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Clinical outcome prediction is major concern to patients with cancer. Various molecular markers in various carcinomas have been identified in the past few decades. However, accurate predictors in chondrosarcoma have not been developed, even though chondrosarcoma is the second most common primary bone tumour. Chondrosarcoma is the cartilage-forming malignancy and shows a wide spectrum of clinicopathological behaviours. The majority of chondrosarcoma grows slowly and rarely metastasises, and adequate surgery leads to a good prognosis. However, wide surgical excision is acquired in high-grade chondrosarcoma, because this tumour is highly resistant to chemotherapy and radiotherapy. To decide best therapy, accurate diagnostic markers are also necessary in chondrosarcoma. It is reported that angiogenesis and lymphangiogenesis increase by chondrosarcoma staging, and they are promoted by leptin and adiponectin. Several microRNAs to regulate vascular endothelial growth factor (VEGF)-A and VEGF-C are also reported. Alpha-methylacyl-CoA racemase and periostin are proposed as new biomarkers for differential diagnosis of enchondroma and chondrosarcoma. This review summarises that chondrosarcoma diagnostic markers are currently reported.

Several studies have suggested that extracellular matrix (ECM) remodeling and the microenvironment are tightly associated with adipogenesis and adipose angiogenesis. In the present study, we demonstrated that transforming growth factor-beta induced (TGFBI) suppresses angiogenesis stimulated by adipocyte-conditioned medium (Ad-CM), both in vitro and in vivo. TGFBI knockout (KO) mice exhibited increased numbers of blood vessels in adipose tissue, and blood vessels from these mice showed enhanced infiltration into Matrigel containing Ad-CM. The treatment of Ad-CM-stimulated SVEC-10 endothelial cells with TGFBI protein reduced migration and tube-forming activity. TGFBI protein suppressed the activation of the Src and extracellular signaling-related kinase signaling pathways of these SVEC-10 endothelial cells. Our findings indicated that TGFBI inhibited adipose angiogenesis by suppressing the activation of Src and ERK signaling pathways, possibly because of the stimulation of the angiogenic activity of endothelial cells.

CCL5 is a member of the CC chemokine family expressed in a wide array of immune and non-immune cells in response to stress signals. CCL5 expression correlates with advanced human breast cancer. However, its functional significance and mode of action have not been established. Here, we show that CCL5-deficient mice are resistant to highly aggressive, triple-negative mammary tumor growth. Hematopoietic CCL5 is dominant in this phenotype. The absence of hematopoietic CCL5 causes aberrant generation of CD11b + /Gr-1 + , myeloid-derived suppressor cells (MDSCs) in the bone marrow in response to tumor growth by accumulating Ly6C hi and Ly6G + MDSCs with impaired capacity to suppress cytotoxicity of CD8 + T cells. These properties of CCL5 are observed in both orthotopic and spontaneous mammary tumors. Antibody-mediated systemic blockade of CCL5 inhibits tumor progression and enhances the efficacy of therapeutic vaccination against non-immunogenic tumors. CCL5 also helps maintain the immunosuppressive capacity of human MDSCs. Our study uncovers a novel, chemokine-independent activity of the hematopoietically derived CCL5 that promotes mammary tumor progression via generating MDSCs in the bone marrow in cooperation with tumor-derived colony-stimulating factors. The study sheds considerable light on the interplay between the hematopoietic compartment and tumor niche. Because of the apparent dispensable nature of this molecule in normal physiology, CCL5 may represent an excellent therapeutic target in immunotherapy for breast cancer as well as a broad range of solid tumors that have significant amounts of MDSC infiltration.

Antigen-presenting cells (APCs), including macrophages and dendritic cells (DCs), play a crucial role in bridging innate and adaptive immunity; thereby, innate immune checkpoint blockade-based therapy is an attractive approach for the induction of sustainable tumor-specific immunity. The interaction between the cluster of differentiation 47 (CD47) on tumor and signal-regulatory protein alpha (SIRPα) on phagocytic cells inhibits the phagocytic function of APCs, acting as a “don’t eat me” signal. Accordingly, CD47 blockade is known to increase tumor cell phagocytosis, eliciting tumor-specific CD8+ T-cell immunity. Here, we introduced a nature-derived nanocage to deliver SIRPγ for blocking of antiphagocytic signaling through binding to CD47 and combined it with prophagocytic stimuli using a metabolic reprogramming reagent for APCs (CpG-oligodeoxynucleotides). Upon delivering the clustered SIRPγ variant, the nanocage showed enhanced CD47 binding profiles on tumor cells, thereby promoting active engulfment by phagocytes. Moreover, combination with CpG potentiated the prophagocytic ability, leading to the establishment of antitumorigenic surroundings. This combination treatment could competently inhibit tumor growth by invigorating APCs and CD8+ T-cells in TMEs in B16F10 orthotopic tumor models, known to be resistant to CD47-targeting therapeutics. Collectively, enhanced delivery of an innate immune checkpoint antagonist with metabolic modulation stimuli of immune cells could be a promising strategy for arousing immune responses against cancer.

A long-term change of a subtidal macroalgal assemblage has been investigated in Maxwell Bay, King George Island (KGI) of the Antarctic coast by a revisit survey after 30 years. Field surveys were done by SCUBA diving at six sites in 2016–2018 to directly compare with the previous survey conducted in 1988–1993 at the same sites. The total number of macroalgal species was similar between the previous and the present survey, 25 and 27 species respectively. However, the macroalgal assemblage changed substantially with the average similarity of 48.2% between the two surveys. Also, the species-level abundance showed a high variability between surveys. On the other hand, over the 30 years interval there was little overall change at the between-site level hierarchical structure in the subtidal communities of Maxwell Bay. The sites near the penguin rookery consistently showed the highest biodiversity, indicating the importance of land-based nutrients input in Antarctic coastal habitats. A noticeable pattern change over 30 years was the increase of Desmarestia complex and Plocamium cartilagineum and the decrease of Himantothallus grandifolius . Both groups are still dominant, but the shift from Himantothallus to Desmarestia-Plocamium may reflects temperature rise on the Maxwell Bay coast compared to the past.

In this study, we investigated the therapeutic effects of c-MET inhibition in ovarian clear cell carcinoma (OCCC). Expression levels of c-MET in the epithelial ovarian cancers (EOCs) and normal ovarian tissues were evaluated using real-time PCR. To test the effects of c-MET inhibitors in OCCC cell lines, we performed MTT and apoptosis assays. We used Western blots to evaluate the expression of c-MET and its down-stream pathway. In vivo experiments were performed to test the effects of c-MET inhibitor on tumor growth in orthotopic mouse xenografts of OCCC cell line RMG1 and a patient-derived tumor xenograft (PDX) model of OCCC. c-MET expression was significantly greater in OCCCs compared with serous carcinomas and normal ovarian tissues (p < 0.001). In in vitro study, inhibition of c-MET using c-MET inhibitors (SU11274 or crizotinib) significantly decreased the proliferation, and increased the apoptosis of OCCC cells. SU11274 decreased expression of the p-c-MET proteins and blocked the phosphorylation of down-stream proteins Akt and Erk. Furthermore, SU11274 treatment significantly decreased the in vivo tumor weight in xenograft models of RMG1 cell and a PDX model for OCCC compared to control (p = 0.004 and p = 0.009, respectively).

Background/Aim: Periostin exists as an extracellular matrix protein in several carcinomas and is related to metastasis and poor prognosis. It is mainly secreted from cancer associated fibroblasts, and not from carcinoma cells. As a tumor microenvironment component, periostin usually mediates tumor cell stemness, metastasis, angiogenesis and lymphangiogenesis. This study aimed to examine the role of periostin in chondrosarcoma. Materials and Methods: To evaluate the effect of periostin on the proliferation of chondrosarcoma cells, MTT assay was performed on SW1353 cells and periostin knockdown SW1353 cells. Migration activity was examined using Boyden chamber. Results: Periostin, secreted from chondrosarcoma cells, was found to support proliferation, and maintain stemness and migration of chondrosarcoma cells. Periostin also induced proliferation and migration of lymphatic endothelial cells. Conclusion: Periostin plays an important role in chondrosarcoma development and disease progression.

The purpose of this study was to describe the clinical characteristics and to assess the contributing factors in patients developing bone metastasis in uterine cervical cancer. Two thousand thirteen patients had a diagnosis of uterine cervical cancer at Samsung Medical Center between June 1994 and December 2011. During the study period, 105 patients with bone metastasis were identified, and their clinicopathologic data were investigated retrospectively. Among 105 patients with bone metastasis, 14 patients were excluded and 91 patients were evaluable. The median bone metastasis-free survival was 27 months (range, 0–279 months). The time to bone metastasis was significantly shorter in patients with adenocarcinoma than in patients with squamous cell carcinoma (median duration, 12 vs 29 months; P = 0.016). In addition, it was shorter in patients with stage IIB to stage IV disease than in those with stage I to stage IIA disease (15 vs 22 months; P = 0.02). The median survival after bone metastasis was 10 months, longer in the patients who received radiotherapy (± chemotherapy) than in the patients who received chemotherapy alone as a salvage therapy (12 vs 7 months; P = 0.01). Initial stage, number of bone metastases, location of involved bone, and coexisting metastatic lesion were not associated with the overall survival of the patients. Our study demonstrates that adenocarcinoma, advanced stage (IIB-IV) and initial multiple bone metastases contribute to earlier bone metastasis. Once bone metastasis was recognized, the survival of these patients was poor and no factors were identified to predict survival of those patients.

Background The aim of this study was to compare the surgical and oncologic outcomes of laparoscopic-assisted radical vaginal hysterectomy (LARVH) with that of laparoscopic radical hysterectomy (LRH) for early-stage cervical cancer. Methods Patients affected by invasive cervical cancer (FIGO stage I–IIA) who had received LARVH ( n  = 89) in our institute between September 2004 and December 2010 were compared with patients treated by LRH ( n  = 105) during the same period. All patient information, surgical and pathological data, and oncological results were prospectively collected. Patients undergoing abdominal radical hysterectomy (ARH) were included for comparison of safety, morbidity, and recurrence rate. Results The mean estimated blood loss (EBL) and return of bowel activity were significantly reduced in the LRH group compared with the LARVH group ( p  = .011 and p  = .002, respectively). Intraoperative complications occurred in 10 patients (11.2 %) in the LARVH group, 6 (5.7 %) in the LRH group, and 3 (3.0 %) in the ARH group. Forest plot analyses of the previous studies showed higher incidence of intraoperative complication in the LARVH group than in LRH group ( p  = .02). Despite the similar overall recurrence rate, stump recurrence seems to be high in the LRH group in the forest plot analysis of previous studies ( p  = 0.08). Conclusions Both LARVH and LRH are safe and effective therapeutic procedures for the management of early-stage cervical cancer, although LRH is characterized by less blood loss and shorter bowel recovery time. Possible higher stump recurrence in the LRH should be further evaluated.

This study was conducted to investigate transforming growth factor beta-induced protein (TGFBI) expression and analyze the clinical and prognostic significance of TGFBI in oropharyngeal squamous cell carcinoma (OPSCC). We evaluated TGFBI expression by immunohistochemistry in 94 patients with OPSCC. For comprehensive analysis, TGFBI expression was subdivided into tumor cell score (T), stroma score (S), and the sum of two scores (TS) calculated using H-score. Clinicopathological features and survival outcomes were compared between groups of high expression and low expression of TGFBI in each area. Overall, 12 patients (12.8%) showed high T score, and 41 patients (43.6%) revealed high S score. Although T score showed no significant difference both in overall survival (OS) (p=0.080) and recurrence free survival (RFS) (p=0.272), high S score patients had significantly worse OS (p=0.003) and worse RFS (p=0.043). High TS score also showed significant association with worse OS (p=0.011) and worse RFS (p=0.021). High S score was an independent prognostic factor predicting shorter OS (HR=6.352, 95%CI=1.206-40.050, p=0.029) and RFS (HR=18.843, 95%CI=1.030-344.799, p=0.048) in the multivariate analysis. High S score of TGFBI was a significant predictor of poor prognosis in OPSCC. TGFBI could be a useful new predictive and prognostic biomarker in OPSCC.