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    The emerging pathogenic and therapeutic importance of the anaplastic lymphoma kinase gene.

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    Authors
    Kelleher, Fergal C
    McDermott, Ray
    Affiliation
    Department of Medical Oncology, Adelaide and Meath Hospital, Dublin, Ireland., fergalkelleher@hotmail.com
    Issue Date
    2012-02-01T10:49:46Z
    MeSH
    Antineoplastic Agents/therapeutic use
    Carcinoma, Non-Small-Cell Lung/genetics/therapy
    *Chromosome Aberrations
    Chromosomes, Human, Pair 2/*genetics
    Drug Synergism
    Gene Amplification
    Humans
    Lung Neoplasms/genetics/therapy
    Lymphoma, Large-Cell, Anaplastic/genetics/therapy
    Mutation/genetics
    Neoplasms/*genetics/therapy
    Neuroblastoma/genetics/therapy
    Protein-Tyrosine Kinases/antagonists & inhibitors/*genetics
    Pyrimidines/therapeutic use
    Pyrroles/therapeutic use
    Receptor Protein-Tyrosine Kinases
    Receptor, IGF Type 1/antagonists & inhibitors
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    Citation
    Eur J Cancer. 2010 Sep;46(13):2357-68. Epub 2010 May 5.
    Journal
    European journal of cancer (Oxford, England : 1990)
    URI
    http://hdl.handle.net/10147/207908
    DOI
    10.1016/j.ejca.2010.04.006
    PubMed ID
    20451371
    Abstract
    The anaplastic lymphoma kinase gene (ALK) is a gene on chromosome 2p23 that has expression restricted to the brain, testis and small intestine but is not expressed in normal lymphoid tissue. It has similarity to the insulin receptor subfamily of kinases and is emerging as having increased pathologic and potential therapeutic importance in malignant disease. This gene was originally established as being implicated in the pathogenesis of rare diseases including inflammatory myofibroblastic tumour (IMT) and ALK-positive anaplastic large cell lymphoma, which is a subtype of non-Hodgkin's lymphoma. Recently the number of diseases in which ALK is implicated in their pathogenesis has increased. In 2007, an inversion of chromosome 2 involving ALK and a fusion partner gene in a subset of non-small cell lung cancer was discovered. In 2008, publications emerged implicating ALK in familial and sporadic cases of neuroblastoma, a childhood cancer of the sympatho-adrenal system. Chromosomal abnormalities involving ALK are translocations, amplifications or mutations. Chromosomal translocations are the longest recognised ALK genetic abnormality. When translocations occur a fusion gene is created between ALK and a gene partner. This has been described in ALK-positive anaplastic large cell lymphoma in which ALK is fused to NPM (nucleolar protein gene) and in non-small cell lung cancer where ALK is fused to EML4 (Echinoderm microtubule-associated protein 4). The most frequently described partner genes in inflammatory myofibroblastic tumour are tropomyosin 3/4 (TMP3/4), however in IMTs a diversity of ALK fusion partners have been found, with the ability to homodimerise a common characteristic. Point mutations and amplification of the ALK gene occur in the childhood cancer neuroblastoma. Therapeutic targeting of ALK fusion genes using tyrosine kinase inhibition, vaccination using an ALK specific antigen and treatment using viral vectors for RNAi are emerging potential therapeutic possibilities.
    Language
    eng
    ISSN
    1879-0852 (Electronic)
    0959-8049 (Linking)
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.ejca.2010.04.006
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