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The initial step of organ infiltration of malignant cells is the interaction with host vascular endothelial cells, which is often mediated by specific combinations of cell adhesion molecules. Cell adhesion molecule 1 (CADM1) is overexpressed in adult T‐cell leukemia/lymphoma (ATL) and provides a cell‐surface diagnostic marker. CADM1 promotes the adhesion of ATL cells to vascular endothelial cells and multiple organ infiltration in mice. However, its binding partner on host cells has not yet been identified. In this study, we show that CADM1 promotes transendothelial migration of ATL cells in addition to the adhesion to vascular endothelial cells. Moreover, CADM1 enhances liver infiltration of mouse T‐cell lymphoma cells, EL4, after tail vein injection, whereas a CADM1 mutant lacking adhesive activity did not. Among the known CADM1‐binding proteins expressed in primary endothelial cells, only CADM1 and CADM4 could induce morphological extension of ATL cells when plated onto glass coated with these proteins. Furthermore, CADM1‐mediated liver infiltration of EL4 cells was canceled in conventional and vascular endothelium‐specific Cadm1 knockout mice, whereas it was not canceled in Cadm4 knockout mice. These results suggest that CADM1 on host vascular endothelial cells is required for organ infiltration of ATL and other T‐cell lymphomas expressing CADM1. Trans‐homophilic interaction CADM1 between T‐lymphoma cells and host vascular endothelial cells is required for organ infiltration of lymphoma cells expressing CADM1.

YAP1, the main Hippo pathway effector, is a potent oncogene and is overexpressed in non‐small‐cell lung cancer (NSCLC); however, the YAP1 expression pattern in small‐cell lung cancer (SCLC) has not yet been elucidated in detail. We report that the loss of YAP1 is a special feature of high‐grade neuroendocrine lung tumors. A hierarchical cluster analysis of 15 high‐grade neuroendocrine tumor cell lines containing 14 SCLC cell lines that depended on the genes of Hippo pathway molecules and neuroendocrine markers clearly classified these lines into two groups: the YAP1‐negative and neuroendocrine marker‐positive group (n = 11), and the YAP1‐positive and neuroendocrine marker‐negative group (n = 4). Among the 41 NSCLC cell lines examined, the loss of YAP1 was only observed in one cell line showing the strong expression of neuroendocrine markers. Immunostaining for YAP1, using the sections of 189 NSCLC, 41 SCLC, and 30 large cell neuroendocrine carcinoma (LCNEC) cases, revealed that the loss of YAP1 was common in SCLC (40/41, 98%) and LCNEC (18/30, 60%), but was rare in NSCLC (6/189, 3%). Among the SCLC and LCNEC cases tested, the loss of YAP1 correlated with the expression of neuroendocrine markers, and a survival analysis revealed that YAP1‐negative cases were more chemosensitive than YAP1‐positive cases. Chemosensitivity test for cisplatin using YAP1‐positive/YAP1‐negative SCLC cell lines also showed compatible results. YAP1‐sh‐mediated knockdown induced the neuroendocrine marker RAB3a, which suggested the possible involvement of YAP1 in the regulation of neuroendocrine differentiation. Thus, we showed that the loss of YAP1 has potential as a clinical marker for predicting neuroendocrine features and chemosensitivity. YAP1 is possibly involved in the regulation of neuroendocrine differentiation of lung tumors. Loss of YAP1 correlated with strong expression of neuroendocrine markers. Loss of YAP1 is a predictor of chemothensitivity in high‐grade neuroendocrine tumors.

YAP 1 , the main Hippo pathway effector, is a potent oncogene and is overexpressed in non‐small‐cell lung cancer ( NSCLC ); however, the YAP 1 expression pattern in small‐cell lung cancer ( SCLC ) has not yet been elucidated in detail. We report that the loss of YAP 1 is a special feature of high‐grade neuroendocrine lung tumors. A hierarchical cluster analysis of 15 high‐grade neuroendocrine tumor cell lines containing 14 SCLC cell lines that depended on the genes of Hippo pathway molecules and neuroendocrine markers clearly classified these lines into two groups: the YAP 1 ‐negative and neuroendocrine marker‐positive group ( n = 11), and the YAP 1 ‐positive and neuroendocrine marker‐negative group ( n = 4). Among the 41 NSCLC cell lines examined, the loss of YAP 1 was only observed in one cell line showing the strong expression of neuroendocrine markers. Immunostaining for YAP 1, using the sections of 189 NSCLC , 41 SCLC , and 30 large cell neuroendocrine carcinoma ( LCNEC ) cases, revealed that the loss of YAP 1 was common in SCLC (40/41, 98%) and LCNEC (18/30, 60%), but was rare in NSCLC (6/189, 3%). Among the SCLC and LCNEC cases tested, the loss of YAP 1 correlated with the expression of neuroendocrine markers, and a survival analysis revealed that YAP 1‐negative cases were more chemosensitive than YAP 1‐positive cases. Chemosensitivity test for cisplatin using YAP 1‐positive/ YAP 1‐negative SCLC cell lines also showed compatible results. YAP 1 ‐sh‐mediated knockdown induced the neuroendocrine marker RAB 3a , which suggested the possible involvement of YAP 1 in the regulation of neuroendocrine differentiation. Thus, we showed that the loss of YAP 1 has potential as a clinical marker for predicting neuroendocrine features and chemosensitivity.

Epitaxial lift-off process enables the separation of III–V device layers from gallium arsenide substrates and has been extensively explored to avoid the high cost of III–V devices by reusing the substrates. Conventional epitaxial lift-off processes require several post-processing steps to restore the substrate to an epi-ready condition. Here we present an epitaxial lift-off scheme that minimizes the amount of post-etching residues and keeps the surface smooth, leading to direct reuse of the gallium arsenide substrate. The successful direct substrate reuse is confirmed by the performance comparison of solar cells grown on the original and the reused substrates. Following the features of our epitaxial lift-off process, a high-throughput technique called surface tension-assisted epitaxial lift-off was developed. In addition to showing full wafer gallium arsenide thin film transfer onto both rigid and flexible substrates, we also demonstrate devices, including light-emitting diode and metal-oxide-semiconductor capacitor, first built on thin active layers and then transferred to secondary substrates. The fabrication of electronic devices depends on semiconductor substrates for device growth. The etching technique implemented here by Cheng et al . allows the reuse of these substrates and suggests a more economic fabrication of electronic devices.

Hepatocellular carcinoma (HCC) is characterized by a notable sex disparity in incidence and tumor aggressiveness. Revealing differences in genetic landscapes between male and female HCCs may expand the understanding of sexual disparities mechanisms and assist the development of precision medicine. Although reports on the sex disparity of HCC are accumulated, studies focusing on sex-related biomarkers among Asian populations remain limited. Here, we conducted a comprehensive genomic profiling analysis to explore differences between male and female patients within a cohort of 195 Taiwanese HCC patients. We did not detect any sex-biased genomic alterations. However, when our investigation extended to the TCGA dataset, we found higher frequencies of gene copy gains in CCNE2 and mutations in CTNNB1 and TP53 among male patients. Besides, we further evaluated the associations between genomic alterations and patients’ prognosis by sex. The results showed that female patients harboring tumors with STAT3 gain and alterations in the JAK–STAT pathway displayed a poor prognosis. These two factors remained independently associated with unfavorable prognosis even after adjusting for the patient’s age and stage characteristics (Hazard ratio = 10.434, 95% CI 3.331–32.677, P < 0.001; Hazard ratio = 2.547, 95% CI 1.195–5.432, P  = 0.016, respectively). In summary, this study provides valuable insights into understanding sex disparity in HCC in the East Asian population. Validation through larger cohorts and extensive sequencing efforts is warranted.

Tumor multifocality and location are prognostic factors for upper tract urothelial carcinoma (UTUC). However, confounding effects can appear when these two factors are analyzed together. Therefore, we aimed to investigate the impact of tumor distribution on the outcomes of multifocal UTUC after radical nephroureterectomy. From the 2780 UTUC patients in the Taiwan UTUC Collaboration Group, 685 UTUC cases with multifocal tumors (defined as more than one tumor lesion in unilateral upper urinary tract) were retrospectively included and divided into three groups: multiple renal pelvic tumors, multiple ureteral tumors, and synchronous renal pelvic and ureteral tumors included 164, 152, and 369 patients, respectively. We found the prevalence of carcinoma in situ was the highest in the synchronous group. In multivariate survival analyses, tumor distribution showed no difference in cancer-specific and disease-free survival, but there was a significant difference in bladder recurrence-free survival. The synchronous group had the highest bladder recurrence rate. In summary, tumor distribution did not influence the cancer-specific outcomes of multifocal UTUC, but synchronous lesions led to a higher rate of bladder recurrence than multiple renal pelvic tumors. We believe that the distribution of tumors reflects the degree of malignant involvement within the urinary tract, but has little significance for survival or disease progression.

Background Nephroureterectomy with bladder cuff excision is the standard treatment for high-risk upper urinary tract urothelial carcinoma (UTUC). The role of minimally invasive surgery in treating locally advanced UTUC remains controversial. This study aimed to compare the outcomes of open , laparoscopic , and robotic surgeries for managing locally advanced UTUC. Methods We retrospectively reviewed 705 patients with locally advanced UTUC from multiple institutions throughout Taiwan. Perioperative outcomes and oncological outcomes, such as cancer-specific survival , overall survival , disease-free survival and bladder-free survival , were compared between the open, laparoscopic and robotic groups. Results The minimally invasive group had better overall and cancer-specific survival (CSS) rates. The 2-year CSS rates of the open, laparoscopic and robotic groups were 71%, 83%, and 77% respectively ( p  < 0.001). The robotic group had similar outcomes to the laparoscopic group. ( p  = 0.061, 0.825, 0.341 for OS, CSS, DFS respectively.) More lymph node dissections were performed and more lymph nodes were harvested in the robotic group ( p  = 0.009). Conclusions Our results demonstrated that minimally invasive surgery, including laparoscopic and robotic surgery, for locally advanced UTUC resulted in oncological outcomes that are non-inferior to those of open surgery.