also found that M-CSF+ monocyte chemoattractant protein-1 and formyl peptide receptor-2 agonists skewed macrophages into an IL-10lowIL-12high M2 profile through modulating the phosphorylation of signal transducer and activator of transcription-3 which exacerbated HCC invasion in vitro and in vivo.[7] More recently, Pan et al. showed that signal regulatory protein-α (SIRP-α) functioned as an important modulator of TAM phenotypic switch in hepatoma

and tumor-derived factors, for example, CSF-1 induced downregulation selleckchem of SIRP-α expression on Mφ, followed by promoting their migration to the tumor which was associated with progression of HCC.[8] More interestingly, Ding et al. showed that distinct activation patterns of TAM in different areas of tumor tissue from patients with HCC, implied that macrophages in those areas may use different strategies to promote the tumor progression and macrophage density may predict the prognosis of HCC patients.[9] Thus, it markedly adds to the information to understand the future relevance of TAM and HCC tumor lesions in the clinical application. In summary, the aforementioned

findings have triggered efforts to target TAM and their associated molecules to modulate pathogenesis of HCC. Finally, it is clear that inhibition of M-CSF/CSF-1 to eliminate the M2-like TAM or switch it to M1-like TAM may have potential in designing novel anticancer strategies for HCC therapy. “
“The availability of seven approved therapies, including five oral

drugs, for chronic hepatitis B has expanded AP24534 ic50 the indications for treatment. The decision to initiate treatment is easy in patients with liver failure, but there continues to be debate regarding when treatment should be initiated in patients with precirrhotic liver disease.1, 2 Recognizing that liver biopsy is not performed 上海皓元医药股份有限公司 on all patients with chronic hepatitis B, the guidelines of the American Association for the Study of Liver Diseases (AASLD)3, 4 and the Asian Pacific Association for the Study of the Liver (APASL)5 primarily rely on alanine aminotransferase (ALT) levels to guide treatment decisions. The AASLD and APASL guidelines recommend treatment for patients with an ALT level higher than 2 times the upper limit of normal (ULN) range and liver biopsy to guide treatment decisions for patients with an ALT level 1 to 2 times ULN, particularly if they are above the age of 40 years. The guidelines of the European Association for the Study of the Liver place more emphasis on liver histology; they recommend treatment for patients with at least a Metavir activity grade of A2 (range = 0-3) or a Metavir fibrosis score of F2 (range = 0-4).6 All three guidelines recommend that patients who are deemed not to be treatment candidates at presentation be monitored so that treatment can be initiated later when the liver disease becomes more active.