1,721,198 research outputs found
CARATTERIZZAZIONE MOLECOLARE DELLA FARMACO-RESISTENZA IN PAZIENTI NAIVE CON EPATITE CRONICA B TRATTATI CON ENTECAVIR
No full textLONG-TREATMENT OF ENTECAVIR IN NUCLEOSIDE-NAÏVE PATIENTS WITH CHRONIC HEPATITIS B INFECTION
The nucleoside analogue (NUC) entecavir (ETV) is a first line option for NUC-naïve patients with chronic hepatitis B, with a remarkable record of efficacy and safety in registration trials, but limited validation in field practice. Aim: to assess the outcome of ETV therapy in real life, previously untreated patients with chronic hepatitis B. Methods: 119 NUC-naïve patients with chronic hepatitis B (57 years, 75% HBeAg negative, 54% cirrhosis), consecutively recruited in A. M. Centro Migliavacca Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, University of Milan, Milan, were treated with ETV 0.5 mg for 36 months. Clinical, laboratory and virology (HBV DNA (LLQ < 12 IU/mL) surveillance was performed every 3 months while the RT resistance pattern was looked for by INNO-LiPA V2-3 at baseline and every 3 months. Results: serum HBV DNA became undetectable in 80% , 93% and 97% of the patients at week 48, 96 and 144, respectively, with time to virological response being significantly affected by baseline viremia (p<0.001). The 96-week cumulative probability of HBV DNA undetectable (< 12 IU/mL ) was 98% in patients without baseline mutations and 93% in patients with baseline mutations. No patient had to discontinue ETV for serious adverse events. Conclusions: ETV monotherapy efficiently suppresses HBV in the vast majority of real-life, NUC-naïve patients with chronic hepatitis B, independently on initial HBeAg status and cirrhosis
Cancer stem cells and therapeutic perspectives
No full textThe cancer stem cell hypothesis suggests that neoplastic clones are maintained exclusively by a rare fraction of cells with stem cell proprieties. Stem cells are defined as cells which are able to both extensively self-renew and differentiate into progenitors. Furthermore, stem cells are also attractive candidates as origin of cancers, as in their long lifespan mutations and epigenetic changes they can increase allowing for increasing evolution toward malignancy.
Herein, we discuss the evidences reported in literature on existence of cancer stem cells in several tumors and mechanisms of the extrinsic and intrinsic circuitry controlling stem cell fate as well as their possible connections to cancer. In particular, the review will focus on recent results on conserved Polycomb Group (PcG) gene family, an epigenetic chromatin modifiers involved in cancer development and also in the maintenance of embryonic and adult stem cells. There are two distinct multiprotein PcG complexes identified, Polycomb repressive complex (PRC) 1 and 2. The fact that either PRC1 Bmil than PRC2 SU(Z)12 components are implicated in self-renewal stem cells and up-regulated in several kind of human cancer, confirm the importance of (dc)regulation of the PcG genes in cancer and stem cell biology. Moreover, Bmil and SU(Z)12 are downstream target of Sonic hedgehog (Shh) and Writ signaling respectively, providing for a connection between epigenetic change regulators (PcG) and developmental-signaling pathways.
Finally, potential therapies using inhibitors acting on cancer stem cell population such as cyclopamine, an inhibitor of hedgehog signalling, 6-bromoindirubin-3'-oxime (BIO) which acts on GSK3 and inhibitors of beta-catenin signaling such as exisulind and the tyrosine-kinase inhibitor ST1571/Gleevac/imatinib will also discuss
New perspectives in the treatment of melanoma : anti-angiogenic and anti-lymphoangiogenic strategies
No full textMelanoma is a significant, worldwide growing public health burden. Single-agent chemotherapy or immunotherapy remains the treatment of election for this disease when systemic therapy is offered. Malignant melanoma of the skin is distinguished by its capability to early metastatic spread by means of lymphatic vessels to regional lymph nodes. Herein new accomplishments on the role of lymphangiogenesis and of angiogenesis in cutaneous melanoma will be discussed, together with the possible application of these discoveries in developing prognostic and therapeutic tools in melanoma metastasis. Furthermore, the present review will summarize the main angiogenic inhibitors reported in the recent patents (2003-2005), with special emphasis on the aspects which have important implications for the prognosis and the treatment of human melanomas
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Failure of adefovir 20 mg to improve suboptimal response in lamivudine resistant hepatitis B patients treated with adefovir 10 mg and lamivudine
No full textNine patients with lamivudine-resistant chronic hepatitis B infection who had been treated with adefovir 10 mg/day and had had a suboptimal response but did not have genotypic resistance to adefovir were treated with high-dose adefovir (20 mg/day). The response to the increased dose of adefovir was compared with the response in 15 patients with a suboptimal response who did not receive an increase in the dose of adefovir. The increase in the dose of adefovir did not lead to a significant reduction in hepatitis B DNA when compared with patients maintained on the standard dose. These data suggest that increasing the dose of adefovir in patients with a suboptimal response does not lead to an improved response
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