Ontogenetic anatomy-based surgical procedures were considered to have the potential to increase survival by 15 to 20%% compared to standard treatment in cervix cancer [8].
High dose rate and pulsed dose rate treatments seem to offer the same results as low-dose rate brachytherapy, particularly in cervix carcinoma.
It is supported by pattern analysis of cancers of the lower genital tract, as well as total mesometrial resection in cervix cancer and ontogenetic surgery for vaginal and vulvar malignancies [4, 5, 6, 7, 8, 9, 10, 11, 12, 13].
One causative agent in cervix carcinogenesis is infection with high risk human papilloma viral subtypes, including HPV-16 and -18 [20].
These data provided a compelling rational for investigation of a phase I clinical trial conducted at our Institution to assess Cidofovir toxicity in cervix patients (PHRC 2006).
In addition, transcriptional activation of the CXCR4 promoter is described in cervix carcinoma [45] and immunohistochemistry has shown high CXCR4 expression on cervix cancer cells [11].
These results suggested that E6/E7 indeed contribute to the metastatic process and raise a rational for its abrogation in cervix cancer patients by using an anti-viral agent, Cidofovir, as a therapeutic tool.
It has been shown that in the absence of p63, the stratified squamous epithelium in cervix and vagina is transformed into a simple columnar epithelium expressing uterine epithelial differentiation markers [15].
What may be purpose of elevated VHR in cervix cancer?
CCL2 mRNA abundance and protein in cervix did not change between gestational days (data not shown).
Significantly, our study is the first to document CEACAM7 expression in cervix.
