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Effects of ALK inhibitory treatment with alectinib in glioblastoma cells

ABSTRACT: Effects of ALK inhibitory treatment with alectinib in glioblastoma cells

PROVIDER: PRJNA588428 | ENA |

REPOSITORIES: ENA

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Effects of ALK inhibitory treatment with alectinib in glioblastoma cells

Project description:Anaplastic lymphoma kinase (ALK) is expressed in around 60% of glioblastomas and conveys tumorigenic function. Therefore, ALK inhibitory strategies with alectinib were investigated in glioblastoma cells. We demonstrated that alectinib inhibited proliferation and clonogenicity of ALK expressing glioblastoma initiating cells, whereas cells without ALK expression or after ALK depletion via knockdown showed primary resistance against alectinib. The aim of this analysis was to investigate molecular mechanisms of alectinib mediated treatment effects in the ALK expressing S24 cells, which represent a primary glioblastoma cell culture, and after knockdown of ALK.

2019-11-09 | GSE140145 | GEO

Alectinib-resistant NSCLC harboring EML4-ALK cells: Parental vs. Alectinib-resistant

Project description:Transcriptional profiling of NSCLC harboring EML4-ALK comparing parental H2228 cells with alectinib resistant H2228 cells. Two-condition experiment, H2228 vs. H2228/CHR cells. Biological replicates: 1 parental replicates, 3 alectinib-resistant replicates.

2015-09-18 | E-GEOD-73167 | biostudies-arrayexpress

Alectinib-resistant NSCLC harboring EML4-ALK cells: Parental vs. Alectinib-resistant

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Gene Changes Following in vitro Alectinib Treatment in EML4-ALK Murine NSCLC Cells

Project description:First line treatment for EML4-ALK fusion-positive lung cancer patient is the use of an ALK tyrosine kinase inhibitor (TKI), such as alectinib. While most patients initially respond to this therapy, many patients often develop relapse, and efficacious therapies for patients with relapse disease are limited. To study EML4-ALK fusion-positive lung cancer, novel murine lung cancer cell lines were generated from C57BL/6 mice using an intratracheally injected Adeno-virus that contains Cas9 and guide RNAs for the EML4-ALK translocation, which leads to the development of lung tumors. Cell lines were derived from these tumors. In an effort to better understand how cells respond to alectinib, we treated EML4-ALK-positive murine cell lines (EA1, EA2, and EA3 cells) in vitro for 1-7 days with either 100nM alectinib or DMSO-control. At each time point, RNA was isolated from each condition. RNA was submitted to RNA-seq. Differential analysis on the RNA-seq data was performed to determine and track gene changes over time between control and treated cells. These data will allow us to better develop novel therapeutics to use in conjunction with alectinib when treating EML4-ALK fusion-positive patients.

2022-11-05 | GSE217115 | GEO

Clinical Characteristics and Spatial transcriptome analysis of Early Resistance to Alectinib in ALK-Positive non-small cell lung cancer: A Retrospective OLCSG Study

Project description:In anaplastic lymphoma kinase (ALK) gene rearrangements positive lung cancer, alectinib has shown good efficacy and is used as a first-line drug. However, some cases show early resistance within 3 months, but the characteristics of these cases have not been established. We analyzed patients with unresectable stage III/IV without indications for radical radiotherapy and recurrent ALK-positive lung cancer who received alectinib for primary ALK-TKI. Spatial transcriptome analysis and immunohistochemical staining revealed upregulation of Annexin A1 (ANXA1) in the early resistant group.

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RNA-seq of human NSCLCL treated with Alectinib, Lorlatinib or Brigatinib

Project description:To better understand the differences between different ALK inhibitors on ALK positive NSCL cell lines, we performed RNA-seq analysis on samples treated with 3 types of ALK inhibitors: Alectinib, Lorlatinib and Brigatinib

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A Home-Based Approach Study to Evaluate the Efficacy and Safety of Alectinib in Locally-Advanced or Metastatic ALK-Positive Solid Tumors

Project description:This study will evaluate the efficacy and safety of alectinib in participants with Anaplastic Lymphoma Kinase (ALK)-positive locally advanced or metastatic solid tumors other than lung cancer.

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Gene Changes Following in vitro Alectinib Treatment in EML4-ALK Murine NSCLC Cells

Project description:Gene Changes Following in vitro Alectinib Treatment in EML4-ALK Murine NSCLC Cells

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Gene expression profiles of Glioblastoma stem cells in which ALK or pleiotrophin expression was suppressed.

Project description:Cancer stem cells are believed to be responsible for tumor initiation and development. Much current research on human brain tumors is focused on the stem-like properties of glioblastoma stem cells. Anaplastic lymphoma kinase (ALK) and its ligand pleiotrophin are required for maintaining the stem-like properties and tumorigenicity of glioblastoma stem cells. Human glioblastoma stem cells (GB2) were infected with a lentivirus expressing an shRNA targeting ALK or pleiotrophin.

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Exploiting the polypharmacology of alectinib for synergistic RNA splicing disruption with RBM39 degraders

Project description:Precise control of pre-mRNA splicing is critical for transcriptome integrity, and its disruption is increasingly recognised as a vulnerability in cancer. Here, we identify a functional interplay between two key splicing regulators, RBM39 and serine/arginine protein kinase 1 (SRPK1), and show that dual targeting of these factors severely compromises splicing fidelity in high-risk neuroblastoma. We use the molecular glue indisulam to degrade RBM39 and repurpose the clinical ALK inhibitor alectinib which potently inhibits SRPK1. Co-treatment with indisulam and alectinib inhibited cell proliferation, induced apoptosis, and caused G2–M arrest in multiple cancer cell lines, including MYCN-amplified neuroblastoma. RNA sequencing revealed enhanced splicing defects preferentially in DNA repair and genome maintenance related genes following combination treatment, leading to R-loop accumulation and increased DNA damage. In the Th-MYCN/ALKF1174L neuroblastoma mouse model, combination therapy induced complete tumour regression and significantly improved survival rates compared with monotherapies. These findings demonstrate that combining indisulam and alectinib is a promising approach to treat aggressive malignancies such as high-risk neuroblastoma, exploiting the previously untapped polypharmacology of alectinib as a clinical RNA splicing inhibitor and supporting the therapeutic value of co-targeting interdependent splicing factors for synergistic benefit.

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