Inflammatory Myofibroblastic Tumor of the Anus: A Case Report.

Inflammatory myofibroblastic tumors (IMTs) are neoplastic lesions characterized by the proliferation of spindle cells with myofibroblastic features and lymphocyte infiltration. Primary lesions can develop in several locations but rarely arise in the colon as described herein. The present case was that of a 69-year-old woman who visited our hospital with complaints of bloody bowel discharge and a prolapsed mass from the anus. A 20-mm tumor was identified on visual and digital examination. Lower gastrointestinal endoscopy revealed a pedunculated, elevated lesion above the dentate line, which showed contrast enhancement on abdominal computed tomography. The patient was preoperatively diagnosed with an anal polyp, which was resected transanally. During the procedure, a mobile tumor coated by anal epithelium was observed at the 11 o'clock position above the dentate line. Deeper parts of the tumor were contiguous with the internal anal sphincter (IAS) muscle. Suspecting a neoplastic lesion, we resected the mass en bloc with part of the IAS. Tumor histopathology after surgery led to a final diagnosis of an IMT of the anus. IMT is difficult to diagnose preoperatively. No adjuvant therapy has been formally established; thus, an adequate surgical margin and close monitoring are essential.

[Two Cases of Surgery Combined with Intraoperative Radiofrequency Ablation for Colorectal Cancer and Synchronous Liver Metastases].

The therapeutic management of simultaneous liver metastasis of colorectal cancer(SCRLM)remains controversial. Although hepatic metastasectomy is the first choice for resectable liver metastasis of colorectal cancer, radiofrequency ablation (RFA)is one of the least invasive application for patients who refuse more invasive treatment such as hepatectomy and longterm systemic chemotherapy or for whom such treatment is not suitable. We report 2 cases of SCRLM treated by surgery combined with intraoperative RFA and adjuvant chemotherapy, raising the possibility of local control in the liver for selected patients.

[Regulation of cellular senescence by Bach1].

The tumor suppressor p53 induces cellular senescence, an irreversible form of proliferation arrest, to inhibit carcinogenesis as well as aging of organs and a body. While the major cause of cellular senescence and aging is oxidative stress, little is known about how the p53 activity is regulated under such conditions. Bach1 inhibits expression of oxidative stress responsive genes by competing with Nrf2, the key activator of oxidative stress response. Bach1 inhibits p53-dependent cellular senescence induced by oxidative stress. Bach1 forms a protein complex with p53, is recruited to p53 target genes, and inhibits their expression. These findings provide completely novel insights into how the activity of p53 is regulated under oxidative stress. Since p53 is the critical tumor suppressor with huge clinical implications, the newly identified mechanism should open new research fields.