Displaying publications 21 - 40 of 153 in total

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  1. Fulltext Role of Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) in Cancer Prevention and Cancer Promotion
    Wong RSY
    Adv Pharmacol Sci, 2019;2019:3418975.
    PMID: 30838040 DOI: 10.1155/2019/3418975
    The nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly prescribed by medical practitioners in many clinical conditions for the symptomatic treatment of pain and fever. Due to their anti-inflammatory properties, these drugs have been investigated for their anticancer effects in numerous studies. This is because chronic inflammation has long been linked to carcinogenesis. As such, anti-inflammatory drugs are believed to play a role in cancer treatment and prevention. In the past few decades, research has shown that NSAIDs may decrease the risk of certain types of cancer. However, there is also a growing body of research that proves the contrary. Furthermore, NSAIDs are well known for many side effects, including some life-threatening ones. This review will discuss the relationship between chronic inflammation and cancer, the role of NSAIDs in cancer prevention and cancer promotion, and some of the potentially lethal side effects of these drugs.
    Matched MeSH terms: Carcinogenesis
  2. Fulltext Clinicopathologic and Molecular Characteristics of Epstein-Barr Virus-Associated Smooth Muscle Tumor Compared With Those of Leiomyoma and Leiomyosarcoma
    Wah NW, Mok Y, Omar N, Chang KTE, Tay TKY, Hue SS, et al.
    Mod Pathol, 2023 Jun;36(6):100127.
    PMID: 36965331 DOI: 10.1016/j.modpat.2023.100127
    Epstein-Barr virus (EBV)-associated smooth muscle tumors (EBV-SMTs) are rare smooth muscle neoplasms exclusively associated with immunosuppression, such as in patients with HIV/AIDS, posttransplant, and congenital immunodeficiency. However, the genomic landscape of EBV-SMTs is poorly understood. Leiomyosarcomas harbor genomic instability and multiple recurrent DNA copy number alterations, whereas leiomyomas lack such changes. Thus, this study aimed to fill this knowledge gap by characterizing copy number alterations in EBV-SMTs and correlating this information with clinicopathologic characteristics. Our study investigated and compared the pathologic characteristics and copy number profiles of 9 EBV-SMTs (from 7 post-transplant and AIDS patients), 6 leiomyomas, and 7 leiomyosarcomas, using chromosomal microarray platforms. Our results showed a lower copy number alteration burden in EBV-SMTs and leiomyoma than in leiomyosarcoma. This contrast in the molecular profile between EBV-SMTs and leiomyosarcoma is concordant with the different clinical behaviors and pathologic characteristics exhibited by these tumors. Despite having an overall copy number alteration profile closer to leiomyoma, recurrent copy number gain of oncogenes, such as RUNX1, CCND2, and ETS2, was found in EBV-SMTs. Epigenetic alterations may play an important role in tumorigenesis as recurrent copy number gains were found in histone deacetylases. A gene enrichment analysis also demonstrated enrichment of genes involved in the host response to viral infection, suggesting that the tumor immune microenvironment may play an important role in EBV-SMT tumorigenesis.
    Matched MeSH terms: Carcinogenesis
  3. Adipose-Derived Mesenchymal Stem Cells Promote Growth and Migration of Lung Adenocarcinoma Cancer Cells
    Zakaria N, Yahaya BH
    Adv Exp Med Biol, 2020;1292:83-95.
    PMID: 31916234 DOI: 10.1007/5584_2019_464
    INTRODUCTION: Mesenchymal stem cells (MSCs) have been used in cancer therapy as vehicles to deliver therapeutic materials such as drugs, apoptosis inducers and cytokines due to their ability to migrate and home at the tumour site. Furthermore, MSCs have been genetically engineered to produce anticancer molecules such as TRAIL that can induce apoptosis of cancer cells. However, MSCs' presence in the tumour microenvironment has shown to be involved in promoting tumour growth and progression. Therefore, the roles of MSCs either promoting or suppressing tumorigenesis need to be investigated.

    METHODS: Human adipose-derived MSCs (Ad-MSCs) and A549 cells are co-cultured together in indirect co-culture system using Transwell insert. Following co-culture, both cells were analysed in terms of growth rate, migration ability, apoptosis and gene expression for genes involved in migration and stemness characteristics.

    RESULTS: The result shows that Ad-MSCs promoted the growth of A549 cells when indirectly co-cultured for 48 and 72 h. Furthermore, Ad-MSCs significantly enhanced the migration rate of A549 cells. The increased in migration rate was in parallel with the significant increase of MMP9. There are no significant changes observed in the expression of TWIST2, CDH2 and CDH1, genes involved in the epithelial-to-mesenchymal transition (EMT). Ad-MSCs also protect A549 cancer cells from undergoing apoptosis and increase the survival of cancer cells.

    CONCLUSION: Secretion of soluble factors from Ad-MSCs has been shown to promote the growth and metastatic characteristics of A549 cancer cells. Therefore, the use of Ad-MSCs in cancer therapy needs to be carefully evaluated in the long-term aspect.

    Matched MeSH terms: Carcinogenesis/genetics; Carcinogenesis/pathology
  4. DNMT1 as a therapeutic target in pancreatic cancer: mechanisms and clinical implications
    Wong KK
    Cell Oncol (Dordr), 2020 Oct;43(5):779-792.
    PMID: 32504382 DOI: 10.1007/s13402-020-00526-4
    BACKGROUND: Pancreatic cancer or pancreatic ductal adenocarcinoma (PDAC) is one of the most devastating cancer types with a 5-year survival rate of only 9%. PDAC is one of the leading causes of cancer-related deaths in both genders. Epigenetic alterations may lead to the suppression of tumor suppressor genes, and DNA methylation is a predominant epigenetic modification. DNA methyltransferase 1 (DNMT1) is required for maintaining patterns of DNA methylation during cellular replication. Accumulating evidence has implicated the oncogenic roles of DNMT1 in various malignancies including PDACs.

    CONCLUSIONS: Herein, the expression profiles, oncogenic roles, regulators and inhibitors of DNMT1 in PDACs are presented and discussed. DNMT1 is overexpressed in PDAC cases compared with non-cancerous pancreatic ducts, and its expression gradually increases from pre-neoplastic lesions to PDACs. DNMT1 plays oncogenic roles in suppressing PDAC cell differentiation and in promoting their proliferation, migration and invasion, as well as in induction of the self-renewal capacity of PDAC cancer stem cells. These effects are achieved via promoter hypermethylation of tumor suppressor genes, including cyclin-dependent kinase inhibitors (e.g., p14, p15, p16, p21 and p27), suppressors of epithelial-mesenchymal transition (e.g., E-cadherin) and tumor suppressor miRNAs (e.g., miR-148a, miR-152 and miR-17-92 cluster). Pre-clinical investigations have shown the potency of novel non-nucleoside DNMT1 inhibitors against PDAC cells. Finally, phase I/II clinical trials of DNMT1 inhibitors (azacitidine, decitabine and guadecitabine) in PDAC patients are currently underway, where these inhibitors have the potential to sensitize PDACs to chemotherapy and immune checkpoint blockade therapy.

    Matched MeSH terms: Carcinogenesis/genetics; Carcinogenesis/pathology
  5. Fulltext NUB1 and FAT10 Proteins as Potential Novel Biomarkers in Cancer: A Translational Perspective
    Arshad M, Abdul Hamid N, Chan MC, Ismail F, Tan GC, Pezzella F, et al.
    Cells, 2021 08 24;10(9).
    PMID: 34571823 DOI: 10.3390/cells10092176
    Cancer increases the global disease burden substantially, but it remains a challenge to manage it. The search for novel biomarkers is essential for risk assessment, diagnosis, prognosis, prediction of treatment response, and cancer monitoring. This paper examined NEDD8 ultimate buster-1 (NUB1) and F-adjacent transcript 10 (FAT10) proteins as novel biomarkers in cancer. This literature review is based on the search of the electronic database, PubMed. NUB1 is an interferon-inducible protein that mediates apoptotic and anti-proliferative actions in cancer, while FAT10 is a ubiquitin-like modifier that promotes cancer. The upregulated expression of both NUB1 and FAT10 has been observed in various cancers. NUB1 protein binds to FAT10 non-covalently to promote FAT10 degradation. An overexpressed FAT10 stimulates nuclear factor-kappa β, activates the inflammatory pathways, and induces the proliferation of cancer. The FAT10 protein interacts with the mitotic arrest deficient 2 protein, causing chromosomal instability and breast tumourigenesis. FAT10 binds to the proliferating cell nuclear antigen protein and inhibits the DNA damage repair response. In addition, FAT10 involves epithelial-mesenchymal transition, invasion, apoptosis, and multiplication in hepatocellular carcinoma. Our knowledge about them is still limited. There is a need to further develop NUB1 and FAT10 as novel biomarkers.
    Matched MeSH terms: Carcinogenesis/metabolism; Carcinogenesis/pathology
  6. Fulltext A Systematic Review of the Effects of Equol (Soy Metabolite) on Breast Cancer
    Hod R, Maniam S, Mohd Nor NH
    Molecules, 2021 Feb 19;26(4).
    PMID: 33669783 DOI: 10.3390/molecules26041105
    Equol is a soy isoflavone metabolite that can be produced by intestinal bacteria. It is lipophilic and resembles natural oestrogens with an affinity to oestrogen receptors. This review is focused on how equol affects breast cancer, as evidenced by in vivo and in vitro studies. Equol is considered chemoprotective in specific endocrine-related pathologies, such as breast cancer, prostate cancer, cardiovascular diseases, and menopausal symptoms. In humans, not everyone can produce equol from gut metabolism. It is postulated that equol producers benefit more than non-equol producers for all the endocrine-related effects. Equol exists in two enantiomers of R-equol and S-equol. Earlier studies, however, did not specify which enantiomer was being used. This review considers equol's type and concentration variations, pathways affected, and its outcome in in vivo and in vitro studies.
    Matched MeSH terms: Carcinogenesis/drug effects; Carcinogenesis/pathology
  7. Fulltext Metabolic reprogramming and dysregulated metabolism: cause, consequence and/or enabler of environmental carcinogenesis?
    Robey RB, Weisz J, Kuemmerle NB, Salzberg AC, Berg A, Brown DG, et al.
    Carcinogenesis, 2015 Jun;36 Suppl 1(Suppl 1):S203-31.
    PMID: 26106140 DOI: 10.1093/carcin/bgv037
    Environmental contributions to cancer development are widely accepted, but only a fraction of all pertinent exposures have probably been identified. Traditional toxicological approaches to the problem have largely focused on the effects of individual agents at singular endpoints. As such, they have incompletely addressed both the pro-carcinogenic contributions of environmentally relevant low-dose chemical mixtures and the fact that exposures can influence multiple cancer-associated endpoints over varying timescales. Of these endpoints, dysregulated metabolism is one of the most common and recognizable features of cancer, but its specific roles in exposure-associated cancer development remain poorly understood. Most studies have focused on discrete aspects of cancer metabolism and have incompletely considered both its dynamic integrated nature and the complex controlling influences of substrate availability, external trophic signals and environmental conditions. Emerging high throughput approaches to environmental risk assessment also do not directly address the metabolic causes or consequences of changes in gene expression. As such, there is a compelling need to establish common or complementary frameworks for further exploration that experimentally and conceptually consider the gestalt of cancer metabolism and its causal relationships to both carcinogenesis and the development of other cancer hallmarks. A literature review to identify environmentally relevant exposures unambiguously linked to both cancer development and dysregulated metabolism suggests major gaps in our understanding of exposure-associated carcinogenesis and metabolic reprogramming. Although limited evidence exists to support primary causal roles for metabolism in carcinogenesis, the universality of altered cancer metabolism underscores its fundamental biological importance, and multiple pleiomorphic, even dichotomous, roles for metabolism in promoting, antagonizing or otherwise enabling the development and selection of cancer are suggested.
    Matched MeSH terms: Carcinogenesis/chemically induced*; Carcinogenesis/metabolism*
  8. Fulltext Environmental immune disruptors, inflammation and cancer risk
    Thompson PA, Khatami M, Baglole CJ, Sun J, Harris SA, Moon EY, et al.
    Carcinogenesis, 2015 Jun;36 Suppl 1:S232-53.
    PMID: 26106141 DOI: 10.1093/carcin/bgv038
    An emerging area in environmental toxicology is the role that chemicals and chemical mixtures have on the cells of the human immune system. This is an important area of research that has been most widely pursued in relation to autoimmune diseases and allergy/asthma as opposed to cancer causation. This is despite the well-recognized role that innate and adaptive immunity play as essential factors in tumorigenesis. Here, we review the role that the innate immune cells of inflammatory responses play in tumorigenesis. Focus is placed on the molecules and pathways that have been mechanistically linked with tumor-associated inflammation. Within the context of chemically induced disturbances in immune function as co-factors in carcinogenesis, the evidence linking environmental toxicant exposures with perturbation in the balance between pro- and anti-inflammatory responses is reviewed. Reported effects of bisphenol A, atrazine, phthalates and other common toxicants on molecular and cellular targets involved in tumor-associated inflammation (e.g. cyclooxygenase/prostaglandin E2, nuclear factor kappa B, nitric oxide synthesis, cytokines and chemokines) are presented as example chemically mediated target molecule perturbations relevant to cancer. Commentary on areas of additional research including the need for innovation and integration of systems biology approaches to the study of environmental exposures and cancer causation are presented.
    Matched MeSH terms: Carcinogenesis/chemically induced; Carcinogenesis/immunology
  9. IGFBP-2 in cervical cancer development
    Kaur G, Balasubramaniam SD, Lee YJ
    Exp Mol Pathol, 2020 04;113:104362.
    PMID: 31870856 DOI: 10.1016/j.yexmp.2019.104362
    OBJECTIVE: Increased expression of insulin-like growth factor binding protein 2, IGFBP-2, is associated with many cancers, though its role in cervical cancer is unclear. The aim of this study was to investigate the expression of IGFBP-2 protein and the transcriptomics profile of genes involved in the IGF signaling pathway during cervical cancer development.

    DESIGN: Immunohistochemical expression of IGFBP-2 protein was semi-quantitatively assessed in tissue microarrays containing 9 normal cervix, 10 low grade cervical intraepithelial neoplasia (LGCIN), 10 high grade cervical intraepithelial neoplasia (HGCIN) and 42 squamous cell carcinoma (SCC) cases. The gene expression profiles of IGFBP-2, IGF-1, IGF-1R, PTEN, MDM2, AKT1 and TP53 were determined in three cervical tissue samples each from normal cervix, human papillomavirus (HPV)-infected LGCIN, HGCIN and SCC, using Human Transcriptome Array 2.0.

    RESULTS: IGFBP-2 protein was highly expressed in the cytoplasm of SCC cells compared to normal cervix (p = .013). The expression was not significantly associated with CIN grade or SCC stage. Transcriptomics profiling demonstrated upregulation of IGFBP-2 and TP53 in HGCIN and SCC compared to normal cervix. IGF-1, IGF-1R and PTEN genes were downregulated in all histological groups. IGF-1 gene was significantly downregulated in SCC (p = .031), while PTEN gene was significantly downregulated in HGCIN (p = .012), compared to normal cervix. MDM2 and AKT1 genes were downregulated in LGCIN and HGCIN, while upregulated in SCC.

    CONCLUSION: In cervical carcinogenesis, IGFBP-2 appears to play an oncogenic role, probably through an IGF-independent mechanism.

    Matched MeSH terms: Carcinogenesis/metabolism*; Carcinogenesis/pathology*
  10. Fulltext Potential role of oxidative stress-induced apoptosis in mediating chromosomal rearrangements in nasopharyngeal carcinoma
    Tan SN, Sim SP, Khoo AS
    Cell Biosci, 2016;6:35.
    PMID: 27231526 DOI: 10.1186/s13578-016-0103-9
    Genetic aberrations have been identified in nasopharyngeal carcinoma (NPC), however, the underlying mechanism remains elusive. There are increasing evidences that the apoptotic nuclease caspase-activated deoxyribonuclease (CAD) is one of the players leading to translocation in leukemia. Oxidative stress, which has been strongly implicated in carcinogenesis, is a potent apoptotic inducer. Most of the NPC etiological factors are known to induce oxidative stress. Although apoptosis is a cell death process, cells possess the potential to survive apoptosis upon DNA repair. Eventually, the surviving cells may carry rearranged chromosomes. We hypothesized that oxidative stress-induced apoptosis may cause chromosomal breaks mediated by CAD. Upon erroneous DNA repair, cells that survive apoptosis may harbor chromosomal rearrangements contributing to NPC pathogenesis. This study focused on the AF9 gene at 9p22, a common deletion region in NPC. We aimed to propose a possible model for molecular mechanism underlying the chromosomal rearrangements in NPC.
    Matched MeSH terms: Carcinogenesis
  11. Fulltext Sp1 and Sp3 Are the Transcription Activators of Human ek1 Promoter in TSA-Treated Human Colon Carcinoma Cells
    Kuan CS, See Too WC, Few LL
    PLoS One, 2016;11(1):e0147886.
    PMID: 26807725 DOI: 10.1371/journal.pone.0147886
    Ethanolamine kinase (EK) catalyzes the phosphorylation of ethanolamine, the first step in the CDP-ethanolamine pathway for the biosynthesis of phosphatidylethanolamine (PE). Human EK exists as EK1, EK2α and EK2β isoforms, encoded by two separate genes, named ek1 and ek2. EK activity is stimulated by carcinogens and oncogenes, suggesting the involvement of EK in carcinogenesis. Currently, little is known about EK transcriptional regulation by endogenous or exogenous signals, and the ek gene promoter has never been studied.
    Matched MeSH terms: Carcinogenesis
  12. Fulltext Identification of Schizosaccharomyces pombe in the guts of healthy individuals and patients with colorectal cancer: preliminary evidence from a gut microbiome secretome study
    Chin SF, Megat Mohd Azlan PIH, Mazlan L, Neoh HM
    Gut Pathog, 2018;10:29.
    PMID: 30008808 DOI: 10.1186/s13099-018-0258-5
    Over the years, genetic profiling of the gut microbiome of patients with colorectal cancer (CRC) using genome sequencing has suggested over-representation of several bacterial taxa. However, little is known about the protein or metabolite secretions from the microbiota that could lead to CRC pathology. Proteomic studies on the role of microbial secretome in CRC are relatively rare. Here, we report the identification of proteins from Schizosaccharomyces pombe found in the stool samples of both healthy individuals and patients with CRC. We found that distinctive sets of S. pombe proteins were present exclusively and in high intensities in each group. Our finding may trigger a new interest in the role of gut mycobiota in carcinogenesis.
    Matched MeSH terms: Carcinogenesis
  13. Fulltext A comprehensive overview of mitochondrial DNA 4977-bp deletion in cancer studies
    Yusoff AAM, Abdullah WSW, Khair SZNM, Radzak SMA
    Oncol Rev, 2019 Jan 14;13(1):409.
    PMID: 31044027 DOI: 10.4081/oncol.2019.409
    Mitochondria are cellular machines essential for energy production. The biogenesis of mitochondria is a highly complex and it depends on the coordination of the nuclear and mitochondrial genome. Mitochondrial DNA (mtDNA) mutations and deletions are suspected to be associated with carcinogenesis. The most described mtDNA deletion in various human cancers is called the 4977-bp common deletion (mDNA4977) and it has been explored since two decades. In spite of that, its implication in carcinogenesis still unknown and its predictive and prognostic impact remains controversial. This review article provides an overview of some of the cellular and molecular mechanisms underlying mDNA4977 formation and a detailed summary about mDNA4977 reported in various types of cancers. The current knowledges of mDNA4977 as a prognostic and predictive marker are also discussed.
    Matched MeSH terms: Carcinogenesis
  14. Fulltext The Role of MicroRNAs in Lung Cancer Metabolism
    Azizi MIHN, Othman I, Naidu R
    Cancers (Basel), 2021 Apr 05;13(7).
    PMID: 33916349 DOI: 10.3390/cancers13071716
    MicroRNAs (miRNAs) are short-strand non-coding RNAs that are responsible for post-transcriptional regulation of many biological processes. Their differential expression is important in supporting tumorigenesis by causing dysregulation in normal biological functions including cell proliferation, apoptosis, metastasis and invasion and cellular metabolism. Cellular metabolic processes are a tightly regulated mechanism. However, cancer cells have adapted features to circumvent these regulations, recognizing metabolic reprogramming as an important hallmark of cancer. The miRNA expression profile may differ between localized lung cancers, advanced lung cancers and solid tumors, which lead to a varying extent of metabolic deregulation. Emerging evidence has shown the relationship between the differential expression of miRNAs with lung cancer metabolic reprogramming in perpetuating tumorigenesis. This review provides an insight into the role of different miRNAs in lung cancer metabolic reprogramming by targeting key enzymes, transporter proteins or regulatory components alongside metabolic signaling pathways. These discussions would allow a deeper understanding of the importance of miRNAs in tumor progression therefore providing new avenues for diagnostic, therapeutic and disease management applications.
    Matched MeSH terms: Carcinogenesis
  15. Fulltext Apoptosis: Dual Role in Aetiology and Cure
    Wynn, Aye Aye, Myint, Ohnmar, Mya, Nang Khin
    Borneo Journal of Medical Sciences, 2019;13(3):5-10.
    MyJurnal
    Apoptosis is a programmed cell death which occurs following a variety of stimuli. Physiologically the process is important for morphogenesis of organs and homeostasis of different types of cells. Apoptotic cell death is responsible for a variety of pathologic states such as elimination of cell death in mutated cells, infected cells, tumour cells and transplant rejection well as the pathological atrophy. In this review, there is discussion about the control of apoptosis, detection methods of apoptosis, its association with infectious and non-communicable diseases. Intracellular microorganisms survive through inhibition of host cell apoptosis as well as they destroy the parenchymal cells causing impaired functions. It plays important role in tumourigenesis. There are possible therapeutic roles of drugs that modify apoptosis in human diseases.
    Matched MeSH terms: Carcinogenesis
  16. Fulltext Chemotaxis movement and attachment of Agrobacterium tumefaciens to Phalaenopsis violacea orchid tissues: an assessment of early factors influencing the efficiency of gene transfer
    Subramaniam, Sreeramanan, Balasubramaniam, Vinod, Poobathy, Ranjetta, Sreenivasan, Sasidharan, Rathinam, Xavier
    Trop Life Sci Res, 2009;20(1):-.
    MyJurnal
    An early step in the Agrobacterium-mediated transformation of Phalaenopsis violacea orchid was investigated to elucidate the plant-bacterium interaction. Directed movement in response to chemical attractants is of crucial importance to Agrobacterium tumefaciens strains. Chemotaxis of A. tumefaciens strains (EHA 101 and 105) towards wounded orchid tissues has been studied by using swarm agar plates. The results obtained indicate a minor role for chemotaxis in determining host specificity and suggest that it could not be responsible for the absence of tumourigenesis in P. violacea orchid under natural conditions. The spectrometric GUS and green fluorescent protein (GFP) assays provided information on the amount of inoculated A. tumefaciens that effectively bound to various orchid tissues. It can be concluded that, at least during the two early steps of interaction, A. tumefaciens appears to be compatible with P. violacea, indicating a potential basis for genetic transformation.
    Matched MeSH terms: Carcinogenesis
  17. Effects of reaction conditions on the emission behaviors of arsenic, cadmium and lead during sewage sludge pyrolysis
    Han H, Hu S, Syed-Hassan SSA, Xiao Y, Wang Y, Xu J, et al.
    Bioresour Technol, 2017 Jul;236:138-145.
    PMID: 28399417 DOI: 10.1016/j.biortech.2017.03.112
    Sewage sludge is an important class of bioresources whose energy content could be exploited using pyrolysis technology. However, some harmful trace elements in sewage sludge can escape easily to the gas phase during pyrolysis, increasing the potential of carcinogenic material emissions to the atmosphere. This study investigates emission characteristics of arsenic, cadmium and lead under different pyrolysis conditions for three different sewage sludge samples. The increased temperature (within 723-1123K) significantly promoted the cadmium and lead emissions, but its influence on arsenic emission was not pronounced. The releasing rate order of the three trace elements is volatile arsenic compounds>cadmium>lead in the beginning of pyrolysis. Fast heating rates promoted the emission of trace elements for the sludge containing the highest amount of ash, but exhibited an opposite effect for other studied samples. Overall, the high ash sludge released the least trace elements almost under all reaction conditions.
    Matched MeSH terms: Carcinogenesis
  18. Fulltext The health benefits of probiotics
    Yap, Wei Boon, Rina Anak Sujang
    Jurnal Sains Kesihatan Malaysia, 2014;12(2):41-44.
    MyJurnal
    There has been a significant increase in research on probiotics-associated health benefits in the last 20 years. Many studies carried out in vitro and clinically show that consumption of probiotics inhibits the growth of pathogenic microorganisms. Furthermore, the consumption of probiotics also enhances the host immune response and decreases the levels of carcinogenesis-inducing enzymes. These positive outcomes have led to the use of probiotics in prevention and treatment of infectious diseases like bacterial or antibiotic associated diarrhea, chronic inflammatory bowel diseases and colon cancer. This review summarises literature pertaining to mechanistic actions of probiotics in improving the well-being of hosts.
    Matched MeSH terms: Carcinogenesis
  19. Fulltext The Dynamic Roles of TGF-β Signalling in EBV-Associated Cancers
    Velapasamy S, Dawson CW, Young LS, Paterson IC, Yap LF
    Cancers (Basel), 2018 Jul 27;10(8).
    PMID: 30060514 DOI: 10.3390/cancers10080247
    The transforming growth factor-β (TGF-β) signalling pathway plays a critical role in carcinogenesis. It has a biphasic action by initially suppressing tumorigenesis but promoting tumour progression in the later stages of disease. Consequently, the functional outcome of TGF-β signalling is strongly context-dependent and is influenced by various factors including cell, tissue and cancer type. Disruption of this pathway can be caused by various means, including genetic and environmental factors. A number of human viruses have been shown to modulate TGF-β signalling during tumorigenesis. In this review, we describe how this pathway is perturbed in Epstein-Barr virus (EBV)-associated cancers and how EBV interferes with TGF-β signal transduction. The role of TGF-β in regulating the EBV life cycle in tumour cells is also discussed.
    Matched MeSH terms: Carcinogenesis
  20. Fulltext Mammary Paget's Disease of the Nipple: Relatively Common but Still Unknown to Many
    Ooi PS, Draman N, Yusoff SSM, Zain WZW, Ganasagaran D, Chua HH
    Korean J Fam Med, 2019 Jul;40(4):269-272.
    PMID: 30486607 DOI: 10.4082/kjfm.17.0143
    Mammary Paget's disease is clinically defined as skin inflammation of the nipple area and is an adenocarcinoma of the epidermis of the nipple. The pathogenesis of mammary Paget's disease is relatively unknown; nonetheless, there are two popular theories that support the underlying carcinoma and de novo carcinogenesis. For the attending medical practitioner, mammary Paget's disease poses a diagnostic and therapeutic dilemma, especially in the absence of a clinically palpable breast mass. We report a rare case of a 48-year-old Malay woman who presented at Hospital Universiti Sains Malaysia, Kelantan, Malaysia with the symptom of skin erosion on the left nipple and unresponsiveness to multiple topical treatments. A full evaluation and assessment of the patient were conducted, and mammary Paget's disease was diagnosed.
    Matched MeSH terms: Carcinogenesis
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