Traditionally a disease has been defined by its clinical presentation and observable characteristics, not by the underlying molecular mechanisms, pathways, and systems biology-related processes specific to a particular patient (ignoring persons-at-risk). A new systems approach to subclinical and/or diseased states and wellness resulted in a new trend in healthcare services, namely, personalized and precision medicine (PPM).

To achieve the implementation of the PPM concept, it is necessary to create a fundamentally new strategy based upon the biomarkers and targets to have a unique impact for the implementation of PPM model into the daily clinical practice and pharma. In this sense, despite breakthroughs in research that have led to an increased understanding of PPM-based human disease, the translation of discoveries into therapies for patients has not kept pace with medical needs. It would be extremely useful to integrate data harvesting from different databanks for applications such as prediction and personalization of further treatment to thus provide more tailored measures for the patients and persons at risk resulting in improved outcomes and more cost-effective use of the latest health care resources including diagnostic (companion ones), preventive and therapeutic (targeted molecular and cellular) etc.

Translational researchers, bio-designers, and manufacturers are beginning to realize the promise of PPM, translating to direct benefit to patients or persons at risk. For instance, companion diagnostics tools and targeted therapies and biomarkers represent important stakes for the pharma, in terms of market access, return on investment, and the image among the prescribers. At the same time, they probably represent only the generation of products resulting in translational research and applications. So, developing medicines and predictive diagnostic tools require changes to traditional clinical trial designs, as well as the use of innovative (adaptive) testing procedures that result in new types of data. Making the best use of those innovations and being ready to demonstrate results for regulatory bodies requires specialized knowledge that many clinical development teams don’t have. The areas where companies are most likely to encounter challenges are data analysis and workforce expertise, biomarker and diagnostic test development, and cultural awareness. Navigating those complexities and ever-evolving technologies will pass regulatory muster and provide sufficient data for a successful launch of PPM, which is a huge task. So, partnering and forming strategic alliances between researchers, bio-designers, clinicians, businesses, regulatory bodies, and government can help ensure an optimal development program that leverages the Academia and industry experience and FDA’s new and evolving toolkit to speed our way to getting new tools into the innovative markets.

Healthcare is undergoing a transformation, and it is imperative to leverage new technologies to support the advent of PPM. This is the reason for developing global scientific, clinical, social, and educational projects in the area of PPM and TraMed to elicit the content of the new trend. The latter would provide a unique platform for dialogue and collaboration among thought leaders and stakeholders in government, academia, industry, foundations, and disease and patient advocacy with an interest in improving the system of healthcare delivery on one hand and drug discovery, development, and translation, on the other one, whilst educating the policy community about issues where biomedical science and policy intersect

Statement of the problem: The current study targeted the frequently reported C/T SNP (rs2981582) of the FGFR2 gene to test the role of this SNP in the susceptibility to breast cancer in Sudanese women. We evaluated the role of FGFR2 gene polymorphism (rs2981582) and some non-genetic risk factors on the risk of breast cancer among Sudanese females. We also evaluated the interactions between known risk factors and C/T SNP of FGFR2. The rs2981582 single nucleotide polymorphism in the Fibroblast Growth Factor Receptor 2 gene has been constantly associated with an increased risk of susceptibility to breast cancer. Methodology and theoretical orientation: DNA was extracted and PCR-RFLP data from 81 cases and 81controls were analyzed. Findings: The risk allele (T allele) of the rs2981582 polymorphism was associated with an increased risk of breast cancer (P-value= 0.0017) (OR =2.2, CI95%=1.34 to 3.53). A significant association was also encountered between cases carrying this polymorphism and a history of benign tumors (P-value = 0.0001), and those with a family history of breast cancer in first-degree relatives (P-value=0.045) (OR=7.22 CI95%=1.047 to 81.2). For genotype risk assessment, breast cancer risk significantly increased with the TT genotype (P-value =0.0023) (OR=1.711 CI95%=1.16 to 4.04) when compared to the other two genotypes (CC and CT). Conclusion and significance: Our findings suggest that FGFR2 rs2981582 is significantly associated with breast cancer susceptibility in Sudanese women and presents a potential biomarker for breast cancer prediction.

Cancer is a leading cause of death worldwide and it is a genetic disease. According to the WHO, approximately 10 million deaths were recorded in 2020. Moringa oleifera (Moringa) grows in the tropical and subtropical regions of the world. It is widely distributed and utilized in India and Africa. Many studies have been indicated that the Moringa’s leaves, pods, roots and seeds are rich in nutrition such as ascorbic acid, calcium, potassium, iron, magnesium, phosphorus, zinc, vitamin A, thiamine, riboflavin, niacin and vitamin B-6. Also, many studies have been conducted to assess the nutritional benefits and the medicinal applications of moringa in the treatment of various diseases as it has potential properties as antioxidant, anticancer, anti-inflammatory, anti-diabetic, anti-cholesterol, anti-hypertensive and antimicrobial agent. This review article explores the anticancer potential biochemical properties of Moringa, its metabolism and the mechanism of action as anticancer agent on several types of cancers.

hand, does not correspond to EBER1 expression

at both cellular and exosomal levels.

Conclusion & Significance: Nuclear- cytoplasmic trafficking of EBER1 seems to be linked to its conserved structure and/or its RPL22- binding. This study, therefore, concludes that SL3 of EBER1 appeared to be crucial in its intracellular transpod and RPL22 was implicated in the process. EBER1-La interaction might not be the sole/direct means through which EBER1 is secreted into exosomes. Since trafficking of EBERs is associated with improved cell-cell communication and the spread of EBV [1], unveiling the mechanisms involved in this transpod is critical to understanding the biology of EBV and its associated diseases.

Abs against myelin basic protein/MBP endowing with proteolytic activity (Ab-proteases with functionality) are of great value to monitor demyelination to illustrate the evolution of multiple sclerosis (MS). Anti-MBP autoAbs from MS patients and mice with EAE exhibited specific proteolytic cleavage of MBP which, in turn, markedly differed between: (i) MS patients and healthy controls; (ii) different clinical MS courses; (iii) EDSS scales of demyelination to correlate with the disability of MS patients to predict the transformation prior to changes of the clinical course.

Ab-mediated proteolysis of MBP was shown to be sequence-specific whilst demonstrating five sites of preferential proteolysis to be located within the immunodominant regions of MBP and to fall inside into 5 sequences fixed. Some of the latter (with the highest encephalitogenic properties) were proved to act as a specific inducer of EAE and to be attacked by the MBP-targeted Ab-proteases in MS patients with the most severe (progradient) clinical courses. The other ones whilst being less immunogenic happened to be EAE inducers very rare but were shown to be attacked by Ab-proteases in MS patients with moderate (remission-type) clinical courses.

The activity of Ab-proteases was first registered at the subclinical stages 1-2 years prior to the clinical illness. About 24% of the direct MS-related relatives were seropositive for low-active Ab-proteases from which 22% of the seropositive relatives established were being monitored for 2 years whilst demonstrating a stable growth of the Ab-associated proteolytic activity. Moreover, some of the low-active Ab-proteases in persons at MS-related risks (at subclinical stages of MS), and primary clinical and MRT manifestations observed were coincided with the activity to have its mid-level reached. Registration in the evolution of highly immunogenic Ab-proteases would illustrate either risks of transformation of subclinical stages into clinical ones, or risks of exacerbations to develop.

The activity of Ab-proteases in combination with the sequence-specificity would confirm a high subclinical and predictive (translational) value of the tools as applicable for personalized monitoring protocols. Ab-proteases can be programmed and re-programmed to suit the needs of the body metabolism or could be designed for the development of principally new catalysts with no natural counterparts. Further studies on targeted Ab-mediated proteolysis may provide a translational tool for predicting demyelination and thus the disability of the MS patients.