Publications by authors named "D P Maxson"

This COMAR Technical Information Statement (TIS) addresses health and safety issues concerning exposure of the general public to radiofrequency (RF) fields from 5G wireless communications networks, the expansion of which started on a large scale in 2018 to 2019. 5G technology can transmit much greater amounts of data at much higher speeds for a vastly expanded array of applications compared with preceding 2-4G systems; this is due, in part, to using the greater bandwidth available at much higher frequencies than those used by most existing networks. Although the 5G engineering standard may be deployed for operating networks currently using frequencies extending from 100s to 1,000s of MHz, it can also operate in the 10s of GHz where the wavelengths are 10 mm or less, the so-called millimeter wave (MMW) band.

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Background: Patients with anaplastic lymphoma kinase (ALK)-positive non-small cell lung cancer (NSCLC) respond to ALK inhibitors. Clinically, the presence of ≥15% cells with rearrangements identified on break-apart fluorescence in situ hybridization (FISH) classifies tumors as positive. Increases in native and rearranged ALK copy number also occur.

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Background: Crizotinib produces high response rates and prolonged PFS in ALK+ NSCLC. Retrospective analyses suggest enhanced sensitivity to pemetrexed in crizotinib naive ALK+ NSCLC. Cross-resistance between crizotinib and pemetrexed has not been previously investigated.

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Background: Fluorescence in situ hybridization (FISH), using break-apart red (3') and green (5') ALK (anaplastic lymphoma kinase) probes, consistently shows rearrangements in <100% of tumor cells in ALK-positive (ALK+) nonsmall cell lung cancer (NSCLC). Increased copy numbers of fused and rearranged signals also occur. Here, correlations are explored between the percentage of ALK+ cells and signal copy number and their association with response to ALK inhibition.

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Background: The discovery of distinct subsets of nonsmall cell lung cancer (NSCLC) characterized by activation of driver oncogenes has greatly affected personalized therapy. It is hypothesized that the dominant oncogene in NSCLC would be associated with distinct patterns of metastatic spread in NSCLC at the time of diagnosis.

Methods: A total of 209 consecutive patients with stage IV nonsquamous NSCLC with an EGFR (epidermal growth factor receptor) mutation (N = 39), KRAS (v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog) mutation (N = 49), ALK (anaplastic lymphoma receptor tyrosine kinase) gene rearrangement (N = 41), or wild-type for all 3 (triple negative, N = 80) were included.

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