Search

Cancers and neurological disorders are two major types of diseases in humans. We developed the concept called the Aberrant Cell Cycle Disease (ACCD) due to the accumulating evidence that shows that two different diseases share the common mechanism of aberrant cell cycle re-entry. The aberrant cell cycle re-entry is manifested as kinase/oncoprotein activation and tumor suppressor (TS) inactivation, which are associated with both tumor growth in cancers and neuronal death in neurological disorders. Therefore, some cancer therapies (e.g., kinase/oncogene inhibition and TS elevation) can be leveraged for neurological treatments. MicroRNA (miR/miRNA) provides a new style of drug-target binding. For example, a single tumor suppressor miRNA (TS-miR/miRNA) can bind to and decrease tens of target kinases/oncogenes, producing much more robust efficacy to block cell cycle re-entry than inhibiting a single kinase/oncogene. In this review, we summarize the miRNAs that are altered in both cancers and neurological disorders, with an emphasis on miRNA drugs that have entered into clinical trials for neurological treatment.

Worldwide, health professionals from all specialties are encouraging patients to reduce alcohol use if not abstain, and abstinence is clearly encouraged for tobacco. However, for users of substances that meet diagnostic criteria for substance use disorder (addiction), reducing use or abstaining will be difficult without appropriate addiction treatment. Moreover, this group is the most at risk and the most likely to benefit from reducing use. We propose research-based arguments to better combine encouragement to reduce or abstain from alcohol and tobacco to systematic screening for addiction and facilitated access to addiction treatment to make alcohol and tobacco preventable deaths truly preventable.

Clinical, epidemiological, and molecular studies have sufficiently highlighted the vitality of vitamin D [25(OH)D and 1,25(OH)2D] in human health and wellbeing. Globally, vitamin D deficiency (VDD) has become a public health concern among all age groups. There is a very high prevalence of VDD per the estimates from several epidemiological studies on different ethnic populations. But, population-specific scales do not support these estimates to define VDD clinically and consistent genetic associations. However, clinical studies have shown the relevance of serum vitamin D screening and oral supplementation in improving health conditions, pointing toward a more prominent role of vitamin D in health and wellness. Routinely, the serum concentration of vitamin D is measured to determine the deficiency and is correlated with physiological conditions and clinical symptoms. Recent research points toward a more inclusive role of vitamin D in different disease pathologies and is not just limited to otherwise bone health and overall growth. VDD contributes to the natural history of systemic ailments, including cardiovascular and systemic immune diseases. Considering its significant impact on premature morbidity and mortality, there is a compelling need to comprehensively review and document the direct and indirect implications of VDD in immune system deregulation, systemic inflammatory conditions, and cardio-metabolism. The recommendations from this review call for furthering our research concerning vitamin D and its direct and indirect implications. [ABSTRACT FROM AUTHOR]

AbstractWe report the development of an immunotherapeutic molecule, a Humanized immunotoxin, for treating hCG-expressing advanced-stage cancers. PiPP, a high-affinity anti-hCG monoclonal antibody, is used in the immunotoxin for ‘homing’ hCG-positive cancer cells. The deimmunized (DI) form of α-Sarcin, a fungal-origin toxin that lacks functional T-cell epitopes, is used in the design to ensure minimal immunogenicity of the immunotoxin for repetitive use in humans. A single-chain variable fragment (scFv) of PiPP was constructed by linking the Humanized VH and VL regions of the antibody. The scFv part of the antibody was further linked to the toxin α-Sarcin (DI) at the gene level and expressed as a recombinant protein in E. coli. The immunotoxin was purified from the bacterial cell lysate and analysed for binding and cytotoxicity to hCG-secreting colorectal and pancreatic cancer cells. The results showed that the scFv(PiPP)-Sarcin immunotoxin was able to bind to colorectal and pancreatic cancer cells and killed approximately 85% of the cells. In vivo testing of the immunotoxin produced results similar to those of in vitro testing against colorectal adenocarcinoma-induced tumours. This immunotoxin could be a promising immunotherapeutic agent for treating colorectal, pancreatic and other terminal-stage hCG-expressing cancers. [ABSTRACT FROM AUTHOR]

Simple Summary: The tumor microenvironment (TME) refers to the area immediately surrounding a cancerous tumor that influences the tumor's behavior and how the immune system reacts to it. Central to the TME environment are special immune cells—tumor-associated macrophages (TAMs)—that, rather than restrict the tumor, actually facilitate tumor growth and metastasis. Thus, targeting these TAMs can help to eliminate cancer. In this article, we review the biology of TAMs and delve into the signaling mechanisms underlying the polarization of macrophage phenotypes, their plasticity, and therapeutic implications. Within the tumor microenvironment, myeloid cells constitute a dynamic immune population characterized by a heterogeneous phenotype and diverse functional activities. In this review, we consider recent literature shedding light on the increasingly complex biology of M2-like immunosuppressive tumor-associated macrophages (TAMs), including their contribution to tumor cell invasion and metastasis, stromal remodeling (fibrosis and matrix degradation), and immune suppressive functions, in the tumor microenvironment (TME). This review also delves into the intricate signaling mechanisms underlying the polarization of diverse macrophage phenotypes, and their plasticity. We also review the development of promising therapeutic approaches to target these populations in cancers. The expanding knowledge of distinct subsets of immunosuppressive TAMs, and their contributions to tumorigenesis and metastasis, has sparked significant interest among researchers regarding the therapeutic potential of TAM depletion or phenotypic modulation. [ABSTRACT FROM AUTHOR]

Background: Palliation to late dysphagia after radiotherapy for nasopharyngeal carcinoma (NPC) continues to be a challenge. Intermittent oro-esophageal tube feeding (IOE) is an emerging enteral nutrition mode that can address nutrition and quality of life issues related to nasogastric tube feeding (NGT). Objectives: This study aims to investigate the effect of IOE versus NGT in late dysphagia after radiotherapy for NPC. Methods: This randomized controlled study included 82 NPC survivors with late dysphagia after radiotherapy. The subjects were randomized divided into the IOE and NGT groups (n1 = n2 = 41). Both groups received standard-of-care rehabilitation. Enteral nutrition supports were administered through IOE or NGT accordingly. This study lasted 2 weeks for each participant. The primary outcome was nutritional status including albumin, hemoglobin, total serum protein, and body mass index. The secondary outcomes were (i) the functional oral intake scale (FOIS), (ii) the penetration-aspiration scale (PAS), (iii) oral transit time (OTT), (iv) hyoid pause time (HPT), (v) pharyngeal transport time (PTT), and (vi) swallowing-quality of life (SWAL-QoL). Results: Three cases quitted the study halfway and there were no significant baseline differences between the IOE (n = 40) and NGT (n = 39) groups. Both time and group effects were significant in all nutritional indicators. The time effect was significant in the FOIS levels, OTT and PTT, while the group effect was not. Either time or group effect were insignificant in the PAS levels and HPT. Both group and time effects were significant in the SWAL-QoL total scores (zGroup = 5.080, P < 0.001; zTime = 18.005, P < 0.001). The significance of time and group effects varied across different dimensions of the SWAL-QoL. Conclusions: Rehabilitation interventions can improve swallowing function among NPC survivors with late dysphagia after radiotherapy. In this population who received standard-of-care rehabilitation, IOE is more conducive to the improvement of nutritional status, and swallowing-related quality of life. Trial registration: ClinicalTrials.gov Identifier: NCT06301763. [ABSTRACT FROM AUTHOR]

Scarce data is available regarding primary immunodeficiency-associated cancers in children in low-middle-income countries. This study aimed to determine the incidence, clinical features and outcomes of primary immunodeficiencies (PIDs)-associated cancers in children presenting to Pakistan's largest public-sector specialised pediatric oncology center. Among 5,748 children with cancers registered over 5 years, only eight patients were found to have PID-associated pediatric malignancies with an incidence of 1.4 per 1,000 cases. The median age at the time of diagnosis was 6.5 years with a male-to-female ratio of 7:1. Only four types of PIDs were found to be associated with cancer in children at our center: Ataxia Telangiectasia in 37.5% (n = 3), hyper-IgE syndrome and IgG deficiency in 25% (each n = 2) and one case (12.5%) of common variable immune deficiency. Six different types of pediatric cancers were associated with PID with a predisposition towards hematological malignancies (n = 7, 87.5%). Only two patients (25%) survived. The median survival of the cohort was 3.5 months. Infection-related mortality was the cause of death in four patients (66%), and the type of PID was the only statistically significant factor associated with the outcome. It is concluded that a lesser proportion of PID-associated pediatric cancers are found in our center as compared to the reported data from high-income countries. PID-associated cancers in children have an abysmal prognosis and infection- related mortality is the major cause of treatment failure. Sensitisation of oncologists to look for any underlying PID, the introduction of PID-screening programs in children and consideration of PID-associated malignancies as a high-risk group for treatment may help improve the outcomes. [ABSTRACT FROM AUTHOR]

Resistance to chemotherapy is a problem of major social and economic importance, when looking at factors like the decrease in life expectancy, the associated therapeutic costs, and a significant number of cancers that resist current chemotherapy. The development of chemotherapeutics for all theoretically possible tumor variants is an approach that requires unreasonable resources. We propose a theoretical model that serves the purpose of overcoming resistance to chemotherapeutic agents used in cancer therapy. The model describes a gene delivery system based on liposomes, which are optically guided to the tumor's location. The main aim of the gene delivery system is inhibiting the activity of enzymes involved in drug metabolism, hence offering the opportunity to use inexpensive chemotherapeutics that are already on the market. This model will reduce the costs of chemotherapy and will assure a positive outcome for patients. [ABSTRACT FROM AUTHOR]

Glycoproteins, representing a significant proportion of posttranslational products, play pivotal roles in various biological processes, such as signal transduction and immune response. Abnormal glycosylation may lead to structural and functional changes of glycoprotein, which is closely related to the occurrence and development of various diseases. Consequently, exploring protein glycosylation can shed light on the mechanisms behind disease manifestation and pave the way for innovative diagnostic and therapeutic strategies. Nonetheless, the study of clinical glycoproteomics is fraught with challenges due to the low abundance and intricate structures of glycosylation. Recent advancements in mass spectrometry‐based clinical glycoproteomics have improved our ability to identify abnormal glycoproteins in clinical samples. In this review, we aim to provide a comprehensive overview of the foundational principles and recent advancements in clinical glycoproteomic methodologies and applications. Furthermore, we discussed the typical characteristics, underlying functions, and mechanisms of glycoproteins in various diseases, such as brain diseases, cardiovascular diseases, cancers, kidney diseases, and metabolic diseases. Additionally, we highlighted potential avenues for future development in clinical glycoproteomics. These insights provided in this review will enhance the comprehension of clinical glycoproteomic methods and diseases and promote the elucidation of pathogenesis and the discovery of novel diagnostic biomarkers and therapeutic targets. [ABSTRACT FROM AUTHOR]

Endomucin (MUC14), encoded by EMCN gene, is an O‐glycosylated transmembrane mucin that is mainly found in venous endothelial cells (ECs) and highly expressed in type H vessels of bone tissue. Its main biological functions include promoting endothelial generation and migration through the vascular endothelial growth factor (VEGF) signaling pathway and inhibiting the adhesion of inflammatory cells to ECs. In addition, it induces angiogenesis and promotes bone formation. Due to the excellent functions of Endomucin in the above aspects, it provides a new research target for the treatment of vascular inflammatory‐related diseases and bone diseases. Based on the current understanding of its function, the research of Endomucin mainly focuses on the above two diseases. As it is known, the progression of cancer is closely related to angiogenesis. Endomucin recently is found to be differentially expressed in a variety of tumors and correlated with survival rate. The biological role of Endomucin in cancer is opaque. This article introduces the research progress of Endomucin in vascular inflammatory‐related diseases and bone diseases, discusses its application value and prospect in the treatment, and collects the latest research situation of Endomucin in tumors, to provide meaningful evidence for expanding the research field of Endomucin. [ABSTRACT FROM AUTHOR]

TRAF2 and NCK interacting kinase (TNIK), a critical interacting protein kinase, is currently receiving wide attention. TNIK is found in various human body organs and tissues and participates in cell motility, proliferation, and differentiation. On the one hand, its aberrant expression is related to the onset and progression of numerous malignant tumors. On the other hand, TNIK is important in neuronal growth, proliferation, differentiation, and synaptic formation. Thus, the novel therapeutic strategies for targeting TNIK offer a promising direction for cancer, neurological or psychotic disorders. Here, we briefly summarized the biological information of TNIK, reviewed the role and regulatory mechanism in cancer and neuropsychiatric diseases, and introduced the research progress of inhibitors targeting TNIK. Taken together, this review hopes to contribute to the in-depth understanding of the function and regulatory mechanism of TNIK, which is of great significance for revealing the role of TNIK in the occurrence and treatment of diseases. [ABSTRACT FROM AUTHOR]

N6-methyladenosine (m6A) represents the most prevalent internal and reversible modification on RNAs. Different cell types display their unique m6A profiles, which are determined by the functions of m6A writers and erasers. M6A modifications lead to different outcomes such as decay, stabilization, or transport of the RNAs. The m6A-encoded epigenetic information is interpreted by m6A readers and their interacting proteins. M6A readers are essential for different biological processes, and the defects in m6A readers have been discovered in diverse diseases. Here, we review the latest advances in the roles of m6A readers in development and diseases. These recent studies not only highlight the importance of m6A readers in regulating cell fate transitions, but also point to the potential application of drugs targeting m6A readers in diseases. [ABSTRACT FROM AUTHOR]

Background: Medical fear is a common psychological reaction in hospitalized children, especially during radiotherapy for central nervous system (CNS) cancers. This fear not only causes negative emotions such as anxiety and depression but also affects children's quality of life and treatment outcomes. It is exacerbated by factors such as unfamiliar environments during radiation therapy and separation from parents. Child Life, as a professional service, offers physical and mental support to children through medical understanding and psychological preparation, addressing their social and psychological needs, among other things. This study aims to construct a comprehensive Child Life intervention program (CCLIP), consisting of four key components: psychological adjustment and preparation, therapeutic play, pain management and coping strategies, and family support. The integration of effective intervention methods aims to reduce medical fear in children undergoing radiotherapy, promote psychological well-being, improve treatment compliance, and enhance quality of life. Methods: This study is a protocol for a randomized controlled trial. Using a random number table method, we plan to recruit 38 eligible children who meet the inclusion criteria and then randomize them into two distinct groups: the intervention group and the control group. The intervention group will receive the CCLIP, and the control group will receive standardized care. Data will be collected through questionnaires and on-site assessments during the one-month intervention period at four distinct time points: the day of admission (T0), the first radiotherapy positioning (T1), mid-radiotherapy (T2), and postradiotherapy (T3). The primary outcome measure is the effectiveness of the CCLIP in reducing medical fear among children receiving radiation treatment for CNS cancers. Secondary outcomes include anxiety, depression, radiation adherence, quality of life among children, and parental satisfaction. Discussion: This study aims to alleviate medical fear among children with CNS tumors undergoing radiotherapy through the implementation of the CCLIP while enhancing their mental health and quality of life. The expected outcomes of this research include providing effective intervention strategies for clinical practice, improving the treatment experience and long-term prognosis of children, and having positive impacts on children and their families. Trial registration: This study is registered at the Chinese Clinical Trial Registry, ChiCTR2400082622. Registered 2 April, 2024. [ABSTRACT FROM AUTHOR]

As global population ageing accelerates, cancer emerges as a predominant cause of mortality. Long non-coding RNAs (lncRNAs) play crucial roles in cancer cell growth and death, given their involvement in regulating downstream gene expression levels and numerous cellular processes. Cell death, especially non-apoptotic regulated cell death (RCD), such as ferroptosis, pyroptosis and necroptosis, significantly impacts cancer proliferation, invasion and metastasis. Understanding the interplay between lncRNAs and the diverse forms of cell death in cancer is imperative. Modulating lncRNA expression can regulate cancer onset and progression, offering promising therapeutic avenues. This review discusses the mechanisms by which lncRNAs modulate nonapoptotic RCDs in cancer, highlighting their potential as biomarkers for various cancer types. Elucidating the role of lncRNAs in cell death pathways provides valuable insights for personalised cancer interventions. [ABSTRACT FROM AUTHOR]

Cancer is a severe illness that significantly threatens human life and health. Anticancer peptides (ACPs) represent a promising therapeutic strategy for combating cancer. In silico methods enable rapid and accurate identification of ACPs without extensive human and material resources. This study proposes a two-stage computational framework called ACP-CapsPred, which can accurately identify ACPs and characterize their functional activities across different cancer types. ACP-CapsPred integrates a protein language model with evolutionary information and physicochemical properties of peptides, constructing a comprehensive profile of peptides. ACP-CapsPred employs a next-generation neural network, specifically capsule networks, to construct predictive models. Experimental results demonstrate that ACP-CapsPred exhibits satisfactory predictive capabilities in both stages, reaching state-of-the-art performance. In the first stage, ACP-CapsPred achieves accuracies of 80.25% and 95.71%, as well as F1-scores of 79.86% and 95.90%, on benchmark datasets Set 1 and Set 2, respectively. In the second stage, tasked with characterizing the functional activities of ACPs across five selected cancer types, ACP-CapsPred attains an average accuracy of 90.75% and an F1-score of 91.38%. Furthermore, ACP-CapsPred demonstrates excellent interpretability, revealing regions and residues associated with anticancer activity. Consequently, ACP-CapsPred presents a promising solution to expedite the development of ACPs and offers a novel perspective for other biological sequence analyses. [ABSTRACT FROM AUTHOR]

Histone variants are the paralogs of core histones (H2A, H2B, H3 and H4). They are stably expressed throughout the cell cycle in a replication-independent fashion and are capable of replacing canonical counterparts under different fundamental biological processes. Variants have been shown to take part in multiple processes, including DNA damage repair, transcriptional regulation and X chromosome inactivation, with some of them even specializing in lineage-specific roles like spermatogenesis. Several reports have recently identified some unprecedented variants from different histone families and exploited their prognostic value in distinct types of cancer. Among the four classes of canonical histones, the H2A family has the greatest number of variants known to date, followed by H2B, H3 and H4. In our prior review, we focused on summarizing all 19 mammalian histone H2A variants. Here in this review, we aim to complete the full summary of the roles of mammalian histone variants from the remaining histone H2B, H3, and H4 families, along with an overview of their roles in cancer biology and their prognostic value in a clinical context. [ABSTRACT FROM AUTHOR]

Furin, a serine protease enzyme located in the Golgi apparatus of animal cells, plays a crucial role in cleaving precursor proteins into their mature, active forms. It is ubiquitously expressed across various tissues, including the brain, lungs, gastrointestinal tract, liver, pancreas, and reproductive organs. Since its discovery in 1990, furin has been recognized as a significant therapeutic target, leading to the active development of furin inhibitors for potential use in antiviral, antibacterial, anticancer, and other therapeutic applications. This review provides a comprehensive overview of the progress in the development and characterization of furin inhibitors, encompassing peptides, linear and macrocyclic peptidomimetics, and non-peptide compounds, highlighting their potential in the treatment of both infectious and non-infectious diseases. [ABSTRACT FROM AUTHOR]

Non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin, diclofenac, ibuprofen, or celecoxib have a well-established and unquestionable role in the human therapeutic arsenal, but still new perspectives are being discovered. This review presents new anti-inflammatory mechanisms of NSAIDs action, other than the classical one, i.e., the inhibition of cyclooxygenase (COX) isoforms leading to the prostanoids synthesis blockage. Literature data show that this group of drugs can activate anti-inflammatory peroxisome proliferator-activated receptor gamma (PPARγ), inhibit pro-inflammatory nuclear factor-κB (NF-κB) activation or modulate the components of the unfolded protein response (UPR) pathway. These alternative pathways induced by NSAIDs may not only enhance their basic anti-inflammatory mechanism of action but also promote other effects of the drugs such as anti-cancer. It was also proved that neuroinflammation, with the involvement of NF-κB, PPARγ and the components of the UPR pathway has an essential impact on the development of central nervous system (CNS) diseases. Thus, it seems possible that these new molecular targets may expand the use of NSAIDs, e.g., in the treatment of cancers and/or CNS disorders. [ABSTRACT FROM AUTHOR]

Circular RNAs (circRNAs) are a unique class of RNA molecules formed through back‐splicing rather than linear splicing. As an emerging field in molecular biology, circRNAs have garnered significant attention due to their distinct structure and potential functional implications. A comprehensive understanding of circRNAs' functions and potential clinical applications remains elusive despite accumulating evidence of their involvement in disease pathogenesis. Recent research highlights their significant roles in various human diseases, but comprehensive reviews on their functions and applications remain scarce. This review provides an in‐depth examination of circRNAs, focusing first on their involvement in non‐neoplastic diseases such as respiratory, endocrine, metabolic, musculoskeletal, cardiovascular, and renal disorders. We then explore their roles in tumors, with particular emphasis on exosomal circular RNAs, which are crucial for cancer initiation, progression, and resistance to treatment. By detailing their biogenesis, functions, and impact on disease mechanisms, this review underscores the potential of circRNAs as diagnostic biomarkers and therapeutic targets. The review not only enhances our understanding of circRNAs' roles in specific diseases and tumor types but also highlights their potential as novel diagnostic and therapeutic tools, thereby paving the way for future clinical investigations and potential therapeutic interventions. [ABSTRACT FROM AUTHOR]

Aims: Advances in treatment have extended the life expectancy of patients with metastatic bone disease (MBD). Patients could experience more skeletal-related events (SREs) as a result of this progress. Those who have already experienced a SRE could encounter another local management for a subsequent SRE, which is not part of the treatment for the initial SRE. However, there is a noted gap in research on the rate and characteristics of subsequent SREs requiring further localized treatment, obligating clinicians to extrapolate from experiences with initial SREs when confronting subsequent ones. This study aimed to investigate the proportion of MBD patients developing subsequent SREs requiring local treatment, examine if there are prognostic differences at the initial treatment between those with single versus subsequent SREs, and determine if clinical, oncological, and prognostic features differ between initial and subsequent SRE treatments. Methods: This retrospective study included 3,814 adult patients who received local treatment – surgery and/or radiotherapy – for bone metastasis between 1 January 2010 and 31 December 2019. All included patients had at least one SRE requiring local treatment. A subsequent SRE was defined as a second SRE requiring local treatment. Clinical, oncological, and prognostic features were compared between single SREs and subsequent SREs using Mann-Whitney U test, Fisher’s exact test, and Kaplan–Meier curve. Results: Of the 3,814 patients with SREs, 3,159 (83%) patients had a single SRE and 655 (17%) patients developed a subsequent SRE. Patients who developed subsequent SREs generally had characteristics that favoured longer survival, such as higher BMI, higher albumin levels, fewer comorbidities, or lower neutrophil count. Once the patient got to the point of subsequent SRE, their clinical and oncological characteristics and one-year survival (28%) were not as good as those with only a single SRE (35%; p < 0.001), indicating that clinicians’ experiences when treating the initial SRE are not similar when treating a subsequent SRE. Conclusion: This study found that 17% of patients required treatments for a second, subsequent SRE, and the current clinical guideline did not provide a specific approach to this clinical condition. We observed that referencing the initial treatment, patients in the subsequent SRE group had longer six-week, 90-day, and one-year median survival than patients in the single SRE group. Once patients develop a subsequent SRE, they have a worse one-year survival rate than those who receive treatment for a single SRE. Future research should identify prognostic factors and assess the applicability of existing survival prediction models for better management of subsequent SREs. Cite this article: Bone Joint Res 2024;13(9):497–506.

Abstract N 6-methyladenosine (m6A) represents the most prevalent internal and reversible modification on RNAs. Different cell types display their unique m6A profiles, which are determined by the functions of m6A writers and erasers. M6A modifications lead to different outcomes such as decay, stabilization, or transport of the RNAs. The m6A-encoded epigenetic information is interpreted by m6A readers and their interacting proteins. M6A readers are essential for different biological processes, and the defects in m6A readers have been discovered in diverse diseases. Here, we review the latest advances in the roles of m6A readers in development and diseases. These recent studies not only highlight the importance of m6A readers in regulating cell fate transitions, but also point to the potential application of drugs targeting m6A readers in diseases.

Abstract Background Medical fear is a common psychological reaction in hospitalized children, especially during radiotherapy for central nervous system (CNS) cancers. This fear not only causes negative emotions such as anxiety and depression but also affects children’s quality of life and treatment outcomes. It is exacerbated by factors such as unfamiliar environments during radiation therapy and separation from parents. Child Life, as a professional service, offers physical and mental support to children through medical understanding and psychological preparation, addressing their social and psychological needs, among other things. This study aims to construct a comprehensive Child Life intervention program (CCLIP), consisting of four key components: psychological adjustment and preparation, therapeutic play, pain management and coping strategies, and family support. The integration of effective intervention methods aims to reduce medical fear in children undergoing radiotherapy, promote psychological well-being, improve treatment compliance, and enhance quality of life. Methods This study is a protocol for a randomized controlled trial. Using a random number table method, we plan to recruit 38 eligible children who meet the inclusion criteria and then randomize them into two distinct groups: the intervention group and the control group. The intervention group will receive the CCLIP, and the control group will receive standardized care. Data will be collected through questionnaires and on-site assessments during the one-month intervention period at four distinct time points: the day of admission (T0), the first radiotherapy positioning (T1), mid-radiotherapy (T2), and postradiotherapy (T3). The primary outcome measure is the effectiveness of the CCLIP in reducing medical fear among children receiving radiation treatment for CNS cancers. Secondary outcomes include anxiety, depression, radiation adherence, quality of life among children, and parental satisfaction. Discussion This study aims to alleviate medical fear among children with CNS tumors undergoing radiotherapy through the implementation of the CCLIP while enhancing their mental health and quality of life. The expected outcomes of this research include providing effective intervention strategies for clinical practice, improving the treatment experience and long-term prognosis of children, and having positive impacts on children and their families. Trial registration This study is registered at the Chinese Clinical Trial Registry, ChiCTR2400082622. Registered 2 April, 2024.

Abstract Worldwide, health professionals from all specialties are encouraging patients to reduce alcohol use if not abstain, and abstinence is clearly encouraged for tobacco. However, for users of substances that meet diagnostic criteria for substance use disorder (addiction), reducing use or abstaining will be difficult without appropriate addiction treatment. Moreover, this group is the most at risk and the most likely to benefit from reducing use. We propose research-based arguments to better combine encouragement to reduce or abstain from alcohol and tobacco to systematic screening for addiction and facilitated access to addiction treatment to make alcohol and tobacco preventable deaths truly preventable.

ABSTRACTRNA-binding proteins (RBPs) play crucial roles in the functions and homoeostasis of various tissues by regulating multiple events of RNA processing including RNA splicing, intracellular RNA transport, and mRNA translation. The Drosophila behavior and human splicing (DBHS) family proteins including PSF/SFPQ, NONO, and PSPC1 are ubiquitously expressed RBPs that contribute to the physiology of several tissues. In mammals, DBHS proteins have been reported to contribute to neurological diseases and play crucial roles in cancers, such as prostate, breast, and liver cancers, by regulating cancer-specific gene expression. Notably, in recent years, multiple small molecules targeting DBHS family proteins have been developed for application as cancer therapeutics. This review provides a recent overview of the functions of DBHS family in physiology and pathophysiology, and discusses the application of DBHS family proteins as promising diagnostic and therapeutic targets for cancers.

Oral cancer became a very common condition. WHO estimates that there are 4 cases of lip and oral cavity cancer for every 100,000 people worldwide. The early diagnosis of cancers is currently a top focus in the health sector. Recent systematic reviews and meta-analyses have identified promising biomarkers for early detection in several original research investigations. However, it is still unclear the quality of these evidence and which biomarker performs the best in terms of early detection. Therefore, the objective was, to map the methodological and reporting quality of available oral squamous cell carcinoma (OSCC) or head/neck squamous cell carcinoma (HNSCC) systematic reviews and meta-analysis. Secondly, to evaluate diagnostic accuracy of salivary biomarkers for common craniofacial cancers and to compare the diagnostic value of different salivary biomarkers.PubMed, Scopus, Web of Science, Embase and Cochrane Library electronic databases were used to map the methodological and reporting quality of the systematic reviews and meta-analysis conducted on the HNSCC, OSCC using the AMSTAR-2 checklist. The inclusion criteria were systematic reviews and meta-analysis published in the topic of HNSCC and OSCC biomarkers. Exclusion criteria were no animal studies; original primary studies, due to limitation of competency in other languages articles with language other than English were excluded. The sensitivity and specificity were calculated for salivary biomarkers and ranked according to network meta-analysis principles.A total of N = 5893 patients were included from four meta-analysis studies. All together, these included n = 37 primary studies. n = 94 biomarkers were pooled from these four meta-analyses and categorised into the stages at which they were detected (I-IV). In OSCC, Chemerin and MMP-9 displayed the highest sensitivity, registering 0.94 (95% CI 0.78, 1.00) and a balanced accuracy of 0.93. Phytosphingosine closely followed, with a sensitivity of 0.91 (95% CI 0.68, 0.99) and a balanced accuracy of 0.87.For HNSCC, the top three biomarkers are Actin, IL-1β Singleplex, and IL-8 ELISA. Actin leads with a sensitivity of 0.91 (95% CI 0.68–0.99), a specificity of 0.67, and an overall accuracy of 0.79. Subsequently, IL-1β Singleplex exhibits a sensitivity of 0.62 (95% CI 0.30–0.88), a specificity of 0.89, and an accuracy of 0.75, followed by IL-8 ELISA with a sensitivity of 0.81 (95% CI 0.54–0.97), a specificity of 0.59, and an accuracy of 0.70.In conclusion, there was highest sensitivity for MMP-9 and chemerin salivary biomarkers. There is need of further more studies to identify biomarkers for HNSCC and OSCC.

Abstract Ataxin-2 (ATXN2) was originally discovered in the context of spinocerebellar ataxia type 2 (SCA2), but it has become a key player in various neurodegenerative diseases. This review delves into the multifaceted roles of ATXN2 in human diseases, revealing its diverse molecular and cellular pathways. The impact of ATXN2 on diseases extends beyond functional outcomes; it mainly interacts with various RNA-binding proteins (RBPs) to regulate different stages of post-transcriptional gene expression in diseases. With the progress of research, ATXN2 has also been found to play an important role in the development of various cancers, including breast cancer, gastric cancer, pancreatic cancer, colon cancer, and esophageal cancer. This comprehensive exploration underscores the crucial role of ATXN2 in the pathogenesis of diseases and warrants further investigation by the scientific community. By reviewing the latest discoveries on the regulatory functions of ATXN2 in diseases, this article helps us understand the complex molecular mechanisms of a series of human diseases related to this intriguing protein.

Abstract Myeloid-derived growth factor (MYDGF) is a novel secreted protein with potent antiapoptotic and tissue-repairing properties that is present in nearly 140 human tissues and cell lines, with the highest abundance in the oral epithelium and skin. Initially, MYDGF was found in bone marrow-derived monocytes and macrophages for cardioprotection and repair after myocardial infarction. Subsequent studies have shown that MYDGF plays an important role in other cardiovascular diseases (e.g., atherosclerosis and heart failure), metabolic disorders, renal disease, autoimmune/inflammatory disorders, and cancers. Although the underlying mechanisms have not been fully explored, the role of MYDGF in health and disease may involve cell apoptosis and proliferation, tissue repair and regeneration, anti-inflammation, and glycolipid metabolism regulation. In this review, we summarize the current progress in understanding the role of MYDGF in health and disease, focusing on its structure, function and mechanisms. The graphical abstract shows the current role of MYDGF in different organs and diseases (Fig. 1).

Abstract Cancer is a complex disease composing systemic alterations in multiple scales. In this study, we develop the Tumor Multi-Omics pre-trained Network (TMO-Net) that integrates multi-omics pan-cancer datasets for model pre-training, facilitating cross-omics interactions and enabling joint representation learning and incomplete omics inference. This model enhances multi-omics sample representation and empowers various downstream oncology tasks with incomplete multi-omics datasets. By employing interpretable learning, we characterize the contributions of distinct omics features to clinical outcomes. The TMO-Net model serves as a versatile framework for cross-modal multi-omics learning in oncology, paving the way for tumor omics-specific foundation models.

There is substantial evidence from clinical and preclinical studies suggesting an association between metformin use and a reduced risk of cancer. However, the effects of metformin use on cancers have not yet been subjected to bibliometric analysis. The goal of this study was to explore the potential effects of metformin use on cancers and to conduct a comprehensive assessment of research hotspots related to the use of metformin on cancers. The results of the literature analysis were visualized using various tools such as Adobe Illustrator CC 2018, VOSviewer, CiteSpace, and the R package "bibliometric." The average annual publications from 2013 to 2023 was 372. In terms of journals and co-cited journals, a total of 1,064 journals published 1958 papers, and Oncotarget published the highest number of papers (n = 153, 7.81%), while Cancer Research (Co-citation = 5,125) was the most frequently cited journal. A total of 25,665 authors participated in the research on metformin use on cancers. Metformin has demonstrated improved outcomes in various types of cancer, including breast cancer (BC), lung cancer (LC), colorectal cancer (CRC), prostate cancer (PC), and pancreatic cancer. This bibliometric analysis reviews the current literature on the clinical data on metformin use on cancers and describes the preclinical evidence illustrating the potential mechanisms of metformin use on various cancers directly or indirectly. [ABSTRACT FROM AUTHOR]

Reports on cases of strongyloidiasis and tuberculosis or aspergillosis coinfection are fragmented in the literature and no large-scale reviews are describing its occurrence across the globe. We identified a total of 230 cases of strongyloidiasis and tuberculosis coinfection amongst 2376 participants with tuberculosis disease from eight epidemiological surveys conducted in Ethiopia (n = 4, 50%); Tanzania (n = 3, 37.5%) and Malaysia (n = 1, 12.5%). Clinical outcomes in these studies were not stated as they were largely descriptive. In addition, there were ten individual case reports of strongyloidiasis and tuberculosis coinfection. Of the ten, four were from the USA (40%), two each from India (20%) and Japan (20%), and one each from the UK (10%) and Argentina (10%). Of the ten, six had favourable outcomes, two were fatal and outcomes were unclear in the remainder. Ten cases of strongyloidiasis and aspergillosis coinfection were identified, five were reported from the USA (50%), and one each from the Netherlands (10%), China (10%), Iran (10%), Colombia (10%) and Italy (10%). Five each had favourable and fatal outcomes. Fatal outcomes in strongyloidiasis and tuberculosis or aspergillosis coinfection were associated with steroid therapy (n = 3), decline for treatment (n = 1), delayed diagnosis (n = 2) and delayed presentation (n = 1). Our findings suggest a significant proportion of individuals living with tuberculosis are also affected with strongyloidiasis, especially in sub-Saharan Africa. However, more studies are required to ascertain the burden of strongyloidiasis and tuberculosis coinfection as few cases were reported from other highly burdened tuberculosis regions. In addition, the role of the attending clinician is critical to reduce morbidities from the coexistence of these clinical entities as a significant number of cases with documented outcomes were fatal. [ABSTRACT FROM AUTHOR]

Liquid biopsy, a noninvasive diagnosis that examines circulating tumor components in body fluids, is increasingly used in cancer management. An overview of relevant literature emphasizes the current state of liquid biopsy applications in cancer care. Biomarkers in liquid biopsy, particularly circulating tumor DNA (ctDNA), circulating tumor RNAs (ctRNA), circulating tumor cells (CTCs), extracellular vesicles (EVs), and other components, offer promising opportunities for early cancer diagnosis, treatment selection, monitoring, and disease assessment. The implementation of liquid biopsy in precision medicine has shown significant potential in various cancer types, including lung cancer, colorectal cancer, breast cancer, and prostate cancer. Advances in genomic and molecular technologies such as next-generation sequencing (NGS) and digital polymerase chain reaction (dPCR) have expanded the utility of liquid biopsy, enabling the detection of somatic variants and actionable genomic alterations in tumors. Liquid biopsy has also demonstrated utility in predicting treatment responses, monitoring minimal residual disease (MRD), and assessing tumor heterogeneity. Nevertheless, standardizing liquid biopsy techniques, interpreting results, and integrating them into the clinical routine remain as challenges. Despite these challenges, liquid biopsy has significant clinical implications in cancer management, offering a dynamic and noninvasive approach to understanding tumor biology and guiding personalized treatment strategies. [ABSTRACT FROM AUTHOR]

Drug resistance plays a vital role in both cancer treatment and prognosis. Especially, early insights into such drug‐induced resistance in acute myeloid leukemia (AML) can help to improve treatment plans, reduce costs, and bring overall positive outcomes for patients. Raman spectroscopy provides precise biomolecular information and can provide all these necessities effectively. In this study, we employed machine learning (ML) discrimination of Raman micro‐spectroscopic data of myelocytic leukemia cell line HL‐60 from its drug‐resistant counterpart HL‐60/MX2. Principal component analysis (PCA), linear discriminant analysis (LDA), and logistic regression (LR) methods were evaluated for their ability to identify and discriminate drug resistance in AML cells. Our study demonstrates the power of ML to classify drug‐induced resistance in AML cells utilizing subtle variations in biomolecular information contained in molecular spectroscopic data by obtaining 94.11% and 97.05% classification accuracies by LDA and LR models, respectively. We also showed that the ML methods are discernable. Our findings depict the importance of automation and its optimal usage in cancer study and diagnosis. The results of our study are expected to take ML‐assisted Raman spectroscopy one step closer to making it a generalized tool in medical diagnosis in the future. [ABSTRACT FROM AUTHOR]

Background: Glucagon-like peptide-1 receptor (GLP1R) agonists have been approved by Food and Drug Administration for management of obesity. However, the causal relationship of GLP1R agonists (GLP1RA) with cancers still unclear. Methods: The available cis-eQTLs for drugs target genes (GLP1R) were used as proxies for exposure to GLP1RA. Mendelian randomizations (MR) were performed to reveal the association of genetically-proxied GLP1RA with 14 common types cancer from large-scale consortia. Type 2 diabetes was used as positive control, and the GWASs data including 80 154 cases and 853 816 controls. Replicating the findings in the FinnGen study and then pooled with meta-analysis. Finally, all the related randomized controlled trails (RCTs) on GLP1RA were systematically searched from PubMed, Embase, and the Cochrane Library to comprehensively synthesize the evidence to validate any possible association with cancers. Result: A total of 22 significant cis-eQTL single-nucleotide polymorphisms were included as genetic instrument. The association of genetically-proxied GLP1RA with significantly decreased type 2 diabetes risk [OR (95%)= 0.82 (0.79-0.86), P< 0.001], which ensuring the effectiveness of identified genetic instruments. The authors found favorable evidence to support the association of GLP1RA with reduced breast cancer and basal cell carcinoma risk [0.92 (0.88-0.96), P<0.001, 0.92 (0.85-0.99), P=0.029, respectively], and with increased colorectal cancer risk [1.12 (1.07-1.18), P< 0.001]. In addition, there was no suggestive evidence to support the association of GLP1RA with ovarian cancer [0.99 (0.90-1.09), P=0.827], lung cancer [1.01 (0.93-1.10), P =0760], and thyroid cancer [0.83 (0.63-1.10), P= 0.187]. Our findings were consistent with the meta-analysis. Finally, 80 RCTs were included in the systematic review, with a low incidence of different kinds of cancer. Conclusions: Our study suggests that GLP1RA may decrease the risk of breast cancer and basal cell carcinoma, but increase the risk of colorectal cancer. However, according to the systematic review of RCTs, the incidence of cancer in patients treated with GLP1RA is low. Larger sample sizes of RCTs with long-term follow-up are necessary to establish the incidence of cancers and evaluate the risk-benefit ratios. [ABSTRACT FROM AUTHOR]

Cancers associated with pathogen infections are gradually becoming important threats to human health globally, and it is of great significance to study the mechanisms of pathogen carcinogenesis. Current mechanistic studies rely on animal and two-dimensional (2D) cell culture models, but traditional methods have been proven insufficient for the rapid modeling of diseases caused by new pathogens. Therefore, research focus has shifted to organoid models, which can replicate the structural and genetic characteristics of the target tissues or organs in vitro, providing new platforms for the study of pathogen-induced oncogenic mechanisms. This review summarizes the application of organoid technology in the studies of four pathogen-associated cancers: gastric cancer linked to Helicobacter pylori, liver cancer associated with hepatitis B virus or hepatitis C virus, colorectal cancer caused by Escherichia coli, and cervical cancer related to human papillomavirus. This review also proposes several limitations of organoid technology to optimize organoid models and advance the treatment of cancer associated with pathogen infections in the future. [ABSTRACT FROM AUTHOR]

Ataxin-2 (ATXN2) was originally discovered in the context of spinocerebellar ataxia type 2 (SCA2), but it has become a key player in various neurodegenerative diseases. This review delves into the multifaceted roles of ATXN2 in human diseases, revealing its diverse molecular and cellular pathways. The impact of ATXN2 on diseases extends beyond functional outcomes; it mainly interacts with various RNA-binding proteins (RBPs) to regulate different stages of post-transcriptional gene expression in diseases. With the progress of research, ATXN2 has also been found to play an important role in the development of various cancers, including breast cancer, gastric cancer, pancreatic cancer, colon cancer, and esophageal cancer. This comprehensive exploration underscores the crucial role of ATXN2 in the pathogenesis of diseases and warrants further investigation by the scientific community. By reviewing the latest discoveries on the regulatory functions of ATXN2 in diseases, this article helps us understand the complex molecular mechanisms of a series of human diseases related to this intriguing protein. [ABSTRACT FROM AUTHOR]

Myeloid-derived growth factor (MYDGF) is a novel secreted protein with potent antiapoptotic and tissue-repairing properties that is present in nearly 140 human tissues and cell lines, with the highest abundance in the oral epithelium and skin. Initially, MYDGF was found in bone marrow-derived monocytes and macrophages for cardioprotection and repair after myocardial infarction. Subsequent studies have shown that MYDGF plays an important role in other cardiovascular diseases (e.g., atherosclerosis and heart failure), metabolic disorders, renal disease, autoimmune/inflammatory disorders, and cancers. Although the underlying mechanisms have not been fully explored, the role of MYDGF in health and disease may involve cell apoptosis and proliferation, tissue repair and regeneration, anti-inflammation, and glycolipid metabolism regulation. In this review, we summarize the current progress in understanding the role of MYDGF in health and disease, focusing on its structure, function and mechanisms. The graphical abstract shows the current role of MYDGF in different organs and diseases (Fig. 1). [ABSTRACT FROM AUTHOR]

Simple Summary: Aldehyde dehydrogenases of the subfamily 1A (ALDH1A) are enzymes involved in the synthesis of retinoic acid, which is necessary for the normal development and maintenance of epithelia, reproduction, memory, and immune function in adults. ALDH1A3, one of the enzymes that belong to the ALD1A subfamily, is also expressed at high levels in many human cancers like glioblastoma and mesothelioma. Herein, we review the role of ALDH1A3 in cancer, showing its relation with excessive proliferation, chemoresistance, and invasiveness. We also illustrate the current attempts to develop ALDH1A3-selective inhibitors and specific fluorescent probes that are potentially useful for cancer therapy and fluorescence-guided tumor resection. Aldehyde dehydrogenases of the subfamily 1A (ALDH1A) are enzymes necessary for the oxidation of all-trans or 9-cis retinal to retinoic acid (RA). Retinoic acid and its derivatives are important for normal development and maintenance of epithelia, reproduction, memory, and immune function in adults. Moreover, in recent years, it has been demonstrated that ALDH1A members are also expressed and functional in several human cancers where their role is not limited to the synthesis of RA. Here, we review the current knowledge about ALDH1A3, one of the 1A isoforms, in cancers with an emphasis on two of the deadliest tumors that affect humans: glioblastoma multiforme and mesothelioma. In both tumors, ALDH1A3 is considered a negative prognostic factor, and its level correlates with excessive proliferation, chemoresistance, and invasiveness. We also review the recent attempts to develop both ALDH1A3-selective inhibitors for cancer therapy and ALDH1A3-specific fluorescent substrates for fluorescence-guided tumor resection. [ABSTRACT FROM AUTHOR]

Background: Nuclear pore complexes (NPCs) are sophisticated and dynamic protein structures that straddle the nuclear envelope and act as gatekeepers for transporting molecules between the nucleus and the cytoplasm. NPCs comprise up to 30 different proteins known as nucleoporins (NUPs). However, a growing body of research has suggested that NPCs play important roles in gene regulation, viral infections, cancer, mitosis, genetic diseases, kidney diseases, immune system diseases, and degenerative neurological and muscular pathologies. Purpose: In this review, we introduce the structure and function of NPCs. Then We described the physiological and pathological effects of each component of NPCs which provide a direction for future clinical applications. Methods: The literatures from PubMed have been reviewed for this article. Conclusion: This review summarizes current studies on the implications of NPCs in human physiology and pathology, highlighting the mechanistic underpinnings of NPC-associated diseases. [ABSTRACT FROM AUTHOR]

Unfortunately, cardiovascular diseases and cancers are still the leading causes of death in developed and developing countries despite the considerable progress made in the prevention and treatment of diseases. Maybe we missed something? Insulin resistance (IR) with associated hyperinsulinemia (Hypein) is a silent pandemic whose prevalence is continually growing in developed and developing countries, now exceeding 51% of the general population. IR/Hypein, despite the vast scientific literature supporting its adverse action on the development of type 2 diabetes, cardiovascular alterations, tumors, neurological disorders, and cellular senescence, is not yet considered an independent risk factor and, therefore, is not screened in the general population and adequately treated. There are now numerous substances, drugs, and natural substances that, in association with the correction of a wrong lifestyle, can help to reduce IR/Hypein. We are convinced that the time has come to implement a prevention plan against this critical risk factor. Therefore, this manuscript aims to highlight IR/Hypein as an independent risk factor for type 2 diabetes, cardiovascular diseases, cancers, cellular senescence, and neuropsychiatric disorders, supporting our conviction with the available scientific literature on the topic. [ABSTRACT FROM AUTHOR]

Background: Lymphoid Cancers (LC), is a heterogeneous monoclonal group of disorder with accumulation of abnormal of lymphocytes in the blood, bone marrow and reticule-endothelia tissue. LC is the commonest hematological cancers and constitutes the 5th most common cancer. Vitamin D, is crucial with respect to outcome and prognosis. However, there is death and inconsistency of data on Vitamin D in LC. Aim: The aim of this review is to determine the role and level of Vitamin D in Lymphoid cancers. Method: A vigorous search was run via various academic search engine, such as Ebsco, Hinari, google scholar, Scopus etc. Conclusion: The role of vitamin D in lymphoid malignancies has been underscore; this review will help to awaken health practioner with bias for lymphoid cancers on the importance of vitamin D with the insight into further research for development of therapeutic intervention. [ABSTRACT FROM AUTHOR]

Background: Previous observational epidemiological studies reported an association between cathepsins and cancer, however, a causal relationship is uncertain. This study evaluated the causal relationship between cathepsins and cancer using Mendelian randomization (MR) analysis. Methods: We used publicly available genome-wide association study (GWAS) data for bidirectional MR analysis. Inverse variance weighting (IVW) was used as the primary MR method of MR analysis. Results: After correction for the False Discovery Rate (FDR), two cathepsins were found to be significantly associated with cancer risk: cathepsin H (CTSH) levels increased the risk of lung cancer (OR = 1.070, 95% CI = 1.027–1.114, P = 0.001, PFDR= 0.009), and CTSH levels decreased the risk of basal cell carcinoma (OR = 0.947, 95% CI = 0.919–0.975, P = 0.0002, PFDR= 0.002). In addition, there was no statistically significant effect of the 20 cancers on the nine cathepsins. Some unadjusted low P-value phenotypes are worth mentioning, including a positive correlation between cathepsin O (CTSO) and breast cancer (OR = 1.012, 95% CI = 1.001–1.025, P = 0.041), cathepsin S (CTSS) and pharyngeal cancer (OR = 1.017, 95% CI = 1.001–1.034, P = 0.043), and CTSS and endometrial cancer (OR = 1.055, 95% CI = 1.012–1.101, P = 0.012); and there was a negative correlation between cathepsin Z and ovarian cancer (CTSZ) (OR = 0.970, 95% CI = 0.949–0.991, P = 0.006), CTSS and prostate cancer (OR = 0.947, 95% CI = 0.902–0.944, P = 0.028), and cathepsin E (CTSE) and pancreatic cancer (OR = 0.963, 95% CI = 0.938–0.990, P = 0.006). Conclusion: Our MR analyses showed a causal relationship between cathepsins and cancers and may help provide new insights for further mechanistic and clinical studies of cathepsin-mediated cancer. [ABSTRACT FROM AUTHOR]

Circular RNAs (circRNAs) are a type of non-coding RNA (ncRNA) that possesses a unique single-stranded circular structure. They are primarily formed through alternative splicing of pre-mRNA (messenger RNA). The primary biological function of circRNAs is to regulate gene expression at both the transcriptional and post-transcriptional levels. Recent studies have increasingly demonstrated a close association between the dysregulation of circRNAs and the progression of diverse cancers, where they can function as either tumor suppressors or oncogenes. circWHSC1 (circNSD2) is a circular ncRNA that originates from the first 2 exons of the Wolf-Hirschhorn syndrome candidate gene (WHSC1). As Chen 2019 discovery that circWHSC1 (circNSD2) functions as a sponge for miRNAs and promotes cancer, this circRNA has garnered significant interest among researchers. circWHSC1 (circNSD2) has been found to be up-regulated in various malignant tumors, including nasopharyngeal carcinoma, lung cancer, breast cancer, liver cancer, colorectal cancer, ovarian cancer, cervical cancer, and endometrial cancer. It exerts its effects on cancer by either inhibiting or promoting the expression of related genes through direct or indirect pathways, ultimately affecting cancer proliferation, invasion, and prognosis. This article provides a comprehensive review and discussion of the biological roles of circWHSC1 (circNSD2) and its target genes in various cancers, as well as the latest research progress on related molecular biological regulatory mechanisms. Furthermore, the potential significance of circWHSC1 (circNSD2) in future clinical applications and transformations is thoroughly analyzed and discussed. [ABSTRACT FROM AUTHOR]

Cancer has been one of the most problematic health issues globally. Typically, all cancers share a common characteristic or cancer hallmark, such as sustaining cell proliferation, evading growth suppressors, and enabling replicative immortality. Indeed, cell cycle regulation in cancer is often found to be dysregulated, leading to an increase in aggressiveness. These dysregulations are partly due to the aberrant cellular signaling pathway. In recent years, circular RNAs (circRNAs) have been widely studied and classified as one of the regulators in various cancers. Numerous studies have reported that circRNAs antagonize or promote cancer progression through the modulation of cell cycle regulators or their associated signaling pathways, directly or indirectly. Mostly, circRNAs are known to act as microRNA (miRNA) sponges. However, they also hold additional mechanisms for regulating cellular activity, including protein binding, RNA-binding protein (RBP) recruitment, and protein translation. This review will discuss the current knowledge of how circRNAs regulate cell cycle-related proteins through the abovementioned mechanisms in different cancers. [ABSTRACT FROM AUTHOR]

Despite decades of basic and clinical research and trials of promising new therapies, cancer remains a major cause of morbidity and mortality due to the emergence of drug resistance to anticancer drugs. These resistance events have a very well-understood underlying mechanism, and their therapeutic relevance has long been recognized. Thus, drug resistance continues to be a major obstacle to providing cancer patients with the intended "cure". PAQR4 (Progestin and AdipoQ Receptor Family Member 4) gene is a recently identified novel protein-coding gene associated with various human cancers and acts through different signaling pathways. PAQR4 has a significant influence on multiple proteins that may regulate various gene expressions and may develop chemoresistance. This review discusses the roles of PAQR4 in tumor immunity, carcinogenesis, and chemoresistance. This paper is the first review, discussing PAQR4 in the pathogenesis of cancer. The review further explores the PAQR4 as a potential target in various malignancies. [ABSTRACT FROM AUTHOR]

Modulation of histone methylation status is regarded as an important mechanism of epigenetic regulation and has substantial clinical potential for the therapy of diseases, including cancer and other disorders. The present study aimed to provide a comprehensive introduction to the enzymology of histone demethylases, as well as their cancerous roles, molecular mechanisms, therapeutic possibilities, and challenges for targeting them, in order to advance drug design for clinical therapy and highlight new insight into the mechanisms of these enzymes in cancer. A series of clinical trials have been performed to explore potential roles of histone demethylases in several cancer types. Numerous targeted inhibitors associated with immunotherapy, chemotherapy, radiotherapy, and targeted therapy have been used to exert anticancer functions. Future studies should evaluate the dynamic transformation of histone demethylases leading to carcinogenesis and explore individual therapy. [ABSTRACT FROM AUTHOR]

Abstract Glycoproteins, representing a significant proportion of posttranslational products, play pivotal roles in various biological processes, such as signal transduction and immune response. Abnormal glycosylation may lead to structural and functional changes of glycoprotein, which is closely related to the occurrence and development of various diseases. Consequently, exploring protein glycosylation can shed light on the mechanisms behind disease manifestation and pave the way for innovative diagnostic and therapeutic strategies. Nonetheless, the study of clinical glycoproteomics is fraught with challenges due to the low abundance and intricate structures of glycosylation. Recent advancements in mass spectrometry‐based clinical glycoproteomics have improved our ability to identify abnormal glycoproteins in clinical samples. In this review, we aim to provide a comprehensive overview of the foundational principles and recent advancements in clinical glycoproteomic methodologies and applications. Furthermore, we discussed the typical characteristics, underlying functions, and mechanisms of glycoproteins in various diseases, such as brain diseases, cardiovascular diseases, cancers, kidney diseases, and metabolic diseases. Additionally, we highlighted potential avenues for future development in clinical glycoproteomics. These insights provided in this review will enhance the comprehension of clinical glycoproteomic methods and diseases and promote the elucidation of pathogenesis and the discovery of novel diagnostic biomarkers and therapeutic targets.

Abstract Circular RNAs (circRNAs) are a unique class of RNA molecules formed through back‐splicing rather than linear splicing. As an emerging field in molecular biology, circRNAs have garnered significant attention due to their distinct structure and potential functional implications. A comprehensive understanding of circRNAs’ functions and potential clinical applications remains elusive despite accumulating evidence of their involvement in disease pathogenesis. Recent research highlights their significant roles in various human diseases, but comprehensive reviews on their functions and applications remain scarce. This review provides an in‐depth examination of circRNAs, focusing first on their involvement in non‐neoplastic diseases such as respiratory, endocrine, metabolic, musculoskeletal, cardiovascular, and renal disorders. We then explore their roles in tumors, with particular emphasis on exosomal circular RNAs, which are crucial for cancer initiation, progression, and resistance to treatment. By detailing their biogenesis, functions, and impact on disease mechanisms, this review underscores the potential of circRNAs as diagnostic biomarkers and therapeutic targets. The review not only enhances our understanding of circRNAs’ roles in specific diseases and tumor types but also highlights their potential as novel diagnostic and therapeutic tools, thereby paving the way for future clinical investigations and potential therapeutic interventions.

Background: Mortality from malignancies in children remains high. Creating awareness of the disease and advocacy for funding of a cancer research center are pertinent. Objective: To determine the incidence and outcome of children with cancers at the University of Abuja Teaching Hospital, Gwagwaglada, Abuja- FCT, Nigeria. Method: This was a 5 year prospective study of all diagnosed cancer patients admitted into the paediatric ward. The type of cancer, method of diagnosis, clinical staging and outcomes were entered and frequency tables generated on Microsoft Excel. Results: Forty-six patients were diagnosed with cancer within the study period. Burkitt's lymphoma was the highest encountred malignancy, while medulloblastoma was least occurring. Only 36.9 percent (N=17) of patients received chemotherapy. Of these, 6.5 percent (n=3) completed therapy. Twenty nine percent of patients died. 4 percent of those that died had commenced chemotherapy. There was a 70 percent treatment default rate. One patient was referred on request to another tertiary center. All other patients were lost to follow up. Conclusion: Management of childhood cancers still poses a problem. Poverty, ignorance and lack of cancer research units contributed to our poor outcome. The greater involvement of government and international non-governmental organizations (NGO) which assist health sector is advocated in the establishment of cancer research centers and the provision of free chemotherapeutic agents.