|LETTER TO THE EDITOR
|Year : 2017 | Volume
| Issue : 1 | Page : 152-153
Transcoelomic spread and ovarian seeding during ovulation: A possible pathogenesis of Krukenberg tumor
Bikash Shah1, Wen-Hao Tang1, Shammi Karn2
1 Department of General Surgery, Zhong Da Hospital, Southeast University, Nanjing 210009, Jiangsu, China
2 Department of Gynecology and Obstetrics, Zhong Da Hospital, Southeast University, Nanjing 210009, Jiangsu, China
|Date of Web Publication||16-May-2017|
Department of General Surgery, Zhong Da Hospital, Southeast University, Nanjing 210009, Jiangsu
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Shah B, Tang WH, Karn S. Transcoelomic spread and ovarian seeding during ovulation: A possible pathogenesis of Krukenberg tumor. J Can Res Ther 2017;13:152-3
Krukenberg tumor is a metastatic ovarian tumor with its primary site being the gastrointestinal (GI) tract. Still the definitive metastatic pathway of Krukenberg tumor is not fully understood, it is in its hypothetical stage. Here, we propose a hypothesis of transcoelomic spread and ruptured ovary during ovulation, providing a seeding site for metastasizing tumor cells as the possible route of metastasis in Krukenberg tumor cases. Many evidence support our hypothesis:
- The most important predictor of Krukenberg tumor is T-stage of the primary carcinomas. Based on the T-stages, the tumor cells could scatter more easily into the peritoneal cavity, facilitating transcoelomic spread. Moreover, in the majority of the metachronous Krukenberg tumor cases, the primary tumor at the GI tract are found to be in its advanced stage (T3 and T4), in which the primary tumor have already invaded the serosal layer. In advance stage of primary GI tumors, the most common way for cancer cells to metastasize is transcoelomic spread 
- Patients with Krukenberg tumors are mostly young females with functioning ovaries. During ovulation, there is disruption of ovarian surface epithelium during the release of an oocyte. Moreover, during the process of wound healing, growth factors are released which promote cells to migrate into the wound area. Thus, detached tumor cells from advanced primary (GI) tumor may get trapped and start colonizing in the wound to form a tumor. During repair, invaginations of the epithelium result in crypts that can pinch off to form epithelial (cortical) inclusion cysts within the underlying stromal compartment. These inclusion cysts are widely believed to be the potential origin of epithelial ovarian cancer. Similarly, it is possible for tumor cells in the peritoneal cavity to get included in the inclusion cysts to form a Krukenberg tumor
- There is bilateral involvement of the ovary in the majority of the Krukenberg tumor cases. Moreover, we also know both the ovary takes part in ovulation predisposing both of them to metastatic disease
- In case of unilateral Krukenberg tumors, the right ovary is more often involved. Moreover, many studies have shown that right ovary is also more frequently involved in ovulation than the left. This may be the reason for more frequent involvement of the right ovary in Krukenberg tumor. We also know due to larger right paracolic gutter, abdominal fluid tend to have greater drainage into the right side, and fact that right ovary is more often involved in ovulation may correlate to be the reason of transcoelomic spread of tumor cells to right ovary
- In the process of transcoelomic seeding, detached tumor cells that have already acquired all the necessary metastatic characteristics are merely transported via peritoneal fluid into the abdominal cavity to a new site. The flow of intraperitoneal fluid is also directed by gravity to its most dependent sites. As per human being, we acquire standing position making ovary an easy access to detached tumor cells.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| > References|| |
Jeung YJ, Ok HJ, Kim WG, Kim SH, Lee TH. Krukenberg tumors of gastric origin versus colorectal origin. Obstet Gynecol Sci 2015;58:32-9.
Qiu L, Yang T, Shan XH, Hu MB, Li Y. Metastatic factors for Krukenberg tumor: A clinical study on 102 cases. Med Oncol 2011;28:1514-9.
Ganapathy N, Venkataraman SS, Daniel R, Aravind RJ, Kumarakrishnan VB. Molecular biology of wound healing. J Pharm Bioallied Sci 2012;4 Suppl 2:S334-7.
Tan DS, Agarwal R, Kaye SB. Mechanisms of transcoelomic metastasis in ovarian cancer. Lancet Oncol 2006;7:925-34.
Järvelä I, Nuojua-Huttunen S, Martikainen H. Ovulation side and cycle fecundity: A retrospective analysis of frozen/thawed embryo transfer cycles. Hum Reprod 2000;15:1247-9.
|This article has been cited by|
||Ovarian Metastasis from Pancreatic Ductal Adenocarcinoma
| ||Joseph R. Habib, Shamsher Pasha, Subhan Khan, Benedict Kinny-Köster, Sami Shoucair, Elizabeth D. Thompson, Jun Yu, Kelly Lafaro, Richard A. Burkhart, William R. Burns, Brigitte M. Ronnett, Christopher L. Wolfgang, Ralph H. Hruban, Jin He, Elliot K. Fishman, Ammar A. Javed |
| ||World Journal of Surgery. 2021; 45(10): 3157 |
|[Pubmed] | [DOI]|
||Intestinal Obstruction Due to Giant Bilateral Krukenberg’s Tumors Synchronous of Colorectal Origin
| ||Naveen Kumar Gaur, Oseen Shaikh, Chellappa Vijayakumar, Uday Kumbhar, Rajesh Nachiappa Ganesh |
| ||Cureus. 2021; |
|[Pubmed] | [DOI]|