[A Case of Sinusoidal Obstruction Syndrome and Nodular Regenerative Hyperplasia after Using Oxaliplatin for Rectal Cancer].

We present a case of a 44-year-old woman with rectal cancer(cT2N3M0, cStage Ⅲb)treated with 4 capecitabine-oxaliplatin( CAPOX)therapy courses, followed by laparoscopic intersphincteric resection. The patient received 7 postoperative, adjuvant CAPOX therapy courses. After 16 months since the final CAPOX administration, computed tomography(CT) revealed multiple liver tumors, showing early enhancement, and a jejunal mesenteric mass suspected to be a gastrointestinal stromal tumor(GIST). To overcome the percutaneous needle biopsy limitation, laparoscopic partial hepatectomy and laparoscopic- assisted partial intestinal resection were performed. Two liver lesions were diagnosed as nodular regenerative hyperplasia( NRH)with sinusoidal obstruction syndrome(SOS), supported by the hyperplasia and sinusoidal dilatation pathological findings, consequential to using oxaliplatin. Considering the rarity of NRH, using oxaliplatin may be proven vital in the differential diagnosis.

A Notch ligand, Delta-like 1 functions as an adhesion molecule for mast cells.

Mast cells (MCs) accumulate in chronic inflammatory sites; however, it is not clear which adhesion molecules are involved in this process. Recently, the expression of Notch ligands was reported to be upregulated in inflammatory sites. Although Notch receptors are known as signaling molecules that can activate integrins, their contributions to the adhesion of MCs have not been studied. In this study, we demonstrated that mouse MCs efficiently adhered to stromal cells forced to express a Notch ligand, Delta-like 1 (Dll1). Surprisingly, the adhesion was a consequence of direct cell-cell interaction between MCs and Dll1-expressing stromal cells rather than activation of downstream effectors of Notch receptor(s)-Dll1. The adhesion of MCs to Dll1-expressing stromal cells remained even when the cell metabolism was arrested. The recognition was blocked only by inhibition of Notch receptor(s)-Dll1 interaction by addition of soluble DLL1, or mAbs against Dll1 or Notch2. Taken together, these results indicate that Notch receptor(s) and Dll1 directly promote the adhesion of MCs to stromal cells by acting as adhesion molecules. This appreciation that Notch receptor-ligand interactions have an adhesion function will provide an important clue to molecular basis of accumulation of MCs to inflammatory sites.