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. 2012 Mar 9;5:8. doi: 10.1186/1756-8722-5-8

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Copyright ©2012 Li et al; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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"Ovarian" serous carcinogenesis. The most common site of the fallopian tube for serous cancer development is the tubal fimbriated end (TFE). Benign tubal epithelia (BTE) are able to form ovarian epithelial inclusions (OEI) through an unclear pathway, then follow low-grade serous carcinoma (LG-SC) development pathway. Within this pathway, there are small amount of OEIs which are derived from ovarian surface epithelia (OSE). It is currently believed that these OSE derived OEIs are barely able to form LG-SCs. In contrast to LG-SC, HG-SC mainly derives from serous tubal intraepithelial carcinoma (STIC), which is able to stick on ovarian surface or get into ovarian stroma and expand to form full blown cancer. There are about 10% or less LG-SCs which can develop into HG-SC upon acquiring p53 mutation.