Baobab Index

Omics biomarkers comprise several molecular entities, including genomic, epigenomic, transcriptomic, proteomic, and metabolomic signatures. They play an essential role in oncology drug development and clinical settings by enabling personalized medicine. In precision oncology, validating biomarkers is a greater challenge than discovering them. The biomarkers discussed here span a wide evidentiary spectrum, from those endorsed in clinical guidelines to those that remain investigational.

The rising demand for novel therapeutics, including antimicrobial, anticancer, and anti-inflammatory agents, underscores the need for new drug discovery strategies. Microbial communities represent rich reservoirs of bioactive compounds encoded by biosynthetic gene clusters (BGCs), yet traditional approaches remain limited by the inability to culture most microorganisms and the frequent rediscovery of known metabolites. Sequence-based metagenomics provides a transformative solution by directly identifying BGCs from environmental DNA. Using NovaSeq X Plus shotgun sequencing, we explored the biosynthetic potential of microbial communities in two previously unstudied brackish springs of the Siwa Oasis, Cleopatra and Fatnas. These ecosystems were dominated by bacteria (99.2%), with archaea being nearly absent (< 0.1%), and the microbial composition consisted largely of mesophilic taxa from Pseudomonadota, Bacteroidota, Actinomycetota, and Planctomycetota, which together accounted for 98.2% of the community. Our integrated bioinformatics pipeline enabled the reconstruction of 37 medium-to-high-quality metagenome-assembled genomes (MAGs), and recovered 147 BGCs mostly from Pseudomonadota, Actinomycetota, and Acidobacteriota phyla. Terpene (n = 23) and ribosomally synthesized and post-translationally modified peptide (RiPPs; n = 22) BGCs predominated within Cleopatra Spring, whereas RiPPs (n = 20) represented the dominant class recovered from Fatnas Spring. None of the recovered gene clusters mapped to experimentally validated entries in the MIBiG database (distance > 0.4), and 96.6% displayed structural divergence from the gene cluster families catalogued in the BGC Atlas. These results highlight the Siwa Oasis as a promising reservoir of unexplored biosynthetic potential and a valuable resource for natural product discovery to address global health challenges.

Pediatric disorders consist of genetic, hematologic, neurologic, autoimmune, and inflammatory diseases. These conditions impose long-term health challenges on children, despite many advancements with conventional medicine. Although conventional treatments increase life expectancy and provide better disease control, many present challenges such as toxicity, insufficient control of the disease, and adverse effects on normal growth, development, and quality of life. Many researchers have shown increased interest in using stem cell therapies as an alternative to current medications to allow for complete, sustainable repair of damaged tissues and modification of disease processes (i.e., using stem cells to regenerate tissue or change the way in which a disease occurs). This paper will provide the current information on stem cells used in the treatment of children and the many different types of stem cells, including: hematopoietic stem cells (and their derivatives), mesenchymal stem cells (and their derivatives), induced pluripotent stem cells, embryonic stem cells, tissue-specific progenitor cells, extracellular vesicles, and bioengineered products. This paper will also discuss what is known about the stem cells listed as well as their methods of action, where they might currently be better utilized, and future uses of these cells in children for a variety of types of pediatric diseases. Because each stem cell type listed has very different scientific background and clinical evidence, there is much variability in the amount of scientific evidence available to support stem cell therapies. For example, hematopoietic stem cell transplantation (HSCT) has over 50 years of clinical experience; thus, there are many studies defining the clinical efficacy and long-term outcomes associated with HSCT. Conversely, while there are many published studies supporting the use of mesenchymal stem cells (MSCs), extracellular vesicles (EVs), gene-edited cells, organoids, and many induced pluripotent stem cell-derived therapies, more evidence (clinical and basic science) is still needed to fully establish efficacy for the use of these various stem cells in children with pediatric diseases. In addition to needing more clinical evidence, stem cell-based therapies face many important challenges to the advancement of these therapies, including (but not limited to) long-term safety assessments, manufacturing standardization, regulatory oversight, ethical concerns, and equitable access to advanced therapies. Addressing these challenges will be important for future advances in the use of regenerative medicine in pediatric patients which will also require the rigorous evaluation of new stem cell therapies, the continued improvement of translational mechanisms, and the ongoing incorporation of new techniques (e.g., genome editing, organoid modeling, EV therapeutics, bioengineering, and artificial intelligence) to advance regenerative medicine and demonstrate its value through safe and reproducible clinical trial results.

Aberrant activation of Aurora A kinase causes mitotic spindle assembly, chromosome segregation, and cell cycle progression, leading to genomic instability as well as disruption of several tumor suppressors. Furthermore, ERK has largely emerged as a survival signaling pathway controlling cell proliferation, differentiation, and metastasis. Unfortunately, this pathway is overexpressed in most of the human malignancies. In efforts to develop innovative inhibitors targeting Aurora A/ERK signaling pathway, a novel series of thiadiazolo-, triazolo-pyrimidine hybrids have been designed, synthesized, and assessed for their ability to block Aurora A/ERK and induce apoptosis. Cytotoxicity of the synthesized hybrids was examined against MCF-7, HCT-116 and A549 cell lines. Among the synthesized hybrids, 9a, 9c, and 14b demonstrated higher cytotoxic action than alisertib and GDC-0994 against the MCF-7 and A549 cancer cell lines. IC

Ethylene functions as a central hormonal regulator controlling diverse metabolic and developmental changes throughout fruit maturation and storage. In this review, we provide an integrative examination of ethylene-dependent networks that coordinate ripening, addressing genetic control mechanisms, climate stress responses, and commercial handling practices. Our analysis focuses on the molecular mechanisms of ethylene production and the downstream signaling components that drive expression of genes necessary for ripening. We also examine how ethylene signaling interfaces with master transcriptional regulators and integrates with other phytohormones, such as abscisic acid, auxin, jasmonic acid, and brassinosteroids to fine-tune the ripening process. Moreover, we address the impact of climate change-related factors, such as heat stress, altered light regimes, elevated CO

This study aimed to assess the protective role of dietary hesperidin (HEP) in Nile tilapia (Oreochromis niloticus) under ammonia stress conditions. The investigation focuses on its capacity to alleviate ammonia-induced metabolic disorders, oxidative stress, and inflammatory responses. For 60 days, 160 Nile tilapia (26.46 ± 0.17 g) were split into four equal groups (control, HEP, AMM, and AMM + HEP). The control and AMM groups were administered a basal diet, whereas the HEP and AMM + HEP groups received a basal diet containing 150 mg HEP/kg. The AMM and AMM + HEP groups were subjected to 0.21 mg/L of un-ionized ammonia. Prolonged exposure to ammonia induced oxidative stress by increasing the malondialdehyde (386.67%); however, it lowered superoxide dismutase (83.26%), catalase (86.38%), and glutathione peroxidase activities (60.72%). Ammonia poisoning elevated the total cholesterol (22.30%), triglycerides (164.04%), low density lipoprotein (41.21%), and very low density lipoprotein (164.06%), while lowering the high density lipoprotein (39.25%), total protein (53.84%), albumin (47.59%), and globulin (61.53%). In addition, ammonia poisoning increased the hepatic function markers, including total bilirubin, direct bilirubin, indirect bilirubin, alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase. Ammonia exposure upregulated the hepatic expression of toll-like receptor-5 (7.21-fold), tumor necrosis factor-α (6.97-fold), nuclear transcription factor kappa β (7.51-fold), interleukin-1β (7.40-fold), interleukin-6 (4.57-fold), interleukin-8 (6.36-fold), and mitogen-activated protein kinase-1 (8.05-fold), while downregulating the interleukin-10 (0.23-fold) expression. Dietary HEP improved the antioxidant capacity and liver functions, alongside ameliorating the inflammatory responses in Nile tilapia during ammonia exposure. Ultimately, ammonia poisoning in Nile tilapia tanks can be mitigated by dietary HEP (150 mg/kg), which will improve fish health and liver functions.

Acute myeloid leukemia (AML) is a genetically heterogeneous and dynamically evolving malignancy in which morphologic remission does not necessarily indicate eradication of disease. Bone marrow examination remains central to diagnosis and response assessment, yet repeated aspiration is invasive, may be affected by hemodilution and spatial sampling, and provides only intermittent snapshots of an evolving clonal process. Liquid biopsy offers a complementary strategy by interrogating circulating cell-free DNA (cfDNA), the leukemia-derived fraction termed circulating tumor DNA (ctDNA), extracellular vesicles, exosomal nucleic acids, and circulating leukemic cells. Among the analytical platforms applicable to these materials, droplet digital polymerase chain reaction (ddPCR) is attractive because it partitions a specimen into thousands of reactions and enables highly precise absolute quantification without a calibration curve. This narrative review critically examines the biological rationale, analytical performance, and clinical evidence supporting ddPCR-based liquid biopsy in AML. The strongest current evidence concerns molecular measurable residual disease (MRD), particularly for NPM1 mutations and selected patient-specific variants, with additional applications in IDH1/2, FLT3-TKD, KIT, CEBPA, DNMT3A, and fusion-transcript monitoring. We discuss the roles of peripheral blood and plasma cfDNA at diagnosis, during induction and consolidation, before and after allogeneic hematopoietic stem-cell transplantation, and at suspected molecular relapse. We also compare ddPCR with multiparameter flow cytometry, reverse-transcription quantitative PCR, and error-corrected next-generation sequencing, emphasizing that analytical sensitivity alone does not establish clinical validity. Major barriers include pre-analytical variation, low and fluctuating ctDNA abundance, assay-specific false-positive droplets, incomplete target coverage, clonal hematopoiesis, and the absence of harmonized thresholds. Emerging multi-analyte strategies that combine mutation tracking, methylation, exosomal RNA, chimerism, and computational modeling may improve robustness. At present, ddPCR is best positioned as a rapid, targeted, and complementary tool embedded in a multimodal MRD framework rather than as a universal replacement for bone marrow or broad genomic profiling.

Vitamin D

Childhood cancers are rare, but incidence has risen modestly in countries with robust registration, partly reflecting improved diagnosis. In high-income countries, cancer is the leading cause of disease-related death in children. Marked inequities in incidence, survival, and research capacity underscore the need for large-scale collaboration to identify environmental, genetic, and contextual determinants of risk. The Childhood Cancer and Leukemia International Consortium (CLIC) was established in 2007 to study the etiology of childhood leukemia and later expanded in 2019 to include other childhood cancers, principally solid tumors. CLIC pools harmonized, individual-level data from case-control and cohort studies, obtained through interviews, record linkage (insurance claims, registries), or geographic information systems, and integrates germline genomic data where available. Membership has grown from 13 studies in 9 countries to 57 studies in 21 countries; recruitment spans the early 1960s to the present and encompasses approximately 150,000 cases across all tumor types and 300,000 controls with clinical, demographic, and exposure data, centralized via harmonized data dictionaries at the Data Coordination Center, established in 2014 at the International Agency for Research on Cancer, and supported by a secure analysis platform. Pooled analyses across diverse populations have implicated parental age, prenatal vitamin or folic acid use, mode of delivery, fetal growth, selected congenital anomalies, occupational or household exposures (e.g., pesticides), paternal smoking, and markers of early-life immune modulation (e.g., breastfeeding, daycare attendance) in leukemia risk, informing carcinogen evaluation and prevention. The integration of genetic ancestry and germline susceptibility data is clarifying ancestry-related differences in leukemia biology and outcomes, while confirming risk loci with population-specific effects. CLIC is now adding polygenic risk scores and exposomic data to refine etiologic subtyping and identify modifiable pathways, while broadening representation from underserved regions through partnership-building and capacity-strengthening.