In addition, patients under octreotide treatment tended to have lower MELD scores than patients undergoing other treatment modalities although there was no overall difference in MELD score between the various groups. In summary, this retrospective Carfilzomib PR-171 analysis of survival of BCLC stage-matched patients with HCC showed that octreotide treatment produces a similar survival benefit as TACE or multimodal therapy as compared to no active treatment. Given the few side effects of long-acting octreotide [Sandostatin LAR] this treatment seems to be a therapeutic option for patients with HCC and needs further randomised controlled studies in BCLC stage-matched patients. Competing interests The authors declare that they have no competing interests. Authors’ contributions JK performed chemoembolization.

MPR recruited patients. MSH and CM were equally involved in the design of the study, patient recruitment, management of the patients, statistical analysis and drafted the manuscript. All authors read an approved the final manuscript.
The mechanisms by which organs undergo repair following injury is of increasing therapeutic interest because targeting either dysregulated or failed repair mechanisms is an attractive alternative to targeting injury mechanisms. Proof of principle that targeting such repair mechanisms can augment normal repair has been established (1). However, there is a paucity of knowledge about normal repair and dysregulation of normal repair in chronic inflammatory diseases.

Working toward this aim, we have recently described a key role for epithelial cell phagocytosis in repair and remodeling of the functional units of the kidney, the nephrons, following severe ischemic injury, a model for acute tubular necrosis in humans (2). In addition to this role for epithelial cells in repair and regeneration, there is now an established literature indicating that in certain circumstances macrophages (Ms) perform crucial roles in repair, not only by engaging in scavenger and debris-clearing functions, but also through paracrine signaling to parenchymal cells that support tissue regeneration (3,�C7). To identify genes that may play roles in repair rather than in injury we performed representational difference analysis of normal rat kidney and kidney subjected to ischemia reperfusion injury (IRI) during the phase of organ repair (8).

This analysis revealed that the gene encoding the transmembrane protein Kim1 (also known as Tim1; see ref. 9) was highly up-regulated during repair. Subsequent analysis indicated that Kim1 functions in repair, at least in part, by functioning as a scavenger receptor on injured epithelial cells (2). In addition to the Kim1 gene, this analysis identified that the Entinostat gene encoding glycoprotein nonmetastatic melanoma B (Gpnmb) was also markedly up-regulated following injury.