Displaying publications 1 - 20 of 153 in total

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  1. Fulltext Reply to Jiménez-Alonso et al., Schooling and Zhao, and Mortazavi: Further discussion on the immunological model of carcinogenesis
    Palmer S, Albergante L, Blackburn CC, Newman TJ
    Proc Natl Acad Sci U S A, 2018 05 08;115(19):E4319-E4321.
    PMID: 29669926 DOI: 10.1073/pnas.1802809115
    Matched MeSH terms: Carcinogenesis*
  2. The role of podoplanin inhibitors in controlling oral cancer progression
    Sayuddin ENEN, Taher M, Arzmi MH, Burhanudin NA, Rostam MA
    Arch Oral Biol, 2024 Jan;157:105841.
    PMID: 37952507 DOI: 10.1016/j.archoralbio.2023.105841
    OBJECTIVE: In this article, we review the current studies on the role of podoplanin in oral cancer and the potential application of podoplanin inhibitors as a therapeutic agent for oral cancer.

    DESIGN: The narrative review approach was conducted, providing a comprehensive perspective of related literature. Publications addressing podoplanin and its inhibitors in the context of oral cancer were retrieved from PubMed and Scopus databases.

    RESULTS: Podoplanin has emerged as a biomarker and therapeutic agent for oral cancer. Numerous studies have reported high podoplanin expression in oral cancer and pre-cancerous lesions compared to normal cells. A specific inhibitor targeting podoplanin may have the potential to prevent oral carcinogenesis via interfering with the pathway of cancerous cells involved in cell proliferation and metastasis. Antibodies, chimeric antigen receptor (CAR)-T cells, cancer-specific mAb (CasMab), synthetic molecules, and lectins are among the materials used as anticancer agents targeting podoplanin. Plant-derived lectins appear to demonstrate a unique advantage against alternative candidates.

    CONCLUSIONS: The use of podoplanin inhibitors in place of existing therapeutic approaches could be a promising and novel approach to the prevention and treatment of oral cancer. Nevertheless, further research is required to investigate the practical application of such inhibitors.

    Matched MeSH terms: Carcinogenesis
  3. Probiotic inhibits oral carcinogenesis: A systematic review and meta-analysis
    Wan Mohd Kamaluddin WNF, Rismayuddin NAR, Ismail AF, Mohamad Aidid E, Othman N, Mohamad NAH, et al.
    Arch Oral Biol, 2020 Oct;118:104855.
    PMID: 32801092 DOI: 10.1016/j.archoralbio.2020.104855
    OBJECTIVES: This systematic review aimed to investigate the effects if probiotics can inhibit oral carcinogenesis.

    DESIGN: PubMed, Web of Science, Scopus, and PLOS databases were searched up to February 2020 to identify randomised controlled trials that fulfilled the eligibility criteria. Joanna Briggs Institute (JBI) Critical Appraisal Tool was used for quality assessment of articles. This review was performed according to the Preferred Reporting Items for Systematic Review and Meta-analysis (PRISMA-P) 2015 protocol guidelines.

    RESULT: The initial search retrieved 774 articles. Of these, only five articles were included in the qualitative synthesis. Two out of the five papers were further analysed for quantitative synthesis in meta-analysis. The majority of the included studies were found to be of "moderate quality". The qualitative synthesis found four probiotics that exhibited potential therapeutic effects in oral carcinogenesis, includingAcetobacter syzygii, AJ2, Lactobacillus plantarum, and Lactobacillus salivarius REN. Among them, the application of L. salivarius REN resulted in a 95 % lower risk for developing oral cancer (p 

    Matched MeSH terms: Carcinogenesis*
  4. E-cadherin: Its dysregulation in carcinogenesis and clinical implications
    Wong SHM, Fang CM, Chuah LH, Leong CO, Ngai SC
    Crit Rev Oncol Hematol, 2018 Jan;121:11-22.
    PMID: 29279096 DOI: 10.1016/j.critrevonc.2017.11.010
    E-cadherin is a transmembrane glycoprotein which connects epithelial cells together at adherens junctions. In normal cells, E-cadherin exerts its tumour suppressing role mainly by sequestering β-catenin from its binding to LEF (Lymphoid enhancer factor)/TCF (T cell factor) which serves the function of transcribing genes of the proliferative Wnt signaling pathway. Despite the ongoing debate on whether the loss of E-cadherin is the cause or effect of epithelial-mesenchymal transition (EMT), E-cadherin functional loss has frequently been associated with poor prognosis and survival in patients of various cancers. The dysregulation of E-cadherin expression that leads to carcinogenesis happens mostly at the epigenetic level but there are cases of genetic alterations as well. E-cadherin expression has been linked to the cellular functions of invasiveness reduction, growth inhibition, apoptosis, cell cycle arrest and differentiation. Studies on various cancers have shown that these different cellular functions are also interdependent. Recent studies have reported a rapid expansion of E-cadherin clinical relevance in various cancers. This review article summarises the multifaceted effect E-cadherin expression has on cellular functions in the context of carcinogenesis as well as its clinical implications in diagnosis, prognosis and therapeutics.
    Matched MeSH terms: Carcinogenesis/genetics; Carcinogenesis/metabolism; Carcinogenesis/pathology
  5. Evidence is insufficient to suggest that probiotics may reduce the risk of oral cancer
    Karpiński TM
    J Evid Based Dent Pract, 2021 12;21(4):101637.
    PMID: 34922715 DOI: 10.1016/j.jebdp.2021.101637
    ARTICLE TITLE AND BIBLIOGRAPHIC INFORMATION: Wan Mohd Kamaluddin et al. Probiotic inhibits oral carcinogenesis: A systematic review and meta-analysis. Arch Oral Biol. 2020 Oct;118:104,855. Doi: 10.1016/j.archoralbio.2020.104855. Epub 2020 Aug 2.

    SOURCE OF FUNDING: The study was funded by International Islamic University Malaysia (P-RIGS18-036-0036).

    TYPE OF STUDY/DESIGN: Systematic review with meta-analysis.

    Matched MeSH terms: Carcinogenesis
  6. Fulltext The Mechanisms of Probiotics, Prebiotics, Synbiotics, and Postbiotics in Oral Cancer Management
    Mohd Fuad AS, Amran NA, Nasruddin NS, Burhanudin NA, Dashper S, Arzmi MH
    Probiotics Antimicrob Proteins, 2023 Oct;15(5):1298-1311.
    PMID: 36048406 DOI: 10.1007/s12602-022-09985-7
    Oral carcinogenesis is preceded by oral diseases associated with inflammation such as periodontitis and oral candidiasis, which are contributed by chronic alcoholism, smoking, poor oral hygiene, and microbial infections. Dysbiosis is an imbalance of microbial composition due to oral infection, which has been reported to contribute to oral carcinogenesis. Therefore, in this review, we summarised the role of probiotics, prebiotics, synbiotics, and postbiotics in promoting a balanced oral microbiome, which may prevent oral carcinogenesis due to oral infections. Probiotics have been shown to produce biofilm, which possesses antibacterial activity against oral pathogens. Meanwhile, prebiotics can support growth and increase the benefit of probiotics. In addition, postbiotics possess antibacterial, anticariogenic, and anticancer properties that potentially aid in oral cancer prevention and treatment. The use of probiotics, prebiotics, synbiotics, and postbiotics for oral cancer management is still limited despite their vast potential, thus, discovering their prospects could herald a novel approach to disease prevention and treatment while participating in combating antimicrobial resistance.
    Matched MeSH terms: Carcinogenesis
  7. Fulltext Health effects of herbicides and its current removal strategies
    Mohd Ghazi R, Nik Yusoff NR, Abdul Halim NS, Wahab IRA, Ab Latif N, Hasmoni SH, et al.
    Bioengineered, 2023 Dec;14(1):2259526.
    PMID: 37747278 DOI: 10.1080/21655979.2023.2259526
    The continually expanding global population has necessitated increased food supply production. Thus, agricultural intensification has been required to keep up with food supply demand, resulting in a sharp rise in pesticide use. The pesticide aids in the prevention of potential losses caused by pests, plant pathogens, and weeds, but excessive use over time has accumulated its occurrence in the environment and subsequently rendered it one of the emerging contaminants of concern. This review highlights the sources and classification of herbicides and their fate in the environment, with a special focus on the effects on human health and methods to remove herbicides. The human health impacts discussion was in relation to toxic effects, cell disruption, carcinogenic impacts, negative fertility effects, and neurological impacts. The removal treatments described herein include physicochemical, biological, and chemical treatment approaches, and advanced oxidation processes (AOPs). Also, alternative, green, and sustainable treatment options were discussed to shed insight into effective treatment technologies for herbicides. To conclude, this review serves as a stepping stone to a better environment with herbicides.
    Matched MeSH terms: Carcinogenesis
  8. Calreticulin and cancer
    Zamanian M, Veerakumarasivam A, Abdullah S, Rosli R
    Pathol Oncol Res, 2013 Apr;19(2):149-54.
    PMID: 23392843 DOI: 10.1007/s12253-012-9600-2
    Calreticulin (CRT) as a multi-functional endoplasmic reticulum protein is involved in a spectrum of cellular processes which ranges from calcium homeostasis and chaperoning to cell adhesion and finally malignant formation and progression. Previous studies have shown a contributing role for CRT in a range of different cancers. This present review will focus on the possible roles of CRT in the progression of malignant proliferation and the mechanisms involved in its contribution to cancer invasion.
    Matched MeSH terms: Carcinogenesis/metabolism*; Carcinogenesis/pathology
  9. The role of Candida albicans candidalysin ECE1 gene in oral carcinogenesis
    Engku Nasrullah Satiman EAF, Ahmad H, Ramzi AB, Abdul Wahab R, Kaderi MA, Wan Harun WHA, et al.
    J Oral Pathol Med, 2020 Oct;49(9):835-841.
    PMID: 32170981 DOI: 10.1111/jop.13014
    Oral squamous cell carcinoma is associated with many known risk factors including tobacco smoking, chronic alcoholism, poor oral hygiene, unhealthy dietary habits and microbial infection. Previous studies have highlighted Candida albicans host tissue infection as a risk factor in the initiation and progression of oral cancer. C albicans invasion induces several cancerous hallmarks, such as activation of proto-oncogenes, induction of DNA damage and overexpression of inflammatory signalling pathways. However, the molecular mechanisms behind these responses remain unclear. A recently discovered fungal toxin peptide, candidalysin, has been reported as an essential molecule in epithelial damage and host recognition of C albicans infection. Candidalysin has a clear role in inflammasome activation and induction of cell damage. Several inflammatory molecules such as IL-6, IL-17, NLRP3 and GM-CSF have been linked to carcinogenesis. Candidalysin is encoded by the ECE1 gene, which has been linked to virulence factors of C albicans such as adhesion, biofilm formation and filamentation properties. This review discusses the recent epidemiological burden of oral cancer and highlights the significance of the ECE1 gene and the ECE1 protein breakdown product, candidalysin in oral malignancy. The immunological and molecular mechanisms behind oral malignancy induced by inflammation and the role of the toxic fungal peptide candidalysin in oral carcinogenesis are explored. With increasing evidence associating C albicans with oral carcinoma, identifying the possible fungal pathogenicity factors including the role of candidalysin can assist in efforts to understand the link between C albicans infection and carcinogenesis, and pave the way for research into therapeutic potentials.
    Matched MeSH terms: Carcinogenesis/genetics
  10. Use of Arbitrary Reference Genes May Lead to Misleading Conclusions
    Tan SC
    Gynecol. Obstet. Invest., 2019;84(5):519-520.
    PMID: 31269498 DOI: 10.1159/000501684
    Matched MeSH terms: Carcinogenesis*
  11. Ferroptosis as a potential target for cancer therapy
    Chen Z, Wang W, Abdul Razak SR, Han T, Ahmad NH, Li X
    Cell Death Dis, 2023 Jul 24;14(7):460.
    PMID: 37488128 DOI: 10.1038/s41419-023-05930-w
    Ferroptosis is a recently discovered essential type of cell death that is mainly characterized by iron overload and lipid peroxidation. Emerging evidence suggests that ferroptosis is a double-edged sword in human cancer. However, the precise underlying molecular mechanisms and their differential roles in tumorigenesis are unclear. Therefore, in this review, we summarize and briefly present the key pathways of ferroptosis, paying special attention to the regulation of ferroptosis as well as its dual role as an oncogenic and as a tumor suppressor event in various human cancers. Moreover, multiple pharmacological ferroptosis activators are summarized, and the prospect of targeting ferroptosis in cancer therapy is further elucidated.
    Matched MeSH terms: Carcinogenesis/genetics
  12. Fulltext CRNDE: A Pivotal Oncogenic Long Non-Coding RNA in Cancers
    Hor YZ, Salvamani S, Gunasekaran B, Yian KR
    Yale J Biol Med, 2023 Dec;96(4):511-526.
    PMID: 38161583 DOI: 10.59249/VHYE2306
    Colorectal Neoplasia Differentially Expressed (CRNDE), a long non-coding RNA that was initially identified as aberrantly expressed in colorectal cancer (CRC) has also been observed to exhibit elevated expression in various other human malignancies. Recent research has accumulated substantial evidence implicating CRNDE as an oncogenic player, exerting influence over critical cellular processes linked to cancer progression. Particularly, its regulatory interactions with microRNAs and proteins have been shown to modulate pathways that contribute to carcinogenesis and tumorigenesis. This review will comprehensively outline the roles of CRNDE in colorectal, liver, glioma, lung, cervical, gastric and prostate cancer, elucidating the mechanisms involved in modulating proliferation, apoptosis, migration, invasion, angiogenesis, and radio/chemoresistance. Furthermore, the review highlights CRNDE's potential as a multifaceted biomarker, owing to its presence in diverse biological samples and stable properties, thereby underscoring its diagnostic, therapeutic, and prognostic applications. This review aims to provide comprehensive insights of CRNDE-mediated oncogenesis and identify CRNDE as a promising target for future clinical interventions.
    Matched MeSH terms: Carcinogenesis/genetics
  13. Fulltext Targeting energy metabolism to eliminate cancer cells
    Shahruzaman SH, Fakurazi S, Maniam S
    Cancer Manag Res, 2018;10:2325-2335.
    PMID: 30104901 DOI: 10.2147/CMAR.S167424
    Adaptive metabolic responses toward a low oxygen environment are essential to maintain rapid proliferation and are relevant for tumorigenesis. Reprogramming of core metabolism in tumors confers a selective growth advantage such as the ability to evade apoptosis and/or enhance cell proliferation and promotes tumor growth and progression. One of the mechanisms that contributes to tumor growth is the impairment of cancer cell metabolism. In this review, we outline the small-molecule inhibitors identified over the past decade in targeting cancer cell metabolism and the usage of some of these molecules in clinical trials.
    Matched MeSH terms: Carcinogenesis
  14. Polymicrobial interactions of Candida albicans and its role in oral carcinogenesis
    Arzmi MH, Dashper S, McCullough M
    J Oral Pathol Med, 2019 Aug;48(7):546-551.
    PMID: 31183906 DOI: 10.1111/jop.12905
    The oral microbiome is composed of microorganisms residing in the oral cavity, which are critical components of health and disease. Disruption of the oral microbiome has been proven to influence the course of oral diseases, especially among immunocompromised patients. Oral microbiome is comprised of inter-kingdom microorganisms, including yeasts such as Candida albicans, bacteria, archaea and viruses. These microorganisms can interact synergistically, mutualistically and antagonistically, wherein the sum of these interactions dictates the composition of the oral microbiome. For instance, polymicrobial interactions can improve the ability of C albicans to form biofilm, which subsequently increases the colonisation of oral mucosa by the yeast. Polymicrobial interactions of C albicans with other members of the oral microbiome have been reported to enhance the malignant phenotype of oral cancer cells, such as the attachment to extracellular matrix molecules (ECM) and epithelial-mesenchymal transition (EMT). Polymicrobial interactions may also exacerbate an inflammatory response in oral epithelial cells, which may play a role in carcinogenesis. This review focuses on the role of polymicrobial interactions between C albicans and other oral microorganisms, including its role in promoting oral carcinogenesis.
    Matched MeSH terms: Carcinogenesis
  15. Circadian rhythms and cancer
    Selvaraj C, Safi SZ, Vijayakumar R
    Adv Protein Chem Struct Biol, 2023;137:135-159.
    PMID: 37709373 DOI: 10.1016/bs.apcsb.2023.05.001
    Circadian rhythms are autonomous oscillators developed by the molecular circadian clock, essential for coordinating internal time with the external environment in a 24-h daily cycle. In mammals, this circadian clock system plays a major role in all physiological processes and severely affects human health. The regulation of the circadian clock extends beyond the clock genes to involve several clock-controlled genes. Hence, the aberrant expression of these clock genes leads to the downregulation of important targets that control the cell cycle and the ability to undergo apoptosis. This may lead to genomic instability and promotes carcinogenesis. Alteration in the clock genes and their modulation is recognized as a new approach for the development of effective treatment against several diseases, including cancer. Until now, there has been a lack of understanding of circadian rhythms and cancer disease. For that, this chapter aims to represent the core components of circadian rhythms and their function in cancer pathogenesis and progression. In addition, the clinical impacts, current clock drugs, and potential therapeutic targets have been discussed.
    Matched MeSH terms: Carcinogenesis
  16. Long-term in vitro expansion of human adipose-derived stem cells showed low risk of tumourigenicity
    Zaman WS, Makpol S, Sathapan S, Chua KH
    J Tissue Eng Regen Med, 2014 Jan;8(1):67-76.
    PMID: 22552847 DOI: 10.1002/term.1501
    In the field of cell-based therapy and regenerative medicine, clinical application is the ultimate goal. However, one major concern is: does in vitro manipulation during culture expansion increases tumourigenicity risk on the prepared cells? Therefore, the aim of this study was to investigate the effect of long-term in vitro expansion on human adipose-derived stem cells (ASCs). The ASCs were harvested from lipo-aspirate samples and cultured until passage 20 (P20), using standard culture procedures. ASCs at P5, P10, P15 and P20 were analysed for morphological changes, DNA damage (Comet assay), tumour suppressor gene expression level (quantitative PCR), p53 mutation, telomerase activity, telomere length determination and in vivo tumourigenicity test. Our data showed that ASCs lost their fibroblastic feature in long-term culture. The population doubling time of ASCs increased with long-term culture especially at P15 and P20. There was an increase in DNA damage at later passages (P15 and P20). No significant changes were observed in both p53 and p21 genes expression throughout the long-term culture. There was also no p53 mutation detected and no significant changes were recorded in the relative telomerase activity (RTA) and mean telomere length (TRF) in ASCs at all passages. In vivo implantation of ASCs at P15 and P20 into the nude mice did not result in tumour formation after 4 months. The data showed that ASCs have low risk of tumourigenicity up to P20, with a total population doubling of 42 times. This indicates that adipose tissue should be a safe source of stem cells for cell-based therapy.
    Matched MeSH terms: Carcinogenesis*
  17. The role of heat shock proteins and glucose regulated proteins in cancer
    Tan JS, Ong Kc KC, Rhodes A
    Malays J Pathol, 2016 Aug;38(2):75-82.
    PMID: 27568663 MyJurnal
    Heat shock proteins (HSPs) are a family of evolutionary conserved proteins that work as molecular chaperones for cellular proteins essential for cell viability and growth as well as having numerous cyto-protective roles. They are sub-categorised based on their molecular weights; amongst which some of the most extensively studied are the HSP90 and HSP70 families. Important members of these two families; Heat shock proteins 70 and heat shock proteins 90 (Hsp70/90), are the glucose regulated proteins (GRP). These stress-inducible chaperones possess distinct roles from that of the other HSPs, residing mostly in the endoplasmic reticulum and mitochondria, but they can also be translocated to other cellular locations. Their ability in adapting to stress conditions in the tumour microenvironment suggests novel functions in cancer. GRPs have been implicated in many crucial steps of carcinogenesis to include stabilization of oncogenic proteins, induction of tumour angiogenesis, inhibition of apoptosis and replicative senescence, and promotion of invasion and metastasis.
    Matched MeSH terms: Carcinogenesis/metabolism*
  18. Linking Benzene, in Utero Carcinogenicity and Fetal Hematopoietic Stem Cell Niches: A Mechanistic Review
    Yusoff NA, Abd Hamid Z, Budin SB, Taib IS
    Int J Mol Sci, 2023 Mar 28;24(7).
    PMID: 37047305 DOI: 10.3390/ijms24076335
    Previous research reported that prolonged benzene exposure during in utero fetal development causes greater fetal abnormalities than in adult-stage exposure. This phenomenon increases the risk for disease development at the fetal stage, particularly carcinogenesis, which is mainly associated with hematological malignancies. Benzene has been reported to potentially act via multiple modes of action that target the hematopoietic stem cell (HSCs) niche, a complex microenvironment in which HSCs and multilineage hematopoietic stem and progenitor cells (HSPCs) reside. Oxidative stress, chromosomal aberration and epigenetic modification are among the known mechanisms mediating benzene-induced genetic and epigenetic modification in fetal stem cells leading to in utero carcinogenesis. Hence, it is crucial to monitor exposure to carcinogenic benzene via environmental, occupational or lifestyle factors among pregnant women. Benzene is a well-known cause of adult leukemia. However, proof of benzene involvement with childhood leukemia remains scarce despite previously reported research linking incidences of hematological disorders and maternal benzene exposure. Furthermore, accumulating evidence has shown that maternal benzene exposure is able to alter the developmental and functional properties of HSPCs, leading to hematological disorders in fetus and children. Since HSPCs are parental blood cells that regulate hematopoiesis during the fetal and adult stages, benzene exposure that targets HSPCs may induce damage to the population and trigger the development of hematological diseases. Therefore, the mechanism of in utero carcinogenicity by benzene in targeting fetal HSPCs is the primary focus of this review.
    Matched MeSH terms: Carcinogenesis/pathology
  19. MicroRNAs and colorectal cancer: clinical potential and regulatory networks
    Osei GY, Adu-Amankwaah J, Koomson S, Beletaa S, Asiamah EA, Smith-Togobo C, et al.
    Mol Biol Rep, 2023 Nov;50(11):9575-9585.
    PMID: 37776413 DOI: 10.1007/s11033-023-08810-w
    Colorectal cancer (CRC) is a serious global health concern, with a high incidence and mortality rate. Although there have been advancements in the early detection and treatment of CRC, therapy resistance is common. MicroRNAs (miRNAs), a type of small non-coding RNA that regulates gene expression, are key players in the initiation and progression of CRC. Recently, there has been growing attention to the complex interplay of miRNAs in cancer development. miRNAs are powerful RNA molecules that regulate gene expression and have been implicated in various physiological and pathological processes, including carcinogenesis. By identifying current challenges and limitations of treatment strategies and suggesting future research directions, this review aims to contribute to ongoing efforts to enhance CRC diagnosis and treatment. It also provides a comprehensive overview of the role miRNAs play in CRC carcinogenesis and explores the potential of miRNA-based therapies as a treatment option. Importantly, this review highlights the exciting potential of targeted modulation of miRNA function as a therapeutic approach for CRC.
    Matched MeSH terms: Carcinogenesis/genetics
  20. Fulltext Revisiting Mitochondria Scored Cancer Progression and Metastasis
    Gundamaraju R, Lu W, Manikam R
    Cancers (Basel), 2021 Jan 23;13(3).
    PMID: 33498743 DOI: 10.3390/cancers13030432
    The Warburg effect has immensely succored the study of cancer biology, especially in highlighting the role of mitochondria in cancer stemness and their benefaction to the malignancy of oxidative and glycolytic cancer cells. Mitochondrial genetics have represented a focal point in cancer therapeutics due to the involvement of mitochondria in programmed cell death. The mitochondrion has been well established as a switch in cell death decisions. The mitochondrion's instrumental role in central bioenergetics, calcium homeostasis, and translational regulation has earned it its fame in metastatic dissemination in cancer cells. Here, we revisit and review mechanisms through which mitochondria influence oncogenesis and metastasis by underscoring the oncogenic mitochondrion that is capable of transferring malignant capacities to recipient cells.
    Matched MeSH terms: Carcinogenesis
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