Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA100655 | ENA |
REPOSITORIES: ENA
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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.
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Project description:Genomic profiling of Anaplastic Large Cell Lymphoma
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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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Project description:Kynureninase is a member of a large family of catalytically diverse but structurally homologous pyridoxal 5'-phosphate (PLP) dependent enzymes known as the aspartate aminotransferase superfamily or alpha-family. The Homo sapiens and other eukaryotic constitutive kynureninases preferentially catalyze the hydrolytic cleavage of 3-hydroxy-l-kynurenine to produce 3-hydroxyanthranilate and l-alanine, while l-kynurenine is the substrate of many prokaryotic inducible kynureninases. The human enzyme was cloned with an N-terminal hexahistidine tag, expressed, and purified from a bacterial expression system using Ni metal ion affinity chromatography. Kinetic characterization of the recombinant enzyme reveals classic Michaelis-Menten behavior, with a Km of 28.3 +/- 1.9 microM and a specific activity of 1.75 micromol min-1 mg-1 for 3-hydroxy-dl-kynurenine. Crystals of recombinant kynureninase that diffracted to 2.0 A were obtained, and the atomic structure of the PLP-bound holoenzyme was determined by molecular replacement using the Pseudomonas fluorescens kynureninase structure (PDB entry 1qz9) as the phasing model. A structural superposition with the P. fluorescens kynureninase revealed that these two structures resemble the "open" and "closed" conformations of aspartate aminotransferase. The comparison illustrates the dynamic nature of these proteins' small domains and reveals a role for Arg-434 similar to its role in other AAT alpha-family members. Docking of 3-hydroxy-l-kynurenine into the human kynureninase active site suggests that Asn-333 and His-102 are involved in substrate binding and molecular discrimination between inducible and constitutive kynureninase substrates.
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Project description:RNA extracted at 240min. Samples are rRNA depleted. Expression measurement of Homo sapiens genes.
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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.
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Project description:Expression data of primary and metastasic tissues from ALK+ NSCLC patients (Anaplastic lymphoma kinase fusion positive non-small cell lung carcinoma)
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