Abstract
Simple SummaryDespite the implementation of efficient screening and vaccination programs, uterine cervical cancer remains a leading cause of cancer-related mortality in women worldwide. New therapeutic approaches have so far failed to improve treatment response and prognosis significantly, especially in patients with recurrent disease or metastases. Further, robust molecular markers to predict therapy response and survival are scarce and their routine use is limited in clinical practice. Accordingly, there is an urgent need to identify and establish molecular markers to predict therapy response and clinical outcome to improve treatment and survival in cervical cancer.Uterine cervical cancer is one of the leading causes of cancer-related mortality in women worldwide. Each year, over half a million new cases are estimated, resulting in more than 300,000 deaths. While less-invasive, fertility-preserving surgical procedures can be offered to women in early stages, treatment for locally advanced disease may include radical hysterectomy, primary chemoradiotherapy (CRT) or a combination of these modalities. Concurrent platinum-based chemoradiotherapy regimens remain the first-line treatments for locally advanced cervical cancer. Despite achievements such as the introduction of angiogenesis inhibitors, and more recently immunotherapies, the overall survival of women with persistent, recurrent or metastatic disease has not been extended significantly in the last decades. Furthermore, a broad spectrum of molecular markers to predict therapy response and survival and to identify patients with high- and low-risk constellations is missing. Implementation of these markers, however, may help to further improve treatment and to develop new targeted therapies. This review aims to provide comprehensive insights into the complex mechanisms of cervical cancer pathogenesis within the context of molecular markers for predicting treatment response and prognosis.
Highlights
Transient infections with human papillomavirus (HPV) are common, with a lifetime probability ranging between 50% and 95% [1]
The findings indicated that a more pronounced decrease in the Circulating Tumor Cells (CTC) count to be associated with a lower risk of death, while patients with a CTC
A recent systematic review and network meta-analysis suggested a greater diversity of the cervicovaginal microbiota in human papillomaviruses (HPV)+ women, while a greater diversity of cervicovaginal microbiota dominated by non-Lactobacilli species expect of Lactobacillus iners was associated with high-risk HPV, CINs and cervical cancer [260,261]
Summary
Transient infections with human papillomavirus (HPV) are common, with a lifetime probability ranging between 50% and 95% [1]. Therapeutic vaccination strategies (e.g., NCT02853604) and adoptive cell therapies (e.g., NCT03108495) are currently being tested [19] In this regard, the FDA recently approved the antibody-drug conjugate (ADC) tisotumab vedotin against tissue factor and monomethyl auristatin E (MMAE) for recurrent or metastatic cervical cancer after efficacy, and safety was demonstrated in the NCT03438396 multicenter, open-label, single arm, phase 2 trial (innovaTV 204/GOG-3023/ENGOT-cx6) [20]. The FDA recently approved the antibody-drug conjugate (ADC) tisotumab vedotin against tissue factor and monomethyl auristatin E (MMAE) for recurrent or metastatic cervical cancer after efficacy, and safety was demonstrated in the NCT03438396 multicenter, open-label, single arm, phase 2 trial (innovaTV 204/GOG-3023/ENGOT-cx6) [20] Despite these advances, survival rates have not improved significantly over the past two decades and especially the prognosis for women with persistent, recurrent or metastatic disease remains poor. These markers, may cover a prerequisite to unravel the molecular pathogenesis and heterogeneity of cervical cancer and will be crucial to further develop novel therapeutic targets and treatment approaches
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