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The persistent infection of high-risk Human papillomavirus (HR-HPV) induced cervical cancer remains a challenge in women worldwide including India. Recent advances in cancer research have paved the way for advanced cancer treatment modalities including immunotherapy by manipulating the function or number of cytotoxic T cells. It is well established that anaphylatoxins like C3a and C5a of complement system influence tumor growth by evading apoptosis leading to progression of cancer. The role of the complement system, particularly the complement regulatory proteins (CRPs) which are important determinants of immune response play a crucial role in carcinogenesis. In a tumor microenvironment (TME) assisted suppression of immune effector cells may be achieved through CRPs. However, recent advances in pharmacogenomics including drug designing and combination of these approaches have provided a holistic understanding of signaling pathways and their crosstalk, to regulate cellular communications.This review describes the role of complement system; particularly CRPs in HPV induced cervical carcinogenesis which may be used for designing anti- HPV or cervical cancer therapeutics.

The role of epigenetics in the etiology of cancer progression is being emphasized for the past two decades to check the impact of chromatin modifiers and remodelers. Histone modifications, DNA methylation, chromatin remodeling, nucleosome positioning, regulation by non-coding RNAs and precisely microRNAs are influential epigenetic marks in the field of progressive cancer sub-types. Furthermore, constant epigenetic changes due to hyper or hypomethylation could efficiently serve as effective biomarkers of cancer diagnosis and therapeutic development. Ongoing research in the field of epigenetics has resulted in the resolutory role of various epigenetic markers and their inhibition using specific inhibitors to arrest their key cellular functions in in-vitro and pre-clinical studies. Although, the mechanism of epigenetics in cancer largely remains unexplored. Nevertheless, various advancements in the field of epigenetics have been made through transcriptome analysis and in-vitro genome targeting technologies to unravel the applicability of epigenetic markers for future cancer therapeutics and management. Therefore, this review emphasizes on recent advances in epigenetic landscapes that could be targeted/explored using novel approaches as personalized treatment modalities for cancer containment.

Breast cancer consists of various subtypes like Her2+, ER/PR+Her2-, ER/PR+Her2+, TNBCs (Triple-Negative Breast Cancers), TPBCs (Triple-Positive Breast Cancers), etc., according to hormonal receptors and Her2 profile. Among these, TNBCs have limited therapeutic interventions, due to lack of receptors for ER, PR and Her2. Apart from BRCA1 and BRCA2, there are certain tumor suppressors and/or oncogenes (PML and RB1) influencing breast cancer, but the precise implication of these genes and their correlation is still not clearly understood. These genes play pivotal role in cell cycle regulation, proliferation, differentiation, survival, and apoptosis. Thus, we sought to identify the role of PML and RB1, and their correlation in breast cancer especially in TNBCs. Data demonstrated that 17% were TNBCs, interestingly among these cases, 72% showed remarkable upregulation of PML and downregulation of RB1; whereas 14% cases showed downregulation of PML and RB1, and 14% cases showed loss of expression of PML and RB1. To further validate our results, we included the data from METABRICS and TCGA datasets. Interestingly, our data showed good concordance with METABRICS and TCGA data showing upregulation of PML and downregulation of RB1 in TNBCs. In addition, we also checked the survivability effect of PML and RB1 through Kaplan-Meier plotter and observed that upregulation of PML and downregulation of RB1 decreases recurrence-free survivability in TNBC cases. Overall, the data suggests a plausible role of PML and RB1 genes in breast cancer patients particularly in TNBCs, where treatment options are limited compared to the other subtypes of breast cancer cases.