Fusions of the tyrosine kinase genes ALK (anaplastic lymphoma kinase), ROS1 (c-ros oncogene 1), or RET (rearranged during transfection) occur in 1%-5% of lung adenocarcinomas (LADCs) and their products constitute therapeutic targets for kinase inhibitory drugs.
Screening of anaplastic lymphoma tyrosine kinase (ALK) gene fusions in non-small cell lung cancer (NSCLC) patients enables the identification of the patients likely to benefit from ALK-targeted therapy.
EGFR(epidermal growth factor receptor) mutations and ALK(anaplastic lymphoma kinase) rearrangement are typical examples of such driver oncogenic mutations found in lung adenocarcinomas.
EML4 (echinoderm microtubule-associated protein-like 4)-ALK (anaplastic lymphoma kinase) was recently identified as a transforming fusion gene in non-small cell lung cancer (NSCLC).
NSCLC with the EML4 (echinoderm microtubule-associated protein-like 4)-ALK (anaplastic lymphoma kinase) fusion gene is also more likely to occur in never smokers and in those with adenocarcinoma histology, and is expected to benefit from ALK inhibitors.
EML4 (echinoderm microtubule-associated protein-like 4)-ALK (anaplastic lymphoma kinase) was recently identified as a transforming fusion gene in non-small cell lung cancer (NSCLC).
NSCLC with the EML4 (echinoderm microtubule-associated protein-like 4)-ALK (anaplastic lymphoma kinase) fusion gene is also more likely to occur in never smokers and in those with adenocarcinoma histology, and is expected to benefit from ALK inhibitors.
<i>Nucleophosmin-anaplastic lymphoma kinase</i> (<i>NPM-ALK)</i> fusion genes resulting from the translocation t(2;5)(p23;q35) are present in almost 90% of childhood ALK-positive anaplastic large-cell lymphomas (ALCL).
Inhibition of EGFR and anaplastic lymphoma kinase (ALK) signaling is highly effective in a subgroup of non-small cell lung cancer (NSCLC) patients with distinct clinicopathologic features.
EGFR(epidermal growth factor receptor) mutations and ALK(anaplastic lymphoma kinase) rearrangement are typical examples of such driver oncogenic mutations found in lung adenocarcinomas.
The expression patterns of PTN, receptor protein tyrosine phosphatase β/ζ, (RPTPβ/ζ), syndecan-1 (SDC1), syndecan-3 (SDC3) and anaplastic lymphoma kinase (ALK) were determined by immunohistochemistry (IHC).
The expression patterns of PTN, receptor protein tyrosine phosphatase β/ζ, (RPTPβ/ζ), syndecan-1 (SDC1), syndecan-3 (SDC3) and anaplastic lymphoma kinase (ALK) were determined by immunohistochemistry (IHC).
The expression patterns of PTN, receptor protein tyrosine phosphatase β/ζ, (RPTPβ/ζ), syndecan-1 (SDC1), syndecan-3 (SDC3) and anaplastic lymphoma kinase (ALK) were determined by immunohistochemistry (IHC).
SATB1 was negatively regulated by STAT5 through microRNA-155, which in turn triggered enhanced expression of T helper type 2 cytokines such as IL-5 and IL-9.In parallel, Sun et al. found that SATB1 expression was up-regulated by promoter demethylation in a subset of cutaneous anaplastic lymphoma and was associated with T helper type 17 polarization in patients with better therapeutic responses.
SATB1 was negatively regulated by STAT5 through microRNA-155, which in turn triggered enhanced expression of T helper type 2 cytokines such as IL-5 and IL-9.In parallel, Sun et al. found that SATB1 expression was up-regulated by promoter demethylation in a subset of cutaneous anaplastic lymphoma and was associated with T helper type 17 polarization in patients with better therapeutic responses.
Accumulating evidence suggest that patients with advanced non-small-cell lung cancer (NSCLC) and specific genomic alterations including epidermal growth factor receptor and microtubule-associated protein-like 4 anaplastic lymphoma kinase could significantly benefit from molecular-targeted therapies compared with chemotherapy.
Accumulating evidence suggest that patients with advanced non-small-cell lung cancer (NSCLC) and specific genomic alterations including epidermal growth factor receptor and microtubule-associated protein-like 4 anaplastic lymphoma kinase could significantly benefit from molecular-targeted therapies compared with chemotherapy.