The process of identification and management of neurological disorder conditions faces challenges, prompting the investigation of novel methods in order to improve diagnostic accuracy. In this study, we conducted a systematic literature review to identify the significance of genetics- and molecular-pathway-based machine learning (ML) models in treating neurological disorder conditions. According to the study\'s objectives, search strategies were developed to extract the research studies using digital libraries. We followed rigorous study selection criteria. A total of 24 studies met the inclusion criteria and were included in the review. We classified the studies based on neurological disorders. The included studies highlighted multiple methodologies and exceptional results in treating neurological disorders. The study findings underscore the potential of the existing models, presenting personalized interventions based on the individual\'s conditions. The findings offer better-performing approaches that handle genetics and molecular data to generate effective outcomes. Moreover, we discuss the future research directions and challenges, emphasizing the demand for generalizing existing models in real-world clinical settings. This study contributes to advancing knowledge in the field of diagnosis and management of neurological disorders.

BACKGROUND: Gliomas pose a significant challenge to effective treatment despite advancements in chemotherapy and radiotherapy. Glioma stem cells (GSCs), a subset within tumors, contribute to resistance, tumor heterogeneity, and plasticity. Recent studies reveal GSCs\' role in therapeutic resistance, driven by DNA repair mechanisms and dynamic transitions between cellular states. Resistance mechanisms can involve different cellular pathways, most of which have been recently reported in the literature. Despite progress, targeted therapeutic approaches lack consensus due to GSCs\' high plasticity.
OBJECTIVE: To analyze targeted therapies against GSC-mediated resistance to radio- and chemotherapy in gliomas, focusing on underlying mechanisms.
METHODS: A systematic search was conducted across major medical databases (PubMed, Embase, and Cochrane Library) up to September 30, 2023. The search strategy utilized relevant Medical Subject Heading terms and keywords related to including \"glioma stem cells\", \"radiotherapy\", \"chemotherapy\", \"resistance\", and \"targeted therapies\". Studies included in this review were publications focusing on targeted therapies against the molecular mechanism of GSC-mediated resistance to radiotherapy resistance (RTR).
RESULTS: In a comprehensive review of 66 studies on stem cell therapies for SCI, 452 papers were initially identified, with 203 chosen for full-text analysis. Among them, 201 were deemed eligible after excluding 168 for various reasons. The temporal breakdown of studies illustrates this trend: 2005-2010 (33.3%), 2011-2015 (36.4%), and 2016-2022 (30.3%). Key GSC models, particularly U87 (33.3%), U251 (15.2%), and T98G (15.2%), emerge as significant in research, reflecting their representativeness of glioma characteristics. Pathway analysis indicates a focus on phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (mTOR) (27.3%) and Notch (12.1%) pathways, suggesting their crucial roles in resistance development. Targeted molecules with mTOR (18.2%), CHK1/2 (15.2%), and ATP binding cassette G2 (12.1%) as frequent targets underscore their importance in overcoming GSC-mediated resistance. Various therapeutic agents, notably RNA inhibitor/short hairpin RNA (27.3%), inhibitors (e.g., LY294002, NVP-BEZ235) (24.2%), and monoclonal antibodies (e.g., cetuximab) (9.1%), demonstrate versatility in targeted therapies. among 20 studies (60.6%), the most common effect on the chemotherapy resistance response is a reduction in temozolomide resistance (51.5%), followed by reductions in carmustine resistance (9.1%) and doxorubicin resistance (3.0%), while resistance to RTR is reduced in 42.4% of studies.
CONCLUSIONS: GSCs play a complex role in mediating radioresistance and chemoresistance, emphasizing the necessity for precision therapies that consider the heterogeneity within the GSC population and the dynamic tumor microenvironment to enhance outcomes for glioblastoma patients.

There is extensive coverage in the existing literature on implant-associated lymphomas like anaplastic large-cell lymphoma, but breast implant-associated squamous cell carcinoma (BIA-SCC) has received limited scholarly attention since its first case in 1992. Thus, this study aims to conduct a qualitative synthesis focused on the underexplored association between breast implants and BIA-SCC. A systematic review was conducted utilizing the PubMed, Web of Science, and Cochrane databases to identify all currently reported cases of BIA-SCC. Additionally, a literature review was performed to identify potential biochemical mechanisms that could lead to BIA-SCC. Studies were vetted for quality using the NIH quality assessment tool. From an initial pool of 246 papers, 11 met the quality criteria for inclusion, examining a total of 14 patients aged between 40 and 81 years. BIA-SCC was found in a diverse range of implants, including those with smooth and textured surfaces, as well as those filled with saline and silicone. The condition notably manifested a proclivity for aggressive clinical progression, as evidenced by a mortality rate approximating 21.4% within a post-diagnostic interval of six months. Our literature review reveals that chronic inflammation, driven by various external factors such as pathogens and implants, can initiate carcinogenesis through epigenetic modifications and immune system alterations. This includes effects from exosomes and macrophage polarization, showcasing potential pathways for the pathogenesis of BIA-SCC. The study highlights the pressing need for further investigation into BIA-SCC, a subject hitherto inadequately addressed in the academic sphere. This necessitates the urgency for early screening and intervention to improve postoperative outcomes. While the review is confined by its reliance on case reports and series, it serves as a valuable reference for future research endeavors.

Colorectal carcinoma (colon and rectum) is currently considered among the most prevalent malignancies of Western societies. The pathogenesis and etiological mechanisms underlying colorectal cancer (CRC) development remain complex and heterogeneous. The homeostasis and function of normal human intestinal cells is highly regulated by microRNAs. Therefore, it is not surprising that mutations and inactivation of these molecules appear to be linked with progression of colorectal tumors. Recent studies have reported significant alterations of microRNA expression in adenomas and CRCs compared with adjacent normal tissues. This observed deviation has been proposed to correlate with the progression and survival of disease as well as with choice of optimal treatment and drug resistance. MicroRNAs can adopt either oncogenic or tumor-suppressive roles during regulation of pathways that drive carcinogenesis. Typically, oncogenic microRNAs termed oncomirs, target and silence endogenous tumor-suppressor genes. On the other hand, tumor-suppressive microRNAs are critical in downregulating genes associated with cell growth and malignant capabilities. By extensively evaluating robust studies, we have emphasized and distinguished a discrete set of microRNAs that can modulate tumor progression by silencing specific driver genes crucial in signaling pathways including Wnt/b-catenin, epidermal growth factor receptor, P53, mismatch repair DNA repair, and transforming-growth factor beta.

Cancer can take years to develop, both at its beginning and during its development. All typical epithelial cancers have a long latency period, sometimes 20 years or more, and if they are clinically detected, distinct genes may include infinite mutations. Long non-coding RNAs (LncRNAs) are a subset of RNAs that regulate many biological processes, including RNA processing, epigenetic control, and signal transduction. Current studies show that lncRNAs, which are dysregulated in cancer, play a significant function in the growth and spread of the illness. LncRNAs have been connected to the overexpression of specific proteins that function in tumors\' spread and growth. Moreover, through translational inhibition, microRNAs (miRNAs) regulates gene expression sequence specifically. Apart from that, non-coding RNAs known as miRNAs, with a length of around 22 nucleotides, controls gene expressions in a sequence-specific way either by preventing translation or degrading messenger RNA (mRNA). Quercetin appears to have a significant role in altering miRNA and lncRNA expression, which is linked to variations in the production of oncogenes, tumor suppressors, and proteins produced from cancer. Quercetin may change the earliest epigenetic modifications related to cancer prevention in addition to its usual antioxidant or anti-inflammatory effects. It would be beneficial to have more in-depth information on how Quercetin modulates miRNAs and lncRNAs to use it as a cancer therapeutic strategy. Here, we go through what is known about Quercetin\'s potential to modulate miRNAs and lncRNAs in various malignancies.

Driven by the limitations and obstacles of the available approaches and medications for multiple sclerosis (MS) that still cannot treat the disease, but only aid in accelerating the recovery from its attacks, the use of naturally occurring molecules as a potentially safe and effective treatment for MS is being explored in model organisms. MS is a devastating disease involving the brain and spinal cord, and its symptoms vary widely. Multiple molecular pathways are involved in the pathogenesis of the disease. The present review showcases the recent advancements in harnessing nature\'s resources to combat MS. By deciphering the molecular pathways involved in the pathogenesis of the disease, a wealth of potential therapeutic agents is uncovered that may revolutionize the treatment of MS. Thus, a new hope can be envisioned in the future, aiming at paving the way toward identifying novel safe alternatives to improve the lives of patients with MS.

This comprehensive review explores the genetic contributions to endometriosis and their potential impact on improving diagnostic techniques. The review begins by defining endometriosis and discussing its prevalence, emphasizing the need for a deeper understanding of the genetic basis of the condition. It highlights recent genome-wide association studies (GWAS) that have identified specific genetic variants associated with endometriosis, shedding light on the molecular pathways and mechanisms involved. The review addresses genetic heterogeneity across different populations and ethnicities, emphasizing the importance of considering population-specific markers in diagnostic approaches. It explores the diagnostic implications of genetic insights, including the potential use of genetic markers for precise and early detection, as well as risk prediction. The review also delves into the integration of genetic information with clinical parameters and imaging findings, and the exploration of multi-omics approaches for a comprehensive understanding of endometriosis. It discusses recent studies on genetic and epigenetic biomarkers, their potential as diagnostic tools, and the need for validation in independent cohorts. The review highlights the impact of new genomic technologies, such as next-generation sequencing, in improving diagnostic accuracy and personalized management. It identifies the challenges and future directions in translating genetic findings into diagnostic tools and emphasizes the transformative potential of genetic insights in endometriosis diagnosis. This review provides a roadmap for future research and underscores the significance of genetic insights in improving diagnostic precision and personalized care for individuals with endometriosis.

Short non-coding RNAs called microRNAs (miRNAs) control gene expression by either inhibiting translation or degrading messenger RNA. MiRNAs are crucial for many biological functions, and the deregulation of their expression is strongly linked to the emergence of cancer. A single miRNA controls several gene expressions, allowing it to simultaneously control a number of cellular signaling pathways. As a result, miRNAs may be used as therapeutic targets as well as biomarkers for the prognosis and diagnosis of different cancers. Recent research has shown that natural compounds like curcumin, resveratrol and quercetin exert their pro-apoptotic and/or anti-proliferative impacts by modulating one and/or more miRNAs, which inhibits the growth of cancer cells, induces apoptosis, or increases the effectiveness of conventional cancer therapies. Here, we summarize the most recent developments in curcumin\'s control over the expression of miRNAs and emphasize the significance of these herbal remedies as a viable strategy in the treatment and prevention of cancer.

Esophageal adenocarcinoma (EAC) is rapidly increasing in incidence and is associated with a poor prognosis. Barrett\'s esophagus (BE) is a known precursor of esophageal adenocarcinoma. This review aims to explore Barrett\'s esophagus, esophageal adenocarcinoma, and the progression from the former to the latter. An overview of the definition, diagnosis, epidemiology, and risk factors for both entities are presented, with special attention being given to the areas of debate in the literature. The progression from Barrett\'s esophagus to esophageal adenocarcinoma is reviewed and the relevant molecular pathways are discussed. The definition of Barrett\'s esophagus remains debated and without international consensus. This, alongside other factors, has made establishing the true prevalence of Barrett\'s esophagus challenging. The degree of dysplasia can be a histological challenge, but is necessary to guide clinical management. The progression of BE to EAC is likely driven by inflammatory pathways, pepsin exposure, upregulation of growth factor pathways, and mitochondrial changes. Surveillance is maintained through serial endoscopic evaluation, with shorter intervals recommended for high-risk features.

Parkinson\'s disease is a neurodegenerative disease whose progression and clinical characteristics have a close bidirectional and multilevel relationship with the process of neuroinflammation. In this context, it is necessary to understand the mechanisms involved in this neuroinflammation-PD link. This systematic search was, hereby, conducted with a focus on the four levels where alterations associated with neuroinflammation in PD have been described (genetic, cellular, histopathological and clinical-behavioral) by consulting the PubMed, Google Scholar, Scielo and Redalyc search engines, including clinical studies, review articles, book chapters and case studies. Initially, 585,772 articles were included, and, after applying the inclusion and exclusion criteria, 84 articles were obtained that contained information about the multilevel association of neuroinflammation with alterations in gene, molecular, cellular, tissue and neuroanatomical expression as well as clinical-behavioral manifestations in PD.