Protein–protein interactions (PPI) are vital in modulating biochemical pathways in many biological processes. Inhibiting PPI is a tremendously important diagnostic and therapeutic strategy in averting pathophysiological cues and disease progression. Targeting PPI as a smart drug discovery tool has been largely overlooked over the years due to their highly dynamic and expansive interfacial areas. However in recent years, researchers have developed new technologies that have the potential to move this approach up the technology development curve and enable the regular discovery of PPI-focused smart drugs. Few drugs are already on the market and some potential drug-like candidates are in clinical trials. In this study we review the application of peptidomimetics as a valuable tool in PPI inhibition in cancer. First, we describe PPI and the general properties of the PPI interface. Next, we discuss the classification of peptidomimetics. Lastly, we focus on the application of peptidomimetics on targeted PPI in cancer pathways.

Endometrial cancer (EC), a prevalent gynecological malignancy, presents significant challenges due to its genetic complexity and heterogeneity. The genomic landscape of EC is underpinned by genetic alterations, such as mutations in PTEN, PIK3CA, and ARID1A, and chromosomal abnormalities. The identification of molecular subtypes—POLE ultramutated, microsatellite instability (MSI), copy number low, and copy number high—illustrates the diverse genetic profiles within EC and underscores the need for subtype-specific therapeutic strategies. The integration of multi-omics technologies such as single-cell genomics and spatial transcriptomics has revolutionized our understanding and approach to studying EC and offers a holistic perspective that enhances the ability to identify novel biomarkers and therapeutic targets. The translation of these multi-omics findings into personalized medicine and precision oncology is increasingly feasible in clinical practice. Targeted therapies such as PI3K/AKT/mTOR inhibitors have demonstrated the potential for improved treatment efficacy tailored to specific genetic alterations. Despite these advancements, challenges persist in terms of variability in patient responses, the integration of genomic data into clinical workflows, and ethical considerations. This review explores the genomic underpinnings of EC, from genes to clinical practice. It highlights the ongoing need for multidisciplinary research and collaboration to address the complexities of EC and improve diagnosis, treatment, and patient outcomes.

Bananas (Musa spp. L.) are grouped on the basis of their genomic origins in relation to Musa acuminata (A genome) and M. balbisiana (B genome). The two ancestral wild seeded diploid species evolved in vastly different geographical areas and contributed several agronomic traits towards the present genetic composition of cultivated bananas. Most cultivated bananas are triploid (AAA, AAB and ABB), some are diploid (AA, BB and AB) and a few are tetraploids (AAAA, AAAB, AABB and ABBB). Limitations on the correct identification of the A and B genomes in Musa have generated need for the development of new and more reliable techniques. Distinguishing the A and the B genome remains practically and theoretically important for banana breeders. The aim of the research was to develop a DNA based A genome specific marker for the identification of the A genome in bananas. A putative marker (600 bp) specific to the A genome was identified by Random Amplified Polymorphic DNA (RAPD) technique. A sequence characterised amplified region (SCAR) marker was developed from the RAPD amplicon. The SCAR primers annealed a 500 bp fragment specific to the A genome in a sample of 22 randomly selected homo- and heterogenomic A genome containing accessions representing different genome combinations. The 500 bp SCAR marker is useful for the identification of the A genome. However an additional 700 bp fragment annealed in all M. balbisiana genotypes and in five of the eight heterogenomic accessions, suggesting lack of differentiation between the A and B genome. This study has provided a 500 bp A genome SCAR marker and recent evidence that the A and B genomes of banana may not be as differentiated as previously considered.