Pelvic Anatomy for Distal Rectal Cancer Surgery

Worldwide, colorectal cancer is the third most common cancer and one of the leading causes of cancer-related deaths. Currently, total mesorectal excision (TME) is considered as the gold standard surgical procedure for rectal cancer. To achieve a good oncologic outcome and functional outcome after TME in distal rectal cancer, exact knowledge regarding the pelvic anatomy including pelvic fascia, pelvic floor, and the autonomic nerve is essential. Accurate TME along the embryologic plane not only reduces local recurrence rate but also preserves urinary and sexual function by minimizing nerve damage. In the past, pelvic floor muscles and autonomic nerves could not be visualized clearly, however, the development of imaging studies and improvements of minimally invasive surgical techniques such as laparoscopic and robotic surgery can clearly show the anatomy of the pelvic region. In this chapter, we will provide accurate anatomy of the rectum and the anal canal, pelvic fascia, and the pelvic autonomic nerve. This anatomical information will be an important indicator for performing an adequate operation for distal rectal cancer

Protein Tyrosine Phosphatases as Potential Regulators of STAT3 Signaling

The signal transducer and activator of transcription 3 (STAT3) protein is a major transcription factor involved in many cellular processes, such as cell growth and proliferation, differentiation, migration, and cell death or cell apoptosis. It is activated in response to a variety of extracellular stimuli including cytokines and growth factors. The aberrant activation of STAT3 contributes to several human diseases, particularly cancer. Consequently, STAT3-mediated signaling continues to be extensively studied in order to identify potential targets for the development of new and more effective clinical therapeutics. STAT3 activation can be regulated, either positively or negatively, by different posttranslational mechanisms including serine or tyrosine phosphorylation/dephosphorylation, acetylation, or demethylation. One of the major mechanisms that negatively regulates STAT3 activation is dephosphorylation of the tyrosine residue essential for its activation by protein tyrosine phosphatases (PTPs). There are seven PTPs that have been shown to dephosphorylate STAT3 and, thereby, regulate STAT3 signaling: PTP receptor-type D (PTPRD), PTP receptor-type T (PTPRT), PTP receptor-type K (PTPRK), Src homology region 2 (SH-2) domain-containing phosphatase 1(SHP1), SH-2 domain-containing phosphatase 2 (SHP2), MEG2/PTP non-receptor type 9 (PTPN9), and T-cell PTP (TC-PTP)/PTP non-receptor type 2 (PTPN2). These regulators have great potential as targets for the development of more effective therapies against human disease, including cancer