Project description:Breast implant-associated anaplastic large cell lymphoma (BIA-ALCL) is an anaplastic lymphoma kinase-negative (ALKneg) T-cell lymphoma. Here, we provide RNA-seq data of four BIA-ALCL and four ALCL cell lines:TLBR-1, TLBR-2, TLBR-3, TLBR-4 and DEL (two replicates), KARPAS-299, KI-JK, SUP-M2 (two replicates), respectively.
Project description:Deregulation of chromatin modifiers, including DNA helicases, are emerging as one of the mechanism underlying the transformation of anaplastic lymphoma kinase negative (ALK−) anaplastic large cell lymphoma (ALCL). We recently identified the DNA helicase HELLS as central for proficient ALK-ALCL proliferation and progression. By performing RNA-sequencing profiling coupled with bioinformatic prediction, we demonstrated that HELLS contributes to an appropriate cytokinesis via the transcriptional regulation of genes involved in cleavage furrow regulation in ALK- anaplastic large cell lymphoma
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.
Project description:Tyrosine kinase receptor anaplastic lymphoma kinase (ALK) is physiologically expressed during embryogenesis. However, chromosomal rearrangements, especially translocations, cause expression of pathogenic ALK fusion proteins that drive tumor formation and maintenance. For instance, the translocation between chromosomes 2 and 5 (t(2;5)) fuses the nucleophosmin 1 (NPM1) gene with ALK, leading to anaplastic large cell lymphoma (ALCL). The constitutive active NPM1::ALK tyrosine kinase drives tumor transformation and tumor cells inevitably depend on ALK kinase activity for survival. For this reason, ALK kinase inhibitors showed great success in treating ALK-positive ALCL. Here, we explored gene expression changes induced by ceritinib, second generation ALK inhibitor, on a representative cell line, SUDHL-1.
Project description:Neuroblastoma is a pediatric solid tumor originating from neural crest cells, which are precursors of the sympathetic nervous system. Amplification of MYCN proto-oncogene is a key factor contributing to poor prognosis of neuroblastoma and is strongly associated with aggressive disease progression. Additionally, the anaplastic lymphoma kinase plays an important role in the pathogenesis of neuroblastoma. Mutation or amplification of anaplastic lymphoma kinase drives oncogenic signaling pathways, such as the MAPK and Ras pathways, which together with MYCN amplification exacerbate tumor malignancy. The use of human induced pluripotent stem cell-derived cranial neural crest cells to establish a neuroblastoma model is expected to be of great significance in studying the pathogenesis of this disease. In this study, we sought to mimic the tumorigenic process of neuroblastoma by overexpressing MYCN and anaplastic lymphoma kinase in cranial neural crest cells derived from human induced pluripotent stem cells. These modified cells when subcutaneously transplanted into immunodeficient mice induced neuroblastoma-like tumors, and could thus be used an in vitro model to study this cancer. Through extensive gene expression profiling and whole exome sequencing of MYCN/anaplastic lymphoma kinase-induced clones, we identified key features of neuroblastoma, including activation of the MAPK signaling pathway and gain of 17q chromosome, which is critical for malignant tumor development. This model provides a valuable platform for studying the biological mechanisms driving anaplastic lymphoma kinase mutations and MYCN amplification in neuroblastoma derived from cranial neural crest cells as well as for exploring potential therapeutic approaches against these targets to improve patient prognosis.
