Do unexpected land auction outcomes bring new information to the real estate market?

Land and real estate are intrinsically related but generally traded in two different markets. Vacant land, being a major "raw material" for development of real estate, is traded by developers who actively manage development risk for profit. Real estate, being a long lived final product, is traded by end-users or investors for use or investment in the secondary market. This study examines price discovery between the two markets. The key question is whether land transactions, in the form of public auctions, convey any new information to the secondary real estate market. Our results suggest unexpected land auction outcomes have both market-wide and local effects on real estate prices. However, the impacts are asymmetric. We found that lower than expected land auction prices have a significant negative market-wide and local impact on real estate prices while higher than expect land auction prices have little or no impact. © Springer Science + Business Media, LLC 2009.published_or_final_versionSpringer Open Choice, 01 Dec 201

Multinationals FDI and uncertainty: A comment

This paper re-examines the model developed by Firoozi [Firoozi, F., 1997. Multinational FDI and uncertainty: an exposition. Journal of Multinational Financial Management 7, 265-273] to study foreign direct investment (FDI) by multinationals facing cost uncertainty. Firoozi shows that a mean-preserving-spread increase in cost uncertainty has an ambiguous effect on the optimal level of FDI. Contrary to his findings, we show that the FDI-uncertainty connection is de facto negative, confined to his model and under reasonable assumptions on multinationals' preferences.link_to_subscribed_fulltex

Liquidity risk and corporate hedging with futures

This paper examines the hedging behaviour of a value-maximizing firm that exists for two periods. The firm faces uncertain income and is subject to tax asymmetries with no loss-offset provisions. The firm has access to unbiased futures contracts in each period for hedging purposes. We impose a liquidity constraint on the firm. Specifically, whenever the net interim loss due to its first-period futures position exceeds a predetermined threshold level, the firm is forced to terminate its risk management program and, therefore, is prohibited from trading the futures contracts in the second period. We show that the liquidity-constrained firm optimally adopts a full-hedge via its second-period futures position to minimize the extent of the income risk and an under-hedge via its first-period futures position to limit the degree of the liquidity risk. © 2011 The Authors. Pacific Economic Review© 2011 Blackwell Publishing Asia Pty Ltd.link_to_subscribed_fulltex

An angiogenic function for E-cadherin in ovarian cancer

Meeting Theme: Harnessing Breakthroughs - Targeting CuresSession - Tumor Biology: Poster Presentations - Angiogenesis 1: Molecular and Cellular Mechanisms: abstract no. 9This journal suppl. entitled: Proceedings: AACR Annual Meeting 2014The loss of E-cadherin, a cell-cell adhesion molecule, is a well-established marker for metastasis of cancer. Although E-cadherin is synthesized as a transmembrane molecule, it can be cleaved of the ectodomain and released in a soluble form (sE-cad), and this accounts a key mechanism for a rapid reduction of functional E-cadherin at the cell surface. Yet, very little is known about how this important protein dictates the metastasis of these tumors. In ovarian cancer, a highly metastatic tumor that is rapidly lethal, sE-cad is highly expressed in the serum and metastatic ascites of ovarian carcinoma patients. Despite many studies focused on the role of E-cadherin loss in weakening cell-cell adhesion, whether sE-cad has biological activity in itself remain virtually unknown. Here we show for the first time that sE-cad can transduce angiogenic signals. sE-cad was also present in the culture supernatant of ovarian cancer lines. sE-cad of supernatant and a recombinant sE-cad-Fc chimera potently stimulated the migration of, permeability, and tubulogenesis by human umbilical vein endothelial cells in vitro. sE-cad also promoted functional neovascularization in a Matrigel implant model in vivo. These effects could be reversed by neutralizing anti-sE-cad, confirming that the effects were sE-cad specific. In addition, we found that sE-cad bound to VE-cadherin, an effect mediated through the phosphatidylinositol 3-kinase/Akt-β-catenin pathway. These results unravel a new and important piece to the complex biology of tumor angiogenesis and metastasis, and provide insights of novel mechanisms regulating angiogenesis. (This study was supported by RGC grant HKU781013). ©2014 American Association for Cancer Research

Loss of BRCA1 regulates autophagy as a cellular stress response in breast and ovarian cancer cells

Poster Session 1 - Autophagy and Altered Mitochondrial Function: abstract no. 3790Inactivation of cell death is a major step in tumor development. The BRCA1 tumor suppressor, which is frequently mutated in human breast and ovarian cancers, is a critical mediator of cell death. Although the role of BRCA1 gene loss for inhibiting apoptosis is well established, little is known regarding its ...link_to_OA_fulltextThe 102nd Annual Meeting of American Association for Cancer Research (AACR), Orlando, FL., 2-6 April 2011

An angiogenic role of E-cadherin-positive exosomes in ovarian cancer

This journal suppl. entitled: Proceedings: AACR 106th Annual Meeting 2015Session - Molecular and Cellular Biology: Poster session - Cell Signaling in Cancer 2: abstract no. 1035Meeting Theme: Bringing Cancer Discoveries to PatientsAngiogenesis, the induction of vasculature, is a vital step for metastasis. Loss of E-cadherin is a well-established marker for tumor metastasis. In ovarian cancer, a highly metastatic tumor that is rapidly lethal, we and others have previously shown the deregulated pattern of E-cadherin and its close association with tumor progression. Although E-cadherin is synthesized as a transmembrane molecule, it can be shed from the cell surface (sE-cad) which accounts for a rapid removal of functional E-cadherin. Here, in addition to ectodomain shedding, we show for the first time that sE-cad can be actively released from ovarian cancer cells in the form of exosomes. These sE-cad-positive exosomes play a critical role in angiogenesis which stimulated the migration, permeability, and tubulogenesis of human umbilical vein endothelial cells in vitro, and promoted functional neovascularization in vivo. In search of the underlying mechanisms by which sE-cad-positive exosomes might regulate angiogenic endothelial cells, which lack E-cadherin, we showed that a novel heterophilic crosstalk between sE-cad and VE-cadherin. Moreover, such angiogenic effect was mediated through activation of the phosphatidylinositol 3-kinase/Akt-beta-catenin signaling cascade. These results uncover a new angiogenic function for sE-cad and a novel paradigm for sE-cad production which may have potential clinical implications (This study was supported by RGC grant HKU781013). ©2015 American Association for Cancer Research

Mergers and investments in cost reduction with private information revisited

This paper re-examines the model developed by Stenbacka (1991) which addresses the investment incentives of an innovating firm operating in anticipation of a merger with its rival in a Cournot duopoly setting. In contrast to Stenbacka, we find that the innovating firm need not always invest more should it conceal rather than reveal its R&D outcome prior to the takeover. Furthermore, we show that the ex ante incentive for the innovating firm to conceal its private information is perfectly consistent with earlier findings in the information sharing literature. (C) 1997 Published by Elsevier Science B.V

c-Met overexpression contributes to the acquired apoptotic resistance of nonadherent ovarian cancer cells through a cross talk mediated by phosphatidylinositol 3-kinase and extracellular signal-regulated kinase 1/2

Ovarian cancer is the most lethal gynecologic cancer mainly because of widespread peritoneal dissemination and malignant ascites. Key to this is the capacity of tumor cells to escape suspension-induced apoptosis (anoikis), which also underlies their resistance to chemotherapy. Here, we used a nonadherent cell culture model to investigate the molecular mechanisms of apoptotic resistance of ovarian cancer cells that may mimic the chemoresistance found in solid tumors. We found that ovarian cancer cells acquired a remarkable resistance to anoikis and apoptosis induced by exposure to clinically relevant doses of two front-line chemotherapeutic drugs cisplatin and paclitaxel when grown in three-dimensional than monolayer cultures. Inhibition of the hepatocyte growth factor (HGF) receptor c-Met, which is frequently overexpressed in ovarian cancer, by a specific inhibitor or small interfering RNA blocked the acquired anoikis resistance and restored chemosensitivity in three-dimensional not in two-dimensional cultures. These effects were found to be dependent on both phosphatidylinositol 3-kinase (PI3K)/Akt and extracellular signal-regulated kinase (ERK) 1/2 signaling pathways. Inhibitors of PI3K/Akt abrogated ERK1/2 activation and its associated anoikis resistance in response to HGF, suggesting a signaling relay between these two pathways. Furthermore, we identified a central role of Ras as a mechanism of this cross talk. Interestingly, Ras did not lie upstream of PI3K/Akt, whereas PI3K/Akt signaling to ERK1/2 involved Ras. These findings shed new light on the apoptotic resistance mechanism of nonadherent ovarian cancer ascites cells and may have important clinical implications. Copyright © 2010 Neoplasia Press, Inc. All rights reserved.link_to_OA_fulltex

c-Met overexpression contributes to the acquired apoptosis resistance of non-adherent ovarian cancer cells through a cross-talk mediated by phosphatidylinositol 3-kinase and extracellular signal-regulated kinase 1/2

Poster Session 29 - Receptor Signaling in Endocrine Related Cancers: abstract no. 1722Ovarian cancer is the most lethal gynecological cancer mainly due to widespread peritoneal dissemination and malignant ascites. Key to this is the capacity of tumor cells to escape suspension-induced apoptosis (anoikis), which also underlies their resistance to chemotherapy. Here we utilized a non-adherent cell culture model to investigate molecular mechanisms of apoptotic resistance of ovarian cancer cells that may mimic the chemoresistance found in solid tumors. We found that ovarian cancer cells acquired a remarkable resistance to anoikis and apoptosis induced by exposure to clinically relevant doses of two front-line chemotherapeutic drugs cisplatin and paclitaxel when grown in three-dimensional (3D) than monolayer cultures. Inhibition of the hepatocyte growth factor (HGF) receptor c-Met, which is frequently overexpressed in ovarian cancer, by a specific inhibitor or small interfering RNA blocked the acquired anoikis resistance and restored chemosensitivity in 3D, not in 2D cultures. These effects were found to be dependent on both phosphatidylinositol 3-kinase (PI3K)/Akt and extracellular-signal regulated kinase (ERK) 1/2 signaling pathways. Inhibitors of PI3K/Akt abrogated ERK1/2 activation and its associated anoikis resistance in response to HGF, suggesting a signaling relay between these two pathways. Furthermore, we identified, as a mechanism of this cross-talk, a central role of Ras. Interestingly, Ras did not lie upstream of PI3K/Akt, whereas PI3K/Akt signaling to ERK1/2 involved Ras. These findings shed new light on the apoptotic resistance mechanism of non-adherent ovarian cancer ascites cells.link_to_OA_fulltextThe 101st Annual Meeting of the American Association for Cancer Research (AACR 2010), Washington D.C., 17-21 April 2010. In AACR Meeting Abstracts, 201

Age of Helicobacter pylori Eradication and Subsequent Risk of Gastric Cancer Development: A Population-Based Study

Presentation Number: 97