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Synergy between molecular biology and imaging science toward mechanism-based biomarkers associated with prostate cancer  [PDF]
Belinda Seto
Journal of Biomedical Science and Engineering (JBiSE) , 2012, DOI: 10.4236/jbise.2012.512A107

Prostate cancer is a heterogeneous disease with subtypes that are characterized by different molecular profiles as a result of chromosomal rearrangements, epigenetic modifications, and activation of various signaling pathways. The subtype heterogeneity contributes to the challenges with a definitive diagnosis and biomarkers for disease progression. The current diagnostic test based on the detection of prostate specific antigen lacks sensitivity and specificity. Imaging plays an important role in characterizing biomarkers and elucidating the underlying molecular mechanisms. For example, 18F-fluoro-2-deoxy glucose is commonly used to assess cancer cell metabolism. More recently, magnetic resonance spectroscopic observations of the in vivo dynamic conversion of hyperpolarized 13C- pyruvate to lactate demonstrate that imaging enables the visualization of molecular processes. Biomarkers have also been developed that reveal aberrant cell growth and proliferation, both hallmarks of cancer. Androgen dependent and independent signaling path- ways underpin prostate cancer pathogenesis as they lead to downstream effect in cell growth, proliferation, survival, and suppression of apoptosis. Molecular imaging with radiolabeled ligands and positron emission tomography/computed tomography has provided quantitative characterization of the interactions between receptors and testosterone or growth factors. These observations, along with data on genetic alterations of the receptor genes, shed light on signal transduction involved in prostate cancer. This review article highlights advances in the understanding of the molecular mechanisms of prostate cancer and the synergy of this knowledge with imaging in characterizing potential biomarkers of the disease.

Isoform-Specific Potentiation of Stem and Progenitor Cell Engraftment by AML1/RUNX1
Shinobu Tsuzuki ,Dengli Hong,Rajeev Gupta,Keitaro Matsuo,Masao Seto,Tariq Enver
PLOS Medicine , 2007, DOI: 10.1371/journal.pmed.0040172
Abstract: Background AML1/RUNX1 is the most frequently mutated gene in leukaemia and is central to the normal biology of hematopoietic stem and progenitor cells. However, the role of different AML1 isoforms within these primitive compartments is unclear. Here we investigate whether altering relative expression of AML1 isoforms impacts the balance between cell self-renewal and differentiation in vitro and in vivo. Methods and Findings The human AML1a isoform encodes a truncated molecule with DNA-binding but no transactivation capacity. We used a retrovirus-based approach to transduce AML1a into primitive haematopoietic cells isolated from the mouse. We observed that enforced AML1a expression increased the competitive engraftment potential of murine long-term reconstituting stem cells with the proportion of AML1a-expressing cells increasing over time in both primary and secondary recipients. Furthermore, AML1a expression dramatically increased primitive and committed progenitor activity in engrafted animals as assessed by long-term culture, cobblestone formation, and colony assays. In contrast, expression of the full-length isoform AML1b abrogated engraftment potential. In vitro, AML1b promoted differentiation while AML1a promoted proliferation of progenitors capable of short-term lymphomyeloid engraftment. Consistent with these findings, the relative abundance of AML1a was highest in the primitive stem/progenitor compartment of human cord blood, and forced expression of AML1a in these cells enhanced maintenance of primitive potential both in vitro and in vivo. Conclusions These data demonstrate that the “a” isoform of AML1 has the capacity to potentiate stem and progenitor cell engraftment, both of which are required for successful clinical transplantation. This activity is consistent with its expression pattern in both normal and leukaemic cells. Manipulating the balance of AML1 isoform expression may offer novel therapeutic strategies, exploitable in the contexts of leukaemia and also in cord blood transplantation in adults, in whom stem and progenitor cell numbers are often limiting.
Functionally Deregulated AML1/RUNX1 Cooperates with BCR-ABL to Induce a Blastic Phase-Like Phenotype of Chronic Myelogenous Leukemia in Mice
Kiyoko Yamamoto, Shinobu Tsuzuki, Yosuke Minami, Yukiya Yamamoto, Akihiro Abe, Koichi Ohshima, Masao Seto, Tomoki Naoe
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0074864
Abstract: Patients in the chronic phase (CP) of chronic myelogenous leukemia (CML) have been treated successfully following the advent of ABL kinase inhibitors, but once they progress to the blast crisis (BC) phase the prognosis becomes dismal. Although mechanisms underlying the progression are largely unknown, recent studies revealed the presence of alterations of key molecules for hematopoiesis, such as AML1/RUNX1. Our analysis of 13 BC cases revealed that three cases had AML1 mutations and the transcript levels of wild-type (wt.) AML1 were elevated in BC compared with CP. Functional analysis of representative AML1 mutants using mouse hematopoietic cells revealed the possible contribution of some, but not all, mutants for the BC-phenotype. Specifically, K83Q and R139G, but neither R80C nor D171N mutants, conferred upon BCR-ABL-expressing cells a growth advantage over BCR-ABL-alone control cells in cytokine-free culture, and the cells thus grown killed mice upon intravenous transfer. Unexpectedly, wt.AML1 behaved similarly to K83Q and R139G mutants. In a bone marrow transplantation assay, K83Q and wt.AML1s induced the emergence of blast-like cells. The overall findings suggest the roles of altered functions of AML1 imposed by some, but not all, mutants, and the elevated expression of wt.AML1 for the disease progression of CML.
Genomic Profiling of Oral Squamous Cell Carcinoma by Array-Based Comparative Genomic Hybridization
Shunichi Yoshioka, Yoshiyuki Tsukamoto, Naoki Hijiya, Chisato Nakada, Tomohisa Uchida, Keiko Matsuura, Ichiro Takeuchi, Masao Seto, Kenji Kawano, Masatsugu Moriyama
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0056165
Abstract: We designed a study to investigate genetic relationships between primary tumors of oral squamous cell carcinoma (OSCC) and their lymph node metastases, and to identify genomic copy number aberrations (CNAs) related to lymph node metastasis. For this purpose, we collected a total of 42 tumor samples from 25 patients and analyzed their genomic profiles by array-based comparative genomic hybridization. We then compared the genetic profiles of metastatic primary tumors (MPTs) with their paired lymph node metastases (LNMs), and also those of LNMs with non-metastatic primary tumors (NMPTs). Firstly, we found that although there were some distinctive differences in the patterns of genomic profiles between MPTs and their paired LNMs, the paired samples shared similar genomic aberration patterns in each case. Unsupervised hierarchical clustering analysis grouped together 12 of the 15 MPT-LNM pairs. Furthermore, similarity scores between paired samples were significantly higher than those between non-paired samples. These results suggested that MPTs and their paired LNMs are composed predominantly of genetically clonal tumor cells, while minor populations with different CNAs may also exist in metastatic OSCCs. Secondly, to identify CNAs related to lymph node metastasis, we compared CNAs between grouped samples of MPTs and LNMs, but were unable to find any CNAs that were more common in LNMs. Finally, we hypothesized that subpopulations carrying metastasis-related CNAs might be present in both the MPT and LNM. Accordingly, we compared CNAs between NMPTs and LNMs, and found that gains of 7p, 8q and 17q were more common in the latter than in the former, suggesting that these CNAs may be involved in lymph node metastasis of OSCC. In conclusion, our data suggest that in OSCCs showing metastasis, the primary and metastatic tumors share similar genomic profiles, and that cells in the primary tumor may tend to metastasize after acquiring metastasis-associated CNAs.
Asset Pricing with Stochastic Habit Formation  [PDF]
Masao Nakagawa
Journal of Mathematical Finance (JMF) , 2012, DOI: 10.4236/jmf.2012.22018
Abstract: This paper examines optimal consumption/portfolio choices under stochastic habit formation in which it is uncertain how deep consumers would become in the habit of consuming in future. By extending Shroder and Skiadas [1] to stochastic habit formation, the optimization problem with stochastic habit forming preferences is transformed into that with simple time-additive preferences. Optimal portfolios are composed of the tangency portfolio and habit hedging portfolio. Resulting risk premia are characterized by consumption beta, which is proportionate to the covariance with consumption changes, and habit beta, defined by using the covariance with habit.
Novel Cathode Materials for Sodium Ion Batteries Derived from Layer Structured Titanate Cs2Ti5O11·(1 + x)H2O  [PDF]
Masao Ohashi
Materials Sciences and Applications (MSA) , 2018, DOI: 10.4236/msa.2018.96037
Abstract: A layer structured titanate Cs2Ti5O11·(1 + x)H2O (x = 0.70) has been prepared in a solid state reaction using Cs2CO3 and anatase type TiO2 at 900°C. Ion exchange reactions of Cs+ in the interlayer space were studied in aqueous solutions. The single phases of Li+, Na+ and H+ exchange products were obtained. The three kinds of resulting titanates were evaluated for use as the cathodes in rechargeable sodium batteries after dehydrations by heating at 200°C in a vacuum. The electrochemical measurements showed that they exhibited the reversible Na+ intercalation-deintercalation in a voltage range of 0.5 - 3.5 V or 0.7 - 4.0 V. The Li+ exchange product showed the best performance of the discharge-charge capacities in this study. The initial Na+ intercalation-deintercalation capacities of the Li2Ti5O11 were 120 mAh/g and 100 mAh/g; the amounts of Na+ correspond to 1.9 and 1.6 of the formula unit, respectively. The titanates are nontoxic, inexpensive and environmentally benign.
Ion Exchange of Layer-Structured Titanate CsxTi2-x/2Mgx/2O4 (x = 0.70) and Applications as Cathode Materials for Both Lithium- and Sodium-Ion Batteries  [PDF]
Masao Ohashi
Materials Sciences and Applications (MSA) , 2019, DOI: 10.4236/msa.2019.102012
Abstract: Cathode materials for rechargeable batteries have been extensively investigated. Sodium-ion batteries are emerging as alternatives to lithium-ion batteries. In this study, a novel cathode material for both lithium- and sodium-ion batteries has been derived from a layered crystal. Layer-structured titanate CsxTi2-x/2Mgx/2O4 (x = 0.70) with lepidocrocite (γ-FeOOH)-type structure has been prepared in a solid-state reaction from Cs2CO3, anatase-type TiO2, and MgO at 800°C. Ion-exchange reactions of Cs+ in the interlayer space were studied in aqueous solutions. The single phases of Li+, Na+, and H+ exchange products were obtained, and these were found to contain interlayer water. The interlayer water in the lithium ion-exchange product was removed by heating at 180°C in vacuum. The resulting titanate Li0.53H0.13Cs0.14Ti1.65Mg0.30O4 was evaluated for use as cathodes in both rechargeable lithium and sodium batteries. The Li+ intercalation-deintercalation capacities were found to be 151 mAh/g and 114 mAh/g, respectively, for the first cycle in the voltage range 1.0 - 3.5 V. The amounts of Li+ corresponded to 0.98 and 0.74 of the formula unit, respectively. The Na+ intercalation-deintercalation capacities were 91 mAh/g and 77 mAh/g, respectively, for the first cycle in the voltage range 0.70 - 3.5 V. The amounts of Na+ corresponded to 0.59 and 0.50 of the formula unit, respectively. The new cathode material derived from the layer-structured titanate is non-toxic, inexpensive, and environmentally benign.
Downregulation of SAV1 plays a role in pathogenesis of high-grade clear cell renal cell carcinoma
Keiko Matsuura, Chisato Nakada, Mizuho Mashio, Takahiro Narimatsu, Taichiro Yoshimoto, Masato Tanigawa, Yoshiyuki Tsukamoto, Naoki Hijiya, Ichiro Takeuchi, Takeo Nomura, Fuminori Sato, Hiromitsu Mimata, Masao Seto, Masatsugu Moriyama
BMC Cancer , 2011, DOI: 10.1186/1471-2407-11-523
Abstract: We performed array CGH and gene expression analysis of 8 RCC cell lines (786-O, 769-P, KMRC-1, KMRC-2, KMRC-3, KMRC-20, TUHR4TKB, and Caki-2), and expression level of mRNA was confirmed by quantitative RT-PCR (qRT-PCR) analysis. We next re-expressed SAV1 in 786-O cells, and analyzed its colony-forming activity. Then, we transfected siRNAs of SAV1 into the kidney epithelial cell line HK2 and renal proximal tubule epithelial cells (RPTECs), and analyzed their proliferation and apoptosis. Furthermore, the activity of YAP1, which is a downstream molecule of SAV1, was evaluated by western blot analysis, reporter assay and immunohistochemical analysis.We found that SAV1, a component of the Hippo pathway, is frequently downregulated in high-grade ccRCC. SAV1 is located on chromosome 14q22.1, where copy number loss had been observed in 7 of 12 high-grade ccRCCs in our previous study, suggesting that gene copy number loss is responsible for the downregulation of SAV1. Colony-forming activity by 786-O cells, which show homozygous loss of SAV1, was significantly reduced when SAV1 was re-introduced exogenously. Knockdown of SAV1 promoted proliferation of HK2 and RPTEC. Although the phosphorylation level of YAP1 was low in 786-O cells, it was elevated in SAV1-transduced 786-O cells. Furthermore, the transcriptional activity of the YAP1 and TEAD3 complex was inhibited in SAV1-transduced 786-O cells. Immunohistochemistry frequently demonstrated nuclear localization of YAP1 in ccRCC cases with SAV1 downregulation, and it was preferentially detected in high-grade ccRCC.Taken together, downregulation of SAV1 and the consequent YAP1 activation are involved in the pathogenesis of high-grade ccRCC. It is an attractive hypothesis that Hippo signaling could be candidates for new therapeutic target.Renal cell carcinoma (RCC) is histopathologically subdivided into various categories, of which clear cell renal cell carcinoma (ccRCC) is the most common subtype, accounting for 70-80% of all RC
Rapamycin and mTOR: a serendipitous discovery and implications for breast cancer
Belinda Seto
Clinical and Translational Medicine , 2012, DOI: 10.1186/2001-1326-1-29
Abstract: Breast cancer is the second most commonly diagnosed cancer, after skin cancer, among U.S. women. In 2012, 227,000 new cases have been reported [1]. Recent developments in computed tomography imaging have improved the early detection of breast cancer, when treatment is most effective [2]. Concomitant with the technological development is the explosion of research findings on the molecular mechanisms of breast cancer. As a result, mechanism-based approaches have become increasingly used as strategies for therapeutic developments. This confluence of technology development in early diagnosis and improved therapeutics has led to a decline in breast cancer death in recent years, although death rates are still higher than all types of cancer other than lung cancer [3].This report describes a tale of discovery that reinforces the serendipitous nature of basic research and the notion that discoveries may lead to unanticipated outcomes in other disciplines. In this particular story, the isolation of the bacterium Streptomyces hygroscopicus from a soil sample three decades ago on a remote island led to intense, multifaceted research that changed the way breast cancer is treated. The identification of rapamycin from Streptomyces hygroscopicus as an antifungal agent, through being an immune inhibitor to being an effective anticancer drug, demonstrates a research continuum driven by clinical observations that were critical in the elucidation of the mTOR pathway. Rapamycin provided the stimulus for research on the complex and pivotal mTOR pathway that transmits signals through which it controls a range of vital biological processes. The dissection of the molecular networks of interacting signaling pathways has led to improved understanding of the transcription, protein synthesis, and metabolic processes that underpin oncogenic transformation. Such knowledge has led to therapeutic developments that yielded targeted drugs for breast cancer patients. For patients who are estrogen and
Viral Genomics and Bioinformatics
Donald Seto
Viruses , 2010, DOI: 10.3390/v2122587
Abstract: From the recognition by Ivanovski in 1892 that tobacco mosaic disease is caused and transmitted by fine pore filtrates [1], viruses have been isolated, characterized, identified and studied from animals, plants, protists, bacteria and even other viruses [2,3]. As human and global public health pathogens that can be highly contagious and have devastating morbidity and mortality consequences, viruses are the focus of much research. The difficult challenge has been to define and study a miniscule “being” with the appropriate tools. In the past, these tools often provided only low-resolution views. A first approach to studying an unknown virus is to know exactly its identity, and to place it into context of other related and non-related viruses. For human and public health, this is important as the identity may provide a course of action to limit the effects of the pathogen. [...]
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