Regulation of epithelial mesenchymal transition (EMT) by Serum Amyloid A 1 (SAA1) is dependent on integrin in esophageal squamous cell carcinoma (ESCC)

Poster abstract: no. B5Esophageal Squamous Cell Carcinoma (ESCC) is the predominant type comprising more than 90% of esophageal cancer, which is a highly metastatic and fatal cancer, and is ranked the eighth in mortality rate in Hong Kong cancer patients (Hong Kong Cancer Registry, Hospital Authority, 2010). Using a functional complementation approach, SAA1 was identified as one of the tumor suppressor gene candidates. The SAA1 is an acute phase protein, which is highly expressed in response to inflammation by the liver. It is also present as a secretary protein in histologically normal human epithelial tissues. The expression of SAA1 was found to be down-regulated in ESCC. Interestingly, the gene expression of SAA1 and the mesenchymal marker N-cadherin was found to be inversely correlated in a panel of ESCC and the immortalized esophageal epithelial cell lines. Therefore, we want to determine whether SAA1 could regulate EMT in ESCC ...postprin

Differential angiogenic roles of serum amyloid A 1 (SAA1) isoforms in esophageal squamous cell carcinoma (ESCC)

Molecular and Cellular Biology - Poster Presentations - Proffered Abstracts - Poster Presentations - Tumor Suppressors 2: abstract no. 1550This journal suppl. entitled: Proceedings: AACR Annual Meeting 2014; April 5-9, 2014 ...Esophageal Caner (EC), a highly metastatic and fatal cancer, is ranked the eighth in mortality rate in Hong Kong cancer patients (Hong Kong Cancer Registry, Hospital Authority, 2010). Esophageal Squamous Cell Carcinoma (ESCC) is the predominant type comprising more than 90% of EC. Using a functional complementation approach, SAA1 was identified as one of the tumor suppressor gene candidates. SAA1 is located at chromosome 11p15.1 and is expressed as a secretary protein in liver, human cultured smooth muscle cells, monocyte-macrophage cell lines, and in histologically-normal human epithelial tissues. Genetic polymorphisms of SAA1 have been identified as a risk factor of diseases such as amyloidosis. Three SAA1 isoforms with two ...postprin

Computational fluid dynamics modeling of symptomatic intracranial atherosclerosis may predict risk of stroke recurrence.

BackgroundPatients with symptomatic intracranial atherosclerosis (ICAS) of ≥ 70% luminal stenosis are at high risk of stroke recurrence. We aimed to evaluate the relationships between hemodynamics of ICAS revealed by computational fluid dynamics (CFD) models and risk of stroke recurrence in this patient subset.MethodsPatients with a symptomatic ICAS lesion of 70-99% luminal stenosis were screened and enrolled in this study. CFD models were reconstructed based on baseline computed tomographic angiography (CTA) source images, to reveal hemodynamics of the qualifying symptomatic ICAS lesions. Change of pressures across a lesion was represented by the ratio of post- and pre-stenotic pressures. Change of shear strain rates (SSR) across a lesion was represented by the ratio of SSRs at the stenotic throat and proximal normal vessel segment, similar for the change of flow velocities. Patients were followed up for 1 year.ResultsOverall, 32 patients (median age 65; 59.4% males) were recruited. The median pressure, SSR and velocity ratios for the ICAS lesions were 0.40 (-2.46-0.79), 4.5 (2.2-20.6), and 7.4 (5.2-12.5), respectively. SSR ratio (hazard ratio [HR] 1.027; 95% confidence interval [CI], 1.004-1.051; P = 0.023) and velocity ratio (HR 1.029; 95% CI, 1.002-1.056; P = 0.035) were significantly related to recurrent territorial ischemic stroke within 1 year by univariate Cox regression, respectively with the c-statistics of 0.776 (95% CI, 0.594-0.903; P = 0.014) and 0.776 (95% CI, 0.594-0.903; P = 0.002) in receiver operating characteristic analysis.ConclusionsHemodynamics of ICAS on CFD models reconstructed from routinely obtained CTA images may predict subsequent stroke recurrence in patients with a symptomatic ICAS lesion of 70-99% luminal stenosis

Regulation of angiogenesis by Serum Amyloid A 1 (SAA1) isoforms via integrin signaling in esophageal squamous cell carcinoma

Session P4-12: Cancer-associated genes 2 (がん関連遺伝子 2): no. P-3059Conference Theme: Deeper insights into cancer biology bringing cures for cancer patient

Caries Management with Non-Metallic Nanomaterials: A Systematic Review

Veena Wenqing Xu, Mohammed Zahedul Islam Nizami, Iris Xiaoxue Yin, Christie Ying Kei Lung, Ollie Yiru Yu, Chun Hung Chu Faculty of Dentistry, The University of Hong Kong, Hong Kong, People’s Republic of ChinaCorrespondence: Chun Hung Chu, Faculty of Dentistry, The University of Hong Kong, 34 Hospital Road, Hong Kong, People’s Republic of China, Tel +852 2859 0287, Fax +852 2858 2532, Email [email protected]: Non-metallic nanomaterials do not stain enamel or dentin. Most have better biocompatibility than metallic nanomaterials do for management of dental caries.Objective: The objective of this study is to review the types, properties and potential uses of non-metallic nanomaterials systematically for managing dental caries.Methods: Two researchers independently performed a literature search of publications in English using PubMed, Scopus and Web of Science. The keywords used were (nanoparticles OR nanocomposites OR nanomaterials) AND (caries OR tooth decay). They screened the titles and abstracts to identify potentially eligible publications of original research reporting non-metallic nanomaterials for caries management. Then, they retrieved and studied the full text of the identified publications for inclusion in this study.Results: Out of 2497 resulting publications, this study included 75 of those. The non-metallic nanomaterials used in these publications were categorized as biological organic nanomaterials (n=45), synthetic organic nanomaterials (n=15), carbon-based nanomaterials (n=13) and selenium nanomaterials (n=2). They inhibited bacteria growth and/or promoted remineralization. They could be incorporated in topical agents (29/75, 39%), dental adhesives (11/75, 15%), restorative fillers (4/75, 5%), dental sealant (3/75, 4%), oral drugs (3/75, 4%), toothpastes (2/75, 3%) and functional candies (1/75, 1%). Other publications (22/75, 29%) do not mention specific applications. However, most publications (67/75, 89%) were in vitro studies. Six publications (6/75, 8%) were animal studies, and only two publications (2/75, 3%) were clinical studies.Conclusion: The literature showed non-metallic nanomaterials have antibacterial and/or remineralising properties. The most common type of non-metallic nanomaterials for caries management is organic nanomaterials. Non-metallic nanomaterials can be incorporated into dental sealants, toothpaste, dental adhesives, topical agents and even candies and drugs. However, the majority of the publications are in vitro studies, and only two publications are clinical studies.Keywords: nanomaterials, nanoparticles, caries, prevention, antibacterial, remineralisatio

SAA1 polymorphisms are associated with variation in antiangiogenic and tumor-suppressive activities in nasopharyngeal carcinoma

Nasopharyngeal carcinoma (NPC) is a cancer that occurs in high frequency in Southern China. A previous functional complementation approach and the subsequent cDNA microarray analysis have identified that serum amyloid A1 (SAA1) is an NPC candidate tumor suppressor gene. SAA1 belongs to a family of acute-phase proteins that are encoded by five polymorphic coding alleles. The SAA1 genotyping results showed that only three SAA1 isoforms (SAA1.1, 1.3 and 1.5) were observed in both Hong Kong NPC patients and healthy individuals. This study aims to determine the functional role of SAA1 polymorphisms in tumor progression and to investigate the relationship between SAA1 polymorphisms and NPC risk. Indeed, we have shown that restoration of SAA1.1 and 1.3 in the SAA1-deficient NPC cell lines could suppress tumor formation and angiogenesis in vitro and in vivo. The secreted SAA1.1 and SAA1.3 proteins can block cell adhesion and induce apoptosis in the vascular endothelial cells. In contrast, the SAA1.5 cannot induce apoptosis or inhibit angiogenesis because of its weaker binding affinity to αVβ3 integrin. This can explain why SAA1.5 has no tumor-suppressive effects. Furthermore, the NPC tumors with this particular SAA1.5/1.5 genotype showed higher levels of SAA1 gene expression, and SAA1.1 and 1.3 alleles were preferentially inactivated in tumor tissues that were examined. These findings further strengthen the conclusion for the defective function of SAA1.5 in suppression of tumor formation and angiogenesis. Interestingly, the frequency of the SAA1.5/1.5 genotype in NPC patients was ~2-fold higher than in the healthy individuals (P=0.00128, odds ratio=2.28), which indicates that this SAA1 genotype is significantly associated with a higher NPC risk. Collectively, this homozygous SAA1.5/1.5 genotype appears to be a recessive susceptibility gene, which has lost the antiangiogenic function, whereas SAA1.1 and SAA1.3 are the dominant alleles of the tumor suppressor phenotype