Sociodemographic inequalities in cigarette, smokeless tobacco, waterpipe tobacco, and electronic cigarette use among adolescents aged 12-16 years in 114 countries: A cross-sectional analysis.

INTRODUCTION: The majority of users of tobacco and nicotine products start using them in adolescence. In order to keep equity considerations at the forefront of tobacco control, it is crucial to assess whether inequalities in prevalence of tobacco and nicotine use exist among adolescents globally. METHODS: We conducted a secondary analysis of Global Youth Tobacco Survey (GYTS) data from 538644 school-based adolescents (79.3% aged 13-15 years) in 114 countries (2013-2019). Data were collected on current (past 30-day) use of cigarettes, smokeless tobacco, waterpipe tobacco and electronic cigarettes. We used weighted Poisson regression models adjusted for sex, pocket money, and age to assess differences in prevalence of current use between boys and girls, and between students with high versus low pocket money. RESULTS: Although there was substantial regional variation, in most countries boys were statistically significantly more likely to report current use of all assessed products (ranging from 50.0% of countries for waterpipe tobacco to 73.3% of countries for electronic cigarettes). Inequalities by sex were less pronounced in Europe compared to other regions. Inequalities by pocket money were less consistent; students with more pocket money were more likely to report current use of cigarettes (vs those with less pocket money) in 61.8% of the countries, but more likely to report current use of smokeless tobacco in only 18.3% of countries. CONCLUSIONS: Globally, boys and adolescents with more pocket money are generally more likely to use a range of tobacco and nicotine products. However, these patterns are not universal and local variations should be taken into consideration to design effective and equitable tobacco control policies.

Role of homeobox genes in cancer: immune system interactions, long non-coding RNAs, and tumor progression.

The intricate interplay between Homeobox genes, long non-coding RNAs (lncRNAs), and the development of malignancies represents a rapidly expanding area of research. Specific discernible lncRNAs have been discovered to adeptly regulate HOX gene expression in the context of cancer, providing fresh insights into the molecular mechanisms that govern cancer development and progression. An in-depth comprehension of these intricate associations may pave the way for innovative therapeutic strategies in cancer treatment. The HOX gene family is garnering increasing attention due to its involvement in immune system regulation, interaction with long non-coding RNAs, and tumor progression. Although initially recognized for its crucial role in embryonic development, this comprehensive exploration of the world of HOX genes contributes to our understanding of their diverse functions, potentially leading to immunology, developmental biology, and cancer research discoveries. Thus, the primary objective of this review is to delve into these aspects of HOX gene biology in greater detail, shedding light on their complex functions and potential therapeutic applications.

Dual role of microRNA-31 in human cancers; focusing on cancer pathogenesis and signaling pathways.

Widespread changes in the expression of microRNAs in cancer result in abnormal gene expression for the miRNAs that control those genes, which in turn causes changes to entire molecular networks and pathways. The frequently altered miR-31, which is found in a wide range of cancers, is one cancer-related miRNA that is particularly intriguing. MiR-31 has a very complicated set of biological functions, and depending on the type of tumor, it may act both as a tumor suppressor and an oncogene. The endogenous expression levels of miR-31 appear to be a key determinant of the phenotype brought on by aberrant expression. Varied expression levels of miR-31 could affect cell growth, metastasis, drug resistance, and other process by several mechanisms like targeting BRCA1-associated protein-1 (BAP1), large tumor suppressor kinase 1 (LATS1) and protein phosphatase 2 (PP2A). This review highlights the current understanding of the genes that miR-31 targets while summarizing the complex expression patterns of miR-31 in human cancers and the diverse phenotypes brought on by altered miR-31 expression.

Exosomal Non-coding RNA Derived from Mesenchymal Stem Cells (MSCs) in Autoimmune Diseases Progression and Therapy; an Updated Review.

Inflammation and autoimmune diseases (AD) are common outcomes of an overactive immune system. Inflammation occurs due to the immune system reacting to damaging stimuli. Exosomes are being recognized as an advanced therapeutic approach for addressing an overactive immune system, positioning them as a promising option for treating AD. Mesenchymal stem cells (MSCs) release exosomes that have strong immunomodulatory effects, influenced by their cell of origin. MSCs-exosomes, being a cell-free therapy, exhibit less toxicity and provoke a diminished immune response compared to cell-based therapies. Exosomal non-coding RNAs (ncRNA), particularly microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) are intricately linked to various biological and functional aspects of human health. Exosomal ncRNAs can lead to tissue malfunction, aging, and illnesses when they experience tissue-specific alterations as a result of various internal or external problems. In this study, we will examine current trends in exosomal ncRNA researches regarding AD. Then, therapeutic uses of MSCs-exosomal ncRNA will be outlined, with a particle focus on the underlying molecular mechanisms.

Inhibitors of the mTOR signaling pathway can play an important role in breast cancer immunopathogenesis.

This study explores the critical role of inhibitors targeting the mammalian target of rapamycin (mTOR) signaling pathway in breast cancer research and treatment. The mTOR pathway, a central regulator of cellular processes, has been identified as a crucial factor in the development and progression of breast cancer. The essay explains the complex molecular mechanisms through which mTOR inhibitors, such as rapamycin and its analogs, exert their anticancer effects. These inhibitors can stop cell growth, proliferation, and survival in breast cancer cells by blocking critical signaling pathways within the mTOR pathway. Furthermore, the essay discusses the implications of using mTOR inhibitors as a comprehensive therapeutic strategy. It emphasizes the potential benefits of combining mTOR inhibitors with other treatment approaches to enhance the effectiveness of breast cancer treatment. The evolving landscape of breast cancer research underscores the significance of mTOR as a therapeutic target and highlights ongoing efforts to improve and optimize mTOR inhibitors for clinical use. In conclusion, the essay asserts that inhibitors of the mTOR signaling pathway offer a promising approach in the fight against breast cancer. These inhibitors provide a focused and effective intervention targeting specific dysregulations within the mTOR pathway. As research advances, the integration of mTOR inhibitors into customized combination therapies holds excellent potential for shaping a more effective and personalized approach to breast cancer treatment, ultimately leading to improved outcomes for individuals affected by this complex and diverse disease.

Multi-Drug Resistance and Breast Cancer Progression via Toll-Like Receptors (TLRs) Signaling.

Toll-like receptors (TLRs) are essential receptors involved in inflammation and innate immunity. Various types of cancer cells, as well as innate immune cells, express TLRs. There is mounting proof that TLRs are critical to the development and spread of cancer as well as metabolism. In breast cancer, up-regulated levels of TLRs have been linked to the aggressiveness of the diseases, worse treatment outcomes, and the emergence of therapeutic resistance. Patients with advanced non-resectable, recurring, and metastatic breast cancer currently have few available treatment choices. An intriguing new strategy is an innate immunity-mediated anticancer immunotherapy, either used alone or in conjunction with existing treatments. In fact, several TLR agonists and antagonists have been used in clinical studies for anti-cancer immunotherapy. Consequently, TLRs serve as critical targets for controlling the course of breast cancer and treatment resistance in addition to being implicated in immune responses against pathogen infection and cancer immunology. In this review, we deliver an overview of the most current findings on TLR involvement in the development of breast cancer and treatment resistance.

An updated study of the relationship between bacterial infections and women's immune system, focusing on bacterial compositions with successful pregnancy.

Genital tract infections can cause a variety of harmful health outcomes, including endometritis, bacterial vaginosis, and pelvic inflammatory disease, in addition to infertility. Anaerobic bacteria, such as Gardnerella vaginalis, Megasphaera spp., and Atopobium vaginae, are more commonly identified in cases of bacterial vaginosis than lactobacilli. It is unknown how the microorganisms that cause pelvic inflammatory diseases and endometritis enter the uterus. Both prospective and retrospective research have connected pelvic inflammatory disorders, chronic endometritis, and bacterial vaginosis to infertility. Similar to bacterial vaginosis, endometritis-related infertility is probably caused by a variety of factors, such as inflammation, immune system recognition of sperm antigens, bacterial toxins, and a higher risk of STDs. Preconception care for symptomatic women may include diagnosing and treating pelvic inflammatory disease, chronic endometritis, and bacterial vaginosis before conception to optimize the results of both natural and assisted reproduction.

Specific small interfering RNAs (siRNAs) for targeting the metastasis, immune responses, and drug resistance of colorectal cancer cells (CRC).

Colorectal cancer (CRC) involves various genetic alterations, with liver metastasis posing a significant clinical challenge. Furthermore, CRC cells mostly show an increase in resistance to traditional treatments like chemotherapy. It is essential to investigate more advanced and effective therapies to prevent medication resistance and metastases and extend patient life. As a result, it is anticipated that small interfering RNAs (siRNAs) would be exceptional instruments that can control gene expression by RNA interference (RNAi). In eukaryotes, RNAi is a biological mechanism that destroys specific messenger RNA (mRNA) molecules, thereby inhibiting gene expression. In the management of CRC, this method of treatment represents a potential therapeutic agent. However, it is important to acknowledge that siRNA therapies have significant issues, such as low serum stability and nonspecific absorption into biological systems. Delivery mechanisms are thus being created to address these issues. In the current work, we address the potential benefits of siRNA therapy and outline the difficulties in treating CRCby focusing on the primary signaling pathways linked to metastasis as well as genes implicated in the multi-drug resistance (MDR) process.

Targeting Hepatic Cancer Stem Cells (CSCs) and Related Drug Resistance by Small Interfering RNA (siRNA).

Tumor recurrence after curative therapy and hepatocellular carcinoma (HCC) cells' resistance to conventional therapies is the reasons for the worse clinical results of HCC patients. A tiny population of cancer cells with a strong potential for self-renewal, differentiation, and tumorigenesis has been identified as cancer stem cells (CSCs). The discovery of CSC surface markers and the separation of CSC subpopulations from HCC cells have been made possible by recent developments in the study of hepatic (liver) CSCs. Hepatic CSC surface markers include epithelial cell adhesion molecules (EpCAM), CD133, CD90, CD13, CD44, OV-6, ALDH, and K19. CSCs have a significant influence on the development of cancer, invasiveness, self-renewal, metastasis, and drug resistance in HCC, and thus provide a therapeutic chance to treat HCC and avoid its recurrence. Therefore, it is essential to develop treatment approaches that specifically and effectively target hepatic stem cells. Given this, one potential treatment approach is to use particular small interfering RNA (siRNA) to target CSC, disrupting their behavior and microenvironment as well as changing their epigenetic state. The characteristics of CSCs in HCC are outlined in this study, along with new treatment approaches based on siRNA that may be used to target hepatic CSCs and overcome HCC resistance to traditional therapies.

The association of metabolic syndrome with telomere length as a marker of cellular aging: a systematic review and meta-analysis.

Background: It has been suggested that metabolic syndrome (MetS) accelerates the aging process, potentially contributing to the development of age-related complications. Available studies examining the relation of MetS to telomere length (TL), a putative biological marker of aging, have yielded inconclusive findings. This meta-analysis was performed to investigate the association between MetS and TL. Methods: A comprehensive systematic search was conducted in PubMed and Scopus databases to identify relevant literature published up to February 2024. Standard mean difference (SMD) and standardized beta coefficient (ß) with their 95% confidence intervals (CI) were used as effect sizes to measure the associations using the random effects model. Results: A total of nine studies, comprising a total sample size of 8,606 participants, were eligible for the meta-analysis. No significant difference in mean TL was found between patients with and without MetS (SMD = -0.03, 95%CI = -0.17 to 0.10), with a significant heterogeneity across the studies (I 2 = 89.7.0%, p ≤ 0.001). In contrast, it was revealed that MetS is negatively related to TL (ß = -0.08, 95%CI = -0.15 to -0.004). In the subgroup analysis, this finding was supported by the International Diabetes Federation (IDF) definition of MetS. Conclusion: This meta-analysis highlighted that MetS may be linked to a shorter TL. Additional studies are required to confirm this finding.

Detailed role of SR-A1 and SR-E3 in tumor biology, progression, and therapy.

The first host defense systems are the innate immune response and the inflammatory response. Among innate immune cells, macrophages, are crucial because they preserve tissue homeostasis and eradicate infections by phagocytosis, or the ingestion of particles. Macrophages exhibit phenotypic variability contingent on their stimulation state and tissue environment and may be detected in several tissues. Meanwhile, critical inflammatory functions are played by macrophage scavenger receptors, in particular, SR-A1 (CD204) and SR-E3 (CD206), in a variety of pathophysiologic events. Such receptors, which are mainly found on the surface of multiple types of macrophages, have different effects on processes, including atherosclerosis, innate and adaptive immunity, liver and lung diseases, and, more recently, cancer. Although macrophage scavenger receptors have been demonstrated to be active across the disease spectrum, conflicting experimental findings and insufficient signaling pathways have hindered our comprehension of the molecular processes underlying its array of roles. Herein, as SR-A1 and SR-E3 functions are often binary, either protecting the host or impairing the pathophysiology of cancers has been reviewed. We will look into their function in malignancies, with an emphasis on their recently discovered function in macrophages and the possible therapeutic benefits of SR-A1 and SR-E3 targeting.

HOXA9 versus HOXB9; particular focus on their controversial role in tumor pathogenesis.

The Homeobox (HOX) gene family is essential to regulating cellular processes because it maintains the exact coordination required for tissue homeostasis, cellular differentiation, and embryonic development. The most distinctive feature of this class of genes is the presence of the highly conserved DNA region known as the homeobox, which is essential for controlling their regulatory activities. Important players in the intricate process of genetic regulation are the HOX genes. Many diseases, especially in the area of cancer, are linked to their aberrant functioning. Due to their distinctive functions in biomedical research-particularly in the complex process of tumor advancement-HOXA9 and HOXB9 have drawn particular attention. HOXA9 and HOXB9 are more significant than what is usually connected with HOX genes since they have roles in the intricate field of cancer and beyond embryonic processes. The framework for a focused study of the different effects of HOXA9 and HOXB9 in the context of tumor biology is established in this study.

Reducing non-communicable diseases among Palestinian populations in Gaza: A participatory comparative and cost-effectiveness modeling assessment.

We sought to assess the effectiveness and cost-effectiveness of potential new public health and healthcare NCD risk reduction efforts among Palestinians in Gaza. We created a microsimulation model using: (i) a cross-sectional household survey of NCD risk factors among 4,576 Palestinian adults aged ≥40 years old in Gaza; (ii) a modified Delphi process among local public health experts to identify potentially feasible new interventions; and (iii) reviews of intervention cost and effectiveness, modified to the Gazan and refugee contexts. The survey revealed 28.6% tobacco smoking, a 40.4% prevalence of hypertension diagnosis (with a 95.6% medication treatment rate), a 25.6% prevalence of diabetes diagnosis (with 95.3% on treatment), a 21.9% prevalence of dyslipidemia (with 79.6% on a statin), and a 9.8% prevalence of asthma or chronic obstructive pulmonary disease (without known treatment). A calibrated model estimated a loss of 9,516 DALYs per 10,000 population over the 10-year policy horizon. The interventions having an incremental cost-effectiveness ratio (ICER) less than three times the GDP per capita of Palestine per DALY averted (<$10,992 per DALY averted)(<$10,992 per DALY averted) included bans on tobacco smoking in indoor and public places [$34 per incremental DALY averted (95% CI: $17, $50)], treatment of asthma using low dose inhaled beclometasone and short-acting beta-agonists [$140 per DALY averted (95% CI: $77, $207)], treatment of breast cancer stages I and II [$730 per DALY averted (95% CI: $372, $1,100)], implementing a mass media campaign for healthier nutrition [$737 per DALY averted (95% CI: $403, $1,100)], treatment of colorectal cancer stages I and II [$7,657 per DALY averted (95% CI: $3,721, $11,639)], and (screening with mammography [$17,054 per DALY averted (95% CI: $8,693, $25,359)]). Despite high levels of NCD risk factors among Palestinians in Gaza, we estimated that several interventions would be expected to reduce the loss of DALYs within common cost-effectiveness thresholds.

miRNAs in radiotherapy resistance of cancer; a comprehensive review.

While intensity-modulated radiation therapy-based comprehensive therapy increases outcomes, cancer patients still have a low five-year survival rate and a high recurrence rate. The primary factor contributing to cancer patients' poor prognoses is radiation resistance. A class of endogenous non-coding RNAs, known as microRNAs (miRNAs), controls various biological processes in eukaryotes. These miRNAs influence tumor cell growth, death, migration, invasion, and metastasis, which controls how human carcinoma develops and spreads. The correlation between the unbalanced expression of miRNAs and the prognosis and sensitivity to radiation therapy is well-established. MiRNAs have a significant impact on the regulation of DNA repair, the epithelial-to-mesenchymal transition (EMT), and stemness in the tumor radiation response. But because radio resistance is a complicated phenomena, further research is required to fully comprehend these mechanisms. Radiation response rates vary depending on the modality used, which includes the method of delivery, radiation dosage, tumor stage and grade, confounding medical co-morbidities, and intrinsic tumor microenvironment. Here, we summarize the possible mechanisms through which miRNAs contribute to human tumors' resistance to radiation.

Synthesis of N,N'-alkylidene bisamides and Suzuki-Miyaura coupling reaction derivatives with Pd organometallic catalyst anchored to channels of mesoporous silica MCM-41.

At first, an organometallic catalyst namely, Pd-DPyE@MCM-41@MNP was prepared through magnetic (Fe3O4) nanoparticles-doped into channels of mesoporous silica MCM-41 and then, anchoring a novel complex composed of di(4-pyridyl)ethylene and palladium on the inner surface of the support. This immobilized catalyst was successfully identified via VSM, ICP-OES, TEM, FTIR, TGA, SEM, BET, XRD, EDX and elemental mapping analyses. After that, it was used as a versatile, heterogeneous, and magnetically reproducible catalyst in the generation of N,N'-alkylidene bisamides (1a-13a, 8-20 min, 90-98%, 50 °C, solvent-free) and Suzuki-Miyaura coupling (SMC) reaction derivatives (1b-26b, 10-140 min, 86-98%, 60 °C, PEG-400). The VSM plot of Pd-DPyE@MCM-41@MNP displays that this nanocatalyst can be easily recycled by applying an external magnetic field. In both synthetic paths, this nanocatalyst was reused at least seven times without palladium leaching and significantly reducing its catalytic performance. Also, stability and heterogeneous nature of catalyst were approved via ICP-OES technique and hot filtration test.

Beneath the Surface: Exploring Hidden Threats of Long-Term Corticosteroid Therapy to Bone Density.

Within the field of medical treatments, corticosteroids are potent substances that efficiently reduce inflammation and immunological responses, making them essential for the management of a wide range of medical ailments. However, continued use of these synthetic drugs presents a serious risk: the onset of osteoporosis brought on by corticosteroids. Determining the complex pathways by which corticosteroids cause a general disturbance in bone metabolism, suppress osteoblast function, increase osteoclast activity, and upset the delicate balance of bone remodelling emphasizes the need for all-encompassing management and prevention approaches. In this review, we aim to expose the complexities of corticosteroid-induced bone loss and urge for personalized, proactive measures to improve long-term therapeutic outcomes.

LncRNA NEAT1 in the pathogenesis of liver-related diseases.

Nuclear paraspeckle assembly transcript 1 (NEAT1) is a long noncoding RNA (lncRNA) that is widely expressed in a variety of mammalian cell types. Altered expression levels of the lncRNA NEAT1 have been reported in liver-related disorders including cancer, fatty liver disease, liver fibrosis, viral hepatitis, and hepatic ischemia. lncRNA NEAT1 mostly acts as a competing endogenous RNA (ceRNA) to sponge various miRNAs (miRs) to regulate different functions. In regard to hepatic cancers, the elevated expression of NEAT1 has been reported to have a relation with the proliferation, migration, angiogenesis, apoptosis, as well as epithelial-mesenchymal transition (EMT) of cancer cells. Furthermore, NEAT1 upregulation has contributed to the pathogenesis of other liver diseases such as fibrosis. In this review, we summarize and discuss the molecular mechanisms by which NEAT1 contributes to liver-related disorders including acute liver failure, nonalcoholic fatty liver disease (NAFLD), liver fibrosis, and liver carcinoma, providing novel insights and introducing NEAT1 as a potential therapeutic target in these diseases.

Synergistic effects of Metformin and Forskolin on oxidative stress induced by diabetes and hepatocellular cancer: An animal study.

AIM: This study proposed to assess the synergistic effects of Forskolin and Metformin (alone and in combination) on glucose, hematological, liver serum, and oxidative stress parameters in diabetic, healthy, and hepatocellular carcinoma (HCC) induced rats. MATERIALS AND METHODS: Eighty male Wistar rats were divided into 10 experimental groups (8 rats for each group), including 1) healthy group, 2) diabetic group, 3) HCC group, 4) diabet + Metformin (300 mg/kg), 5) diabet + Forskolin (100 mg/kg), 6) diabet + Metformin (300 mg/kg) & Forskolin (100 mg/kg), 7) HCC + Metformin (300 mg/kg), 8) HCC + Forskolin (100 mg/kg), 9) HCC + Metformin (300 mg/kg) & Forskolin (100 mg/kg), and 10) healthy group + Metformin (300 mg/kg) & Forskolin (100 mg/kg). The rats were administrated Forskolin/Metformin daily for 8 weeks. Glucose, hematological, and liver serum parameters were measured and compared among the groups. The levels of malondialdehyde (MDA), and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx), as well as 8-hydroxydeoxyguanosine (8 OHdG) levels, were also measured. RESULTS: The average blood glucose reduction in diabetic rats with the Forskolin, Metformin, and Forskolin + Metformin treatments was 43.5%, 47.1%, and 53.9%, respectively. These reduction values for HCC rats after the treatments were 21.0%, 16.2%, and 23.7%, respectively. For all the diabetic and HCC rats treated with Forskolin/Metformin, the MDA, SOD, and GPx levels showed significant improvement compared with the diabetic and HCC groups (P < 0.05). Although the rats treated with Forskolin + Metformin experienced a higher reduction in oxidative stress of blood and urine samples compared to the Forskolin group, the differences between this group and rats treated with Metformin were not significant for all parameters. CONCLUSION: Metformin and Forskolin reduced oxidative stress in diabetic and HCC-induced rats. The results indicated that the combination of agents (Metformin & Forskolin) had greater therapeutic effects than Forskolin alone in reducing glucose levels in diabetic rats. However, the ameliorative effects of combining Metformin and Forskolin on blood and urine oxidative stress were not statistically higher than those of Metformin alone.

Transcarotid versus transfemoral transcatheter aortic valve replacement: A systematic review and meta-analysis.

BACKGROUND: In the 2021 Transcatheter Valve Therapy (TVT) registry, 8.9 % of patients underwent TAVR via access sites other than the femoral artery. Transthoracic approaches may be contraindicated in some patients and may be associated with poorer outcomes. Therefore other alternative access routes are increasingly being performed. We conducted a systematic review of the literature on transcarotid transcatheter aortic valve replacement (TC-TAVR) and meta-analysis comparing outcomes of TC-TAVR and other access routes. METHODS: We comprehensively searched for controlled randomized and non-randomized studies from 4 online databases. We presented data using risk ratios (95 % confidence intervals) and measured heterogeneity using Higgins' I2. RESULTS: Sixteen observational studies on transcarotid TAVR were included in the analysis; 4 studies compared TC-TAVR vs TF-TAVR. The mean age and STS score for patients undergoing TC-TAVR were 80 years and 7.6 respectively. For TF-TAVR patients, mean age and STS score were 81.2 years and 6.5 respectively. There was no difference between patients undergoing TC-TAVR and TF-TAVR in the following 30-day outcomes: MACE [8.4 % vs 6.7 %; OR 1.32 (95 % CI 0.71-2.46 p = 0.38) I2 = 0 %], mortality [5.6 % vs 4.0 %; OR 0.42 (95 % CI 0.60-3.37, P = 0.42) I2 = 0 %] and stroke [0.7 % vs 2.3 %; OR 0.49 (95 % CI 0.09-2.56, P = 0.40) I2 = 0 %]. There was no difference in 30-day major vascular complications [0.7 % vs 3 %; OR 0.55 (95 % CI 0.06-5.29, P = 0.61) I2 = 39 %], major bleeding [0.7 % vs 3.8 %; OR 0.39 (95 % CI 0.09-1.67, P = 0.21) I2 = 0 %], and moderate or severe aortic valve regurgitation [8.6 % vs 9.9 %; OR 0.89 (95 % CI 0.48-1.65, P = 0.72) I2 = 0 %]. CONCLUSION: There are no significant differences in mortality, stroke MACE and major or life-threatening bleeding or vascular complications when TC-TAVR is compared to TF-TAVR approaches.

Nucleic acid vaccines-based therapy for triple-negative breast cancer: A new paradigm in tumor immunotherapy arena.

Nucleic acid vaccines (NAVs) have the potential to be economical, safe, and efficacious. Furthermore, just the chosen antigen in the pathogen is the target of the immune responses brought on by NAVs. Triple-negative breast cancer (TNBC) treatment shows great promise for nucleic acid-based vaccines, such as DNA (as plasmids) and RNA (as messenger RNA [mRNA]). Moreover, cancer vaccines offer a compelling approach that can elicit targeted and long-lasting immune responses against tumor antigens. Bacterial plasmids that encode antigens and immunostimulatory molecules serve as the foundation for DNA vaccines. In the 1990s, plasmid DNA encoding the influenza A nucleoprotein triggered a protective and targeted cytotoxic T lymphocyte (CTL) response, marking the first instance of DNA vaccine-mediated immunity. Similarly, in vitro transcribed mRNA was first successfully used in animals in 1990. At that point, mice were given an injection of the gene encoding the mRNA sequence, and the researchers saw the production of a protein. We begin this review by summarizing our existing knowledge of NAVs. Next, we addressed NAV delivery, emphasizing the need to increase efficacy in TNBC.