•Build a large-scale 3D shape retrieval benchmark that supports multi-modal queries.•Evaluate the 26 3D shape retrieval methods using 3 types of metrics.•Solicit and identify state-of-the-art methods ...and promising related techniques.•Perform detailed analysis on diverse methods w.r.t accuracy and efficiency.•Make benchmark and evaluation tools freely available to the community.
Large-scale 3D shape retrieval has become an important research direction in content-based 3D shape retrieval. To promote this research area, two Shape Retrieval Contest (SHREC) tracks on large scale comprehensive and sketch-based 3D model retrieval have been organized by us in 2014. Both tracks were based on a unified large-scale benchmark that supports multimodal queries (3D models and sketches). This benchmark contains 13680 sketches and 8987 3D models, divided into 171 distinct classes. It was compiled to be a superset of existing benchmarks and presents a new challenge to retrieval methods as it comprises generic models as well as domain-specific model types. Twelve and six distinct 3D shape retrieval methods have competed with each other in these two contests, respectively. To measure and compare the performance of the participating and other promising Query-by-Model or Query-by-Sketch 3D shape retrieval methods and to solicit state-of-the-art approaches, we perform a more comprehensive comparison of twenty-six (eighteen originally participating algorithms and eight additional state-of-the-art or new) retrieval methods by evaluating them on the common benchmark. The benchmark, results, and evaluation tools are publicly available at our websites (http://www.itl.nist.gov/iad/vug/sharp/contest/2014/Generic3D/, 2014, http://www.itl.nist.gov/iad/vug/sharp/contest/2014/SBR/, 2014).
Research of 3D shape retrieval has been popular recently. However, only small amount of research has focused on partial 3D shape retrieval. In this paper, we propose new features KAZE+VLAD for ...partial 3D shape retrieval. In KAZE+VLAD, firstly, extracts the KAZE as local features from Depth Buffer images generated from multiple view points of the 3D Object. Secondly, integrates local features into features of 3D object by encoding method. We used VLAD for encoding method. We used a modified Princeton Segmentation Benchmark, and conducted comparative experiments between our proposed and previous features.
Mucin 1 C‐terminal subunit (MUC1‐C) has been introduced as a key regulator for acquiring drug resistance in various cancers, but the functional role of MUC1‐C in urothelial carcinoma (UC) cells ...remains unknown. We aimed to elucidate the molecular mechanisms underlying the acquisition of cisplatin (CDDP) resistance through MUC1‐C oncoprotein in UC cells. MUC1‐C expression was examined immunohistochemically in tumor specimens of 159 UC patients who received CDDP‐based perioperative chemotherapy. As a result, moderate to high MUC1‐C expression was independently associated with poor survival in UC patients. Using human bladder cancer cell lines and CDDP‐resistant (CR) cell lines, we compared the expression levels of MUC1‐C, multiple drug resistance 1 (MDR1), the PI3K‐AKT‐mTOR pathway, and x‐cystine/glutamate transporter (xCT) to elucidate the biological mechanisms contributing to the acquisition of chemoresistance. MUC1‐C was strongly expressed in CR cell lines, followed with MDR1 expression via activation of the PI3K‐AKT‐mTOR pathway. MUC1‐C also stabilized the expression of xCT, which enhanced antioxidant defenses by increasing intracellular glutathione (GSH) levels. MUC1 down‐regulation showed MDR1 inhibition along with PI3K‐AKT‐mTOR pathway suppression. Moreover, it inhibited xCT stabilization and resulted in significant decreases in intracellular GSH levels and increased reactive oxygen species (ROS) generation. The MUC1‐C inhibitor restored sensitivity to CDDP in CR cells and UC murine xenograft models. In conclusion, we found that MUC1‐C plays a pivotal role in the acquisition of CDDP resistance in UC cells, and therefore the combined treatment of CDDP with a MUC1‐C inhibitor may become a novel therapeutic option in CR UC patients.
Our present study demonstrated that mucin 1 C‐terminal peptide (MUC1‐C) plays a pivotal role in the acquisition of cisplatin (CDDP) resistance via multiple drug resistance 1 regulation and x‐cystine/glutamate transporter stabilization in urothelial cancer cells. The combined treatment of CDDP with a MUC1‐C inhibitor, GO‐203, may become a novel therapeutic option in CDDP‐resistant UC patients.
We report the synthesis of 2 nm copper nanocrystals (Cu NCs) via a microwave-assisted polyol method without using additional protective and reducing agents. The Cu NCs are oxidation resistant and ...exhibit photoluminescence and highly stable properties in a colloidal dispersion.
This study aimed to clarify the clinical characteristics and oncological outcomes of patients with upper tract urothelial carcinoma (UTUC) who developed muscle‐invasive bladder cancer (MIBC) after ...radical nephroureterectomy (RNU). We identified 966 pTa‐4N0‐2M0 patients with UTUC who underwent RNU and clarified the risk factors for MIBC progression after initial intravesical recurrence (IVR). We also identified 318 patients with primary pT2‐4N0‐2M0 MIBC to compare the oncological outcomes with those of patients with UTUC who developed or progressed to MIBC. Furthermore, immunohistochemical examination of p53 and FGFR3 expression in tumor specimens was performed to compare UTUC of MIBC origin with primary MIBC. In total, 392 (40.6%) patients developed IVR after RNU and 46 (4.8%) developed MIBC at initial IVR or thereafter. As a result, pT1 stage on the initial IVR specimen, concomitant carcinoma in situ on the initial IVR specimen, and no intravesical adjuvant therapy after IVR were independent factors for MIBC progression. After propensity score matching adjustment, primary UTUC was a favorable indicator for cancer‐specific death compared with primary MIBC. Subgroup molecular analysis revealed high FGFR3 expression in non‐MIBC and MIBC specimens from primary UTUC, whereas low FGFR3 but high p53 expression was observed in specimens from primary MIBC tissue. In conclusion, our study demonstrated that patients with UTUC who develop MIBC recurrence after RNU exhibited the clinical characteristics of subsequent IVR more than those of primary UTUC. Of note, MIBC subsequent to UTUC may have favorable outcomes, probably due to the different molecular biological background compared with primary MIBC.
We conducted a multicenter cohort study describing the clinicopathological characteristics of muscle‐invasive bladder recurrence developed after surgical management of upper tract urothelial carcinoma.
Tumor necrosis factor‐α (TNF‐α) is involved in epithelial‐mesenchymal transition (EMT) and expression of CD44, a cancer stem cell marker, in several cancers. This study was performed to clarify the ...significance of TNF‐α and CD44 in clear cell renal cell carcinomas (ccRCCs). Expression of TNF‐α and CD44 was examined by immunohistochemistry in 120 ccRCCs. Involvement of TNF‐α in EMT and induction of CD44 was analyzed by monitoring expression of EMT‐related genes and CD44, and invasion in cultured ccRCC cell lines. TNF‐α and CD44 were immunolocalized mainly to carcinoma cells of high‐grade ccRCCs with positive correlations with primary tumor stage. A positive correlation was also obtained between TNF‐α and CD44 expression, and co‐upregulation of TNF‐α and CD44 was associated with primary tumor stage, distant metastasis, and poor prognosis. TNF‐α enhanced migration and invasion of ccRCC cells together with down‐regulation of E‐cadherin expression and up‐regulation of matrix metalloproteinase 9 and CD44 expression. TNF‐α also up‐regulated the expression of TNF‐α itself in ccRCC cells. Among the 25 ccRCC patients treated with sunitinib for metastatic disease, high CD44 expression was associated with poor treatment outcome. Importantly, residual carcinoma cells in the sunitinib‐treated metastatic ccRCCs were strongly positive for CD44, and the CD44 expression was significantly higher in the tumors from the sunitinib‐treated patients than in those from untreated ones. Our data show that TNF‐α plays an important role in progression of ccRCCs by inducing EMT and CD44 expression, and suggest that CD44 induced by TNF‐α may be involved in the resistance to the sunitinib treatment.
What's New?
Cancer‐related inflammation helps tumors spread like wildfire, and TNF‐α gets that inflammation going. In some cancers, TNF‐α drives cells toward metastasis and boosts expression of CD44, a marker of cancer stem cells. What is the role of TNF‐α in clear cell renal cell carcinoma (ccRCC)? These authors found that TNF‐α expression correlates with CD44 expression, and both are associated with tumor stage and poor prognosis. In addition, when patients were treated with sunitinib, the ones that didn't respond well to the treatment had high CD44 expression, suggesting that TNF‐α can bolster chemotherapy resistance by driving up CD44 levels.
The development of systemic therapies, including vascular endothelial growth factor‐tyrosine kinase inhibitors (VEGF‐TKI) and mammalian target of rapamycin (mTOR) inhibitors, represents a major ...breakthrough in the treatment of patients with renal cell carcinoma (RCC). However, inherent resistance is observed in some patients and acquired resistance commonly develops in many patients within several months of the initiation of systemic therapies. Since these treatments rarely cure patients, their aim is to suppress tumor progression and prolong survival. Therefore, the establishment of dependable criteria that predict responses and resistance to systemic therapies is clinically important, and the underlying molecular mechanisms also need to be elucidated for the future development of more effective therapies. We herein review recent advances in research on the molecular mechanisms underlying resistance, with a focus on morphological characteristics, tumor angiogenesis, and the tumor immune microenvironment in RCC and their relationships with VEGF‐TKI treatments. Recent therapies using immune checkpoint inhibitors (ICI) and newly developed VEGF‐TKI also appear to be effective for advanced RCC, with stable and durable responses to ICI being observed in some RCC patients. These new drugs and their outcomes have been briefly described.
The purpose of this article is to review the recent advances in renal cell carcinoma (RCC) from a pathological point of view. Because the genetic features and morphological characteristics have ...become major criteria for the classification of RCC, special techniques, such as immunohistochemistry, are essential to the differential diagnosis of renal tumors. Metastasis is frequently observed among the RCC patients with curative nephrectomy, and extracellular matrix‐degrading enzymes, such as matrix metalloproteinases (MMP) and heparanase, play a key role in invasion and metastasis of RCC. Snail and Slug, transcription factors of epithelial‐mesenchymal transition (EMT), accelerate cancer cell invasion through downregulation of E‐cadherin and up‐regulation of MMP. Therapies targeted at the vascular endothelial growth factor pathway have become the standard treatment of metastatic RCC. Although they lead to tumor shrinkage mainly by inhibiting angiogenesis, they have typically been associated with drug resistance. The mechanism of the resistance remains largely unknown, but complex events including re‐activation of angiogenesis, EMT and cancer stem cells, and immune escape are implicated in the refractory response to the therapy. Recent advances of the research on RCC have caused the changes of classification and therapy, and pathologists should take overall view of these as integrated pathology.
Cisplatin (CDDP)-based chemotherapy is the gold standard treatment for many types of cancer. However, the phenotypic hallmark of tumors often changes after CDDP treatment, with the acquisition of ...epithelial-to-mesenchymal transition (EMT) and platinum resistance. Furthermore, the mechanisms by which cancer cells acquire EMT under the control of CDDP remain unclear. Following an investigation of urothelial carcinoma (UC) before and after the acquisition of platinum resistance, we offer the new target TNFAIP2, which led to EMT and tumor invasion in platinum-treated UC cells. TNFAIP2 expression in cancer was examined at the protein and transcriptional levels. A potential target for TNFAIP2 during EMT was assessed by microarray. Clinically, upregulated TNFAIP2 expression was identified as a significant predictor of mortality following surgery in three different cohorts of patients with UC (n = 156, n = 119, and n = 54). Knockdown of TNFAIP2 resulted in upregulation of E-cadherin expression and downregulation of TWIST1 expression, which decreased motile function in platinum-resistant UC cells. TNFAIP2 overexpression led to downregulation of E-cadherin expression and upregulation of TWIST1 expression in platinum-naïve UC cells. Clinical investigation of matched pre- and post-CDDP-treated UC sections confirmed upregulation of TNFAIP2 expression in CDDP-treated tumors but downregulation of E-cadherin expression. Global gene expression analysis following TNFAIP2 knockdown identified MTDH as a positive regulator of TNFAIP2-derived EMT acquisition in cancer cells. The present results suggest a relationship between TNFAIP2 and EMT in cancers under the control of CDDP, in which MTDH expression levels in cancer cells are vital for promoting TNFAIP2-derived EMT acquisition.
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