Current Therapeutic Strategies (current + therapeutic_strategy)

Distribution by Scientific Domains


Selected Abstracts


Liver cancer stem cells: implications for a new therapeutic target

LIVER INTERNATIONAL, Issue 7 2009
Terence Kin Wah Lee
Abstract Hepatocellular carcinoma (HCC) is an aggressive tumour with a poor prognosis. Current therapeutic strategies against this disease target mostly rapidly growing differentiated tumour cells. However, the result is often dismal due to the chemoresistant nature of this tumour type. Recent research efforts on stem cells and cancer biology have shed light on new directions for the eradication of cancer stem cells (CSCs) in HCC. The liver is a distinctive organ with the ability of tissue renewal in response to injury. Based on the hypothesis that cancer development is derived from the hierarchy of the stem cell system, we will briefly discuss the origin of liver stem cells and its relation to HCC development. We will also summarize the current CSC markers in HCC and discuss their relevance to the treatment of this deadly disease. [source]


New insights into the regulation of iron homeostasis

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 5 2006
R. Deicher
Abstract Hepcidin evolves as a potent hepatocyte-derived regulator of the body's iron distribution piloting the flow of iron via, and directly binding, to the cellular iron exporter ferroportin. The hepcidin-ferroportin axis dominates the iron egress from all cellular compartments that are critical to iron homeostasis, namely placental syncytiotrophoblasts, duodenal enterocytes, hepatocytes and macrophages of the reticuloendothelial system. The gene that encodes hepcidin expression (HAMP) is subject to regulation by proinflammatory cytokines, such as IL-6 and IL-1; excessive hepcidin production explains the relative deficiency of iron during inflammatory states, eventually resulting in the anaemia of inflammation. The haemochromatosis genes HFE (the human leukocyte antigen-related gene), TfR2 (the transferrin receptor-2 gene) and HJV (the haemojuvelin gene) potentially facilitate the transcription of HAMP. Disruption of each of the four genes leads to a diminished hepatic release of hepcidin consistent with both a dominant role of hepcidin in hereditary haemochromatosis and an upstream regulatory role of HFE, TfR2 and HJV on HAMP expression. The engineered generation of hepcidin agonists, mimetics or antagonists could largely broaden current therapeutic strategies to redirect the flow of iron. [source]


Multifunctional host defense peptides: antiparasitic activities

FEBS JOURNAL, Issue 22 2009
Amram Mor
Whereas significant knowledge is accumulating on the antibacterial and antifungal properties of host defense peptides (HDPs) and their synthetic mimics, much less is known of their activities against parasites. A variety of in vitro and in vivo antiparasitic assays suggest that these notorious antimicrobial compounds could represent a powerful tool for the development of novel drugs to fight parasites in the vertebrate host or to complement current therapeutic strategies, albeit the fact that HDPs essentially act by nonspecific mechanisms casts serious doubt on their ability to exert sufficient selectivity to be considered ideal candidates for drug development. This minireview summarizes recent efforts to assess the antiparasitic properties of HDPs and their synthetic derivatives, focusing on two of the most used models ,Plasmodium and Leishmania species , for antiparasitic assays against the different development stages. [source]


Peripheral T-cell lymphomas, unspecified (or not otherwise specified): a review

HEMATOLOGICAL ONCOLOGY, Issue 1 2008
Delvys Rodriguez-Abreu
Abstract Peripheral T-cell lymphomas (PTCL) comprises a heterogeneous group of haematological tumours, which originate from mature T-cells, and constitute less than 15% of all non-Hodgkin's lymphomas (NHLs) in adults. The current WHO classification recognizes nine distinct clinicopathologic peripheral T-cell NHLs, being the ,unspecified variant' (PTCL-U) the most common subtype. These neoplasms often present in advanced stage at diagnosis, and most commonly have an aggressive clinical course requiring prompt treatment. The rarity of these tumours requires additional studies to better understand their biology and search for new therapies which may hopefully improve the dismal outcome of most patients. This review aims to describe the pathobiological aspects as well the clinical characteristics and current therapeutic strategies of the PTCLs, with special attention to the group of PTCL-U Copyright 2007 John Wiley & Sons, Ltd. [source]


REVIEW: An Approach for Neuroprotective Therapies of Secondary Brain Damage after Excitotoxic Retinal Injury in Mice

CNS: NEUROSCIENCE AND THERAPEUTICS, Issue 5 2010
Yasushi Ito
SUMMARY Background: Many current therapeutic strategies for several eye diseases, such as glaucoma, retinal ischemia, and optic neuropathy, are focused on protection of the retinal ganglion cells (RGCs). In fact, loss of visual field, including irreversible blindness, is caused by RGC damage in these diseases. However, recent evidence suggests that the RGC damage extends to visual center in brain: the visual impairment induced by these diseases may result not only from RGC loss, but also from neuronal degeneration within the visual center in brain. Objective: To protect neurons within the visual center in the brain, as well as retinal treatment, for the prevention of visual disorder in these diseases. Methods: Once considered difficult to study the visual center in brain following RGCs loss, because obtaining the human samples that are suitable for the study may be difficult. In addition, the monkey, mainly used as glaucomatous model, is relatively high cost and needs to long experiment-span. Here, we focused on mice, because of their high degree of availability, relatively low cost, and amenability to experimental and genetic manipulation. Conclusion: In this review, we describe time-dependent alterations in the visual center in brain following RGCs loss, and whether some drugs prevent the neuronal damage of the visual center in the brain. [source]