PubMedCrossRef Tucidinostat 43. Higham CE, Chung TT, Lawrance J, Drake WM, Trainer PJ: Long-term experience of pegvisomant therapy as a treatment for acromegaly. Clin Endocrinol (Oxf) 2009,71(1):86–91.CrossRef 44. Marazuela M, Paniagua AE,

Gahete MD, Lucas T, Alvarez-Escolá C, Manzanares R, Cameselle-Teijeiro J, Luque-Ramirez M, Luque RM, Fernandez-Rodriguez E, Castaño JP, Bernabeu I: Somatotroph tumor progression during pegvisomant therapy: a clinical and molecular study. J Clin Endocrinol Metabol 2011,96(2):E251-E259.CrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions AB and LDM had the idea for this research, took responsibility for the design of this work and wrote the manuscript. AB and FV performed all statistical analyses. FV, RI, MP, RB, MP, AG, LT, SC have made substantial contributions in acquisition of data, laboratory analyses and interpretation of data for each involved center. MA, PG, AF,

VT, AP have been involved in revising critically the manuscript see more and have given final approval of the version to be published.”
“Background Hepatocellular carcinoma is the sixth most common malignancy and the third most common cause of cancer-related death worldwide [1], but the disease progression of HCC remains poorly understood. A previous study showed that the local tumor immune microenvironment plays an important role in cancer suppression and promotion and that one of the main TEW-7197 cost factors leading to tumor immune tolerance in the local tumor microenvironment is the influence of CD4+/CD25+/FOXP3+ regulatory T cells (Tregs) [2]. The number of Tregs increases in response to infection by pathogenic microorganisms, including the hepatitis B virus; this increase inhibits CD4+ and CD8+ T-cell activation, proliferation and cytokine secretion, thus affecting the host immune response to infection and leading to chronic infection [3–6]. This phenomenon indicates that the FOXP3 gene may play a role in inflammation and chronic infections such as hepatitis B, which HAS1 may increase the risk of carcinoma. FOXP3 is a specific molecular marker

of Tregs that plays an important role in the development of Tregs and their inhibitory functions [7, 8]. Increased levels of FOXP3+ Tregs in the peripheral blood and tumor tissue have been reported in patients with various types of cancer, including ovarian [9, 10], breast [11], hepatocellular carcinoma [12] and other tumors [13]; the accumulation of Tregs in local lymph nodes or in tumors is associated with a less favorable prognosis [9–14]. Although Tregs are the major cell type expressing FOXP3, it has recently been demonstrated that the tumor cell itself can express FOXP3, such as pancreatic cancer [15], melanoma [16] and other tumor types [17], and the function of FOXP3 may represent a new mechanism of immune evasion in cancers.