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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.

Simple Summary Breast cancer prevalence is a major challenge worldwide due to the lack of early diagnostics and treatment modalities. In this era of technological advancements, researchers are exploring several grey areas in breast cancer research, which may lead to the appropriate point of care, non-invasive and diagnostic aid for early breast cancer detection and management. Exosome-based research, an emerging area, endeavors to locate and elucidate the role of exosomes in breast cancer diagnostics, immune response and clinical outcomes. This review may provide insights on small extracellular vesicles research and their role in breast cancer. Future extensive studies on exosome biology in conjunction with cancer genetics shall undoubtedly open up new vistas in exosome-based diagnostics for early cancer detection and therapeutics. Abstract Despite the recent advancements in therapeutics and personalized medicine, breast cancer remains one of the most lethal cancers among women. The prognostic and diagnostic aids mainly include assessment of tumor tissues with conventional methods towards better therapeutic strategies. However, current era of gene-based research may influence the treatment outcome particularly as an adjunct to diagnostics by exploring the role of non-invasive liquid biopsies or circulating markers. The characterization of tumor milieu for physiological fluids has been central to identifying the role of exosomes or small extracellular vesicles (sEVs). These exosomes provide necessary communication between tumor cells in the tumor microenvironment (TME). The manipulation of exosomes in TME may provide promising diagnostic/therapeutic strategies, particularly in triple-negative breast cancer patients. This review has described and highlighted the role of exosomes in breast carcinogenesis and how they could be used or targeted by recent immunotherapeutics to achieve promising intervention strategies.

Cancer is a highly proliferative disease, which is caused due to the loss of regulation of cell cycle and apoptosis, DNA damage, faulty repair system etc. The cancer microenvironment plays a pivotal role in disease progression as they contain different types of innate and adaptive immune cells. The most important molecules that establish a correlation between inflammation, innate immunity, adaptive immunity, and cancer are the molecules released by inflammatory cells in cancer microenvironment. These molecules secreted by the immune cells, which might activate a pro-tumorigenic and anti-tumorigenic response in cancer. In inflammatory microenvironment, the equilibrium state of immunosuppressive and immunostimulatory signals are important in tumor suppression. The immunotherapeutic approaches could be more effective in cancer treatment. However, advancement in immunobiology and cancer are improving the prospects of immunotherapy alone and/or in combination with the conventional therapies. Thus, the review attempts to highlight a promising and futuristic immunotherapeutic approach in combination with conventional treatment modalities.

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.

Background: Most oral squamous cell carcinomas are preceded by premalignant lesions like leukoplakia, erythroplakia etc. Identification of these lesions by molecular markers and intervention at an early stage can reduce mortality, morbidity and cost of treatment associated with oral cancer. Extracellular signal regulated kinase 1 (ERK 1) is one of the various markers involved in carcinogenesis.Methods: We studied the expression of ERK 1 in twenty-five oral premalignant lesion biopsies using immunohistochemistry (IHC) and western blot analysis.Results: Ninety-two percent of premalignant lesions showed positive expression of ERK 1 on IHC and the same were confirmed by western blot analysis. ERK 1 expression was increased in premalignant lesions as compared to peripheral normal tissue but the difference between them was not statistically significant. On comparing the level of expression of peripheral normal and premalignant tissue on IHC, moderate and high level of expressions were significantly higher in premalignant lesions (24%) than peripheral normal tissue (12%).Conclusions: There was an increased expression of ERK 1 in oral premalignant lesions as compared to peripheral normal tissue, although, this difference was not statistically significant.