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Br J Cancer
2008 May 06;989:1536-9. doi: 10.1038/sj.bjc.6604341.
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EML4-ALK fusion transcript is not found in gastrointestinal and breast cancers.
Fukuyoshi Y
,
Inoue H
,
Kita Y
,
Utsunomiya T
,
Ishida T
,
Mori M
.
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Fusion genes have been identified as chromosomal rearrangements in certain cancers, such as leukaemia, lymphoma, and sarcoma. The EML4-ALK (EML4: echinoderm microtubule-associated-protein-like 4; ALK: anaplastic lymphoma kinase) fusion gene has been identified as an oncogene in non-small-cell lung cancer (NSCLC). This study examined the presence of this fusion transcript in gastrointestinal and breast cancers. We evaluated the expression of the EML4-ALK transcript in 104 lung cancer cases and in 645 gastrointestinal and breast cancer samples. Only one of the lung cancer samples tested positive for the EML4-ALK fusion transcript, whereas none were detected in 555 gastrointestinal and 90 breast cancer cases. Our data suggest that the EML4-ALK fusion transcript is not present in gastrointestinal or breast cancers and is specific to NSCLC.
Figure 1. Screening of specimens for EML4âALK mRNA. Representative cases of lung, liver, and oesophageal carcinoma were subjected to reverse transcription-polymerase chain reaction with primers for EML4âALK fusion transcript. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA is also shown. Marker, 100âbp DNA ladder.
Figure 2. Schematic of reverse transcription-polymerase chain reaction revealing fusion of EML4 with ALK in a case with non-small-cell lung cancer (adenocarcinoma). Line graph shows the position and automated DNA sequencing of the fusion points (identical to the variant 1 transcript).
Figure 3. EML4âALK genomic alterations in non-small-cell lung cancer. Results from three representative cases are shown. EML4âALK genomic fusion was found in case 3. Marker, λ/HindIII.
Figure 4. The breakpoints in EML4 and ALK genes. The upper figure shows the structure of EML4âALK variant 1 described by Soda et al (2007) and the lower figure shows the structure of EML4âALK that we found. The middle figure shows a wild-type EML4âALK. Filled and open arrows indicate breakpoints.
Druker,
Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia.
2006, Pubmed
Druker,
Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia.
2006,
Pubmed
Druker,
Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr-Abl positive cells.
1996,
Pubmed
Hirasaki,
BAC clones related to prognosis in patients with esophageal squamous carcinoma: an array comparative genomic hybridization study.
2007,
Pubmed
Inamura,
EML4-ALK fusion is linked to histological characteristics in a subset of lung cancers.
2008,
Pubmed
,
Echinobase
Inoue,
The expression of tumor-rejection antigen "MAGE" genes in human gastric carcinoma.
1995,
Pubmed
Mitelman,
Fusion genes and rearranged genes as a linear function of chromosome aberrations in cancer.
2004,
Pubmed
Mitelman,
The impact of translocations and gene fusions on cancer causation.
2007,
Pubmed
Perner,
TMPRSS2:ERG fusion-associated deletions provide insight into the heterogeneity of prostate cancer.
2006,
Pubmed
Rikova,
Global survey of phosphotyrosine signaling identifies oncogenic kinases in lung cancer.
2007,
Pubmed
Soda,
Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer.
2007,
Pubmed
,
Echinobase
Tomlins,
Distinct classes of chromosomal rearrangements create oncogenic ETS gene fusions in prostate cancer.
2007,
Pubmed
Tomlins,
Recurrent fusion of TMPRSS2 and ETS transcription factor genes in prostate cancer.
2005,
Pubmed