Cervical cancer

Cervical cancer begins when healthy cells on the surface of the cervix change or become infected with certain types of human papillomavirus (HPV) and grow out of control to become a tumor. HPV causes more than 90% of all cases of cervical cancer and a long-term infection of HPV on the cervix can result in a cancerous tumor which can be malignant and spread to other parts of the body. Cervical cancer typically takes over 10 to 20 years to develop from precancerous changes. The two main types of cervical cancers are squamous cell carcinoma (80% to 90%), which start in the cells on the outer surface covering of the cervix, and adenocarcinoma (10% to 20%), which start in the glandular cells that line the lower birth canal in the internal portion of the cervix. The squamous and glandular cells meet at the opening of the cervix at the squamocolumnar junction, which is the location where most cervical cancers start. Cervical cancer is both the fourth-most common type of cancer and the fourth-most common cause of death from cancer in women worldwide.

Figure 1. The volcano plot shows the adjusted p-value compared to the difference in average protein expression (NPX) for all proteins in cervical cancer compared to all other cancers. The lollipop plot shows the top 10 most important proteins resulting from the cancer prediction model with importance scores ranging between 0 to 100.

Pan-cancer protein panel

7 proteins have been selected by the model to predict cervical cancer (Table 1). The origin of most of these proteins according to the Human Protein Atlas is rather heterogeneous, but a few show enriched expression in normal female tissues. The top protein for cervical cancer (GLO1) is a mitochondrial enzyme (lyase) with low tissue specificity, but this protein has earlier been implicated in cancer (Santarius T et al. (2010)). In an earlier study on cervical cancer patients (Berggrund M et al. (2019)), few up-regulated proteins were found and all differentially expressed proteins with significance were downregulated, such as PTX3 also with lower levels in our study.