Published online Oct 27, 2016. doi: 10.4240/wjgs.v8.i10.660
Peer-review started: June 18, 2016
First decision: July 27, 2016
Revised: August 14, 2016
Accepted: August 27, 2016
Article in press: August 29, 2016
Published online: October 27, 2016
Processing time: 130 Days and 10.7 Hours
Malignant neoplasms of the appendix are rare and represent less than 1% of gastrointestinal cancers. Goblet cell carcinoids (GCC) tumors are a distinctive group of heterogeneous appendiceal neoplasm that exhibit unique clinical and pathologic features. This review focuses on the current diagnostic procedures, pathogenesis, possible signaling mechanisms and treatment options for GCC. Perspectives for future research are discussed. The tumor likely arises from pluripotent intestinal epithelial crypt base stem cells. Previous findings of Notch signaling as a tumor suppressor in Neuroendocrine tumors may have a similar role in this tumor too. Loss of Notch signaling may be the driver mutation with other successive downstream mutations likely favors them into progressing and behavior similar to poorly differentiated adenocarcinoma with minimal neuroendocrine differentiation. A multidisciplinary approach is suggested for optimal outcomes. Surgery remains the main treatment modality. Simple appendectomy may be sufficient in early stages while right hemicolectomy is recommended for advanced tumors. Cytoreductive surgery with heated intraperitoneal chemotherapy may improve survival in a select few with metastatic peritoneal disease. These tumors have an unpredictable behavior even in early stages and local recurrence and delayed metastases may be seen. Lifelong surveillance is warranted.
Core tip: Goblet cell carcinoids tumors are a distinctive group of heterogeneous appendiceal neoplasm that exhibit unique clinical and pathologic features. The pathogenesis is unclear however the tumor likely arises from pluripotent intestinal epithelial crypt base stem cells. Loss of Notch signaling may be the driver mutation with other successive downstream mutations likely favors them into progressing and behavior similar to poorly differentiated adenocarcinoma with minimal neuroendocrine differentiation. Surgery remains the main treatment modality. We discuss the clinical implications of this cancer focusing on the tumor biology, mutations, signaling mechanisms and management.