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Background/Aim: The Archer FusionPlex platform is widely used for comprehensive fusion-gene detection in cancer tissues. This platform separately displays results for strong-evidence and weak-evidence fusion candidates (WEFCs). Distinctive fusion patterns are frequently found in the weak-evidence category and information about the patterns is clinically essential. Patients and Methods: We describe the type and frequency of WEFCs observed using the FusionPlex Sarcoma Panel (S Panel) and the FusionPlex ALK, RET, and ROS1 ver2 Panel (ARR Panel). Results: A total of 97 specimens were examined and 620 candidates were detected and categorized as WEFCs. A median of five WEFCs were detected per sample. In the S Panel group, there were 13 WEFCs with a frequency of more than 1%. In the ARR Panel group, a total of 16 WEFCs were detected with a frequency of more than 1%. Conclusion: Specific WEFCs were detected according to the panel selected. [ABSTRACT FROM AUTHOR]

The prognosis of stage IVb non-small cell lung cancer (NSCLC) patients with multiple distant metastases or involvement of different extra-thoracic sites is poor. The prognosis following salvage surgery for patients with more than five metastases has been reported as most unfavourable. The following case is of a 71-year-old man with a 9-year survival duration after being diagnosed with stage IVb ALK-rearranged lung adenocarcinoma, who was treated for 6 years with whole-brain radiotherapy, pemetrexed-based chemotherapy, ALK-tyrosine kinase inhibitors (TKIs) including ceritinib and alectinib, and salvage sublobar resection of the primary lung cancer and who obtained treatment-free remission (TFR) for more than 3 years following surgery. [ABSTRACT FROM AUTHOR]

Monitoring exhaled breath is a very attractive, noninvasive screening technique for early diagnosis of diseases, especially lung cancer. However, the technique provides insufficient accuracy because the exhaled air has many crucial volatile organic compounds (VOCs) at very low concentrations (ppb level). We analyzed the breath exhaled by lung cancer patients and healthy subjects (controls) using gas chromatography/mass spectrometry (GC/MS), and performed a subsequent statistical analysis to diagnose lung cancer based on the combination of multiple lung cancer-related VOCs. We detected 68 VOCs as marker species using GC/MS analysis. We reduced the number of VOCs and used support vector machine (SVM) algorithm to classify the samples. We observed that a combination of five VOCs (CHN, methanol, CH3CN, isoprene, 1-propanol) is sufficient for 89.0% screening accuracy, and hence, it can be used for the design and development of a desktop GC-sensor analysis system for lung cancer. [ABSTRACT FROM AUTHOR]

Various volatile organic compounds (VOCs) in breath exhaled by patients with lung cancer, healthy controls, and patients with lung cancer who underwent surgery for resection of cancer were analyzed by gas condenser-equipped gas chromatography-mass spectrometry (GC/MS) for development of an exhaled breath monitoring prototype system involving metal oxide gas sensors, a gas condenser, and gas chromatography columns. The gas condenser-GC/MS analysis identified concentrations of 56 VOCs in the breath exhaled by the test population of 136 volunteers (107 patients with lung cancer and 29 controls), and selected four target VOCs, nonanal, acetoin, acetic acid, and propanoic acid, for use with the condenser, GC, and sensor-type prototype system. The prototype system analyzed exhaled breath samples from 101 volunteers (74 patients with lung cancer and 27 controls). The prototype system exhibited a level of performance similar to that of the gas condenser-GC/MS system for breath analysis. [ABSTRACT FROM AUTHOR]

We previously reported the results of bacterial artificial chromosome array comprehensive genomic hybridization of malignant pleural mesotheliomas (MPMs), including two cases with high-level amplification in the 11q22 locus. In this study, we found that the YAP1 gene encoding a transcriptional coactivator was localized in this amplified region and overexpressed in both cases, suggesting it as a candidate oncogene in this region. We analyzed the involvement of YAP1 in MPM proliferation, as well as its functional and physical interaction with Merlin encoded by the neurofibromatosis type 2 (NF2) tumor suppressor gene, which is frequently mutated in MPMs. YAP1-RNA interference suppressed growth of a mesothelioma cell line NCI-H290 with NF2 homozygous deletion, probably through cell-cycle arrest and apoptosis induction, whereas YAP1 transfection promoted the growth of MeT-5A, an immortalized mesothelial cell line. We also found that the introduction of NF2 into NCI-H290 induced phosphorylation at serine 127 of YAP1, which was accompanied by reduction of nuclear localization of YAP1, whereas nuclear localization of a YAP1 S 127A mutant was not affected. Furthermore, results of immunoprecipitation and in vitro pull-down assays indicated a physical interaction between Merlin and YAP1. These results suggest that YAP1 is involved in mesothelial cell growth and that the transcriptional coactivator activity of YAP1 is functionally inhibited by Merlin through the induction of phosphorylation and cytoplasmic retention of YAP1. This is the first report of negative regulatory signaling from Merlin to YAP1 in mammalian cells. Future studies of transcriptional targets of YAP1 in MPMs may shed light on the molecular mechanisms of MPM development and lead to new therapeutic strategies. [ABSTRACT FROM AUTHOR]