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PMID: 20451371 Published · ppublish English Journal Article Review

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

European journal of cancer (Oxford, England : 1990) ·Vol. 46 ·No. 13 ·2010-09-00 ·Pages 2357-68

Kelleher FC, McDermott R

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.

MeSH Terms
Anaplastic Lymphoma Kinase 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
Chemicals
Antineoplastic Agents GSK 1838705A Pyrimidines Pyrroles ALK protein, human Anaplastic Lymphoma Kinase Protein-Tyrosine Kinases Receptor Protein-Tyrosine Kinases Receptor, IGF Type 1
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Kelleher Fergal C
Department of Medical Oncology, Adelaide and Meath Hospital, Dublin, Ireland. fergalkelleher@hotmail.com
McDermott Ray
Article Info
Journal
European journal of cancer (Oxford, England : 1990)
Abbr.
Eur J Cancer
ISSN
1879-0852
Published
2010-09-00
Epub
2010-00-05
Pages
2357-68
Language
English
Region
England
NLM ID
9005373
Subset
IM
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