Bashdar Mahmud Hussen

The cytogenetic equivalents of oncogene amplification are well-known in cancer cells as homogeneously staining regions (HSR) or double minutes (DM). We previously described similar amplifications of satellite-DNA (Sat-DNA) in advanced prostate cancer. In this study, we systematically screened for Sat-DNA amplification in 47 breast cancer (BCa) samples, which is a prevalent malignancy in women. Interphase fluorescence in situ hybridization (iFISH) was applied using 23 Sat-DNA probes and a probe for ErbB2/Her2 gene amplification. ErbB2/Her2 gene amplification was identified in 20 of the studied BCA samples; 13 showed an HSR pattern and seven showed a DM pattern by iFISH. Additionally, the application of 23 Sat-DNA probes revealed massive chromosome instability (CIN) in all samples studied. Notably, 15 out of 47 BCa samples displayed amplification of one or two Sat-DNAs. Each was detectable as HSR-like structures in 13 out of 15 cases. In two cases, Sat-DNA was amplified as DMs. Sat-III-DNA (1q12/HSat3 and D9Z3) was involved in nine cases, and α-Sat-DNA derived from chromosomes 9, 11, 17 and 18 showed amplification in nine cases. Sat-DNA amplification was positively aligned with advance in tumor grade, Ki67 concentration and positive ErbB2/Her2 immunohistochemistry status and/or gene amplification. Four selected cases with α-Sat-DNA amplification showed enhanced α-Sat-RNA-expression between 1.4- and 9.7-fold, while two cases without α-Sat-DNA amplification showed such RNA-presence only at very low levels. Overall, Sat-DNA amplification may be an overlooked feature of advanced solid tumors, as demonstrated here for BCa and in previous studies for prostate cancer and liposarcoma.

Gasotransmitters, including nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H₂S), play an important role in normal physiological processes in the body, such as neurotransmission, synaptic plasticity, and neuroinflammation. Dysregulation of signaling pathways of gasotransmitters contributes to the pathophysiology of autism spectrum disorder (ASD), which is a neurodevelopmental disorder characterized by deficits in social communication and the presence of restricted interests and repetitive behaviors. This systematic review aims to identify the potential role of gasotransmitters in ASD pathophysiology and their correlation with ASD severity. Following PRISMA guidelines, we conducted a systematic review by searching PubMed and Google Scholar databases in May 2024. We included studies that investigated the role of NO, H₂S, and CO in ASD between 2000 and 2024. We extracted data on the type of gasotransmitters, the model of the study (human or animal model), in vivo or in vitro, and the main role of these gasotransmitters as a risk factor or protective factor obtained findings. Out of 81 published papers screened from the databases, 39 reports were assessed for eligibility. After excluding studies that mentioned NO and CO as environmental pollutants, short communication, editorial letters, narrative reviews, systematic reviews, and meta-analyses, 28 original articles satisfied the inclusion and exclusion criteria. Results indicate a correlation between gasotransmitters and ASD, which contributed to the severity of ASD and its symptoms. An increase in gasotransmitters causes additional complications for individuals with ASD and can be mentioned as a risk factor or biomarker for ASD, except H₂S. The link between these endogenous gaseous molecules and ASD remains unclear; this systematic review offers strong evidence of the significant correlation between gasotransmitters and autism spectrum disorder.

Stem-cell therapy is a revolutionary frontier in modern medicine, offering enormous capacity to transform the treatment landscape of numerous debilitating illnesses and injuries. This review examines the revolutionary frontier of treatments utilizing stem cells, highlighting the distinctive abilities of stem cells to undergo regeneration and specialized cell differentiation into a wide variety of phenotypes. This paper aims to guide researchers, physicians, and stakeholders through the intricate terrain of stem-cell therapy, examining the processes, applications, and challenges inherent in utilizing stem cells across diverse medical disciplines. The historical journey from foundational contributions in the late 19th and early 20th centuries to recent breakthroughs, including ESC isolation and iPSC discovery, has set the stage for monumental leaps in medical science. Stem cells’ regenerative potential spans embryonic, adult, induced pluripotent, and perinatal stages, offering unprecedented therapeutic opportunities in cancer, neurodegenerative disorders, cardiovascular ailments, spinal cord injuries, diabetes, and tissue damage. However, difficulties, such as immunological rejection, tumorigenesis, and precise manipulation of stem-cell behavior, necessitate comprehensive exploration and innovative solutions. This manuscript summarizes recent biotechnological advancements, critical trial evaluations, and emerging technologies, providing a nuanced understanding of the triumphs, difficulties, and future trajectories in stem cell-based regenerative medicine. Future directions, including precision medicine integration, immune modulation strategies, advancements in gene-editing technologies, and bioengineering synergy, offer a roadmap in stem cell treatment. The focus on stem-cell therapy’s potential highlights its significant influence on contemporary medicine and points to a future in which individualized regenerative therapies will alleviate various medical disorders.

Cancer is a broad name for a group of diseases in which abnormal cells grow out of control and are characterized by their complexity and recurrence. Although there has been progress in cancer therapy with the entry of precision medicine and immunotherapy, cancer incidence rates have increased globally. Non-coding RNAs in the form of circular RNAs (circRNAs) play crucial roles in the pathogenesis, clinical diagnosis, and therapy of different diseases, including cancer. According to recent studies, circRNAs appear to serve as accurate indicators and therapeutic targets for cancer treatment. However, circRNAs are promising candidates for cutting-edge cancer therapy because of their distinctive circular structure, stability, and wide range of capabilities; many challenges persist that decrease the applications of circRNA-based cancer therapeutics. Here, we explore the roles of circRNAs as a replacement for cancer therapy, highlight the main challenges facing circRNA-based cancer therapies, and discuss the key strategies to overcome these challenges to improve advanced innovative therapies based on circRNAs with long-term health effects.

Breast cancer (BC) is considered as the most frequent cancer among women and a significant contributor to mortality. The CRISPR/Cas9 gene-editing tool has promising applications for BC drug resistance. It is a unique and creative approach that has lately attracted attention and can be used to fix gene alterations related to multidrug resistance. Recent research has effectively investigated and targeted particular genes linked to BC treatment resistance using CRISPR/Cas9 gene editing, including those linked to hormone receptor signaling, drug efflux transporters, and DNA repair pathways. The CRISPR/Cas9 technology's selective disruption or mutation of these genes provides valuable information about their role in resistance and paves the path for cutting-edge treatment options. CRISPR/Cas9 gene editing can overcome BC treatment resistance by identifying crucial genetic variables and revealing new therapeutic targets Despite the advantages, there are limitations in the study on CRISPR/Cas9-based gene editing for BC treatment resistance, for example, off-target effects and the improvement of delivery techniques are still major issues. Successful clinical translation depends on methods to improve the specificity and effectiveness of CRISPR/Cas9 editing and to solve these constraints. This review aims to explore the possibility of CRISPR/Cas9 gene editing as an innovative method of combating BC medication resistance.

Gastrointestinal cancers are a huge worldwide health concern, which includes a wide variety of digestive tract cancers. Circular RNAs (circRNAs), a kind of non-coding RNA (ncRNAs), are a family of single-stranded, covalently closed RNAs that have become recognized as crucial gene expression regulators, having an impact on several cellular functions in cancer biology. The gut microbiome, which consists of several different bacteria, actively contributes to the regulation of host immunity, inflammation, and metabolism. CircRNAs and the gut microbiome interact significantly to greatly affect the growth of GI cancer. Several studies focus on the complex functions of circRNAs and the gut microbiota in GI cancers, including esophageal cancer, colorectal cancer, gastric cancer, hepatocellular cancer, and pancreatic cancer. It also emphasizes how changed circRNA expression profiles and gut microbiota affect pathways connected to malignancy as well as how circRNAs affect hallmarks of gastrointestinal cancers. Furthermore, circRNAs and gut microbiota have been recommended as biological markers for therapeutic targets as well as diagnostic and prognostic purposes. Targeting circRNAs and the gut microbiota for the treatment of gastrointestinal cancers is also being continued to study. Despite significant initiatives, the connection between circRNAs and the gut microbiota and the emergence of gastrointestinal cancers remains poorly understood. In this study, we will go over the most recent studies to emphasize the key roles of circRNAs and gut microbiota in gastrointestinal cancer progression and therapeutic options. In order to create effective therapies and plan for the future gastrointestinal therapy, it is important to comprehend the functions and mechanisms of circRNAs and the gut microbiota.

Colorectal cancer (CRC) is ranked as the world's third-most prevalent cancer, and metastatic CRC considerably increases cancer-related fatalities globally. A number of complex mechanisms that are strictly controlled at the molecular level are involved in metastasis, which is the primary reason for death in people with CRC. Recently, it has become clear that exosomes, which are small extracellular vesicles released by non-tumorous and tumorigenic cells, play a critical role as communication mediators among tumor microenvironment (TME). To facilitate communication between the TME and cancer cells, non-coding RNAs (ncRNAs) play a crucial role and are recognized as potent regulators of gene expression and cellular processes, such as metastasis and drug resistance. NcRNAs are now recognized as potent regulators of gene expression and many hallmarks of cancer, including metastasis. Exosomal ncRNAs, like miRNAs, circRNAs, and lncRNAs, have been demonstrated to influence a number of cellular mechanisms that contribute to CRC metastasis. However, the molecular mechanisms that link exosomal ncRNAs with CRC metastasis are not well understood. This review highlights the essential roles that exosomal ncRNAs play in the progression of CRC metastatic disease and explores the therapeutic choices that are open to patients who have CRC metastases. However, exosomal ncRNA treatment strategy development is still in its early phases; consequently, additional investigation is required to improve delivery methods and find novel therapeutic targets as well as confirm the effectiveness and safety of these therapies in preclinical and clinical contexts.