cecelia and Gibney, Geoffrey T and Koomen, John M and Smalley, Keiran S. M
PROTEOMICS, ISSN 1615-9853, 01/2015, Volume 15, Issue 2-3, pp. 327 - 339
Basal and kinase inhibitor driven adaptive signaling has been examined in a panel of melanoma cell lines using phosphoproteomics in conjunction with pathway... 
Signaling | NRAS | BRAF | Biomedicine | Phosphoproteomics | Melanoma | CELLS | QUANTITATIVE PROTEOMICS | BIOCHEMISTRY & MOLECULAR BIOLOGY | INHIBITOR RESISTANCE | BIOCHEMICAL RESEARCH METHODS | ACQUIRED-RESISTANCE | CANCER | METASTATIC MELANOMA | MEK INHIBITION | PKC-DELTA | MUTATIONS | MEDIATES RESISTANCE | Melanoma - metabolism | Membrane Proteins - genetics | Humans | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Melanoma - pathology | Sulfonamides - pharmacology | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Mitogen-Activated Protein Kinase Kinases - metabolism | GTP Phosphohydrolases - metabolism | Signal Transduction - drug effects | GTP Phosphohydrolases - genetics | Melanoma - genetics | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Cell Line, Tumor | Indoles - pharmacology | Membrane Proteins - metabolism | Protein Kinase Inhibitors - pharmacology | Mutation | Phosphorylation - drug effects | Proto-Oncogene Proteins B-raf - metabolism | Proteins | Glucose metabolism | Synthesis | Gene mutations | Glycogen | Analysis | Cellular signal transduction | Biological response modifiers | Phosphotransferases | Phosphorylation | Regulators | Adaptive systems | Protein kinase C | Divergence | Peptides | Phosphotyrosine | Homology | Kinases | Phosphatase | Signal transduction | Epidermal growth factor | Cell cycle | Protein-tyrosine kinase receptors | Protein-tyrosine kinase | Genotypes | Tyrosine | Tensin | Cyclin-dependent kinases | Stat3 protein | Extracellular signal-regulated kinase | Glycogen synthase kinase 3 | MAP kinase | Phospholipase C | Phospholipase | Cell lines | Cytoskeleton | Transduction | Interferon | PTEN protein | Guanosinetriphosphatase | Protein-tyrosine-phosphatase | Index Medicus | phosphoproteomics | melanoma | signaling
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10. Full Text Phosphoproteomic analysis of basal and therapy-induced adaptive signaling networks inBRAFandNRASmutant melanoma
by Fedorenko, Inna V and Fang, Bin and Munko, Ana Cecelia and Gibney, Geoffrey T and Koomen, John M and Smalley, Keiran S. M
PROTEOMICS, ISSN 1615-9853, 01/2015, Volume 15, Issue 2-3, pp. 327 - 339
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11. Full Text Fibronectin induction abrogates the BRAF inhibitor response of BRAF V600E/PTEN-null melanoma cells
by Fedorenko, I.V and Abel, E.V and Koomen, J.M and Fang, B and Wood, E.R and Chen, Y.A and Fisher, K.J and Iyengar, S and Dahlman, K.B and Wargo, J.A and Flaherty, K.T and Sosman, J.A and Sondak, V.K and Messina, J.L and Gibney, G.T and Smalley, K.S.M
Oncogene, ISSN 0950-9232, 03/2016, Volume 35, Issue 10, pp. 1225 - 1235
The mechanisms by which some melanoma cells adapt to Serine/threonine-protein kinase B-Raf (BRAF) inhibitor therapy are incompletely understood. In the present... 
ACTIVATION | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | E-CADHERIN | DRUG-RESISTANCE | BRAF(V600E) | CELL BIOLOGY | ONCOLOGY | ADAPTIVE RESISTANCE | GROWTH | GENETICS & HEREDITY | RAF INHIBITORS | EXTRACELLULAR-MATRIX | B-RAF | Proto-Oncogene Proteins B-raf - deficiency | Cell Survival - drug effects | PTEN Phosphohydrolase - genetics | RNA, Small Interfering - genetics | PTEN Phosphohydrolase - deficiency | Humans | Myeloid Cell Leukemia Sequence 1 Protein - metabolism | Melanoma - pathology | Fibronectins - metabolism | Gene Knockdown Techniques | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Xenograft Model Antitumor Assays | Animals | Signal Transduction - drug effects | Proto-Oncogene Proteins B-raf - genetics | Proteomics | Cell Line, Tumor | Female | Mice | Protein Kinase Inhibitors - pharmacology | Gene Expression Regulation, Neoplastic - drug effects | Integrin alpha5beta1 - metabolism | Gene mutations | Melanoma | Cellular signal transduction | Genetic aspects | Models | Gene expression | Health aspects | Proteins | Mutation | Cellular biology | Kinases | Index Medicus
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12. Full Text Evaluating melanoma drug response and therapeutic escape with quantitative proteomics
by Rebecca, Vito W and Wood, Elizabeth and Fedorenko, Inna V and Paraiso, Kim H. T and Haarberg, H. Eirik and Chen, Yi and Xiang, Yun and Sarnaik, Amod and Gibney, Geoffrey T and Sondak, Vernon K and Koomen, John M and Smalley, Keiran S. M
Molecular and Cellular Proteomics, ISSN 1535-9476, 2014, Volume 13, Issue 7, pp. 1844 - 1854
The evolution of cancer therapy into complex regimens with multiple drugs requires novel approaches for the development and evaluation of companion biomarkers.... 
PHASE-II TRIAL | HSP90 INHIBITOR | NRAS | BIOCHEMICAL RESEARCH METHODS | BRAF INHIBITOR RESISTANCE | TARGETED MEK INHIBITION | ABSOLUTE QUANTIFICATION | PROTEINS | CANCER | REPRODUCIBILITY | TANESPIMYCIN | Azabicyclo Compounds - pharmacology | Neoplasm Transplantation | Humans | Drug Resistance, Neoplasm | NF-kappa B - metabolism | Transplantation, Heterologous | Chromatography, High Pressure Liquid | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Receptor, Platelet-Derived Growth Factor beta - antagonists & inhibitors | Piperidines - pharmacology | RNA Interference | Melanoma - genetics | Mass Spectrometry | Indoles - pharmacology | Phthalic Acids - pharmacology | Receptor, Platelet-Derived Growth Factor beta - metabolism | MAP Kinase Kinase 1 - antagonists & inhibitors | Membrane Proteins - genetics | Mice, SCID | Sulfonamides - pharmacology | beta Catenin - genetics | Animals | MAP Kinase Signaling System - drug effects | Wnt Signaling Pathway - genetics | GTP Phosphohydrolases - genetics | HSP90 Heat-Shock Proteins - antagonists & inhibitors | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Proteomics | Cell Line, Tumor | Benzimidazoles - pharmacology | Biomarkers, Tumor - genetics | Mice | Mice, Inbred BALB C | RNA, Small Interfering | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Index Medicus | Research
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13. Full Text XL888 Limits Vemurafenib-Induced Proliferative Skin Events by Suppressing Paradoxical MAPK Activation
by Phadke, Manali and Gibney, Geoffrey T and Rich, Carolyn J and Fedorenko, Inna V and Chen, Y. Ann and Kudchadkar, Ragini R and Sondak, Vernon K and Weber, Jeffrey and Messina, Jane L and Smalley, Keiran S.M
Journal of Investigative Dermatology, ISSN 0022-202X, 10/2015, Volume 135, Issue 10, pp. 2542 - 2544
HSP90 | MEK INHIBITION | PATHWAY | RAF | INHIBITOR RESISTANCE | BRAF INHIBITORS | MELANOMA-CELLS | MUTATIONS | SQUAMOUS-CELL CARCINOMAS | DERMATOLOGY | Azabicyclo Compounds - pharmacology | Immunohistochemistry | Skin Neoplasms - pathology | Skin Neoplasms - drug therapy | Tissue Culture Techniques | Humans | Melanoma - pathology | Sulfonamides - pharmacology | Mitogen-Activated Protein Kinase Kinases - metabolism | Drug Interactions | Melanoma - genetics | Melanoma - drug therapy | Sensitivity and Specificity | Skin Neoplasms - genetics | Mitogen-Activated Protein Kinase Kinases - drug effects | Indoles - pharmacology | Cell Proliferation - drug effects | Biopsy, Needle | Phthalic Acids - pharmacology | Skin - drug effects | Skin - pathology | Index Medicus | melanoma | SCC | BRAF | keratoacanthoma
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14. Full Text Inhibition of autophagy enhances the effects of the AKT inhibitor MK‐2206 when combined with paclitaxel and carboplatin in BRAF wild‐type melanoma
by Rebecca, Vito W and Massaro, Renato R and Fedorenko, Inna V and Sondak, Vernon K and Anderson, Alexander R. A and Kim, Eunjung and Amaravadi, Ravi K and Maria‐Engler, Silvya S and Messina, Jane L and Gibney, Geoffrey T and Kudchadkar, Ragini R and Smalley, Keiran S. M
Pigment Cell & Melanoma Research, ISSN 1755-1471, 05/2014, Volume 27, Issue 3, pp. 465 - 478
This study investigates the mechanism of action behind the long‐term responses (12–16 months) of two BRAF WT melanoma patients to the AKT inhibitor MK ‐2206 in... 
melanoma | apoptosis | BRAF | AKT | autophagy | chemotherapy | Chemotherapy | Autophagy | Melanoma | Apoptosis | CANCER-CELLS | CONTROLLED-TRIAL | MUTANT MELANOMA | IMPROVED SURVIVAL | OPEN-LABEL | CELL-SURVIVAL | CELL BIOLOGY | DERMATOLOGY | METASTATIC MELANOMA | IN-VITRO | NRAS | ONCOLOGY | MUTATIONS | Clone Cells - drug effects | Reactive Oxygen Species - metabolism | Skin Neoplasms - drug therapy | Heterocyclic Compounds, 3-Ring - pharmacology | Humans | Melanoma - enzymology | Male | Neoplasm Proteins - antagonists & inhibitors | Molecular Targeted Therapy | Autophagy - drug effects | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Skin Neoplasms - enzymology | Female | Neoplasm Proteins - genetics | Paclitaxel - administration & dosage | Spheroids, Cellular | Skin Neoplasms - pathology | Tumor Stem Cell Assay | Carboplatin - administration & dosage | Melanoma - pathology | Drug Synergism | Protein Kinase Inhibitors - administration & dosage | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Proto-Oncogene Proteins B-raf - genetics | Heterocyclic Compounds, 3-Ring - administration & dosage | Melanoma - drug therapy | Aged | Protein Kinase Inhibitors - pharmacology | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Drug Resistance, Neoplasm - drug effects | Antimitotic agents | Antioxidants | Analysis | Antineoplastic agents | Cancer | Index Medicus
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15. Full Text Senescent fibroblasts in melanoma initiation and progression: An integrated theoretical, experimental, and clinical approach
by Kim, Eunjung and Rebecca, Vito and Fedorenko, Inna V and Messina, Jane L and Mathew, Rahel and Maria-Engler, Silvya S and Basanta, David and Smalley, Keiran S. M and Anderson, Alexander R. A
Cancer Research, ISSN 0008-5472, 12/2013, Volume 73, Issue 23, pp. 6874 - 6885
We present an integrated study to understand the key role of senescent fibroblasts in driving melanoma progression. Based on the hybrid cellular automata... 
GROWTH-FACTOR-BETA | ONCOLOGY | MECHANOCHEMICAL MODEL | KINETICS | MOUSE | SYSTEMS | STROMA | MALIGNANT-MELANOMA | MUTATIONS | CANCER | BASEMENT-MEMBRANE | Models, Theoretical | Skin Neoplasms - pathology | Skin - cytology | Fibroblasts - physiology | Humans | Cells, Cultured | Cellular Senescence - physiology | Melanoma - pathology | Tumor Microenvironment - physiology | Disease Progression | Skin Neoplasms - physiopathology | Skin Physiological Phenomena | Homeostasis - physiology | Cell Transformation, Neoplastic - pathology | Melanoma - physiopathology | Index Medicus
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16. Full Text Ligand-Independent EPHA2 signaling drives the adoption of a targeted Therapy-Mediated metastatic melanoma phenotype
by Paraiso, Kim H. T and Das Thakur, Meghna and Fang, Bin and Koomen, John M and Fedorenko, Inna V and John, Jobin K and Tsao, Hensin and Flaherty, Keith T and Sondak, Vernon K and Messina, Jane L and Pasquale, Elena B and Villagra, Alejandro and Rao, Uma N and Kirkwood, John M and Meier, Friedegund and Sloot, Sarah and Gibney, Geoffrey T and Stuart, Darrin and Tawbi, Hussein and Smalley, Keiran S. M
Cancer Discovery, ISSN 2159-8274, 2015, Volume 5, Issue 3, pp. 264 - 273
Many patients with BRAF inhibitor resistance can develop disease at new sites, suggesting that drug-induced selection pressure drives metastasis. Here, we used... 
CELLS | INVASION | MEK INHIBITION | ONCOLOGY | MUTANT MELANOMA | ACQUIRED-RESISTANCE | BRAF | RECEPTORS | UP-REGULATION | PLASTICITY | VEMURAFENIB | Melanoma - metabolism | Humans | Receptor, EphA2 - metabolism | Drug Resistance, Neoplasm | Proteome | Phosphatidylinositol 3-Kinases - metabolism | Melanoma - pathology | Molecular Targeted Therapy | Phosphoproteins - metabolism | Protein Interaction Mapping | Protein Interaction Maps | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Neoplasm Metastasis | Phenotype | Signal Transduction - drug effects | Melanoma - drug therapy | Protein Binding | Ligands | Protein Kinase Inhibitors - pharmacology | Proteomics - methods | Proto-Oncogene Proteins c-akt - metabolism | Proto-Oncogene Proteins B-raf - metabolism | Index Medicus
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17. Full Text Long-term effects of BRAF inhibitors in melanoma treatment: friend or foe?
by Sloot, Sarah and Fedorenko, Inna V and Smalley, Keiran SM and Gibney, Geoffrey T
Expert Opinion on Pharmacotherapy, ISSN 1465-6566, 04/2014, Volume 15, Issue 5, pp. 589 - 592
The clinical development of selective BRAF inhibitors for metastatic BRAF V600 mutant melanoma patients has been a major breakthrough in targeted therapeutics.... 
vemurafenib | melanoma | BRAF | paradoxical oncogenesis | MAPK | dabrafenib | Dabrafenib | Paradoxical oncogenesis | Vemurafenib | Melanoma | MEK INHIBITION | IMPROVED SURVIVAL | PHARMACOLOGY & PHARMACY | MUTATIONS | Skin Neoplasms - pathology | Skin Neoplasms - drug therapy | Humans | Melanoma - enzymology | Oximes - therapeutic use | Antineoplastic Agents - therapeutic use | Melanoma - pathology | MAP Kinase Signaling System | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Neoplasm Metastasis | Skin Neoplasms - enzymology | Sulfonamides - therapeutic use | Protein Kinase Inhibitors - therapeutic use | Melanoma - drug therapy | Indoles - therapeutic use | Imidazoles - therapeutic use | Index Medicus
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18. Full Text Paradoxical oncogenesis and the long term consequences of BRAF inhibition in melanoma
by Gibney, Geoffrey T and Messina, Jane L and Fedorenko, Inna V and Sondak, Vernon K and Smalley, Keiran S.M
Nature reviews. Clinical oncology, ISSN 1759-4774, 7/2013, Volume 10, Issue 7, pp. 390 - 399
The clinical benefits of BRAF inhibition in patients with advanced-stage BRAF -mutant melanoma are now well established. Although the emergence of cutaneous... 
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19. Full Text Amuvatinib has cytotoxic effects against NRAS- but not BRAF-mutant melanoma
by Fedorenko, Inna V and Fang, Bin and Koomen, John M and Gibney, Geoffrey T and Smalley, Keiran S.M
Melanoma research, ISSN 0960-8931, 10/2014, Volume 24, Issue 5, pp. 448 - 453
Effective targeted therapy strategies are still lacking for the 15–20% of melanoma patients whose melanomas are driven by oncogenic NRAS . We here report on... 
MP470 | RTK | melanoma | NRAS | BRAF | amuvatinib
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20. Full Text Abstract 5222: A novel mechanism of microenvironment-mediated drug resistance in BRAF V600E melanoma with loss of PTEN
by Fedorenko, Inna V and Paraiso, Kim H.T and Rebecca, Vito W and Wood, Elizabeth and Koomen, John and Messina, Jane and Smalley, Keiran
Cancer Research, ISSN 0008-5472, 04/2012, Volume 72, Issue 8 Supplement, pp. 5222 - 5222
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