Displaying publications 1 - 20 of 87 in total

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  1. Nenny Noorina Saaid, Reena Rahayu Md Zin, Siti Aishah Md Ali, Sharifah Noor Akmal Syed Hussain, Zulkifli Zainuddin, Zubaidah Zakaria
    Sains Malaysiana, 2014;43:1317-1326.
    The identification of chromosomal aberrations in prostate cancer has been widely studied with several known oncogenes and tumor suppressor genes have successfully been discovered. The most frequent aberrations detected in western population were losses in chromosome 5q, 6q, 8p, 13q, 16q, 17p, 18q and gains of 7p/q and 8q. The purpose of this study was to determine the chromosomal aberrations among Malaysian men of Southeast Asia population and discover those potential genes within that chromosomal aberrant region. Thirty-six formalin-fixed paraffin embedded specimens consist of eight organ-confined prostate cancer cases, five with capsular invasion, 14 showed metastasis and nine cases had no tumor stage recorded, were analyzed by array CGH technique. Chromosomal losses were frequently detected at 4q, 6q, 8p, 13q, 18q while gains at 7q, 11q, 12p, 16q and 17q. Gain of 16q24.3 was statistically significant with tumor size. Gains of 6q25.1 and Xq12 as well as losses of 3p13-p1.2 and 13q33.1-q33.3 were significantly correlated with Gleason grade whereas 12p13.31 gain was associated with bone metastasis. Several potential genes have also been found within that aberrant region which is myopodin (4q26-q27), ROBO1 (3p13-p11.2), ERCC5 (13q33.1-q33.3) and CD9 (12p13.31), suggesting that these genes may play a role in prostate cancer progression. The chromosomal aberrations identified by array CGH analysis could provide important clues to discover potential genes associated with prostate tumorigenesis of Malaysian men.
    Matched MeSH terms: Cell Transformation, Neoplastic
  2. Tegginamani AS, Shivakumar VH, Ismail SMB, Abraham MT, Fernandes BA, Zamzuri ATB
    J Coll Physicians Surg Pak, 2022 Feb;32(2):256-258.
    PMID: 35108805 DOI: 10.29271/jcpsp.2022.02.256
    Oral leukoplakia is the most common potentially malignant oral disorder. Oral leukoplakia's malignant potential is independent of the histopathological grade, and the malignant transformation rate varies greatly from 3% to 50% even in the case of severe epithelial dysplasia. Ethnic & environmental variables may contribute to this variation. C-kit immunohistochemistry was performed on 15 oral leukoplakia (OL), two oral squamous cell carcinoma (OSCC), and two dentigerous cysts (DC). The objective of this study was to evaluate the c-kit expression in oral leukoplakia. The use of various immunohistochemical markers to differentiate between OLs with a high and low risk of malignant transformation has been investigated. Only four OL exhibited a faint cytoplasmic expression in basal cells. Whereas, OSCC and DC were devoid of c-kit expression. Thus, this may not be a unique marker for identifying OL at high-risk. Further research with larger sample size is required. Key Words: CD 117, Disease progression, Oral dysplasia, Oral leukoplakia, Risk prediction.
    Matched MeSH terms: Cell Transformation, Neoplastic
  3. Yaacob, H.B., Ngeow, W.C., Tan, P.L., Zainal Arif, A.R.
    Ann Dent, 2002;9(1):-.
    MyJurnal
    The controversy on malignant transformation of oral lichen planus has always intrigued researchers. We present a case of lichenoid lesion and squamous cell carcinoma of the tongue, occurring in a middle aged Indian lady. The diagnosis and timing of these lesions is discussed.
    Matched MeSH terms: Cell Transformation, Neoplastic
  4. Ismail SB, Kumar SK, Zain RB
    J Oral Sci, 2007 Jun;49(2):89-106.
    PMID: 17634721
    Lichen planus, a chronic autoimmune, mucocutaneous disease affects the oral mucosa (oral lichen planus or OLP) besides the skin, genital mucosa, scalp and nails. An immune mediated pathogenesis is recognized in lichen planus although the exact etiology is unknown. The disease most commonly affects middle-aged females. Oral lichenoid reactions (OLR) which are considered variants of OLP, may be regarded as a disease by itself or as an exacerbation of an existing OLP, by the presence of medication (lichenoid drug reactions) or dental materials (contact hypersensitivity). OLP usually presents as white striations (Wickham's striae), white papules, white plaque, erythema, erosions or blisters. Diagnosis of OLP is established either by clinical examination only or by clinical examination with histopathologic confirmation. Direct immunofluorescence examination is only used as an adjunct to the above method of diagnosis and to rule out specific autoimmune diseases such as pemphigus and pemphigoid. Histopathologic features of OLP and OLR are similar with suggestions of certain discriminatory features by some authors. Topical corticosteroids are the treatment of choice for OLP although several other medications have been studied including retinoids, tacrolimus, cyclosporine and photodynamic therapy. Certain OLP undergo malignant transformation and the exact incidence and mechanisms are still controversial. In this paper, etiopathogenesis, diagnosis, management and malignant transformation of OLP and OLR have been reviewed.
    Matched MeSH terms: Cell Transformation, Neoplastic
  5. Ghazali N, Bakri MM, Zain RB
    J Oral Pathol Med, 2003 Aug;32(7):383-92.
    PMID: 12846784
    Some oral verrucal lesions may constitute parts of the clinicopathological spectrum of proliferative verrucous leukoplakia (PVL). Because of its idiopathic yet sinister nature, it is possible that PVL may exist in other populations. The aim of this study was to review the clinicopathological features of persistent, multifocal, oral verrucal lesions in Malaysian population.
    Matched MeSH terms: Cell Transformation, Neoplastic/pathology
  6. Cheah PL, Looi LM, Lin HP, Yap SF
    Pathology, 1991 Jan;23(1):66-8.
    PMID: 1648195
    A case of primary hepatocellular carcinoma (PHC) developing in a 10 year old boy who contracted Hepatitis B virus (HBV) infection in the course of maintenance phase chemotherapy for acute lymphoblastic leukemia was seen at University Hospital, Kuala Lumpur. This case is of interest in that it (1) supports an etiological relationship between HBV infection and PHC, (2) manifested a distinctly short malignant transformation time, and (3) draws attention to the possible contributory role of chemotherapy in increasing the risk of developing PHC.
    Matched MeSH terms: Cell Transformation, Neoplastic*
  7. 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: Cell Transformation, Neoplastic
  8. Zakaria N, Yusoff NM, Zakaria Z, Lim MN, Baharuddin PJ, Fakiruddin KS, et al.
    BMC Cancer, 2015;15:84.
    PMID: 25881239 DOI: 10.1186/s12885-015-1086-3
    Despite significant advances in staging and therapies, lung cancer remains a major cause of cancer-related lethality due to its high incidence and recurrence. Clearly, a novel approach is required to develop new therapies to treat this devastating disease. Recent evidence indicates that tumours contain a small population of cells known as cancer stem cells (CSCs) that are responsible for tumour maintenance, spreading and resistant to chemotherapy. The genetic composition of CSCs so far is not fully understood, but manipulation of the specific genes that maintain their integrity would be beneficial for developing strategies to combat cancer. Therefore, the goal of this study isto identify the transcriptomic composition and biological functions of CSCs from non-small cell lung cancer (NSCLC).
    Matched MeSH terms: Cell Transformation, Neoplastic/genetics; Cell Transformation, Neoplastic/metabolism
  9. Liu C, Hirakawa H, Tanaka K, Mohd Saaya F, Nenoi M, Fujimori A, et al.
    Dose Response, 2019 03 04;17(1):1559325819833840.
    PMID: 30858771 DOI: 10.1177/1559325819833840
    Radiotherapy (RT) treats cancer effectively with high doses of ionizing radiation (IR) to killing cancer cells and shrinking tumors while bearing the risk of developing different side effects, including secondary cancer, which is most concerning for long-term health consequences. Genomic instability (GI) is a characteristic of most cancer cells, and IR-induced GI can manifest as delayed homologous recombination (HR). Radioadaptive response (RAR) is capable of reducing genotoxicity, cell transformation, mutation, and carcinogenesis, but the rational evidence describing its contributions to the reduction of radiation risk, in particular, carcinogenesis, remains fragmented. In this work, to investigate the impact of RAR on high-dose, IR-induced GI measured as delayed HR, the frequency of recombinant cells was comparatively studied under RAR-inducible and -uninducible conditions in the nucleated cells in hematopoietic tissues (bone marrow and spleen) using the Rosa26 Direct Repeat-green fluorescent protein (RaDR-GFP) homozygote mice. Results demonstrated that the frequency of recombinant cells was significantly lower in hematopoietic tissues under RAR-inducible condition. These findings suggest that reduction in delayed HR may be at least a part of the mechanisms underlying decreased carcinogenesis by RAR, and application of RAR would contribute to a more rigorous and scientifically grounded system of radiation protection in RT.
    Matched MeSH terms: Cell Transformation, Neoplastic
  10. Mazlina S, Shiraz MA, Hazim MY, Amran AR, Zulkarnaen AN, Wan Muhaizan WM
    J Laryngol Otol, 2006 Jul;120(7):597-9.
    PMID: 16672089
    Inverted papilloma is a rare, benign tumour representing only 0.5 to 4 per cent of all sinonasal neoplasms; its involvement of the middle ear is extremely rare. We present a case of multicentric inverted papilloma in the sinonasal region and middle ear in a 54-year-old man. The patient later developed neck metastasis secondary to malignant transformation of the inverted papilloma in the middle ear.
    Matched MeSH terms: Cell Transformation, Neoplastic
  11. Senarath NH, Jayasooriya PR, Siriwardena BSMS, Tilakaratne WM
    Asian Pac J Cancer Prev, 2021 Aug 01;22(8):2313-2321.
    PMID: 34452541 DOI: 10.31557/APJCP.2021.22.8.2313
    BACKGROUND: Epithelial dysplasia (ED) at oral cancer excision margins is a frequent finding. Dysplastic epithelium at excision margins may not be similar to dysplasia in Oral potentially malignant disorders (OPMD) as malignant transformation has already taken place. Therefore, management of ED at excision margins should be different to that of OPMD. ED creates a dilemma in relation to further management of cancer patients, since there are no accepted guidelines. Therefore, the objective of this review is to analyze  existing literature and to arrive at evidence based recommendations for the management of ED at excision margins.

    METHODS: A comprehensive string was run on PubMed, Medscape and Medline. The final outcome included 113 studies. Finally, the most relevant 10 articles were critically assessed for inclusion and exclusion criteria against various parameters.

    RESULTS AND CONCLUSIONS:   Severe and Moderate ED need re-excision in order to improve prognosis. There is not enough sound evidence for the management of Mild ED at excision margins of oral squamous cell carcinoma. Guidelines for the management of ED at excision margins should be formulated after comprehensive multi center studies using lager cohorts of patients.
    .

    Matched MeSH terms: Cell Transformation, Neoplastic/pathology*
  12. Hamizah S, Roslida AH, Fezah O, Tan KL, Tor YS, Tan CI
    Asian Pac J Cancer Prev, 2012;13(6):2533-9.
    PMID: 22938417
    Annona muricata L (Annonaceae), commonly known as soursop has a long, rich history in herbal medicine with a lengthy recorded indigenous use. It had also been found to be a promising new anti-tumor agent in numerous in vitro studies. The present investigation concerns chemopreventive effects in a two-stage model of skin papillomagenesis. Chemopreventive effects of an ethanolic extract of A. muricata leaves (AMLE) was evaluated in 6-7 week old ICR mice given a single topical application of 7,12-dimethylbenza(α)anthracene (DMBA 100 μg/100 μl acetone) and promotion by repeated application of croton oil (1% in acetone/ twice a week) for 10 weeks. Morphological tumor incidence, burden and volume were measured, with histological evaluation of skin tissue. Topical application of AMLE at 30, 100 and 300 mg/kg significantly reduced DMBA/croton oil induced mice skin papillomagenesis in (i) peri-initiation protocol (AMLE from 7 days prior to 7 days after DMBA), (ii) promotion protocol (AMLE 30 minutes after croton oil), or (iii) both peri-initiation and promotion protocol (AMLE 7 days prior to 7 day after DMBA and AMLE 30 minutes after croton oil throughout the experimental period), in a dose dependent manner (p<0.05) as compared to carcinogen-treated control. Furthermore, the average latent period was significantly increased in the AMLE-treated group. Interestingly, At 100 and 300 mg/ kg, AMLE completely inhibited the tumor development in all stages. Histopathological study revealed that tumor growth from the AMLE-treated groups showed only slight hyperplasia and absence of keratin pearls and rete ridges. The results, thus suggest that the A.muricata leaves extract was able to suppress tumor initiation as well as tumor promotion even at lower dosage.
    Matched MeSH terms: Cell Transformation, Neoplastic/chemically induced; Cell Transformation, Neoplastic/drug effects
  13. Ramanujam TM, Ramesh JC, Goh DW, Wong KT, Ariffin WA, Kumar G, et al.
    J Pediatr Surg, 1999 Nov;34(11):1684-6.
    PMID: 10591570
    Here the first case in the literature of both mesenchymal hamartoma and malignant mesenchymoma occurring in a 6-year-old male child, at different times and at different sites in the liver, and also the possible malignant transformation of a mesenchymal hamartoma is reported. The tumor developed from a lesion in the right lobe that was overlooked initially during a left lateral segmentectomy at 18 months of age for a mesenchymal hamartoma. Malignant mesenchymoma is a rare and aggressive tumor. The origin of this tumor is not well understood. There has been no direct support to the hypothesis that malignant mesenchymoma may be the malignant counterpart of mesenchymal hamartoma. The authors provide clinical and histopathologic evidence in our case that suggests the possibility of malignant mesenchymoma arising from a mesenchymal hamartoma. This case emphasizes the need for complete removal of mesenchymal hamartoma and the need for long-term follow-up to detect multifocal lesion or malignant transformation.
    Matched MeSH terms: Cell Transformation, Neoplastic/pathology*
  14. Thomson PJ, Goodson ML, Smith DR
    J Oral Pathol Med, 2017 Nov;46(10):888-895.
    PMID: 28833670 DOI: 10.1111/jop.12625
    BACKGROUND: Oral potentially malignant disorders harbour variable and unpredictable risk for squamous carcinoma development. Whilst current management strategies utilise histopathological diagnoses, dysplasia grading and targeted intervention for "high-risk" lesions, clinicians are unable to predict malignant potential.

    METHODS: Detailed, retrospective clinico-pathological analysis of potentially malignant lesions undergoing malignant transformation, from a 590 patient cohort treated by interventional laser surgery and followed for a mean of 7.3 years, was undertaken. Clinical outcome was documented at study census date (31 December 2014).

    RESULTS: A total of 99 patients (16.8%) developed cancer: 71 (12%) seen "unexpectedly" upon excision and 28 (4.8%) progressing to malignancy at a median of 87.3 months post-surgery. Thirty "unexpected" excisions were micro-invasive (42.3%) arising primarily in severely dysplastic precursors (75%) at ventro-lateral tongue and floor of mouth sites (54.5%); 1 patient (1.4%) had a cancer-related death, whilst 58 (81.7%) were disease free. A total of 19 of 28 "progressive" cancers (67.9%) arose at new sites, with erythroleukoplakia a significant predictor of malignancy (P = .0019). Nine (32.1%) developed at the same precursor site, with 6 (77.7%) on the ventro-lateral tongue and floor of mouth. Three (10.7%) were micro-invasive, 9 patients (32.1%) died from metastatic disease and 12 (42.9%) were disease free (P < .001).

    CONCLUSION: Squamous carcinoma may arise at the site of a precursor lesion as transformation or new-site development via field cancerisation. Whilst interventional surgery facilitates early diagnosis and treatment of occult disease, thus reducing risk from same-site transformation, new-site cancer is a significant long-term risk for patients with potentially malignant disorder.

    Matched MeSH terms: Cell Transformation, Neoplastic*
  15. Lim JS, Tang SP, Siar CH
    Asian Pac J Cancer Prev, 2009;10(6):1071-4.
    PMID: 20192586
    BACKGROUND: Conventional methods for writing case notes detailing the progress of oral lichen planus (OLP), a precancerous condition that requires long-term surveillance, is both time-consuming and tedious for the busy clinician.

    OBJECTIVES: To design and perform a simple surveillance on OLP patients based on colour-coded topography mouth maps (TMM).

    MATERIALS AND METHODS: Three colour-coded TMM were employed: red for OLP in high risk oral mucosal sites, yellow for cases showing improvement and green for asymptomatic lesions at each recall visit. In this preliminary study, these were applied on 30 histologically confirmed OLP individuals attending the Oral Medicine Clinic at the Department of Oral Pathology, Oral Medicine and Periodontology, Faculty of Dentistry, University of Malaya. The sites and extent of OLP lesions were charted on either red, yellow or green TMM based on defined criteria. This surveillance evaluated OLP in relation to patientandapos;s age, race, gender, underlying systemic conditions, oral habits, initial onset of OLP, oral manifestations and presence/absence of clinically suspicious areas.

    RESULTS: Study sample comprised 4 (13.3%) Malays, 9 (30.0%) Chinese and 17 (56.7%) Indians. Most OLP patients belong to the green TMM (n= 14, 46.6%) group followed by red (n= 11, 36.7%) and yellow (n= 5, 16.7%) groups. Of the 11 cases with red TMM, rebiopsy was performed on 4 cases but no dysplasia was detected. Any local confounding factors namely periodontal disease or faulty dental restorations were managed accordingly.

    CONCLUSIONS: TMM is simple to use and aided the clinicians in terms of time saving and patient management. Hence, follow-up of OLP patients can be carried out more efficiently and appropriately. TMM can be used for surveillance of other oral precancerous lesions and conditions.

    Matched MeSH terms: Cell Transformation, Neoplastic/pathology*
  16. Mansor NA, Yusof N, Tang YL, Ithnin A, Azma RZ, Tumian NR, et al.
    Malays J Pathol, 2018 Aug;40(2):191-197.
    PMID: 30173238 MyJurnal
    INTRODUCTION: Essential thrombocythaemia (ET) is a chronic myeloproliferative neoplasm (MPN) characterised by persistent thombocytosis. It is an indolent disorder but transformation to myelofibrosis (MF), acute myeloid leukaemia (AML) or myelodyplastic syndrome (MDS) has been reported.

    CASE REPORT: We described a patient with ET whose disease evolved into MDS with fibrosis and complex karyotype after 15 years of stable disease. She was asymptomatic and was on hydroxyurea (HU) treatment until recently when she presented with worsening anaemia. Physical examination showed mild splenomegaly. Full blood picture showed leukoerythroblastic picture with presence of 3% circulating blasts and background of dysplastic features such as hypogranular cytoplasm and nuclear hyposegmentation of neutrophils. The bone marrow aspiration was haemodiluted but revealed presence of 6% blast cells, trilineage dysplasia and predominant erythroid precursors (60%). Trephine biopsy showed no excess of blast cells and normal quantity of erythroid precursors, but there was increased in fibrosis (WHO grade 2) and presence of dysmegakaryopoeisis such as nuclear hypolobation, multinucleation and micromegakaryocytes. Cytogenetic study showed complex karyotype; monosomy of chromosome 2, chromosome 5, chromosome 18 and presence of a marker chromosome (42~44, XX,-2,-5,-18,+mar). Fluorescence in situ hybridisation (FISH) showed 5q deletion (CSF1R and EGR1).

    CONCLUSION: The findings were consistent with transformation of ET to MDS with fibrosis and complex karyotype. ET progression to MDS is considered rare. The presence of complex karyotype and fibrosis in MDS are associated with unfavourable outcome.

    Matched MeSH terms: Cell Transformation, Neoplastic/genetics*
  17. Chieng CK, Say YH
    Tumour Biol., 2015 Sep;36(10):8107-20.
    PMID: 25983001 DOI: 10.1007/s13277-015-3530-z
    As the cellular prion protein (PrP(C)) has been implicated in carcinogenesis, we aimed to investigate the effects of cancer cell-specific PrP(C) overexpression from the invasion, metastasis, and apoptosis aspects, by performing cell motility assays, cell proliferation assays under anchorage-dependent and anchorage-independent conditions, and apoptosis evasion when subjected to multiple anti-cancer drugs. Overexpression of PrP(C) in LS 174T was achieved by stable transfection. PrP(C) overexpression was shown to increase cell proliferation in anchorage-dependent and anchorage-independent manners, as shown by more viable cells in 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, more colonies formed in soft agar assay and increased resistance to anoikis in poly-2-hydroxyethyl methacrylate-coated surface. PrP(C) overexpression also increased cell motility and invasiveness of LS 174T. Cell adhesion to extracellular matrix using collagen- and fibronectin-coated surfaces revealed increased cell attachment in LS 174T cells overexpressing PrP(C). Analysis of apoptotic and necrotic cells by propidium iodide/annexin V-fluorescein isothiocyanate microscopy and 7-amino-actinomycin D/annexin V-phycoerythrin flow cytometry revealed that PrP(C) overexpression attenuated doxorubicin-induced apoptosis. Human apoptosis antibody array with 35 apoptosis-related proteins revealed that three inhibitor of apoptosis proteins (IAPs)-survivin, X-linked inhibitor of apoptosis protein (XIAP), and cellular inhibitor of apoptosis protein-1 (cIAP-1)-were upregulated in LS 174T cells overexpressing PrP(C) in doxorubicin-induced apoptosis. In conclusion, the overexpression of PrP(C) could enhance the invasiveness and survival of LS 174T colorectal cancer cells, indicating that PrP(C) plays a role in colorectal cancer biology.
    Matched MeSH terms: Cell Transformation, Neoplastic/pathology*
  18. Kavitha N, Vijayarathna S, Jothy SL, Oon CE, Chen Y, Kanwar JR, et al.
    Asian Pac J Cancer Prev, 2014;15(18):7489-97.
    PMID: 25292018
    MicroRNAs (miRNAs) are short non-coding RNAs of 20-24 nucleotides that play important roles in carcinogenesis. Accordingly, miRNAs control numerous cancer-relevant biological events such as cell proliferation, cell cycle control, metabolism and apoptosis. In this review, we summarize the current knowledge and concepts concerning the biogenesis of miRNAs, miRNA roles in cancer and their potential as biomarkers for cancer diagnosis and prognosis including the regulation of key cancer-related pathways, such as cell cycle control and miRNA dysregulation. Moreover, microRNA molecules are already receiving the attention of world researchers as therapeutic targets and agents. Therefore, in-depth knowledge of microRNAs has the potential not only to identify their roles in cancer, but also to exploit them as potential biomarkers for cancer diagnosis and identify therapeutic targets for new drug discovery.
    Matched MeSH terms: Cell Transformation, Neoplastic/pathology*
  19. Ahmed Adam MA, Tabana YM, Musa KB, Sandai DA
    Oncol Rep, 2017 Mar;37(3):1321-1336.
    PMID: 28184933 DOI: 10.3892/or.2017.5424
    The chemical nature of most of the mycotoxins makes them highly liposoluble compounds that can be absorbed from the site of exposure such as from the gastrointestinal and respiratory tract to the blood stream where it can be dissimilated throughout the body and reach different organs such as the liver and kidneys. Mycotoxins have a strong tendency and ability to penetrate the human and animal cells and reach the cellular genome where it causes a major mutagenic change in the nucleotide sequence which leads to strong and permanent defects in the genome. This defect will eventually be transcribed, translated and lead to the development of cancer. In this review, the chemical and physical nature of mycotoxins, the action of mycotoxins on the cellular genome and its effect on humans, mycotoxins and their carcinogenicity and mycotoxins research gaps are discussed, and new research areas are suggested. The research review posed various questions. What are the different mycotoxins that can cause cancer, what is the role of mycotoxins in causing cancer and what types of cancers can be caused by mycotoxins? These questions have been selected due to the significant increase in the mycotoxin contamination and the cancer incidence rate in the contemporary world. By revealing and understanding the role of mycotoxins in developing cancer, measures to reduce the risks and incidents of cancer could be taken.
    Matched MeSH terms: Cell Transformation, Neoplastic/chemically induced; Cell Transformation, Neoplastic/genetics; Cell Transformation, Neoplastic/pathology*
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