Complexation of Gold Nanoparticles with Radiolytically Generated Thiocyanate Radicals ((SCN)₂^•-)

Pulse radiolytically generated (SCN)2•- radicals bind strongly to the gold nanoparticle surface, with an apparent equilibrium constant of 4.7 × 103 M-1. The resultant complex has a strong absorption band at 390 nm which quickly undergoes chemical changes to yield an oxidation product, [Au(SCN)2]-, with an absorption maximum at 320 nm. The spectral changes associated with the chemical interaction between SiO2/Al2O3-stabilized gold nanoparticles and (SCN)2•- are elucidated using time-resolved transient absorption spectroscopy

MOESM7 of Markers of MEK inhibitor resistance in low-grade serous ovarian cancer: EGFR is a potential therapeutic target

Additional file 7: Table S5. Compusyn data from selumetinib/trametinib and erlotinib drug combinations in MEKi-re LGSC cell lines

MOESM2 of Markers of MEK inhibitor resistance in low-grade serous ovarian cancer: EGFR is a potential therapeutic target

Additional file 2: Figure S1. Preclinical MEKi evaluation in novel LGSC cell lines

MOESM4 of Markers of MEK inhibitor resistance in low-grade serous ovarian cancer: EGFR is a potential therapeutic target

Additional file 4: Table S3. List of proteins differentially expressed between MEKi-se and MEKi-re LGSC cell lines (results from the RPPA and SPSS analysis)

MOESM5 of Markers of MEK inhibitor resistance in low-grade serous ovarian cancer: EGFR is a potential therapeutic target

Additional file 5: Table S4. EGFR information on LGSC cell lines

MOESM8 of Markers of MEK inhibitor resistance in low-grade serous ovarian cancer: EGFR is a potential therapeutic target

Additional file 8: Figure S3. Effects of trametinib and erlotinib combination on LGSC cell lines by WB analysis

Markers of MEK inhibitor resistance in low-grade serous ovarian cancer: EGFR is a potential therapeutic target.

Background: Although low-grade serous ovarian cancer (LGSC) is rare, case-fatality rates are high as most patients present with advanced disease and current cytotoxic therapies are not overly effective. Recognizing that these cancers may be driven by MAPK pathway activation, MEK inhibitors (MEKi) are being tested in clinical trials. LGSC respond to MEKi only in a subgroup of patients, so predictive biomarkers and better therapies will be needed. Methods: We evaluated a number of patient-derived LGSC cell lines, previously classified according to their MEKi sensitivity. Two cell lines were genomically compared against their matching tumors samples. MEKi-sensitive and MEKi-resistant lines were compared using whole exome sequencing and reverse phase protein array. Two treatment combinations targeting MEKi resistance markers were also evaluated using cell proliferation, cell viability, cell signaling, and drug synergism assays. Results: Low-grade serous ovarian cancer cell lines recapitulated the genomic aberrations from their matching tumor samples. We identified three potential predictive biomarkers that distinguish MEKi sensitive and resistant lines: Conclusions: KRAS mutations and the protein expression of EGFR and PKC-alpha should be evaluated as predictive biomarkers in patients with LGSC treated with MEKi. Combination therapy using a MEKi with EGFR inhibition may represent a promising new therapy for patients with MEKi-resistant LGSC. </h3

Supplementary Data from Multiomics Characterization of Low-Grade Serous Ovarian Carcinoma Identifies Potential Biomarkers of MEK Inhibitor Sensitivity and Therapeutic Vulnerability

Supplementary Data from Multiomics Characterization of Low-Grade Serous Ovarian Carcinoma Identifies Potential Biomarkers of MEK Inhibitor Sensitivity and Therapeutic Vulnerabilit

Supplementary Data from Multiomics Characterization of Low-Grade Serous Ovarian Carcinoma Identifies Potential Biomarkers of MEK Inhibitor Sensitivity and Therapeutic Vulnerability

Supplementary Data from Multiomics Characterization of Low-Grade Serous Ovarian Carcinoma Identifies Potential Biomarkers of MEK Inhibitor Sensitivity and Therapeutic Vulnerabilit