Different Types Of Cancer Research Articles

Comprehensive analysis indicated that NDE1 is a potential biomarker for pan-cancer and promotes bladder cancer progression.

The nuclear distribution E homologue 1 (NDE1) is a crucial dynein binding partner. The NDE1 protein has the potential to disrupt the normal functioning of centrosomes, leading to a compromised ability to generate spindles and ensure precise separation of chromosomes during cell division. The potential consequences of this phenomenon include genomic instability, malignant transformation and the proliferation of neoplastic growths. However, studies examining the connection between NDE1 and cancer is still very rare. The expression level, prognostic impact, gene change, DNA methylation, protein interaction, mRNA m6A modification, ceRNA network, associated gene and function enrichment, and immune-related effects of NDE1 in pan-cancer were examined using a range of online analytic tools and the R software package. The CCK-8 test, transwell assay, scratch assay and colony formation assay were used to confirm the effects of NDE1 on the proliferation, invasion and metastasis of bladder cancer cells. Numerous tumour types have elevated NDE1, which is linked to a bad prognosis. NDE1 is an excellent diagnostic tool for many different types of cancer. Numerous malignancies have been linked to genetic changes in NDE1. NDE1 was connected to TMB, MSI, several immunological checkpoint genes and immune cell infiltration. NDE1 is linked to a number of immunological subtypes. NDE1 could affect how well immunotherapy works to treat different types of cancer. NDE1 was mostly associated with cell cycle, chromosomal segregation, DNA replication and mitotic segregation, according to GO and KEGG analyses. NDE1 physically binds to PAFAH1B1 and DCTN1, respectively. The proliferation, invasion and metastasis of bladder cancer cells may be prevented by NDE1 knockdown. Furthermore, knockdown of NDE1 promoted the apoptosis of bladder cancer cells. High expression of NDE1 is present in a variety of tumours, which is linked to a bad prognosis for cancer. Knockdown of NDE1 inhibited the proliferation, invasion and metastasis of bladder cancer cells, and promoted the apoptosis. For a number of malignancies, NDE1 may be a biomarker for immunotherapy and prognosis.

TEMPORARY REMOVAL: Impact of time of diagnosis on out-of-pocket costs of cancer treatment, a side effect of health insurance design in Australia

The Extended Medicare Safety Net (EMSN) in Australia was designed to provide financial assistance to patients with high out-of-pocket (OOP) costs for medical treatment. The EMSN works on a calendar year basis. Once a patient incurs a specified amount of OOP costs, the EMSN provides additional financial benefits for the remainder of the calendar year. Its design is similar to many types of insurance products that have large deductibles and are applied on a calendar year basis. This study examines if the annual quarter within which a patient is diagnosed with cancer has an impact on the OOP costs incurred for treatment. We use administrative linked data from the Sax Institute's 45 and Up Study. Our results indicate that the timing of cancer diagnosis has a significant impact on OOP costs. Specifically, patients diagnosed in the fourth quarter of the calendar year experience significantly higher OOP costs compared to those diagnosed in the first quarter of the year. This pattern persists after controlling for different types of cancer and different stages of cancer and robustness checks. These findings have important implications for the design of the EMSN, as well as other insurance products.

An approach to diagnosis of prostate cancer using fuzzy logic

<p><span>Early diagnosis of cancers is a major requirement for patients and a complicated job for the oncologist. If it is diagnosed early, it could have made the patient more likely to live. For a few decades, fuzzy logic emerged as an emphatic technique in the identification of diseases like different types of cancers. The recognition of cancer diseases mostly operated with inexactness, inaccuracy, and vagueness. This paper aims to design the fuzzy expert system (FES) and its implementation for the detection of prostate cancer. Specifically, prostate-specific antigen (PSA), prostate volume (PV), age, and percentage free PSA (%FPSA) are used to determine prostate cancer risk (PCR), while PCR serves as an output parameter. Mamdani fuzzy inference method is used to calculate a range of PCR. The system provides a scale of risk of prostate cancer and clears the path for the oncologist to determine whether their patients need a biopsy. This system is fast as it requires minimum calculation and hence comparatively less time which reduces mortality and morbidity and is more reliable than other economic systems and can be frequently used by doctors.</span></p>

Disruption of cyclin D1 degradation leads to the development of mantle cell lymphoma

Cyclin D1 has been recognized as an oncogene due to its abnormal upregulation in different types of cancers. Here, we demonstrated that cyclin D1 is SUMOylated, and we identified Itch as a specific E3 ligase recognizing SUMOylated cyclin D1 and mediating SUMO-induced ubiquitination and proteasome degradation of cyclin D1. We generated cyclin D1 mutant mice with mutations in the SUMOylation site, phosphorylation site, or both sites of cyclin D1, and found that double mutant mice developed a Mantle cell lymphoma (MCL)-like phenotype. We showed that arsenic trioxide (ATO) enhances cyclin D1 SUMOylation-mediated degradation through inhibition of cyclin D1 deSUMOylation enzymes, leading to MCL cell apoptosis. Treatment of severe combined immunodeficiency (SCID) mice grafted with MCL cells with ATO resulted in a significant reduction in tumor growth. In this study, we provide novel insights into the mechanisms of MCL tumor development and cyclin D1 regulation and discover a new strategy for MCL treatment.

Dopamine Polymerization-Mediated Surface Functionalization toward Advanced Bacterial Therapeutics.

ConspectusBacteria-based therapy has spotlighted an unprecedented potential in treating a range of diseases, given that bacteria can be used as both drug vehicles and therapeutic agents. However, the use of bacteria for disease treatment often suffers from unsatisfactory outcomes, due largely to their suboptimal bioavailability, dose-dependent toxicity, and low targeting colonization. In the past few years, substantial efforts have been devoted to tackling these difficulties, among which methods capable of integrating bacteria with multiple functions have been extensively pursued. Different from conventional genetic engineering and modern synthetic bioengineering, surface modification of bacteria has emerged as a simple yet flexible strategy to introduce different functional motifs. Polydopamine, which can be easily formed via in situ dopamine oxidation and self-polymerization, is an appealing biomimetic polymer that has been widely applied for interfacial modification and functionalization. By virtue of its catechol groups, polydopamine can be efficiently codeposited with a multitude of functional elements on diverse surfaces.In this Account, we summarize the recent advances from our group with a focus on the interfacial polymerization-mediated functionalization of bacteria for advanced microbial therapy. First, we present the optimized strategy for bacterial surface modification under cytocompatible conditions by in situ dopamine polymerization. Taking advantage of the hydrogen bonding, π-π stacking, Michael addition, and Schiff base reaction with polydopamine, diverse functional small molecules and macromolecules are facilely codeposited onto the bacterial surface. Namely, monomodal, dual-modal, and multimodal surface modification of bacteria can be achieved by dopamine self-deposition, codeposition with a unitary composition, and codeposition with a set of multiple components, respectively. Second, we outline the regulation of bacterial functions by surface modification. The formed polydopamine surface endows bacteria with the ability to resist in vivo insults, such as gastrointestinal tract stressors and immune clearance, resulting in greatly improved bioavailability. Integration with specific ligands or therapeutic components enables the modified bacteria to increase targeting accumulation and colonization at lesion sites or play synergistic effects in disease treatment. Bacteria codeposited with different bioactive moieties, such as protein antigens, antibodies, and immunoadjuvants, are even able to actively interact with the host, particularly to elicit immune responses by either suppressing immune overactivation to promote the reversion of pathological inflammations or provoking protective innate and/or adaptive immunity to inhibit pathogenic invaders. Third, we highlight the applications of surface-modified bacteria as multifunctional living therapeutics in disease treatment, especially alleviating inflammatory bowel diseases via oral delivery and intervening in different types of cancer through systemic or intratumoral injection. Finally, we discuss the challenges and prospects of dopamine polymerization-mediated multifunctionalization for preparing advanced bacterial therapeutics as well as their bench to bedside translation. We anticipate that this Account can provide an insightful overview of bacterial therapy and inspire innovative thinking and new efforts to develop next-generation living therapeutics for treating various diseases.

Anticorpos biespecíficos em neoplasias hematológicas

Introduction: Immunotherapy is the new frontier in cancer treatment, challenging traditional views regarding the treatment of malignancy. It includes treatment with checkpoint inhibitors, monoclonal antibodies, chimeric antigen receptor T cells (CAR-T), and bispecific monoclonal antibodies (BsAbs). BsAbs are drugs composed of a single monoclonal antibody, which has two binding domains that can bind to two different antigens simultaneously, which is the great advantage of this therapy over others. Therefore, BsAbs have revolutionized clinical outcomes for different types of cancer, especially hematological ones, bringing good results and hope to patients with lymphomas, leukemias and multiple myeloma. Objective: The present research aims to provide an updated overview of BsAbs treatment applied to the main hematological neoplasms, as well as describe its classification and mechanism of action. Material and Methods: This is a literature review based on articles published in the last 9 years (2015-2023) in the PubMed database (Medline), relating hematological malignancies and BsAbs, using the keyword: “Bispecific antibody”. Results: A total of 1,530 articles were found, of which 48 were included in the development of this review article. Conclusions: BsAbs redirect the immune system cells action, generating a new therapeutic response, proving to be an innovative alternative in immunotherapy, being a vanguard option that combines molecular biology engineering and the immune system biological activity.

Investigating the overlap of machine learning algorithms in the final results of RNA-seq analysis on gene expression estimation

Advances in computer science in combination with the next-generation sequencing have introduced a new era in biology, enabling advanced state-of-the-art analysis of complex biological data. Bioinformatics is evolving as a union field between computer Science and biology, enabling the representation, storage, management, analysis and exploration of many types of data with a plethora of machine learning algorithms and computing tools. In this study, we used machine learning algorithms to detect differentially expressed genes between different types of cancer and showing the existence overlap to final results from RNA-sequencing analysis. The datasets were obtained from the National Center for Biotechnology Information resource. Specifically, dataset GSE68086 which corresponds to PMID:200,068,086. This dataset consists of 171 blood platelet samples collected from patients with six different tumors and healthy individuals. All steps for RNA-sequencing analysis (preprocessing, read alignment, transcriptome reconstruction, expression quantification and differential expression analysis) were followed. Machine Learning- based Random Forest and Gradient Boosting algorithms were applied to predict significant genes. The Rstudio statistical tool was used for the analysis.

Marine-Derived Anticancer Agents Targeting Apoptotic Pathways: Exploring the Depths for Novel Cancer Therapies.

Extensive research has been conducted on the isolation and study of bioactive compounds derived from marine sources. Several natural products have demonstrated potential as inducers of apoptosis and are currently under investigation in clinical trials. These marine-derived compounds selectively interact with extrinsic and intrinsic apoptotic pathways using a variety of molecular mechanisms, resulting in cell shrinkage, chromatin condensation, cytoplasmic blebs, apoptotic bodies, and phagocytosis by adjacent parenchymal cells, neoplastic cells, or macrophages. Numerous marine-derived compounds are currently undergoing rigorous examination for their potential application in cancer therapy. This review examines a total of 21 marine-derived compounds, along with their synthetic derivatives, sourced from marine organisms such as sponges, corals, tunicates, mollusks, ascidians, algae, cyanobacteria, fungi, and actinobacteria. These compounds are currently undergoing preclinical and clinical trials to evaluate their potential as apoptosis inducers for the treatment of different types of cancer. This review further examined the compound's properties and mode of action, preclinical investigations, clinical trial studies on single or combination therapy, and the prospective development of marine-derived anticancer therapies.

Comprehensive assessment of TECENTRIQ® and OPDIVO®: analyzing immunotherapy indications withdrawn in triple-negative breast cancer and hepatocellular carcinoma.

Atezolizumab (TECENTRIQ®) and nivolumab (OPDIVO®) are both immunotherapeutic indications targeting programmed cell death 1 ligand 1 (PD-L1) and programmed cell death 1 (PD-1), respectively. These inhibitors hold promise as therapies for triple-negative breast cancer (TNBC) and hepatocellular carcinoma (HCC) and have demonstrated encouraging results in reducing the progression and spread of tumors. However, due to their adverse effects and low response rates, the US Food and Drug Administration (FDA) has withdrawn the approval of atezolizumab in TNBC and nivolumab in HCC treatment. The withdrawals of atezolizumab and nivolumab have raised concerns regarding their effectiveness and the ability to predict treatment responses. Therefore, the current study aims to investigate the immunotherapy withdrawal of PD-1/PD-L1 inhibitors, specifically atezolizumab for TNBC and nivolumab for HCC. This study will examine both the structural and clinical aspects. This review provides detailed insights into the structure of the PD-1 receptor and its ligands, the interactions between PD-1 and PD-L1, and their interactions with the withdrawn antibodies (atezolizumab and nivolumab) as well as PD-1 and PD-L1 modifications. In addition, this review further assesses these antibodies in the context of TNBC and HCC. It seeks to elucidate the factors that contribute to diverse responses to PD-1/PD-L1 therapy in different types of cancer and propose approaches for predicting responses, mitigating the potential risks linked to therapy withdrawals, and optimizing patient outcomes. By better understanding the mechanisms underlying responses to PD-1/PD-L1 therapy and developing strategies to predict these responses, it is possible to create more efficient treatments for TNBC and HCC.

Betulinic acid induces apoptosis of HeLa cells via ROS-dependent ER stress and autophagy in vitro and in vivo.

Betulinic acid (BA), a naturally occurring lupane-type triterpenoid, possesses a wide range of potential activities against different types of cancer. However, the molecular mechanisms involved in anti-cervical cancer about BA were rarely investigated. Herein, the role of BA in cervical cancer suppression by ROS-mediated endoplasmic reticulum stress (ERS) and autophagy was deeply discussed. The findings revealed that BA activated Keap1/Nrf2 pathway and triggered mitochondria-dependent apoptosis due to ROS production. Furthermore, BA increased the intracellular Ca2+ levels, inhibited the expression of Beclin1 and promoted the expression of GRP78, LC3-II, and p62 associated with ERS and autophagy. Besides, BA initiated the formation of autophagosomes and inhibited autophagic flux by the co-administration of BA with 3-methyladenine (3-MA) and chloroquine (CQ), respectively. The in vivo experiment manifested that hydroxychloroquine (HCQ) enhanced the apoptosis induced by BA. For the first time, we demonstrated that BA could initiate early autophagy, inhibit autophagy flux, and induce protective autophagy in HeLa cells. Thus, BA could be a potential chemotherapy drug for cervical cancer, and inhibition of autophagy could enhance the anti-tumor effect of BA. However, the interactions of signaling factors between ERS-mediated and autophagy-mediated apoptosis deserve further attention.

Illuminating the neuropeptide Y4 receptor and its ligand pancreatic polypeptide from a structural, functional, and therapeutic perspective

The neuropeptide Y4 receptor (Y4R), a rhodopsin-like G protein-coupled receptor (GPCR) and the hormone pancreatic polypeptide (PP) are members of the neuropeptide Y family consisting of four receptors (Y1R, Y2R, Y4R, Y5R) and three highly homologous peptide ligands (neuropeptide Y, peptide YY, PP). In this family, the Y4R is of particular interest as it is the only subtype with high affinity to PP over NPY. The Y4R, as a mediator of PP signaling, has a pivotal role in appetite regulation and energy homeostasis, offering potential avenues for the treatment of metabolic disorders such as obesity. PP as anorexigenic peptide is released postprandial from the pancreas in response to food intake, induces satiety signals and contributes to hamper excessive food intake. Moreover, this system was also described to be associated with different types of cancer: overexpression of Y4R have been found in human adenocarcinoma cells, while elevated levels of PP are related to the development of pancreatic endocrine tumors. The pharmacological relevance of the Y4R advanced the search for potent and selective ligands for this receptor subtype, which will be significantly progressed through the elucidation of the active state PP-Y4R cryo-EM structure. This review summarizes the development of novel PP-derived ligands, like Obinepitide as dual Y2R/Y4R agonist in clinical trials or UR-AK86c as small hexapeptide agonist with picomolar affinity, as well as the first allosteric modulators that selectively target the Y4R, e.g. VU0506013 as potent Y4R positive allosteric modulator or (S)-VU0637120 as allosteric antagonist. Here, we provide valuable insights into the complex physiological functions of the Y4R and PP and the pharmacological relevance of the system in appetite regulation to open up new avenues for the development of tool compounds for targeted therapies with potential applications in metabolic disorders.

Exploring the potential of EphA2 receptor signaling pathway: a comprehensive review in cancer treatment.

The protein encoded by the ephrin type-A receptor 2 (EphA2) gene is a member of the ephrin receptor subfamily of the receptor tyrosine kinase family (RTKs). Eph receptors play a significant role in various biological processes, particularly cancer progression, development, and pathogenesis. They have been observed to regulate cancer cell growth, migration, invasion, tumor development, invasiveness, angiogenesis, and metastasis. To target EphA2 activity, various molecular, genetic, biochemical, and pharmacological strategies have been extensively tested in laboratory cultures and animal models. Notably, drugs, such as dasatinib, initially designed to target the kinase family, have demonstrated an additional capability to target EphA2 activity. Additionally, a novel monoclonal antibody named EA5 has emerged as a promising option to counteract the effects of EphA2 overexpression and restore tamoxifen sensitivity in EphA2-transfected MCF-7 cells during in vitro experiments. This antibody mimicked the binding of Ephrin A to EphA2. These methods offer potential avenues for inhibiting EphA2 activity, which could significantly decelerate breast cancer progression and restore sensitivity to certain drugs. This review article comprehensively covers EphA2's involvement in multiple malignancies, including ovarian, colorectal, breast, lung, glioma, and melanoma. Furthermore, we discuss the structure of EphA2, the Eph-Ephrin signaling pathway, various EphA2 inhibitors, and the mechanisms of EphA2 degradation. This article provides an extensive overview of EphA2's vital role in different types of cancers and outlines potential therapeutic approaches to target EphA2, shedding light on the underlying molecular mechanisms that make it an attractive target for cancer treatment.

Targeting EphA2: a promising strategy to overcome chemoresistance and drug resistance in cancer.

Erythropoietin-producing hepatocellular A2 (EphA2) is a vital member of the Eph tyrosine kinase receptor family and has been associated with developmental processes. However, it is often overexpressed in tumors and correlates with cancer progression and worse prognosis due to the activation of its noncanonical signaling pathway. Throughout cancer treatment, the emergence of drug-resistant tumor cells is relatively common. Since the early 2000s, researchers have focused on understanding the role of EphA2 in promoting drug resistance in different types of cancer, as well as finding efficient and secure EphA2 inhibitors. In this review, the current knowledge regarding induced resistance by EphA2 in cancer treatment is summarized, and the types of cancer that lead to the most cancer-related deaths are highlighted. Some EphA2 inhibitors were also investigated. Regardless of whether the cancer treatment has reached a drug-resistance stage in EphA2-overexpressing tumors, once EphA2 is involved in cancer progression and aggressiveness, targeting EphA2 is a promising therapeutic strategy, especially in combination with other target-drugs for synergistic effect. For that reason, monoclonal antibodies against EphA2 and inhibitors of this receptor should be investigated for efficacy and drug toxicity.

MiR-125 in Breast Cancer Etiopathogenesis: An Emerging Role as a Biomarker in Differential Diagnosis, Regenerative Medicine, and the Challenges of Personalized Medicine.

Breast Cancer (BC) is one of the most common cancer types worldwide, and it is characterized by a complex etiopathogenesis, resulting in an equally complex classification of subtypes. MicroRNA (miRNA or miR) are small non-coding RNA molecules that have an essential role in gene expression and are significantly linked to tumor development and angiogenesis in different types of cancer. Recently, complex interactions among coding and non-coding RNA have been elucidated, further shedding light on the complexity of the roles these molecules fulfill in cancer formation. In this context, knowledge about the role of miR in BC has significantly improved, highlighting the deregulation of these molecules as additional factors influencing BC occurrence, development and classification. A considerable number of papers has been published over the past few years regarding the role of miR-125 in human pathology in general and in several types of cancer formation in particular. Interestingly, miR-125 family members have been recently linked to BC formation as well, and complex interactions (competing endogenous RNA networks, or ceRNET) between this molecule and target mRNA have been described. In this review, we summarize the state-of-the-art about research on this topic.

The CDK Inhibitor Dinaciclib Improves Cisplatin Response in Nonseminomatous Testicular Cancer: A Preclinical Study.

Most patients with testicular germ cell tumors (GCTs) are treated with cisplatin (CP)-based chemotherapy. However, some of them may develop CP resistance and therefore represent a clinical challenge. Cyclin-dependent kinase 5 (CDK5) is involved in chemotherapy resistance in different types of cancer. Here, we investigated the possible role of CDK5 and other CDKs targeted by dinaciclib in nonseminoma cell models (both CP-sensitive and CP-resistant), evaluating the potential of the CDK inhibitor dinaciclib as a single/combined agent for the treatment of advanced/metastatic testicular cancer (TC). The effects of dinaciclib and CP on sensitive and resistant NT2/D1 and NCCIT cell viability and proliferation were evaluated using MTT assays and direct count methods. Flow cytometry cell-cycle analysis was performed. The protein expression was assessed via Western blotting. The in vivo experiments were conducted in zebrafish embryos xenografted with TC cells. Among all the CDKs analyzed, CDK5 protein expression was significantly higher in CP-resistant models. Dinaciclib reduced the cell viability and proliferation in each cell model, inducing changes in cell-cycle distribution. In drug combination experiments, dinaciclib enhances the CP effect both in vitro and in the zebrafish model. Dinaciclib, when combined with CP, could be useful for improving nonseminoma TC response to CP.

NTRK Therapy among Different Types of Cancers, Review and Future Perspectives.

Neurotrophic tyrosine receptor kinase (NTRK) has been a remarkable therapeutic target for treating different malignancies, playing an essential role in oncogenic signaling pathways. Groundbreaking trials like NAVIGATE led to the approval of NTRK inhibitors by the Food and Drug Administration (FDA) to treat different malignancies, significantly impacting current oncology treatment. Accurate detection of NTRK gene fusion becomes very important for possible targeted therapy. Various methods to detect NTRK gene fusion have been applied widely based on sensitivity, specificity, and accessibility. The utility of different tests in clinical practice is discussed in this study by providing insights into their effectiveness in targeting patients who may benefit from therapy. Widespread use of NTRK inhibitors in different malignancies could remain limited due to resistance mechanisms that cause challenges to medication efficacy in addition to common side effects of the medications. This review provides a succinct overview of the application of NTRK inhibitors in various types of cancer by emphasizing the critical clinical significance of NTRK fusion gene detection. The discussion also provides a solid foundation for understanding the current challenges and potential changes for improving the efficacy of NTRK inhibitor therapy to treat different malignancies.

Alternative polyadenylation quantitative trait methylation mapping in human cancers provides clues into the molecular mechanisms of APA

Genetic variants are involved in the orchestration of alternative polyadenylation (APA) events, while the role of DNA methylation in regulating APA remains unclear. We generated a comprehensive atlas of APA quantitative trait methylation sites (apaQTMs) across 21 different types of cancer (1,612 to 60,219 acting in cis and 4,448 to 142,349 in trans). Potential causal apaQTMs in non-cancer samples were also identified. Mechanistically, we observed a strong enrichment of cis-apaQTMs near polyadenylation sites (PASs) and both cis- and trans-apaQTMs in proximity to transcription factor (TF) binding regions. Through the integration of ChIP-signals and RNA-seq data from cell lines, we have identified several regulators of APA events, acting either directly or indirectly, implicating novel functions of some important genes, such as TCF7L2, which is known for its involvement in type 2 diabetes and cancers. Furthermore, we have identified a vast number of QTMs that share the same putative causal CpG sites with five different cancer types, underscoring the roles of QTMs, including apaQTMs, in the process of tumorigenesis. DNA methylation is extensively involved in the regulation of APA events in human cancers. In an attempt to elucidate the potential underlying molecular mechanisms of APA by DNA methylation, our study paves the way for subsequent experimental validations into the intricate biological functions of DNA methylation in APA regulation and the pathogenesis of human cancers. To present a comprehensive catalog of apaQTM patterns, we introduce the Pancan-apaQTM database, available at https://pancan-apaqtm-zju.shinyapps.io/pancanaQTM/.

Autoimmunity and Cancer: Two Stations on the Same Continuum.

Autoimmunity has been associated with different types of cancer, including hematological malignancies like lymphomas, and solid tumors. Additionally, the potential role of medication-induced immunosuppression should be considered. Our study aimed to investigate the relationship between autoimmunity and the development of cancer, as well as the impact of immunosuppressive drugs on increasing cancer risk. The study sample was composed of patients who developed cancer after the administration of biological agents for the treatment of autoimmune disorders. Selected patients were treated in our hospital between 1st January 2011 and 31st December 2021 and followed up in internal medicine, gastroenterology, or dermatology consult. From 434 patients with autoimmune diseases using biological agents, only 20 developed cancer, which was our final study sample. The data analysis was performed using the IQVIR package version 2.0.2 (IQVIA, Durham, NC). A p-value of <0.05 was considered statistically significant. We found a significant correlation between long-term corticosteroid therapy and an increased risk of cancer. However, the effect of biological therapies on cancer risk was not statistically significant. It's worth noting that our sample size was small, so we cannot extrapolate these findings. Physicians need to be aware that treating autoimmune diseases with immunosuppressive therapies may contribute to the development of cancer. Further research is needed to determine the impact of such treatments on cancer prognosis.

Optimal gene therapy network: Enhancing cancer classification through advanced AI-driven gene expression analysis

Gene therapy is an advanced medical approach that aims to find solutions for various cancers by identifying optimal gene expressions. In this context, computer-aided detection of gene expressions becomes a research challenge, where artificial intelligence methods are employed to classify cancer types. However, traditional machine learning models must be improved for accurately classifying cancers, leading to unsatisfactory quantitative performance. Therefore, this work implemented the optimal gene therapy network (OGT-Net) for identifying the different types of cancers from the gene expression sequences. Initially, the dataset pre-processing operation normalizes the dataset, which maintains the uniform nature of all records in the dataset. Then, the light gradient boosting model (LGBM) extracts the correlated features from the pre-processed dataset, which contains the relationship among the pre-processed gene expression data. In addition, interrupt-based Harris Hawk optimization (IHHO) extracts the optimal features from LGBM data, decreasing the total number of features by removing redundant gene sequences. Then, a customized deep learning convolution neural network (DLCNN) is used to categorize diseases using gene expression datasets based on lymphography, colon, lung, ovarian, and prostate cancers. The simulation results reveal that the proposed OGT-Net improved performance on various datasets compared to existing approaches, with an average accuracy of 91.128 %, precision of 90.836 %, recall of 91.25 %, and F1-score of 90.7 %.

CRISPR-Based Multiplex Detection of Human Papillomaviruses for One-Pot Point-of-Care Diagnostics.

The World Health Organization's global initiative toward eliminating high-risk Human Papillomavirus (hrHPV)-related cancers recommends DNA testing over visual inspection in all settings for primary cancer screening and HPV eradication by 2100. However, multiple hrHPV types cause different types of cancers, and there is a pressing need for an easy-to-use, multiplex point-of-care diagnostic platform for detecting different hrHPV types. Recently, CRISPR-Cas systems have been repurposed for point-of-care detection. Here, we established a CRISPR-Cas multiplexed diagnostic assay (CRISPRD) to detect cervical cancer-causing hrHPVs in one reaction (one-pot assay). We harnessed the compatibility of thermostable AapCas12b, TccCas13a, and HheCas13a nucleases with isothermal amplification and successfully detected HPV16 and HPV18, along with an internal control in a single-pot assay with a limit of detection of 10 copies and 100% specificity. This platform offers a rapid and practical solution for the multiplex detection of hrHPVs, which may facilitate large-scale hrHPV point-of-care screening. Furthermore, the CRISPRD platform programmability enables it to be adapted for the multiplex detection of any two nucleic acid biomarkers as well as internal control.