The Experts below are selected from a list of 14529 Experts worldwide ranked by ideXlab platform
Andre M. Oliveira - One of the best experts on this subject based on the ideXlab platform.
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Anaplastic Lymphoma Kinase immunoreactivity correlates with alk gene rearrangement and transcriptional up regulation in non small cell lung carcinomas
Human Pathology, 2009Co-Authors: Jennifer M. Boland, Xiaoke Wang, Ping Yang, Sibel Erdogan, George Vasmatzis, Lori S. Tillmans, Michele Johnson, Lisa M. Peterson, Kevin C. Halling, Andre M. OliveiraAbstract:Summary Recently, the fusion gene EML4 - ALK was identified in non–small cell lung carcinoma, which could be a potential therapeutic target. We investigated the prevalence of Anaplastic Lymphoma Kinase protein expression in these tumors by immunohistochemistry and correlated the results with data from ALK molecular studies. Gene expression profiling was performed on 35 adenocarcinomas to identify cases with ALK gene up-regulation, which was correlated with protein overexpression by immunohistochemistry. Immunohistochemistry was also performed on an independent cohort consisting of 150 adenocarcinomas and 150 squamous cell carcinomas to evaluate the utility of Anaplastic Lymphoma Kinase immunostaining as a screening tool. Florescence in situ hybridization for the ALK locus and reverse transcriptase–polymerase chain reaction for EML4-ALK were performed on tumors positive for Anaplastic Lymphoma Kinase by immunohistochemistry. Transcriptional up-regulation of ALK was identified in 2 (6%) of 35 adenocarcinomas by gene expression profiling. These 2 cases were positive for Anaplastic Lymphoma Kinase by immunohistochemistry, whereas the remaining 33 cases were completely negative. In the independent cohort, Anaplastic Lymphoma Kinase immunostaining was positive in 1 of 150 squamous cell carcinomas and in 3 of 150 adenocarcinomas. The 6 cases positive for Anaplastic Lymphoma Kinase by immunohistochemistry showed evidence of ALK locus rearrangement by florescence in situ hybridization but were negative for EGFR and KRAS mutation. The presence of EML4-ALK fusion transcript was confirmed in 2 cases by reverse transcriptase–polymerase chain reaction. In conclusion, Anaplastic Lymphoma Kinase immunoreactivity in non–small cell lung carcinomas was associated with transcriptional up-regulation, ALK locus rearrangement, and the presence of EML4-ALK fusion transcript. Anaplastic Lymphoma Kinase immunohistochemistry may have utility as a screening tool or as a surrogate marker for the molecular techniques to detect the EML4-ALK fusion gene in these tumors.
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Anaplastic Lymphoma Kinase immunoreactivity correlates with ALK gene rearrangement and transcriptional up-regulation in non–small cell lung carcinomas
Human pathology, 2009Co-Authors: Jennifer M. Boland, Xiaoke Wang, Ping Yang, Sibel Erdogan, George Vasmatzis, Lori S. Tillmans, Michele Johnson, Lisa M. Peterson, Kevin C. Halling, Andre M. OliveiraAbstract:Summary Recently, the fusion gene EML4 - ALK was identified in non–small cell lung carcinoma, which could be a potential therapeutic target. We investigated the prevalence of Anaplastic Lymphoma Kinase protein expression in these tumors by immunohistochemistry and correlated the results with data from ALK molecular studies. Gene expression profiling was performed on 35 adenocarcinomas to identify cases with ALK gene up-regulation, which was correlated with protein overexpression by immunohistochemistry. Immunohistochemistry was also performed on an independent cohort consisting of 150 adenocarcinomas and 150 squamous cell carcinomas to evaluate the utility of Anaplastic Lymphoma Kinase immunostaining as a screening tool. Florescence in situ hybridization for the ALK locus and reverse transcriptase–polymerase chain reaction for EML4-ALK were performed on tumors positive for Anaplastic Lymphoma Kinase by immunohistochemistry. Transcriptional up-regulation of ALK was identified in 2 (6%) of 35 adenocarcinomas by gene expression profiling. These 2 cases were positive for Anaplastic Lymphoma Kinase by immunohistochemistry, whereas the remaining 33 cases were completely negative. In the independent cohort, Anaplastic Lymphoma Kinase immunostaining was positive in 1 of 150 squamous cell carcinomas and in 3 of 150 adenocarcinomas. The 6 cases positive for Anaplastic Lymphoma Kinase by immunohistochemistry showed evidence of ALK locus rearrangement by florescence in situ hybridization but were negative for EGFR and KRAS mutation. The presence of EML4-ALK fusion transcript was confirmed in 2 cases by reverse transcriptase–polymerase chain reaction. In conclusion, Anaplastic Lymphoma Kinase immunoreactivity in non–small cell lung carcinomas was associated with transcriptional up-regulation, ALK locus rearrangement, and the presence of EML4-ALK fusion transcript. Anaplastic Lymphoma Kinase immunohistochemistry may have utility as a screening tool or as a surrogate marker for the molecular techniques to detect the EML4-ALK fusion gene in these tumors.
Xiaoke Wang - One of the best experts on this subject based on the ideXlab platform.
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Fusion of dynactin 1 to Anaplastic Lymphoma Kinase in inflammatory myofibroblastic tumor.
Human pathology, 2012Co-Authors: Xiaoke Wang, Chandra Krishnan, Edward P. Nguyen, Kevin J. Meyer, Jennifer L. Oliveira, Ping Yang, Michele R. Erickson-johnson, Michael J. Yaszemski, Avudaiappan MaranAbstract:Summary Inflammatory myofibroblastic tumor is an uncommon neoplasm that occurs more often in younger patients. Approximately 50% of inflammatory myofibroblastic tumors are characterized by Anaplastic Lymphoma Kinase fusion genes, more commonly TPM3–Anaplastic Lymphoma Kinase and TPM4–Anaplastic Lymphoma Kinase . Herein, we report a novel fusion of dynactin 1 to Anaplastic Lymphoma Kinase in a neck inflammatory myofibroblastic tumor diagnosed in a 7-year-old girl. Histologic evaluation showed a perineurioma-like bland spindle cell neoplasm with positive immunohistochemical staining for Anaplastic Lymphoma Kinase, S-100, and CD34 but negative for epithelial membrane antigen. Standard cytogenetic analysis showed a der(2)t(2;12)(p23;q11). Fluorescence in situ hybridization demonstrated separation of the Anaplastic Lymphoma Kinase locus. 5′-rapid amplification of complementary DNA ends polymerase chain reaction identified an in-frame fusion of dynactin 1 exon 16 on chromosome 2 to Anaplastic Lymphoma Kinase exon 20. Reverse transcription-polymerase chain reaction with specific primers and direct sequencing confirmed the fusion. The structure of the fusion protein retains the cytoskeleton-associated protein–glycine domain and coiled coil domain of dynactin 1 and the receptor tyrosine Kinase domain of Anaplastic Lymphoma Kinase. This novel fusion gene is structurally similar to other previously described Anaplastic Lymphoma Kinase fusion genes and may be associated with the unusual morphology and immunophenotype of this tumor.
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Anaplastic Lymphoma Kinase immunoreactivity correlates with alk gene rearrangement and transcriptional up regulation in non small cell lung carcinomas
Human Pathology, 2009Co-Authors: Jennifer M. Boland, Xiaoke Wang, Ping Yang, Sibel Erdogan, George Vasmatzis, Lori S. Tillmans, Michele Johnson, Lisa M. Peterson, Kevin C. Halling, Andre M. OliveiraAbstract:Summary Recently, the fusion gene EML4 - ALK was identified in non–small cell lung carcinoma, which could be a potential therapeutic target. We investigated the prevalence of Anaplastic Lymphoma Kinase protein expression in these tumors by immunohistochemistry and correlated the results with data from ALK molecular studies. Gene expression profiling was performed on 35 adenocarcinomas to identify cases with ALK gene up-regulation, which was correlated with protein overexpression by immunohistochemistry. Immunohistochemistry was also performed on an independent cohort consisting of 150 adenocarcinomas and 150 squamous cell carcinomas to evaluate the utility of Anaplastic Lymphoma Kinase immunostaining as a screening tool. Florescence in situ hybridization for the ALK locus and reverse transcriptase–polymerase chain reaction for EML4-ALK were performed on tumors positive for Anaplastic Lymphoma Kinase by immunohistochemistry. Transcriptional up-regulation of ALK was identified in 2 (6%) of 35 adenocarcinomas by gene expression profiling. These 2 cases were positive for Anaplastic Lymphoma Kinase by immunohistochemistry, whereas the remaining 33 cases were completely negative. In the independent cohort, Anaplastic Lymphoma Kinase immunostaining was positive in 1 of 150 squamous cell carcinomas and in 3 of 150 adenocarcinomas. The 6 cases positive for Anaplastic Lymphoma Kinase by immunohistochemistry showed evidence of ALK locus rearrangement by florescence in situ hybridization but were negative for EGFR and KRAS mutation. The presence of EML4-ALK fusion transcript was confirmed in 2 cases by reverse transcriptase–polymerase chain reaction. In conclusion, Anaplastic Lymphoma Kinase immunoreactivity in non–small cell lung carcinomas was associated with transcriptional up-regulation, ALK locus rearrangement, and the presence of EML4-ALK fusion transcript. Anaplastic Lymphoma Kinase immunohistochemistry may have utility as a screening tool or as a surrogate marker for the molecular techniques to detect the EML4-ALK fusion gene in these tumors.
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Anaplastic Lymphoma Kinase immunoreactivity correlates with ALK gene rearrangement and transcriptional up-regulation in non–small cell lung carcinomas
Human pathology, 2009Co-Authors: Jennifer M. Boland, Xiaoke Wang, Ping Yang, Sibel Erdogan, George Vasmatzis, Lori S. Tillmans, Michele Johnson, Lisa M. Peterson, Kevin C. Halling, Andre M. OliveiraAbstract:Summary Recently, the fusion gene EML4 - ALK was identified in non–small cell lung carcinoma, which could be a potential therapeutic target. We investigated the prevalence of Anaplastic Lymphoma Kinase protein expression in these tumors by immunohistochemistry and correlated the results with data from ALK molecular studies. Gene expression profiling was performed on 35 adenocarcinomas to identify cases with ALK gene up-regulation, which was correlated with protein overexpression by immunohistochemistry. Immunohistochemistry was also performed on an independent cohort consisting of 150 adenocarcinomas and 150 squamous cell carcinomas to evaluate the utility of Anaplastic Lymphoma Kinase immunostaining as a screening tool. Florescence in situ hybridization for the ALK locus and reverse transcriptase–polymerase chain reaction for EML4-ALK were performed on tumors positive for Anaplastic Lymphoma Kinase by immunohistochemistry. Transcriptional up-regulation of ALK was identified in 2 (6%) of 35 adenocarcinomas by gene expression profiling. These 2 cases were positive for Anaplastic Lymphoma Kinase by immunohistochemistry, whereas the remaining 33 cases were completely negative. In the independent cohort, Anaplastic Lymphoma Kinase immunostaining was positive in 1 of 150 squamous cell carcinomas and in 3 of 150 adenocarcinomas. The 6 cases positive for Anaplastic Lymphoma Kinase by immunohistochemistry showed evidence of ALK locus rearrangement by florescence in situ hybridization but were negative for EGFR and KRAS mutation. The presence of EML4-ALK fusion transcript was confirmed in 2 cases by reverse transcriptase–polymerase chain reaction. In conclusion, Anaplastic Lymphoma Kinase immunoreactivity in non–small cell lung carcinomas was associated with transcriptional up-regulation, ALK locus rearrangement, and the presence of EML4-ALK fusion transcript. Anaplastic Lymphoma Kinase immunohistochemistry may have utility as a screening tool or as a surrogate marker for the molecular techniques to detect the EML4-ALK fusion gene in these tumors.
Baoan Chen - One of the best experts on this subject based on the ideXlab platform.
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Crizotinib as a personalized alternative for targeted Anaplastic Lymphoma Kinase rearrangement in previously treated patients with non-small-cell lung cancer
Drug design development and therapy, 2015Co-Authors: Liting Guo, Haijun Zhang, Weiwei Shao, Baoan ChenAbstract:Crizotinib, the first clinically designed and synthesized as a tyrosine Kinase inhibitor targeting mesenchymal-epithelial transition factor, indicating marked anticancer activity in patients with advanced, Anaplastic Lymphoma Kinase-positive non-small-cell lung cancer, was approved by the US Food and Drug Administration in 2011. In this review, we focus on the efficacy of crizotinib compared with chemotherapy in advanced Anaplastic Lymphoma Kinase-positive lung cancer and present the role of crizotinib as a personalized alternative in previously treated patients with non-small-cell lung cancer.
Jennifer M. Boland - One of the best experts on this subject based on the ideXlab platform.
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Anaplastic Lymphoma Kinase immunoreactivity correlates with alk gene rearrangement and transcriptional up regulation in non small cell lung carcinomas
Human Pathology, 2009Co-Authors: Jennifer M. Boland, Xiaoke Wang, Ping Yang, Sibel Erdogan, George Vasmatzis, Lori S. Tillmans, Michele Johnson, Lisa M. Peterson, Kevin C. Halling, Andre M. OliveiraAbstract:Summary Recently, the fusion gene EML4 - ALK was identified in non–small cell lung carcinoma, which could be a potential therapeutic target. We investigated the prevalence of Anaplastic Lymphoma Kinase protein expression in these tumors by immunohistochemistry and correlated the results with data from ALK molecular studies. Gene expression profiling was performed on 35 adenocarcinomas to identify cases with ALK gene up-regulation, which was correlated with protein overexpression by immunohistochemistry. Immunohistochemistry was also performed on an independent cohort consisting of 150 adenocarcinomas and 150 squamous cell carcinomas to evaluate the utility of Anaplastic Lymphoma Kinase immunostaining as a screening tool. Florescence in situ hybridization for the ALK locus and reverse transcriptase–polymerase chain reaction for EML4-ALK were performed on tumors positive for Anaplastic Lymphoma Kinase by immunohistochemistry. Transcriptional up-regulation of ALK was identified in 2 (6%) of 35 adenocarcinomas by gene expression profiling. These 2 cases were positive for Anaplastic Lymphoma Kinase by immunohistochemistry, whereas the remaining 33 cases were completely negative. In the independent cohort, Anaplastic Lymphoma Kinase immunostaining was positive in 1 of 150 squamous cell carcinomas and in 3 of 150 adenocarcinomas. The 6 cases positive for Anaplastic Lymphoma Kinase by immunohistochemistry showed evidence of ALK locus rearrangement by florescence in situ hybridization but were negative for EGFR and KRAS mutation. The presence of EML4-ALK fusion transcript was confirmed in 2 cases by reverse transcriptase–polymerase chain reaction. In conclusion, Anaplastic Lymphoma Kinase immunoreactivity in non–small cell lung carcinomas was associated with transcriptional up-regulation, ALK locus rearrangement, and the presence of EML4-ALK fusion transcript. Anaplastic Lymphoma Kinase immunohistochemistry may have utility as a screening tool or as a surrogate marker for the molecular techniques to detect the EML4-ALK fusion gene in these tumors.
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Anaplastic Lymphoma Kinase immunoreactivity correlates with ALK gene rearrangement and transcriptional up-regulation in non–small cell lung carcinomas
Human pathology, 2009Co-Authors: Jennifer M. Boland, Xiaoke Wang, Ping Yang, Sibel Erdogan, George Vasmatzis, Lori S. Tillmans, Michele Johnson, Lisa M. Peterson, Kevin C. Halling, Andre M. OliveiraAbstract:Summary Recently, the fusion gene EML4 - ALK was identified in non–small cell lung carcinoma, which could be a potential therapeutic target. We investigated the prevalence of Anaplastic Lymphoma Kinase protein expression in these tumors by immunohistochemistry and correlated the results with data from ALK molecular studies. Gene expression profiling was performed on 35 adenocarcinomas to identify cases with ALK gene up-regulation, which was correlated with protein overexpression by immunohistochemistry. Immunohistochemistry was also performed on an independent cohort consisting of 150 adenocarcinomas and 150 squamous cell carcinomas to evaluate the utility of Anaplastic Lymphoma Kinase immunostaining as a screening tool. Florescence in situ hybridization for the ALK locus and reverse transcriptase–polymerase chain reaction for EML4-ALK were performed on tumors positive for Anaplastic Lymphoma Kinase by immunohistochemistry. Transcriptional up-regulation of ALK was identified in 2 (6%) of 35 adenocarcinomas by gene expression profiling. These 2 cases were positive for Anaplastic Lymphoma Kinase by immunohistochemistry, whereas the remaining 33 cases were completely negative. In the independent cohort, Anaplastic Lymphoma Kinase immunostaining was positive in 1 of 150 squamous cell carcinomas and in 3 of 150 adenocarcinomas. The 6 cases positive for Anaplastic Lymphoma Kinase by immunohistochemistry showed evidence of ALK locus rearrangement by florescence in situ hybridization but were negative for EGFR and KRAS mutation. The presence of EML4-ALK fusion transcript was confirmed in 2 cases by reverse transcriptase–polymerase chain reaction. In conclusion, Anaplastic Lymphoma Kinase immunoreactivity in non–small cell lung carcinomas was associated with transcriptional up-regulation, ALK locus rearrangement, and the presence of EML4-ALK fusion transcript. Anaplastic Lymphoma Kinase immunohistochemistry may have utility as a screening tool or as a surrogate marker for the molecular techniques to detect the EML4-ALK fusion gene in these tumors.
Ping Yang - One of the best experts on this subject based on the ideXlab platform.
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Fusion of dynactin 1 to Anaplastic Lymphoma Kinase in inflammatory myofibroblastic tumor.
Human pathology, 2012Co-Authors: Xiaoke Wang, Chandra Krishnan, Edward P. Nguyen, Kevin J. Meyer, Jennifer L. Oliveira, Ping Yang, Michele R. Erickson-johnson, Michael J. Yaszemski, Avudaiappan MaranAbstract:Summary Inflammatory myofibroblastic tumor is an uncommon neoplasm that occurs more often in younger patients. Approximately 50% of inflammatory myofibroblastic tumors are characterized by Anaplastic Lymphoma Kinase fusion genes, more commonly TPM3–Anaplastic Lymphoma Kinase and TPM4–Anaplastic Lymphoma Kinase . Herein, we report a novel fusion of dynactin 1 to Anaplastic Lymphoma Kinase in a neck inflammatory myofibroblastic tumor diagnosed in a 7-year-old girl. Histologic evaluation showed a perineurioma-like bland spindle cell neoplasm with positive immunohistochemical staining for Anaplastic Lymphoma Kinase, S-100, and CD34 but negative for epithelial membrane antigen. Standard cytogenetic analysis showed a der(2)t(2;12)(p23;q11). Fluorescence in situ hybridization demonstrated separation of the Anaplastic Lymphoma Kinase locus. 5′-rapid amplification of complementary DNA ends polymerase chain reaction identified an in-frame fusion of dynactin 1 exon 16 on chromosome 2 to Anaplastic Lymphoma Kinase exon 20. Reverse transcription-polymerase chain reaction with specific primers and direct sequencing confirmed the fusion. The structure of the fusion protein retains the cytoskeleton-associated protein–glycine domain and coiled coil domain of dynactin 1 and the receptor tyrosine Kinase domain of Anaplastic Lymphoma Kinase. This novel fusion gene is structurally similar to other previously described Anaplastic Lymphoma Kinase fusion genes and may be associated with the unusual morphology and immunophenotype of this tumor.
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Anaplastic Lymphoma Kinase immunoreactivity correlates with alk gene rearrangement and transcriptional up regulation in non small cell lung carcinomas
Human Pathology, 2009Co-Authors: Jennifer M. Boland, Xiaoke Wang, Ping Yang, Sibel Erdogan, George Vasmatzis, Lori S. Tillmans, Michele Johnson, Lisa M. Peterson, Kevin C. Halling, Andre M. OliveiraAbstract:Summary Recently, the fusion gene EML4 - ALK was identified in non–small cell lung carcinoma, which could be a potential therapeutic target. We investigated the prevalence of Anaplastic Lymphoma Kinase protein expression in these tumors by immunohistochemistry and correlated the results with data from ALK molecular studies. Gene expression profiling was performed on 35 adenocarcinomas to identify cases with ALK gene up-regulation, which was correlated with protein overexpression by immunohistochemistry. Immunohistochemistry was also performed on an independent cohort consisting of 150 adenocarcinomas and 150 squamous cell carcinomas to evaluate the utility of Anaplastic Lymphoma Kinase immunostaining as a screening tool. Florescence in situ hybridization for the ALK locus and reverse transcriptase–polymerase chain reaction for EML4-ALK were performed on tumors positive for Anaplastic Lymphoma Kinase by immunohistochemistry. Transcriptional up-regulation of ALK was identified in 2 (6%) of 35 adenocarcinomas by gene expression profiling. These 2 cases were positive for Anaplastic Lymphoma Kinase by immunohistochemistry, whereas the remaining 33 cases were completely negative. In the independent cohort, Anaplastic Lymphoma Kinase immunostaining was positive in 1 of 150 squamous cell carcinomas and in 3 of 150 adenocarcinomas. The 6 cases positive for Anaplastic Lymphoma Kinase by immunohistochemistry showed evidence of ALK locus rearrangement by florescence in situ hybridization but were negative for EGFR and KRAS mutation. The presence of EML4-ALK fusion transcript was confirmed in 2 cases by reverse transcriptase–polymerase chain reaction. In conclusion, Anaplastic Lymphoma Kinase immunoreactivity in non–small cell lung carcinomas was associated with transcriptional up-regulation, ALK locus rearrangement, and the presence of EML4-ALK fusion transcript. Anaplastic Lymphoma Kinase immunohistochemistry may have utility as a screening tool or as a surrogate marker for the molecular techniques to detect the EML4-ALK fusion gene in these tumors.
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Anaplastic Lymphoma Kinase immunoreactivity correlates with ALK gene rearrangement and transcriptional up-regulation in non–small cell lung carcinomas
Human pathology, 2009Co-Authors: Jennifer M. Boland, Xiaoke Wang, Ping Yang, Sibel Erdogan, George Vasmatzis, Lori S. Tillmans, Michele Johnson, Lisa M. Peterson, Kevin C. Halling, Andre M. OliveiraAbstract:Summary Recently, the fusion gene EML4 - ALK was identified in non–small cell lung carcinoma, which could be a potential therapeutic target. We investigated the prevalence of Anaplastic Lymphoma Kinase protein expression in these tumors by immunohistochemistry and correlated the results with data from ALK molecular studies. Gene expression profiling was performed on 35 adenocarcinomas to identify cases with ALK gene up-regulation, which was correlated with protein overexpression by immunohistochemistry. Immunohistochemistry was also performed on an independent cohort consisting of 150 adenocarcinomas and 150 squamous cell carcinomas to evaluate the utility of Anaplastic Lymphoma Kinase immunostaining as a screening tool. Florescence in situ hybridization for the ALK locus and reverse transcriptase–polymerase chain reaction for EML4-ALK were performed on tumors positive for Anaplastic Lymphoma Kinase by immunohistochemistry. Transcriptional up-regulation of ALK was identified in 2 (6%) of 35 adenocarcinomas by gene expression profiling. These 2 cases were positive for Anaplastic Lymphoma Kinase by immunohistochemistry, whereas the remaining 33 cases were completely negative. In the independent cohort, Anaplastic Lymphoma Kinase immunostaining was positive in 1 of 150 squamous cell carcinomas and in 3 of 150 adenocarcinomas. The 6 cases positive for Anaplastic Lymphoma Kinase by immunohistochemistry showed evidence of ALK locus rearrangement by florescence in situ hybridization but were negative for EGFR and KRAS mutation. The presence of EML4-ALK fusion transcript was confirmed in 2 cases by reverse transcriptase–polymerase chain reaction. In conclusion, Anaplastic Lymphoma Kinase immunoreactivity in non–small cell lung carcinomas was associated with transcriptional up-regulation, ALK locus rearrangement, and the presence of EML4-ALK fusion transcript. Anaplastic Lymphoma Kinase immunohistochemistry may have utility as a screening tool or as a surrogate marker for the molecular techniques to detect the EML4-ALK fusion gene in these tumors.
