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Afatinib and Selumetinib in Advanced KRAS Mutant and PIK3CA Wildtype Non-small Cell Lung Cancer

ABSTRACT: This is a multi-center open-label proof-of-concept study consisting of two parts: PART A - a phase I dose-finding study (3 + 3 classical design) evaluating the RP2D of afatinib in combination with selumetinib in KRASm NSCLC; and PART B - a randomized phase II study investigating the progression free survival and safety of selumetinib/afatinib combination therapy compared to standard of care chemotherapy in KRASm NSCLC.

DISEASE(S): Gastrointestinal Neoplasms,Colorectal Neoplasms,Carcinoma, Non-small-cell Lung,Pancreatic Neoplasms,Neoplasms,Digestive System Neoplasms

PROVIDER: 2190517 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Afatinib and selumetinib in advanced KRAS mutant positive and PIK3CA wildtype non-small cell lung cancer and colorectal cancer

Project description:Primary objectives: Part A: To determine the recommended phase 2 dose and schedule (RP2D) of the selumetinib/afatinib combination in patients with KRASm and PIK3CAwt NSCLC and CRC Part B: To determine the progression free survival (PFS) of the selumetinib/afatinib combination compared to standard of care therapy in patients with KRASm and PIK3CAwt , NSCLC and CRC Primary endpoints: Part A: Incidence of dose-limiting toxicities (DLTs) Part B: Progression free survival (PFS) per RECIST version 1.1

| 2533271 | ecrin-mdr-crc

Selumetinib

Project description:Selumetinib

| PRJNA712989 | ENA

Expression data from tumor lungs after continuous vs. pulsatile selumetinib treatment in KRASG12C GEMM

Project description:KRAS is one of the driver oncogenes in non-small cell lung cancer (NSCLC), but remains refractory to current modalities of targeted pathway inhibition, which include inhibiting downstream kinase MEK to circumvent KRAS activation. Here, we show that pulsatile, rather than continuous, treatment with MEK inhibitors (MEKis) maintains T cell activation and better control tumor growth and survival. We used microarrays to examine the MAPK signaling pathway suppression from tumor lungs of KRASG12C GEMM after continuous vs. pulsatile treatment of selumetinib.

2019-09-11 | GSE126202 | GEO

Selumetinib in adults with NF1 and inoperable plexiform neurofibroma

Project description:The MEK inhibitor selumetinib induces objective responses and provides clinical benefit in children with neurofibromatosis type 1 (NF1) and inoperable plexiform neurofibromas (PNs). To evaluate whether similar outcomes were possible in adult patients, in whom PN growth is generally slower than in pediatric patients, an open-label phase 2 study of selumetinib in adults with NF1 PNs was conducted. Correlative analysis included extraction of RNA followed by sequencing. Samples include paired specimens collected before and on treatment.

2024-10-07 | GSE277520 | GEO

Copy number analysis of selumetinib-resistant CRC cells lines

Project description:Copy number analysis to compare parental colorectal cancer cell lines and their selumetinib-resistant derivatives and identify gene copy changes that might contribute to resistance

2019-03-11 | GSE126367 | GEO

RNA sequencing analysis of selumetinib-resistant CRC cells lines

Project description:RNA sequencing analysis to compare parental colorectal cancer cell lines and their selumetinib-resistant derivatives and identify expression changes and/or mutations that might contribute to resistance

2019-03-11 | GSE126109 | GEO

Changes in mRNA Expression by schedule-dependent combination of 5-FU and selumetinib

Project description:Anti-tumor effect of the combination between 5-FU and selumetinib was treatment schedule-dependent in BRAF or KRAS mutant CRC cells. Treatment of 5-FU for 2 days followed by selumetinib for another 2 days exhibited synergism for cell viability, whereas single or reversely combined treatment showed antagonism Microarray analysis revealed the distinct groups of genes underlying the efficacy for schedule-dependent treatment.

2020-12-30 | GSE89531 | GEO

Gene expression profiling during treatment of COLO205 cells with selumetinib

Project description:Here, we investigate gene expression response of the BRAFV600E mutant cell line COLO205 to the MEK inhibitor selumetinib / AZD6244 / ARRY-142886. Although selumetinib causes long term G1 arrest, we observe cells stochastically entering the cell cycle without re-activation of ERK and initiation of a normal proliferative gene expression programme. Genes encoding DNA replication and repair factors are downregulated during G1 arrest, but many of these are transiently induced when cells escaping arrest enter S and G2. Nonetheless, mRNAs encoding key DNA replication factors including the MCM replicative helicase complex, PCNA and TIPIN remain at very low abundance.

2021-03-23 | GSE168602 | GEO

Gene expression profiling during treatment of HT29 cells with selumetinib

2021-09-12 | GSE183859 | GEO

Gene expression profiling of MDA231, BT549, and SUM159PT cells after selumetinib treatment or DUSP4 siRNA knockdown

Project description:MDA231, BT549, and SUM159PT basal-like breast cancer cell lines were transfected with non-targeting siRNA (siCONTROL), siRNA targeting DUSP4 (siDUSP4), or siCONTROL + 4 or 24 hr of 1uM selumetinib. Cells were harvested at 96 hr post-siRNA transfection. Data were Log2 RMA normalized. We sought to identify changes in gene expression after MEK inhibition, or after loss of DUSP4 function in breast cancer cell lines.

2013-09-03 | E-GEOD-41816 | biostudies-arrayexpress

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