Cancer is rapidly increasing worldwide and urgent global action towards cancer control is required. Consistent with global trends, Canada is expected to experience a near doubling in new cases and cancer deaths between 2020-2040; population growth and ageing being the primary drivers. The projected increased cancer incidence and its associated costs is expected to further exacerbate socioeconomic inequities. Focused actions to prevent cancer, to detect it earlier when more treatable, and, to lower the risk of recurrence, must be prioritized. Almost half of all cancers are preventable, caused by risk factors that are potentially avoidable and modifiable. Integrating cancer prevention with care-based models is necessary and represents the most cost-effective and sustainable approach to control cancer. To be effective, prevention efforts must consider the cancers impacting local populations and understand how community and individual factors interact within the spatial and temporal contexts in which people live. This study is part of the Nova Scotia Community Cancer Matrix project which profiles the cancers impacting communities over time; measuring associations between cancer and socioeconomic status (SES); and determining how the joint spatial distribution of cancers can be used to address inequities, identify priority populations and strengthen prevention efforts. Using Bayesian inference to model spatio-temporal variations in 58,206 cases diagnosed in 301 communities between 2001-2017, across 10 preventable cancer types, we report significant disparities in cancer risk across communities based on sex and community SES. The work highlights the utility of small-area mapping to identify at-risk communities and understand how community-SES impacts risk. It also uncovers significant inequities rooted in the differential distribution of material and social capacity, operating beyond the control of individuals. The approach is implementable to other regions to inform and strengthen prevention efforts aiming at reducing the burden of cancer or that of other diseases.

Breast cancer (BCa) is a heterogeneous disease, initially responsive to hormone therapy but often developing resistance to both hormonal and chemotherapy treatments. Novel therapeutic strategies are needed for drug-resistant BCa. Genistein, a phytoestrogen structurally similar to estrogen, competes with estrogen for receptor binding and exhibits anti-cancer effects. In this study, we investigated the cellular and metabolic impacts of genistein, alone or in combination with chemotherapy, in two human BCa cell lines-one estrogen receptor-positive (ER+) and one estrogen receptor-negative (ER-). We observed a strong synergistic effect on cell viability at low concentrations of genistein and chemotherapy, resulting in reduced clonogenic capacity and impaired cell migration. Genistein alone modulated cellular energy metabolism, notably reducing ATP production in MCF7 (ER+) cells. This metabolic shift was linked to a decreased dependence on fatty acids for energy, coupled with a decrease in the rate-limiting mitochondrial translocase CPT1 required for fatty acid oxidation, alongside with an increase in intracellular fatty acid levels. While the most significant changes occurred in ER+ cells, ER- cells also showed responses to genistein treatment. Collectively, our findings suggest that low genistein concentrations, in combination with conventional chemotherapy, induces synergistic anti-cancer effects, promoting cellular senescence.

Black women bear a disproportionately higher burden of cervical cancer than any ethnic/racial group. Patient's cancer risk perceptions and patient-provider communication behavior may influence uptake of cervical cancer screening with Papanicolaou (Pap) test. We examined the association of cancer risk perceptions and patient-provider communication behavior and Pap test uptake. Black women completed a cross-sectional survey on sociodemographic, cancer perceptions, and perceived patient-centered communication behaviors. Multiple linear regression models were fitted to explore the association of perceptions and patient communication behaviors. Women (N = 116) average age was 40 ± 12.7 years and 73% had ever received a Pap test. Women who agreed with the statement that it seemed like everything causes cancer had over four times the odds of having had a Pap test (OR = 4.40, 95% CI = 1.38-13.97, p = .012) while those that responded that when they think about cancer, they automatically think of death had 73% lower odds of having had a Pap test (OR = 0.27, 95% CI = 0.08-0.95, p = .040). The odds of Pap test completion were over 4-fold among those who said their health care provider always or usually gave them the chance to ask health-related questions, compared to those who responded sometimes or never (OR = 4.11, 95% CI = 1.36-12.44; p = .012). Interventions to dispel myths and promote effective patient-provider communications are warranted to address anecdotal cancer risk perceptions and promote patient engagements.

Fumarate hydratase (FH) is a key enzyme in the Krebs cycle and cellular energy metabolism, playing a crucial role in tumorigenesis. It is considered a prognostic, diagnostic, and therapeutic target for many types of cancer. Therefore, FH is a popular scientific subject in cancer research. The current study aimed to identify cancer research in the WoS database and examine studies conducted on FH molecules using bibliometric indicators.

The keywords "fumarate hydratase" OR fumarase" AND "cancer OR tumor OR neoplasm" were used to search the WoS database. This search was performed using abstracts, titles, and keywords. The "Article" and "Review" options were used to access the data of papers published between 2002 and March 2024.

A total of 840 publications (616 articles and 224 reviews) were published by the end of March 2024. Research output on FH and cancer has significantly increased recently, with the highest number of publications in 2020 (n = 69, 8.214%). The most commonly used language was English (n = 823, 97.976%), and the USA led in productivity, contributing 306 studies (36.429%). The University of Helsinki is the most productive affiliation with 138 published articles. The researcher who conducted most studies (n = 58, 6.904%) was also the most-cited author, with 1562 citations. In the current bibliometric study, "hereditary leiomyomatosis", "mutations", and "renal-cell cancer" were frequently included in publications.

This bibliometric study provides a quantitative overview of FH research in oncology and presents the most recent FH status in cancer research.

Inflammation is a complex and finely tuned component of the host defense mechanism, responding sensitively to a range of physical, chemical, and biological stressors. Current research is advancing our grasp of both cellular and molecular mechanisms that initiate and regulate interactions within inflammatory pathways. Substantial evidence now indicates a profound link between inflammation, innate immunity, and cancer. Dysregulation of inflammatory pathways is known to be a pivotal factor in the induction, growth, and metastasis of tumors through multiple mechanistic pathways. Basically, the tumor microenvironment (TME), characterized by dynamic interplay between cancerous cells and surrounding inflammatory and stromal cells, plays a central role in these processes. Increasingly, controlled acute inflammation is being explored as a promising therapeutic tool in certain types of cancer. However, inflammatory cells in the TME exhibit remarkable plasticity, with shifting phenotypic and functional roles that facilitate cancer cell survival, proliferation, and migration, especially under chronic inflammatory conditions. Additionally, signaling molecules associated with the innate immune system, like chemokines, are co-opted by malignant cells to support invasion, migration, and metastasis. These findings underscore the need for deeper insights into the mechanisms connecting inflammation to cancer pathology, which could pave the way for innovative diagnostic approaches and targeted anti-inflammatory therapies to counter tumor development. The current review underlines the critical involvement of inflammation in cancer development, examining the connection between the immune system, key inflammatory mediators, biomarkers, and their associated pathways in cancer. We also discuss the impact of inflammation-targeted therapies on anticancer signaling pathways. Furthermore, we review major anti-inflammatory drugs with potential applications in oncology, assessing how inflammation is modulated in cancer management. Lastly, we outline an overview of ongoing discoveries in the field, highlighting both the challenges and the therapeutic promise of targeting inflammation in cancer therapy.

Bisphenol A (BPA) is a high-production-volume industrial chemical and component of commonly used plastic products. However, it is also an endocrine-disrupting chemical that can negatively affect human health. It is not yet known whether it is associated with the development of epithelial ovarian cancer (EOC), a severe and highly fatal human disease. Therefore, the purpose of this study was to determine the concentrations of BPA in the urine of women with EOC or epithelial borderline ovarian tumors (EBOTs) using gas chromatography tandem mass spectrometry (GC-MS/MS) and find their possible associations with kidney function at the molecular level, urine and blood biochemical parameters related to metabolism, anti-Müllerian hormone (AMH) (a marker of ovarian reserve/fertility), and lifestyle habits determined via a questionnaire in comparison to healthy controls. The results suggest that the unadjusted or urine-specific-gravity-adjusted BPA levels were significantly increased in women with EOC/EBOT. The unadjusted BPA was significantly positively associated with urinary creatinine (p = 0.007) in all women with EOC/EBOT after adjustment for age, body mass index, and pregnancy using multiple linear regression analysis. This may be related to kidney injury. However, no association was found between urinary BPA and serum AMH levels in women. Women with ovarian malignancies were more exposed to plastic products for storing foods and drinks. Some lifestyle habits, including refilling plastic bottles, correlate with higher urinary BPA levels across the entire cohort of women. When considering EOC or EBOT, it is necessary to consider the potential higher exposure of women to BPA, as reflected in their urine and lifestyle habits.

Oral epithelial dysplasia (OED) is a histological diagnosis that carries an increased risk of the individual developing oral squamous cell carcinoma. We assessed the information needs (IN) and explored the sources of education used by individuals with OED using a validated OED-specific measurement.

A total of 102 adults with OED from the oral medicine clinic of a dental hospital in Central London were selected using convenience sampling. A cross-sectional survey was conducted in which participants completed the 33-item Oral Epithelial Dysplasia Informational Needs Questionnaire (ODIN-Q), which assessed IN and gathered perspectives on patient education.

Approximately two-thirds of the participants (n = 66, 64%) reported meeting the IN, whereas the remaining participants (n = 36, 35%) did not. The mean and median total scores from the questionnaire were 2.43 (± 0.38) and 2.6, respectively, indicating a low sufficient level of IN. Most participants (n = 80, 78%) preferred one-on-one meetings as the primary mode of obtaining information, followed by written materials (n = 64, 62%), audiovisual resources (n = 24, 23%), and group discussions (n = 8, 0.7%).

Some topics were insufficiently met, necessitating additional educational efforts, such as risk factors and lifestyle modifications, physical and psychological impacts, awareness of potential complications, and seeking medical and psychological support. Sex and degree of dysplasia were associated with the levels of IN. These findings may guide future longitudinal research on OED IN assessment, support the creation of tailored educational tools, and facilitate further evaluation of the psychometric properties of the ODIN-Q.

This study aims to explore how cancer-related risk factors cluster among college students in Guam. Using the 2021-2022 Pacific Islands Cohort of College Students data, we conducted a latent class analysis (LCA) to organize the sample into classes based on clustering cancer risk factors, including tobacco use, binge drinking, low fruit/vegetable intake, physical inactivity, betel nut use, overweight/obesity, depression, and anxiety. Among the 577 college students surveyed, results show a high prevalence of low fruit/vegetable intake, overweight/obesity, depression, and anxiety. The LCA identified three classes, each defined by different clustering cancer risk behaviors. All classes showed high prevalence of low fruit/vegetable intake. Class 1 had the highest rates of tobacco use, betel nut use, and binge drinking. Class 2 had the highest rates of physical inactivity, depression, and anxiety. Class 3 had the lowest rates of betel nut use, overweight/obese, depression, and anxiety when compared with Classes 1 and 2. The clustering of risk behaviors highlights the need for targeted interventions and prevention strategies among Guam's youth, aiming to address these behaviors and potentially reduce cancer risk in the region.

Endocrine-disrupting chemicals (EDCs), including known and unknown parent compounds, their metabolites, and transformation products, are pervasive in daily life, posing increasing risks to human health and the environment. This study employed a high-resolution mass spectrometry-based nontargeted screening approach, integrating polar (HILIC) and reversed-phase separations to expand the chemical space coverage and, supported by open-science tools and resources, evaluated urinary chemical profiles to assess internal EDC exposure. Among 106 annotated biomarkers of exposure, six exhibited significantly higher normalized intensities in patients with ovarian malignancies compared to healthy controls (p < 0.05). This suggests their greater exposure to phthalates (diethylhexyl phthalate and diethyl phthalate), pesticides (metolachlor metabolite and 4-nitrophenol), a UV filter (benzophenone-1), and an industrial byproduct (4-methyl-2-nitrophenol). These compounds may interfere with hormonal regulation, potentially contributing to cancer development. While these findings highlight potential differences in internal EDC exposure, the study primarily demonstrates the applicability of nontargeted urinary profiling for chemical exposure assessment. By providing new insights into EDCs burden and its pathological implications, this work contributes to advancing next-generation chemical risk assessment within the European Partnership for the Assessment of Risks from Chemicals initiative and supports the development of preventive strategies to mitigate environmental cancer risks.

Cancer remains a significant global health challenge, with its progression shaped by complex and multifactorial mechanisms. Recent research suggests that the vagus nerve could play a critical role in mediating communication between the tumor microenvironment and the central nervous system (CNS). This review highlights the diversity of vagal afferent receptors, which could position the vagus nerve as a unique pathway for transmitting immune, metabolic, mechanical, and chemical signals from tumors to the CNS. Such signaling could influence systemic disease progression and tumor-related responses. Additionally, the vagus nerve's interactions with the microbiome and the renin-angiotensin system (RAS)-both implicated in cancer biology-further underscore its potential central role in modulating tumor-related processes. Contradictions in the literature, particularly concerning vagal fibers, illustrate the complexity of its involvement in tumor progression, with both tumor-promoting and tumor-suppressive effects reported depending on cancer type and context. These contradictions often overlook certain experimental biases, such as the failure to distinguish between vagal afferent and efferent fibers during vagotomies or the localized parasympathetic effects that cannot always be extrapolated to the systemic level. By focusing on the homeostatic role of the vagus nerve, understanding these mechanisms could open the door to new perspectives in cancer research related to the vagus nerve and lead to potential therapeutic innovations.

In this study, we synthesised a series of self-assembling glycoconjugates derived from bhilawanol under environmentally friendly conditions in good yields. These self-assembling glycoconjugates displayed anti-cancer activity toward HeLa cells at an IC50 value of 125 μM with minimal side effects, holding immense potential in cancer therapeutics.

The search for new molecules in cancer therapeutics is essential for overcoming treatment limitations, targeting evolving cancer characteristics, minimizing side effects, and advancing scientific knowledge. In this context, a series of benzo[d]thiazole-isatin conjugates (6a-6m) has been synthesized successfully in three steps with excellent yields (>90%). The preliminary antiproliferative results demonstrate that these synthetic derivatives are comparable to the well-known tyrosine kinase inhibitor (TKI) sunitinib. Moreover, the evaluation of their cytotoxicity has revealed outstanding activity against various cancer cell lines, including A549, HePG2, MDA-MB-231, and SGC7901. This significant efficacy highlights their potential as effective anti-cancer agents. Mechanism of action (MoA) studies revealed that compound 6g arrests the A549 and HepG2 cells at S phase, and the compound 6g on HepG2 cells results in a large number of cell necroses. Binding affinity of 6g with EGFR and cyclin-dependent kinase 2 (CDK2) kinase gives better results than reference drugs gefitinib and roscovitine, respectively.

The human microbiome has always been an important determinant of health and recently, its role has also been described in cancer. The altered microbiome could aid cancer progression, modulate chemoresistance and significantly alter drug efficacy. The broad implications of microbes in cancer have prompted researchers to investigate the microbe-cancer axis and identify whether modifying the microbiome could sensitize cancer cells for therapy and improve the survival outcome of cancer patients. The preclinical data has shown that enhancing the number of specific microbial species could restore the patients' response to cancer drugs and the microbial biomarkers may play a vital role in cancer diagnostics. The elucidation of detailed interactions of the human microbiota with cancer would not only help identify the novel drug targets but would also enhance the efficacy of existing drugs. The field exploring the emerging roles of microbiome in cancer is at a nascent stage and an in-depth scientific perspective on this topic would make it more accessible to a wider audience. In this review, we discuss the scientific evidence connecting the human microbiome to the origin and progression of cancer. We also discuss the potential mechanisms by which microbiota affects initiation of cancer, metastasis and chemoresistance. We highlight the significance of the microbiome in therapeutic outcome and evaluate the potential of microbe-based cancer therapy.

Metal sulfide nanomaterials (MeSNs) are highly promising for biomedical applications due to their low toxicity, good dispersibility, high stability, adjustable particle sizes, and good biocompatibility. Their unique chemical and light-conversion properties also enable them to function as photothermal or photodynamic agents, enhancing chemodynamic therapy (CDT) of tumors. This makes MeSNs valuable as photo-enhanced CDT nanoagents, advancing precision and multi-modal tumor treatment. This review examines recent advancements in MeSNs for photo-enhanced chemodynamic tumor ablation, comparing their effectiveness in CDT. It highlights the roles of photothermal, photodynamic, and photocatalytic effects in enhancing treatment efficacy. MeSN-based nanoreactors are categorized by composition into iron sulfide, copper sulfide, other unary, and multi-MeSNs for their applications in tumor therapy. Additionally, this review discusses challenges, limitations, and future biomedical applications of MeSNs, offering insights into their potential for next-generation cancer treatments.

Epilepsy is a neurological disorder characterized by repeated convulsions. Antiepileptic drugs (AEDs) are the main course of therapy for epilepsy. These medications are given according to each patient's personal medical history and the types of seizures they suffer. They have been employed for decades to manage epilepsy, thus delivering relief from seizures through numerous mechanisms of action. Aside from their anticonvulsant attributes, current evidence suggests that certain AEDs may display potential inhibitory effects against cancer invasion and metastasis. This review explored the complicated interactions between the modes of action of AEDs and the pathways causing cancer, and the potential impact of AEDs on the invasion and metastasis of various forms of cancer, while addressing their associated side effects. For example, valproic acid inhibits histone deacetylase, causing hyperacetylation of genes, especially those regulating cell cycle, culminating in cell cycle arrest. Topiramate inhibits carbonic anhydrase, thus disrupting the acidic microenvironment needed for cancer cells to thrive. Lacosamide increases the slow inactivation of the voltage gated Na+ channel, thus inhibiting the growth, proliferation, and metastasis of many cancers. Although drug development is a complex task due to regulatory, intellectual property, and economic challenges, researchers are exploring drug repurposing tactics to overcome these challenges and to find new therapeutic alternatives for diseases like cancer. Thus, drug repurposing is considered among the most effective ways to develop drug candidates using novel properties and therapeutic characteristics, and this review also discusses these issues.

The increasing global burden of cancer necessitates innovative approaches to prevention and treatment. Lifestyle factors such as diet, physical activity, and smoking significantly contribute to cancer. At the same time, current guidelines are based on a one-size-fits-all approach, which limits their effectiveness across diverse populations. Obesity is a well-documented risk factor for cancer, directly affecting 13 types of cancer. The complex interplay of genetic, metabolic, hormonal, and environmental factors in obesity's etiology highlights the need for more tailored approaches to obesity-related cancers. This perspective article advocates for a shift toward an integrative, personalized approach that considers a variety of intrinsic and extrinsic factors associated with the etiology of obesity-related cancers. Lifestyle-based cancer prevention strategies should be tailored to an individual's biological profile, demographic background, behaviors, and environmental exposures. Following a diagnosis, a comprehensive treatment approach should consider how these genetic, physiological, lifestyle, and environmental factors interact in the onset and progression of the disease while also taking cancer type and stage into account. This approach paves the way for more precise and effective strategies in tackling cancer. Fulfilling collaboration across research, healthcare, and policy sectors is essential to achieve these goals.

Background: Globally, colorectal cancer (CRC) is the third-most diagnosed cancer among males and the second-most diagnosed cancer among females. In cancer, stem cells are a subset of neoplastic cells capable of tumorigenesis and exhibit properties like normal stem cells. Moreover, they are resistant to conventional cancer treatments and can repopulate the tumor following treatment. Cancer cells are stimulated to undergo apoptosis by photodynamic therapy (PDT), which involves a light source, a photosensitizer, and reactive oxygen species. Methods: In this study, colon cancer stem cells were isolated from colon cancer cells and characterized using flow cytometry and immunofluorescence techniques. To treat colon cancer stem cells (CCSCs), single-walled carbon nanotubes (SWCNTs) were coupled with hyaluronic acid (HA) and loaded with chlorin-e6 (Ce6). Nanobiocomposite toxicity was assessed using CCSCs with two fluences of 5 J/cm2 and 10 J/cm2. The cellular changes were observed at 24 and 48 h using microscopy, Results: LDH cytotoxicity assay, and cell death induction by annexin propidium iodide assay. An intracellular analysis of reactive oxygen species (ROS) detected oxidative stress within CCSCs. Conclusions: Overall, the results showed that the newly synthesized nanobiocomposite enhanced the ability of PDT to act as a photosensitizer carrier and induced cell death in CCSCs.

Although community engagement has had a substantial presence in public health research, community input to inform geospatial and health analyses remains underutilized and novel. This article reports on community engagement activities to solicit stakeholder perspectives on the role of neighborhood conditions in health and cancer. We discuss how this community input refined an a priori conceptual model to be tested in the larger Families, Friends, and Neighborhoods Study.

We conducted semistructured virtual interviews with 82 stakeholders (e.g., community and faith leaders, educators, and healthcare workers) across four states (Maryland, Connecticut, Alabama, and Missouri). Participants discussed the impact where a person lives can have on their health and cancer risk. We subsequently convened a virtual group discussion with 17 randomly selected interviewees. Our study team individually reviewed discussion notes, which were synthesized into a consensus document.

In addition to constructs from the original conceptual model, participants identified neighborhood-level factors not present in the original model, including K-12 educational quality, local property investment, homelessness, public transportation infrastructure, proximity to healthcare facilities, environmental toxin exposures, access to healthy foods, and cost of living. These factors will be incorporated into the Families, Friends, and Neighborhoods Study analytic models.

Although geospatial analyses in health research have not traditionally employed community engagement techniques, this study illustrates the value of informing multilevel analytic models with the lived experiences of those negatively affected by neighborhood conditions that underlie the risk, prevention, and screening behaviors driving cancer incidence and mortality.

Future social epidemiology research can be enriched through community engagement.

Benzimidazole scaffolds have potent anticancer activity due to their structure similarity to nucleoside. In addition, benzimidazoles could function as hydrogen donors or acceptors and bind to different drug targets that participate in cancer progression. The literature had many anticancer agents containing benzimidazole cores that gained much interest. Provoked by our endless interest in benzimidazoles as anticancer agents, we summarized the successful trials of the benzimidazole scaffolds in this concern. Moreover, we discuss the substantial opportunities in cancer treatment using benzimidazole-based drugs that may direct medicinal chemists for a compelling future design of more active chemotherapeutic agents with potential clinical applications. The uniqueness of this work lies in the highlighted benzimidazole scaffold hybridization with different molecules and benzimidazole-metal complexes, detailed mechanisms of action, and the IC50 of the developed compounds determined by different laboratories after 2015.

This study synthesized a series of Schiff base derivatives featuring a 1,2,4-triazole framework and characterized through FT-IR, 1H NMR, 13C NMR, 19F NMR, MS, and elemental analysis. Subsequently, the inhibitory activities of these compounds were systematically evaluated in vitro against human carbonic anhydrase (hCA) isozymes I and II, acetylcholinesterase (AChE), and butyrylcholinesterase (BChE). The results revealed that compounds 5a and 5c were particularly effective against cholinesterase enzymes, demonstrating their potential for neuroprotective applications. Meanwhile, compounds 5f and 5g exhibited remarkable inhibition of hCA I and II isozymes, suggesting their promise as selective inhibitors for therapeutic areas. Furthermore, molecular docking analyses revealed strong and specific interactions between the active compounds and enzyme binding sites, further supported by molecular dynamics simulations. Additionally, ADMET profiling of all compounds indicated favourable pharmacokinetic properties. The ADMET results suggest that these compounds hold significant potential for clinical applications in central nervous system and various disorders. These findings strongly suggest that the synthesized compounds are promising candidates for addressing unmet therapeutic needs in neurodegenerative and metabolic disorders, with potential applications in multi-enzyme targeting therapies.

Due to rapid westernization, Korean dietary habits have emerged as significant risk factors for chronic disease and cancer. Despite this transition, Korea's cancer prevention guidelines have remained consistent since their establishment about 18 years ago. This study aimed to investigate the degree of awareness and practice to global dietary guidelines among Korean adults and identify demographic and lifestyle factors associated with low practice. A cross-sectional survey conducted in 2023 included 4,000 adults and assessed their awareness and practice of four global recommendations: "Eat a diet rich in whole grains," "Limit consumption of processed meat," "Limit consumption of sugar-sweetened beverages," and "Limit consumption of fast and other processed foods." While more than half of the participants recognized the guidelines' importance for cancer prevention, implementation rates remained below 40%. Furthermore, over 80% of the respondents expressed a compelling requirement for updated and tailored dietary guidelines. Younger individuals, those who were physically inactive, individuals who had not received prior nutrition education, and participants with obesity were more likely to exhibit low practice, particularly to guidelines limiting processed foods and sugary beverages intake. These findings highlight the need to revise Korea's cancer prevention recommendations by incorporating global dietary practices and addressing the westernized eating patterns prevalent within the population. Efforts should focus on promoting these updated guidelines through targeted education and public health interventions that improve practice, especially in high-risk groups, and effectively mitigate the burden of diet-related cancers in Korea.

Pleckstrin homology-like domain family A, member 3 (PHLDA3) is a p53-regulated tumor suppressor protein that suppresses AKT-mediated survival and oncogenic signaling. The PHLDA3 gene has garnered significant attention due to its multifaceted roles in tumorigenesis, metastasis, and invasion. This review explores the complex interactions between PHLDA3 and key cellular processes involved in cancer, emphasizing its regulatory mechanisms and clinical relevance. PHLDA3 has been found to be a critical regulator of metastatic pathways, particularly through its influence on the epithelial-mesenchymal transition (EMT) and in cellular invasion. Its interactions with pivotal signaling pathways, such as the Phosphoinositide 3-kinases/Protein kinase B (PI3K/AKT), p53, and Wnt/β-catenin pathways, highlight its multifunctional roles in various cancer types. Additionally, we discuss the potential of PHLDA3 as both a prognostic biomarker and a therapeutic target, offering new insights into its potential in treating advanced-stage malignancies. This review provides a detailed analysis of the role of PHLDA3 in cancer progression, including metastasis and invasion, underscoring its therapeutic potential.

The leucine-rich repeat containing protein (NLR) canonical inflammasome family includes Nod-like receptor protein 3 (NLRP3). Via the mediation of apoptosis proteins and immunological reactions, it controls the pathogenesis of malignancy. Experimental studies showed a relationship among lymphogenesis, cancer metastasis, and NLRP3 expression. Natural products have also been used as lead-based substances in a number of investigations to speed up the creation of novel, specific NLRP3 inhibitors. Via the mediation of apoptotic proteins and immunological responses, it controls the pathogenesis of malignancy. Moreover, it was recently noted that among human cancers, chemotherapy activates NLRP3. Induction of NLRP3 could encourage the generation of IL-1β and IL-22 to facilitate the propagation of malignancy. Additionally, prior research has demonstrated that the usage of NLRP3 in cancer therapy may result in resistance to drugs. The depletion of NLRP3 could affect the survival of cells. Natural products have been used as lead materials in a number of studies to help generate novel, specific NLRP3 antagonists more quickly. In the present review, we examine the mechanism behind the beneficial effects of the natural substances on the inhibition of cancer growth and progression, with special focus on NLRP3 regulation.

Background and Aims: Several epidemiological studies have investigated the relationship between anthropometric factors and breast cancer (BC), but the results, particularly for premenopausal BC, remain inconsistent and contradictory. The aim of this systematic review is to present an overview of studies examining the association between obesity and BC risk in African women, by menopausal status. Methods: PubMed, Scopus, Web of Science, and Google Scholar were searched until 17 February 2025 to identify published articles. The review included original studies, with no restrictions on publication date or language. The exposures studied were height, weight, body mass index (BMI), waist circumference (WC), hip circumference (HC), and waist-to-hip ratio (WHR). The quality of the studies was assessed using the National Institute of Health (NIH). Study selection and data extraction were carried out by two authors separately. Results: A total of fifteen case-control studies were included in this systematic review, comprising 45,056 subjects (7221 cases and 37,835 controls). Among them, fourteen studies reported stratified results for pre- and postmenopausal women, and one reported findings for only premenopausal BC. We found that BMI was associated with an increased risk of BC in both premenopausal and postmenopausal women, though the associations varied across studies. Height was associated with an increased risk of pre- and postmenopausal BC. WHR was positively associated with BC in pre- and postmenopausal women, while WC showed a positive association with the risk of postmenopausal BC, and inconsistent results with premenopausal BC. Finally, a higher HC was positively associated with premenopausal and postmenopausal BC. Conclusions: The risk of developing BC is higher in obese postmenopausal women. The protective role of BMI has not been demonstrated in African premenopausal women. WHR is a risk factor for premenopausal and postmenopausal BC. There is a need to study the influence of stages of overweight and obesity on BC risk in a large sample of African women in-depth.

Tumors often exhibit greater stiffness compared to normal tissues, primarily due to increased deposition within the tumor stroma. Collagen, proteoglycans, laminin, and fibronectin are key components of the extracellular matrix (ECM), interacting to facilitate ECM assembly. Enhanced fiber density and cross-linking within the ECM result in elevated matrix stiffness and interstitial fluid pressure, subjecting tumors to significant physical stress during growth. This mechanical stress is transduced intracellularly via integrins, the Rho signaling pathway, and the Hippo signaling pathway, thereby promoting tumor invasion. Additionally, mechanical pressure fosters glycolysis in tumor cells, boosting energy production to support metastasis. Mechanical cues also regulate macrophage polarization, maintaining an inflammatory microenvironment conducive to tumor survival. In summary, mechanical signals within tumors play a crucial role in tumor growth and invasion. Understanding these signals and their involvement in tumor progression is essential for advancing our knowledge of tumor biology and enhancing therapeutic approaches.

The association between serum folate concentrations and the mortality of cancer remains unclear. We aim to investigate the association of serum folate concentrations with all-cause and cause-specific mortality among American adults with cancer.

This cohort study included 4535 patients with cancer from National Health and Nutrition Examination Survey (NHANES) 1999 to 2016 and NHANES III (1988-1994). Death outcomes were ascertained by linkage to National Death Index records through 31 December 2019. Cox proportional hazards model and two-piecewise Cox proportional hazards model were used to calculate hazard ratios and 95% confidence intervals for the associations between folate concentrations and the risk of mortality.

During a median follow-up of 37,792 person-years, there were 1998 all-cause deaths and 616 cancer deaths. Non-linear and L-shaped associations were observed between serum folate concentrations and the risk of all-cause and cancer mortality among patients with cancer. Notably, the mortality rates reached a plateau at 23.7 ng/mL for all-cause mortality and 23.57 ng/mL for cancer mortality. When folate levels fell below these thresholds, the risk of all-cause and cancer mortality decreased by approximately 2.1% (HR 0.979; 95% CI 0.969-0.989) and 3.6% (HR 0.964; 95% CI 0.948-0.981), respectively, with each unit increase in the folate concentration up to the thresholds.

Our study reveals that low serum folate concentrations are linked to an elevated risk of cancer mortality among individuals with cancer within a certain range and supplementation of folate in cancer patients to achieve specific serum folate level threshold (23.7 ng/mL) might reduce the risk of cancer mortality.

Several studies have demonstrated that dietary patterns identified by a posteriori and hybrid methods are associated with gastrointestinal (GI) cancer risk and mortality. These studies applied different methods for analyzing dietary data and reported inconsistent findings.

This systematic review and meta-analysis were aimed to determine the association between dietary patterns, derived using principal component analysis (PCA) and reduced rank regression (RRR), and GI cancer risk and GI cancer-caused mortality.

Articles published up to June 2023 in English were eligible for inclusion. The Medline, SCOPUS, Cochrane Library, CINHAL, PsycINFO, ProQuest, and Web of Sciences databases were used to identify prospective studies. The Preferred Reporting Item for Systematic Review and Meta-analysis Protocol 2020 was used to report results.

A total of 28 studies were eligible for inclusion. Varied approaches to deriving dietary patterns were used, including PCA (n = 22), RRR (n = 2), combined PCA and RRR (n = 1), cluster analysis (CA; n = 2) and combined PCA and CA (n = 1).

Two dietary patterns, "healthy" and "unhealthy," were derived using PCA and RRR. The healthy dietary pattern was characterized by a higher intake of fruits, whole grains, legumes, vegetables, milk, and other dairy products, whereas the unhealthy dietary pattern was characterized by a higher intake of red and processed meat, alcohol, and both refined and sugar-sweetened beverages. The findings indicated that the PCA-derived healthy dietary pattern was associated with an 8% reduced risk (relative risk [RR], 0.92; 95% CI, 0.87-0.98), and the unhealthy dietary pattern was associated with a 14% increased risk (RR, 1.14; 95% CI, 1.07-1.22) of GI cancers. Similarly, the RRR-derived healthy dietary pattern (RR, 0.83; 95% CI, 0.61-1.12) may be associated with reduced risk of GI cancers. In contrast, the RRR-derived unhealthy dietary pattern (RR, 0.93; 95% CI, 0.57-1.52) had no association with a reduced risk of GI cancers. Similarly, evidence suggested that PCA-derived healthy dietary patterns may reduce the risk of death from GI cancers, whereas PCA-derived unhealthy dietary patterns may increase the risk.

Findings from prospective studies on the association of PCA-derived dietary patterns and the risk of GI cancers support the evidence of healthy and unhealthy dietary patterns as either protective or risk-increasing factors for GI cancers and for survivorship, respectively. The findings also suggest that the RRR-derived healthy dietary pattern reduces the risk of GI cancers (albeit with low precision), but no association was found for the RRR-derived unhealthy dietary pattern. Prospective studies are required to further clarify disparities in the association between PCA- and RRR-derived dietary patterns and the risk of GI cancers. Systematic review registration: PROSPERO registration no. CRD42022321644.

Epigenetics is currently considered the investigation of inheritable changes in gene expression that do not rely on DNA sequence alteration. Significant epigenetic procedures are involved, such as DNA methylations, histone modifications, and non-coding RNA actions. It is confirmed through several investigations that epigenetic changes are associated with the formation, development, and metastasis of various cancers, such as colorectal cancer (CRC). The difference between epigenetic changes and genetic mutations is that the former could be reversed or prevented; therefore, cancer treatment and prevention could be achieved by restoring abnormal epigenetic events within the neoplastic cells. These treatments, consequently, cause the anti-tumour effects augmentation, drug resistance reduction, and host immune response stimulation. In this article, we begin our survey by exploring basic epigenetic mechanisms to understand epigenetic tools and strategies for treating colorectal cancer in monotherapy and combination with chemotherapy or immunotherapy.

Several primary prevention strategies, including chemoprevention, prophylactic surgery and lifestyle modifications, have been shown to reduce the risk of breast cancer (BC) and prostate cancer (Pca). However, the uptake of these preventive measures is considered suboptimal, limiting their impact on cancer prevention. A personalised primary prevention strategy has yet to be tested for cancer prevention. Therefore, we aim to determine the feasibility, acceptability and potential benefits and harms of this strategy in women and men at high risk of BC and Pca.

This is a two-arm, parallel-group mixed-methods pilot randomised controlled trial with a 1:1 allocation. The study aims to recruit 60 women and 60 men at high risk of BC and PCa in two specialised sites: the Breast Diseases Center and the Department of Urologic Oncology of the CHU de Québec-Université Laval, Canada. Assessments include intentions to uptake, actual uptake rates of primary preventive measures and decision regret. Feasibility and acceptability of the intervention and the study will be measured by quantifying the recruitment rate, appropriateness of randomisation process and satisfaction metrics. Data will be collected using mixed methods. Quantitative measures will be assessed at baseline and 6 months post randomisation. Quantitative analysis will include descriptive statistics for all variables of interest. Generalised linear mixed models with random intercepts will be used to assess the overall intervention effect. Semistructured interviews will be conducted at the end of follow-up, and a thematic analysis will be performed using NVivo to understand participants' perspectives.

The protocol was approved by the Institutional Review Board of CHU de Québec-Université Laval (4 October 2022; 2023-6315). The findings of the study will be published in a peer-reviewed journal and disseminated at national and international conferences and through social media.

The protocol for this study was registered with the International Clinical Trials Registry (ISRCTN15749766) https://doi.org/10.1186/ISRCTN15749766).

Bladder cancer is a public health concern, with smoking and occupational exposure being major risk factors. However, specific risks in women, particularly hormonal, lifestyle, and environmental factors, are underexplored. This study aimed to assess these risk factors in women, focusing on smoking, occupational exposure, recurrent urinary tract infections (UTIs), body mass index (BMI), menopausal status, and family history of cancer.

This retrospective cohort study included 850 women diagnosed with bladder cancer (2018-2023) and age-matched controls. Data on smoking, occupational exposure, UTIs, BMI, menopausal status, and family history were collected from medical records: multivariate logistic regression and propensity score matching identified independent risk factors. Subgroup analysis explored interactions between menopausal status and other factors.

Smoking (OR = 2.15, p = 0.002), occupational exposure (OR = 1.89, p = 0.007), and recurrent UTIs (OR = 1.72, p = 0.013) were significant risk factors, particularly in post-menopausal women. Menopausal status amplified the effects of smoking and UTIs but was not an independent predictor. BMI and family history showed no significant associations.

Smoking, occupational exposure, and recurrent UTIs are key risk factors for bladder cancer in women, especially post-menopausal women, highlighting the need for targeted prevention strategies.

Cancer is a complex global health challenge that requires novel and holistic approaches to treatment and prevention. Polyherbal medicines, composed of multiple plants with historical use in traditional medicine, have gained popularity due to their safety, cost-effectiveness, and accessibility. However, selecting the right plants and determining optimal combinations for enhanced biological effects remains challenging. To address this, a molecular docking study was conducted, targeting proteins implicated in cancer pathogenesis. The study identified bioactive compounds with strong binding energies, guiding the selection of polyherbal formulations for further experimentation. Using response surface methodology, various combinations of plant extracts were screened for their antioxidant properties and phytochemical content. Among the formulations tested, PHEE (Polyherbal Ethanolic Extract), comprising 70% soursop leaf, 5% jackfruit leaf, 5% orange peel, 15% citrus juice, and 5% apple fruit ethanolic extracts, exhibited the most potent biological activities, followed by SLEE (Soursop Leaf Ethanolic Extract), a 100% soursop leaf ethanolic extract. Design Expert Software predicted soursop leaf extract as a key contributor to desirable outcomes, attributed to its rich phytochemical composition. Cell-based assays revealed varying cytotoxic effects of the extracts on leukemia cells, with PHEE showing the highest potency (IC50 = 2.50 μg/mL), followed closely by SLEE (IC50 = 2.90 μg/mL). These effects are potentially due to the abundant acetogenins and flavonoids present in the extracts. However, caution is warranted regarding their cytotoxicity to normal cells. Apoptotic studies confirmed the ability of both PHEE and SLEE to induce programmed cell death, further supporting their potential as anticancer agents. This research underscores the importance of strategic plant combinations in polyherbal formulations and highlights PHEE as a promising candidate for further investigation in cancer treatment.

In recent decades, there has been significant worldwide interest in the emergence of a new invasive species known as Achatina fulica. This is due to its dangerous habits for the environment, its biological characteristics and the fact that it is the intermediate host of several nematode parasites, such as Angiostrongylus cantonensis. This land snail species is native to tropical African countries, but has been introduced, accidentally or deliberately, to other parts of the world to be used for different purposes and is now established in a large part of the tropics. Since the 1980s, hundreds of researchers have been interested in the beneficial properties of its mucus, ranging from the antimicrobial and anticancer properties to the use of its powdered shell as a biocatalyst. This literature review aims to objectively describe the positive and negative aspects associated with the spread of A. fulica, highlighting in particular the opportunities for the local populations deriving from a conscious exploitation of this mollusc.

It is widely accepted that cancer mostly arises from random spontaneous mutations triggered by environmental factors. Our theory challenges the idea of the random somatic mutation theory (SMT). The SMT does not fit well with Charles Darwin's theory of evolution in that the same relatively few mutations would occur so frequently and that these mutations would lead to death rather than survival of the fittest. However, it would fit well under the theory of evolution, if we were to look at it from the vantage point of pathogens and their supporting microbial communities colonizing humans and mutating host cells for their own benefit, as it does give them an evolutionary advantage and they are capable of selecting genes to mutate and of inserting their own DNA or RNA into hosts. In this article, we provide evidence that tumors are actually complex microbial communities composed of various microorganisms living within biofilms encapsulated by a hard matrix; that these microorganisms are what cause the genetic mutations seen in cancer and control angiogenesis; that these pathogens spread by hiding in tumor cells and M2 or M2-like macrophages and other phagocytic immune cells and traveling inside them to distant sites camouflaged by platelets, which they also reprogram, and prepare the distant site for metastasis; that risk factors for cancer are sources of energy that pathogens are able to utilize; and that, in accordance with our previous unifying theory of disease, pathogens utilize melanin for energy for building and sustaining tumors and metastasis. We propose a paradigm shift in our understanding of what cancer is, and, thereby, a different trajectory for avenues of treatment and prevention.

Cancers are a class of disorders that entail uncontrollably unwanted cell development with dissemination. One in six fatalities globally is attributed to cancer, a global health issue. The analysis of the entire DNA sequence and how it expresses itself in tumor cells is known as cancer genomics. The development of novel cancer treatments has been facilitated because of the genomics method. COL10A1 gene, a short chain collagen, and an interstitial matrix component, acts as a predictive biomarker for cancer prognosis. Recognizing the fundamental consequences of mutations in the COL10A1 gene and its expression in cancer is crucial. Analyzing the COL10A1 gene expression with a data set and gene expression patterns shows the level of display of the tumor. Examining the therapeutic techniques of COL10A1 gene expression leads to early detection, screening, radiation therapy, and advanced developments. This review highlights the value of the COL10A1 gene in breast, gastric, pancreatic, lung, and colorectal cancers, emphasizing its role in gene expression patterns and therapeutic techniques.

Prostate cancer (PCa) is the most commonly detected malignancy in men worldwide. PCa is a slow-growing cancer with the absence of symptoms at early stages. The pathogenesis has not been entirely understood including the key risk factors related to PCa development like diet and microbiota derived metabolites. Microbiota may influence the host's immunological responses, inflammatory responses, and metabolic pathways, which may be crucial for the development and metastasis. Similarly, short-chain fatty acids, methylamines, hippurate, bile acids, and other metabolites generated by microbiota may have potential roles in cancer inflammation and progression of cancer. Most studies have focused on the role of metabolites and their pathways involved in chronic inflammation, tumor initiation, proliferation, and progression. In summary, the review discusses the role of microbiota and microbial-derived metabolite-built strategies in inflammation and progression of the PCa.

Extracellular Vesicles (EVs) based cancer research reveals several complicated sides of cancer. EVs are classified as several subpopulations such as microvesicles, apoptotic bodies, and exosomes. In cancer, exosomes play a significant role as a cellular messenger in tumor development and progression. Tumor-derived exosomes (TEXs) are also a theranostic tool for cancer. Tumor virus-infected cell-derived EVs promote cancer development. Exosomes (a subpopulation of EVs) play a significant role in converting noninfecting cells to infected cells. It transports several biological active cargo (DNA, RNA, protein, and virions) towards the noninfected cells. This cellular transport enhances infection rates via reprogramming of noninfected cells. In this review, we explore tumor viruses, exosomes and tumor viruses interlink, the theranostic landscape of exosomes in tumor virus-associated cancer and the future orientation of exosomes-based virus oncology.

Lung cancer is the leading cause of fatalities related to cancer globally. There are numerous ways to treat lung cancer, including surgery, chemotherapy, and radiation. Since these treatments have not yet shown satisfactory results, more research into the underlying mechanisms and different approaches to therapy and prevention are needed. Animal models are essential to the study of lung cancer because they offer priceless information about the etiology, course, and possible treatments for the illness. The therapeutic application of phytochemicals and medicinal plants to treat cancer-related compounds has gained attention subsequently. In addition to discussing the molecular carcinogenic and antitumor effects of the herbal treatment Ocimum sanctum (OS) in connection to lung cancer, this review will address the current awareness regarding lung cancer in animal models. The multitude of animal models used in lung cancer research-such as genetically modified mice, carcinogen-induced models, and xenograft induction-provides a solid foundation for understanding the illness. By easing the examination of the environmental and genetic factors involved and enhancing the analysis of possibilities for treatment, these models eventually assist in the further development of lung cancer therapy. Additionally, using the herb plant OS is essential for both treating and preventing lung cancer. Standardizing dosages and enforcing laws on the use of herbal medications require more in-depth investigation.

Breast cancer causes the deaths of approximately 685,000 women annually, posing a severe threat to women's health. Consequently, there is an urgent need for low-cost, low-toxicity and effective therapeutic methods to prevent or mitigate breast cancer progression. PDBP are natural, non-toxic, and affordable substances and have demonstrated excellent anti-breast cancer activities in inhibiting proliferation, migration, and invasion, and promoting apoptosis both in vitro and in vivo, thus effectively preventing or inhibiting breast cancer. However, there are no comprehensive reviews summarizing the effects and mechanisms of PDBP on the treatment of breast cancer. Therefore, this review described the inhibitory effects and mechanisms of active peptides from different plant protein sources on breast cancer. Additionally, we summarized the advantages and preparation methods of plant protein-derived anticancer peptide-encapsulated nanoparticles and their effects in inhibiting breast cancer. This review provides a scientific basis for understanding the anti-breast cancer mechanisms of PDBP and offers guidance for the development of therapeutic adjuvants enriched with these peptides.

Cancer remains a major global health challenge with a high mortality rate, as evidenced by the rise in new cases every year. Conventional diagnostic methods like PET scans, MRIs, and biopsies, despite being widely used, suffer from significant drawbacks such as high radiation exposure, difficulty in distinguishing malignant from benign tumors, and invasiveness. Early detection, which is crucial for improving treatment outcomes and survival rates, is hindered by the asymptomatic nature of early-stage cancer and the limitations of current diagnostic tools. Cancer biomarkers, detectable in body fluids, offer valuable diagnostic information, and recent advances in nanotechnology have led to the development of highly sensitive nano-biosensors. This review explores recent advancements (2022-2024) in the field of ultrasensitive nano-biosensors, emphasizing the strategic integration of nanomaterials to enhance sensitivity and accuracy in cancer biomarker detection. It highlights how precise nanomaterial positioning in sensor components like electrodes and bioreceptors enables early cancer diagnosis at low biomarker concentrations. These innovations underscore the transformative potential of nanomaterials in revolutionizing early cancer diagnostics, improving patient care, and enhancing survival outcomes.

The prevalence and death due to cancer have been rising over the past few decades, and eliminating tumour cells without sacrificing healthy cells remains a difficult task. Due to the low specificity and solubility of drug molecules, patients often require high dosages to achieve the desired therapeutic effects. Silica nanoparticles (SiNPs) can effectively deliver therapeutic agents to targeted sites in the body, addressing these challenges. Using SiNPs as vehicles for anti-cancer drug delivery has emerged as a promising strategy due to their unique structural properties, biocompatibility, and versatility. This review explores the various aspects of SiNPs in cancer therapy, highlighting their synthesis, functionalization, and application in delivering chemotherapeutic agents, photosensitizers, and nucleic acids. SiNPs offer advantages such as high drug loading capacity, controlled release, and targeted delivery, enhancing therapeutic efficacy and reducing systemic toxicity. Moreover, this review aims to provide an in-depth understanding of the current state and prospects of SiNPs in revolutionizing cancer treatment and improving patient outcomes.

The NIH policy on sex as biological variable (SABV) emphasized the importance of sex-based differences in precision oncology. Over 50% of clinically actionable oncology genes are sex-biased, indicating differences in drug efficacy. Research has identified sex differences in non-reproductive cancers, highlighting the need for comprehensive sex-based cancer data. We therefore developed OncoSexome, a multidimensional knowledge base describing sex-based differences in cancer (https://idrblab.org/OncoSexome/) across four key topics: antineoplastic drugs and responses (SDR), oncology-related biomarkers (SBM), risk factors (SRF) and microbial landscape (SML). SDR covers sex-based differences in 2051 anticancer drugs; SBM describes 12 551 sex-differential biomarkers; SRF illustrates 350 sex-dependent risk factors; SML demonstrates 1386 microbes with sex-differential abundances associated with cancer development. OncoSexome is unique in illuminating multifaceted influences of biological sex on cancer, providing both external and endogenous contributors to cancer development and describing sex-based differences for the broadest oncological classes. Given the increasing global research interest in sex-based differences, OncoSexome is expected to impact future precision oncology practices significantly.