Nanophytotherapeutics for Cancer

Phytochemicals have been attributed beneficial health properties, mainly their anticancer potential. Cancer treatment seeks to shrink the tumor and kill cancer cells; however, the conventional treatment available frequently fails due to the emergence of drug-resistant cell lines. Plant-derived compounds have been studied for their potential anticancer effects or as adjuvant drug to conventional treatment. However, some of the physicochemical properties and stability characteristics of the phytocompounds generate biopharmaceuticals difficulties that limit their efficacy and clinical applications in oncology. In this sense, nanomedicine offers an alternative for the development of biocompatible, biodegradable, safe, and efficacy phytoformulations. Nanostructured delivery systems show immense potential in the bioavailability of phytodrugs by providing better alternatives to conventional dosage forms, through improving physicochemical and biopharmaceutical properties of the phytocompounds and along with it to enhance the therapeutic efficacy.

Potential Cancer Biomarkers

Extensive studies in the field of oncology are able to identify potential cancer biomarkers with tumor-specific molecular characteristics that exceed or complement those of existing biomarkers. However, there are challenges in the development and clinical validation of the cancer biomarkers due to the complexity of the biological process involved. Standalone or integrative approach of broad range of biomolecules, their expression pattern, epigenetic alterations, and metabolic effects are well studied in the cancer research. The potential cancer biomarkers need to be studied extensively with advanced technologies to bring about a great change in cancer screening and therapy. This chapter provide an overview on recent studies about potential cancer biomarkers. Also, specific characteristics of potential biomarkers in three common types of cancer are discussed.

Synthesis, Crystal Structure and Theoretical Investigations of (3-(2-Chlorophenyl)-5-Tosyl-1,3,3a,4,5,9b-Hexahydroisoxazolo[4,3-c]Quinolin-3a-yl)Methanamine

In the title compound (3-(2-chlorophenyl)-5-tosyl-1,3,3a,4,5,9b-hexahydroisoxazolo[4,3-c]quinolin-3a-yl)methanamine (3-CPTHIQM), the Thorpe–Ingold effect causes the S atom's tetrahedral geometry to be deformed, with O-S-O and N-S-C angles diverging from ideal tetrahedral values. The crystal packing features C—H⋯O hydrogen-bond inter¬actions.The supramolecular interactions were confirmed and quantified using Hirshfeld surface analysis. Quantum chemical calculations of sulfonamide are calculated at DFT/B3LYP/6-311++G(d,p) basis set. The NLO properties were calculated at the same level of theory. Furthermore, frontier molecular orbitals (FMOs) and molecular electrostatic potential (MEP) surfaces were calculated and analyzed in detail. In a molecular docking study, the investigated sulfonamide compound is evaluated as a new potential cancer inhibitor.

Impact of the APOBEC3A/B deletion polymorphism on risk of ovarian cancer

A germline 29.5-kb deletion variant removes the 3’ end of the APOBEC3A gene and a large part of APOBEC3B, creating a hybrid gene that has been linked to increased APOBEC3 activity and DNA damage in human cancers. We genotyped the APOBEC3A/B deletion in hospital-based samples of 1398 Norwegian epithelial ovarian cancer patients without detected BRCA1/2 germline mutations and compared to 1,918 healthy female controls, to assess the potential cancer risk associated with the deletion. We observed an association between APOBEC3A/B status and reduced risk for ovarian cancer (OR = 0.75; CI = 0.61–0.91; p = 0.003) applying the dominant model. Similar results were found in other models. The association was observed both in non-serous and serous cases (dominant model: OR = 0.69; CI = 0.50–0.95; p = 0.018 and OR = 0.77; CI = 0.62–0.96; p = 0.019, respectively) as well as within high-grade serous cases (dominant model: OR = 0.79; CI = 0.59–1.05). For validation purposes, we mined an available large multinational GWAS-based data set of > 18,000 cases and > 26,000 controls for SNP rs12628403, known to be in linkage disequilibrium with the APOBEC3A/B deletion. We found a non-significant trend for SNP rs12628403 being linked to reduced risk of ovarian cancer in general and similar trends for all subtypes. For clear cell cancers, the risk reduction reached significance (OR = 0.85; CI = 0.69–1.00).