Displaying publications 61 - 80 of 86 in total

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  1. 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*
  2. Patel S, Murphy D, Haralambieva E, Abdulla ZA, Wong KK, Chen H, et al.
    Biomark Insights, 2014;9:77-84.
    PMID: 25232277 DOI: 10.4137/BMI.S16553
    FAS-associated protein with death domain (FADD) is a major adaptor protein involved in extrinsic apoptosis, embryogenesis, and lymphocyte homeostasis. Although abnormalities of the FADD/death receptor apoptotic pathways have been established in tumorigenesis, fewer studies have analyzed the expression and role of phosphorylated FADD (pFADD). Our identification of FADD as a lymphoma-associated autoantigen in T-cell lymphoma patients raises the possibility that pFADD, with its correlation with cell cycle, may possess role(s) in human T-cell lymphoma development. This immunohistochemical study investigated pFADD protein expression in a range of normal tissues and lymphomas, particularly T-cell lymphomas that require improved therapies. Whereas pFADD was expressed only in scattered normal T cells, it was detected at high levels in T-cell lymphomas (eg, 84% anaplastic large cell lymphoma and 65% peripheral T cell lymphomas, not otherwise specified). The increased expression of pFADD supports further study of its clinical relevance and role in lymphomagenesis, highlighting phosphorylation of FADD as a potential therapeutic target.
    Matched MeSH terms: Cell Transformation, Neoplastic
  3. Teh AH, Symonds E, Bull C, Clifton P, Fenech M
    Mutat Res Rev Mutat Res, 2012 05 22;751(1):64-75.
    PMID: 22627043 DOI: 10.1016/j.mrrev.2012.05.001
    Folate and methionine are critical for one-carbon metabolism impacting DNA synthesis, repair, and methylation processes, as well as polyamine synthesis. These micronutrients have been implicated in colorectal cancer risk. There are, however, inconsistencies within the literature, with some studies showing restriction to have tumour-inhibitory effects, whereas others suggest excess to have adverse outcomes. We conducted a review of the published data to examine the accumulated evidence for involvement of dietary folate and/or methionine restriction or excess in intestinal tumour development in the Apc(Min/+) mouse model, which is genetically prone to develop such cancers. Thirteen publications were selected for evaluation based on the following inclusion criteria: (i) use of Apc(Min/+) mouse model; (ii) interventions using dietary folate and/or methionine; and (iii) primary outcome measures focused on intestinal tumour development. We found that nutritional modulation of folate and methionine was shown to have different effects on intestinal cancer in the Apc(Min/+) mouse, depending on the dosage, duration and timing of intervention, and interaction of the Apc(Min/+) genotype with other genetic factors affecting folate and DNA methylation metabolism. Although some studies showed that folate deficiency before tumorigenesis tended to increase risk of tumour formation, there are inconsistencies regarding whether excess folate post-weaning or after tumour initiation increases intestinal tumour burden. Altogether, the pooled data do not appear to indicate a difference in effect on intestinal tumour incidence between post-weaning diets that are folate deficient or folate adequate. The Apc(Min/+) mouse is a useful model for assessment of the impact of dietary folate on intestinal tumour development, but further research is required to understand the reasons for these inconsistencies amongst studies based on likely mechanisms, including modulation of nucleotide synthesis, DNA methylation, and chromosomal instability, which may affect the rate of cellular division and its control.
    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. 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
  6. Fernandez SH
    Malays J Pathol, 1999 Dec;21(2):117-21.
    PMID: 11068417
    An 86-year-old man presented with a painless, pea-sized growth over the left angle of his jaw, which had been gradually enlarging over two years. A clinical diagnosis of pilar cyst was made. Histopathological examination of the mass revealed a malignant proliferating trichilemmal tumour. During follow-up 4 months later, a palpable small upper jugular lymph node was noted at the left side of the neck. Biopsy revealed a metastatic malignant trichilemmal tumour. This case illustrates a rare malignant tumour which is a challenge to clinical diagnosis.
    Matched MeSH terms: Cell Transformation, Neoplastic
  7. Arjungi KN
    Arzneimittelforschung, 1976;26(5):951-6.
    PMID: 786304
    Areca cattechu Linn is commonly known as areca nut or betel nut. It is a very widely cultivated plant in eastern countries like India, Bangladesh, Ceylon, Malaya, the Philippines and Japan. The importance of this nut is due to its use for chewing purposes. It had an important place as a pharmaceutical in Ayurveda--the ancient Indian system of medicine--also in the Chinese medicinal practices. The pharmaceutical importance of areca nut is due to the presence of an alkaloid, arecoline. Synthetic arecoline hydrobromide is also shown to possess numerous pharmacological properties. Chewing of "betel quid" or areca nut is a typical oriental habit. Betel quid comprises betel leaf, areca nut, catechu, lime and sometimes also tobacco. It is shown that there exists a correlationship between betel quid or areca nut chewing habit and oral cancer. A number of investigators have been able to produce cellular changes such as leukoplakia by application of betel quid or areca nut extract to the buccal mucosa of different animal.
    Matched MeSH terms: Cell Transformation, Neoplastic
  8. Boyle ST, Mittal P, Kaur G, Hoffmann P, Samuel MS, Klingler-Hoffmann M
    J Proteome Res, 2020 10 02;19(10):4093-4103.
    PMID: 32870688 DOI: 10.1021/acs.jproteome.0c00511
    Tumorigenesis involves a complex interplay between genetically modified cancer cells and their adjacent normal tissue, the stroma. We used an established breast cancer mouse model to investigate this inter-relationship. Conditional activation of Rho-associated protein kinase (ROCK) in a model of mammary tumorigenesis enhances tumor growth and progression by educating the stroma and enhancing the production and remodeling of the extracellular matrix. We used peptide matrix-assisted laser desorption/ionization mass spectrometry imaging (MALDI-MSI) to quantify the proteomic changes occurring within tumors and their stroma in their regular spatial context. Peptides were ranked according to their ability to discriminate between the two groups, using a receiver operating characteristic tool. Peptides were identified by liquid chromatography tandem mass spectrometry, and protein expression was validated by quantitative immunofluorescence using an independent set of tumor samples. We have identified and validated four key proteins upregulated in ROCK-activated mammary tumors relative to those expressing kinase-dead ROCK, namely, collagen I, α-SMA, Rab14, and tubulin-β4. Rab14 and tubulin-β4 are expressed within tumor cells, whereas collagen I is localized within the stroma. α-SMA is predominantly localized within the stroma but is also expressed at higher levels in the epithelia of ROCK-activated tumors. High expression of COL1A, the gene encoding the pro-α 1 chain of collagen, correlates with cancer progression in two human breast cancer genomic data sets, and high expression of COL1A and ACTA2 (the gene encoding α-SMA) are associated with a low survival probability (COLIA, p = 0.00013; ACTA2, p = 0.0076) in estrogen receptor-negative breast cancer patients. To investigate whether ROCK-activated tumor cells cause stromal cancer-associated fibroblasts (CAFs) to upregulate expression of collagen I and α-SMA, we treated CAFs with medium conditioned by primary mammary tumor cells in which ROCK had been activated. This led to abundant production of both proteins in CAFs, clearly highlighting the inter-relationship between tumor cells and CAFs and identifying CAFs as the potential source of high levels of collagen 1 and α-SMA and associated enhancement of tissue stiffness. Our research emphasizes the capacity of MALDI-MSI to quantitatively assess tumor-stroma inter-relationships and to identify potential prognostic factors for cancer progression in human patients, using sophisticated mouse cancer models.
    Matched MeSH terms: Cell Transformation, Neoplastic
  9. Arcana Thirumorthy, De-Ming Chau, Khatijah Yusoff, Abhi Veerakumarasivam
    MyJurnal
    Introduction: Bladder cancer is associated with high risk of tumour recurrence and therapeutic resistance. Cancer stem cells (CSC) within a particular tumour are postulated to drive tumorigenesis and influence tumour behaviour. Recent studies have shown that Newcastle disease virus (NDV) is able to selectively kill and exert a strong oncolytic effect against various cancer types. However little is known about the oncolytic effect of NDV against CSC. In this study, the oncolytic effect of NDV against putative bladder CSC was examined. Methods: Putative bladder CSC was selectively grown in the form of 3D-spheroids from six different bladder cancer cell lines. The spheroid cells were characterised for their stemness properties to ensure that these cells truly represent CSC. This was conducted via the analysis of CSC associated genes and cell surface markers expression. Subsequently, the oncolytic effect of the wild-type NDV-AF2240 strain against the bladder cancer spheroids was investigated. Results: All the spheroids expressed significantly high levels of CSC-associated genes. Flow-cytometry analysis revealed that the expression pattern of the CSC-associated surface markers was different in the spheroid cells; suggesting heterogeneity in the expression signatures of these cells. The infection of spheroids with NDV showed that the NDV was able to target bladder cancer spheroids but there was a spectrum of response across the different spheroids. Intriguingly, NDV was able to persistently infect bladder cancer spheroids that were not sensitive towards NDV infection as the presence of NDV viral genes were detected in the spheroid cells. The NDV persistently infected bladder cancer spheroids were resistant to superinfection and developed an antiviral state by expressing low levels of interferon-beta (IFN-b). NDV persistency of infection affects the process of epithelial to mesenchymal transition (EMT) of cancer cells as the spheroid forming ability of an established NDV persistently infected bladder cancer cell line, EJ28-PI was shown to be impaired. The EJ28-PI cells expressed significantly high levels of the EN2 gene. Knockdown of the EN2 expression reduced the viability of EJ28-PI cells; suggesting a role for EN2 in mediating NDV persistency of infection in cancer cells. Conclusion: Bladder CSC gene expression signatures influence the efficacy of NDV-mediated oncolysis. Our current work is focused on identifying genes and signalling pathways that influence NDV-mediated oncolysis us-ing whole-transcriptomic sequencing. The findings of this study can potentially be used to enhance the efficacy of NDV-mediated oncolysis and accelerate the translation of NDV as an oncotherapeutic agent in the clinic.
    Matched MeSH terms: Cell Transformation, Neoplastic
  10. Tegginamani AS, Shivakumar VH, Kallarakkal TG, Ismail SM, Abraham MT, Bin Zamzuri AT
    J Oral Maxillofac Pathol, 2020 09 09;24(2):400.
    PMID: 33456258 DOI: 10.4103/jomfp.JOMFP_272_19
    Background: Oral potentially malignant disorders have a risk for malignant transformation but are difficult to reliably identify and predict which patients are at the risk for malignant transformation. OCT4 has been hypothesized to play a key oncogenic driver in a variety of solid tumors. A deeper understanding of the aberrant molecular pathways which lead to carcinogenesis needs to be identified by the potential markers.

    Aims: To assess the OCT4 stemness factor in oral leukoplakia for its potential risk to malignant transformation.

    Settings and Design: 20 cases of oral leukoplakia were obtained from archives at Oral Cancer Research & Coordinating center (OCRCC) Malaysia Subjects and Methods: 20 cases of oral leukoplakia were assessed by OCT4 immunohistochemically. Oral squamous cell carcinoma was used as a control.

    Result: no expression of OCT 4 was observed in any cases of oral leukoplakia.

    Conclusion: The molecular mechanisms of Oct4 regulation and in particular of its switch on and off in tissues depends upon its microenvironment, which makes it challenging in fundamental and applied research fields of regenerative medicine and cancer therapy. It's better that patients should undergo multiple biopsies for the early detection of malignant transformation with close follow-up during the first two to three years, a large amount of work remains to be done with multi-marker panel investigation, as cure rates have remained constant over three decades.

    Matched MeSH terms: Cell Transformation, Neoplastic
  11. Yeong LT, Abdul Hamid R, Saiful Yazan L, Khaza'ai H, Mohtarrudin N
    BMC Complement Altern Med, 2015;15(1):431.
    PMID: 26638207 DOI: 10.1186/s12906-015-0954-3
    Drastic increment of skin cancer incidence has driven natural product-based chemoprevention as a promising approach in anticancer drug development. Apart from its traditional usages against various ailments, Ardisia crispa (Family: Myrsinaceae) specifically its triterpene-quinone fraction (TQF) which was isolated from the root hexane extract (ACRH) was recently reported to exert antitumor promoting activity in vitro. This study aimed at determining chemopreventive effect of TQF against chemically-induced mouse skin tumorigenesis as well as elucidating its possible pathway(s).
    Matched MeSH terms: Cell Transformation, Neoplastic/drug effects
  12. Pabalan N, Jarjanazi H, Ozcelik H
    J Gastrointest Cancer, 2014 Sep;45(3):334-41.
    PMID: 24756832 DOI: 10.1007/s12029-014-9610-2
    BACKGROUND: Reported associations of capsaicin with gastric cancer development have been conflicting. Here, we examine 10 published articles that explore these associations using 2,452 cases and 3,996 controls.

    METHODS: We used multiple search strategies in MEDLINE through PubMed to seek for suitable articles that had case-control design with gastric cancer as outcome.

    RESULTS: The outcomes of our study shows protection (odds ratio [OR] 0.55, P = 0.003) and susceptibility (OR 1.94, P = 0.0004), both significant with low and medium-high intake of capsaicin, respectively, although under relatively heterogeneous conditions (P(heterogeneity) = <0.0001). Outlier analysis resulted in loss of overall heterogeneity (P = 0.14) without affecting the pooled ORs. Among the subgroups, low intake elicited protection in both Korean (OR 0.37) and Mexican (OR 0.63) populations while high intake rendered these subgroups susceptible (OR 2.96 and OR 1.57, respectively). These subgroup values were highly significant (P = 0.0001-0.01) obtained in heterogeneous conditions (P(heterogeneity) 

    Matched MeSH terms: Cell Transformation, Neoplastic/drug effects
  13. Patil S, Warnakulasuriya S, Raj T, Sanketh DS, Rao RS
    J Investig Clin Dent, 2016 Nov;7(4):417-423.
    PMID: 26075572 DOI: 10.1111/jicd.12166
    OBJECTIVE: Exophytic oral verrucous hyperplasia (OVH) is a new entity described by an expert working group from South Asia. First reported in Taiwan, there are no reports so far from an Indian population. The aim was to use the microscopic features described by the expert group to differentiate OVH from other oral verruco-papillary lesions in an Indian archive.

    MATERIALS AND METHODS: In a retrospective multicentre study, using pathology archives, 188 verruco-papillary lesions were retrieved from pathology archives. A proforma listing histopathological criteria for OVH based on published guidelines (Annals of Dentistry, University of Malaya, 2013) was used. Patients' demographic and clinical data were transcribed from patient charts. The Pearson chi-square test was used to determine associations between clinical and histopathological features.

    RESULTS: Of 188 oral verruco-papillary lesions that were evaluated, based on microscopic features the cases were reclassified as OVH (57), verrucous carcinoma (VC) (84), oral squamous cell carcinoma (16), and other verruco-papillary lesions (31). Both OVH (70%) and VC (60%) showed male predominance and commonly affected buccal mucosa (OVH 74% and VC 57%). Absence of downward growth of the hyperplastic epithelium into lamina propria when compared with the level of the basement membrane of the adjacent normal epithelium was a distinct feature in OVH. Keratin plugging, epithelial dysplasia and subepithelial lymphocytic infiltration were found to be significantly different (P 

    Matched MeSH terms: Cell Transformation, Neoplastic/pathology
  14. Amin I, Koh BK, Asmah R
    J Med Food, 2004;7(1):7-12.
    PMID: 15117546
    This study investigated the effect of cacao liquor extract (CLE) on tumor marker enzymes--alkaline phosphatase (ALP), gamma-glutamyl transpeptidase (GGT), glutathione-S-transferase (GST), and glutathione reductase (GR) activities--in plasma and/or liver of hepatocarcinogenic rats, which were induced with diethylnitrosamine and 2-acetylaminofluorene. Twenty-nine male Sprague-Dawley rats (weighing 150-330 g) were divided into four groups (n = 6-8): normal control group (N), normal group + CLE (NE), cancer group (C), and cancer group + CLE (CE). Analysis of variance showed significant differences (P
    Matched MeSH terms: Cell Transformation, Neoplastic/drug effects
  15. Stebbing J, Zhang H, Xu Y, Lit LC, Green AR, Grothey A, et al.
    Oncogene, 2015 Apr 16;34(16):2103-14.
    PMID: 24909178 DOI: 10.1038/onc.2014.129
    Kinase suppressor of Ras-1 (KSR1) facilitates signal transduction in Ras-dependent cancers, including pancreatic and lung carcinomas but its role in breast cancer has not been well studied. Here, we demonstrate for the first time it functions as a tumor suppressor in breast cancer in contrast to data in other tumors. Breast cancer patients (n>1000) with high KSR1 showed better disease-free and overall survival, results also supported by Oncomine analyses, microarray data (n=2878) and genomic data from paired tumor and cell-free DNA samples revealing loss of heterozygosity. KSR1 expression is associated with high breast cancer 1, early onset (BRCA1), high BRCA1-associated ring domain 1 (BARD1) and checkpoint kinase 1 (Chk1) levels. Phospho-profiling of major components of the canonical Ras-RAF-mitogen-activated protein kinases pathway showed no significant changes after KSR1 overexpression or silencing. Moreover, KSR1 stably transfected cells formed fewer and smaller size colonies compared to the parental ones, while in vivo mouse model also demonstrated that the growth of xenograft tumors overexpressing KSR1 was inhibited. The tumor suppressive action of KSR1 is BRCA1 dependent shown by 3D-matrigel and soft agar assays. KSR1 stabilizes BRCA1 protein levels by reducing BRCA1 ubiquitination through increasing BARD1 abundance. These data link these proteins in a continuum with clinical relevance and position KSR1 in the major oncoprotein pathways in breast tumorigenesis.
    Matched MeSH terms: Cell Transformation, Neoplastic/genetics
  16. Masre SF, Rath N, Olson MF, Greenhalgh DA
    Oncogene, 2017 May 04;36(18):2529-2542.
    PMID: 27991921 DOI: 10.1038/onc.2016.402
    To study ROCK2 activation in carcinogenesis, mice expressing 4-hydroxytamoxifen (4HT)-activated ROCK2 (K14.ROCK(er)) were crossed with mice expressing epidermal-activated ras(Ha) (HK1.ras(1205)). At 8 weeks, 4HT-treated K14.ROCK(er)/HK1.ras(1205) cohorts exhibited papillomas similar to HK1.ras(1205) controls; however, K14.ROCK(er)/HK1.ras(1205) histotypes comprised a mixed papilloma/well-differentiated squamous cell carcinoma (wdSCC), exhibiting p53 loss, increased proliferation and novel NF-κB expression. By 12 weeks, K14.ROCK(er)/HK1.ras(1205) wdSCCs exhibited increased NF-κB and novel tenascin C, indicative of elevated rigidity; yet despite continued ROCK2 activities/p-Mypt1 inactivation, progression to SCC required loss of compensatory p21 expression. K14.ROCK(er)/HK1.ras(1205) papillomatogenesis also required a wound promotion stimulus, confirmed by breeding K14.ROCK(er) into promotion-insensitive HK1.ras(1276) mice, suggesting a permissive K14.ROCK(er)/HK1.ras(1205) papilloma context (wound-promoted/NF-κB(+)/p53(-)/p21(+)) preceded K14.ROCK(er)-mediated (p-Mypt1/tenascin C/rigidity) malignant conversion. Malignancy depended on ROCK(er)/p-Mypt1 expression, as cessation of 4HT treatment induced disorganized tissue architecture and p21-associated differentiation in wdSCCs; yet tenascin C retention in connective tissue extracellular matrix suggests the rigidity laid down for conversion persists. Novel papilloma outgrowths appeared expressing intense, basal layer p21 that confined endogenous ROCK2/p-Mypt1/NF-κB to supra-basal layers, and was paralleled by restored basal layer p53. In later SCCs, 4HT cessation became irrelevant as endogenous ROCK2 expression increased, driving progression via p21 loss, elevated NF-κB expression and tenascin C-associated rigidity, with p-Mypt1 inactivation/actinomyosin-mediated contractility to facilitate invasion. However, p21-associated inhibition of early-stage malignant progression and the intense expression in papilloma outgrowths, identifies a novel, significant antagonism between p21 and ras(Ha)/ROCK2/NF-κB signalling in skin carcinogenesis. Collectively, these data show that ROCK2 activation induces malignancy in ras(Ha)-initiated/promoted papillomas in the context of p53 loss and novel NF-κB expression, whereas increased tissue rigidity and cell motility/contractility help mediate tumour progression.
    Matched MeSH terms: Cell Transformation, Neoplastic/genetics
  17. Mustafa Z, Shamsuddin HS, Ideris A, Ibrahim R, Jaafar H, Ali AM, et al.
    Biomed Res Int, 2013;2013:248507.
    PMID: 23586025 DOI: 10.1155/2013/248507
    Oncolytic viruses have been extensively evaluated for anticancer therapy because this virus preferentially infects cancer cells without interfering with normal cells. Newcastle Disease Virus (NDV) is an avian virus and one of the intensively studied oncolytic viruses affecting many types of cancer including glioma. Nevertheless, the capability of NDV infection on heterogeneous glioma tissue in a cerebrospinal fluid atmosphere has never been reported. Recently, Rac1 is reported to be required for efficient NDV replication in human cancer cells and established a link between tumourigenesis and sensitivity to NDV. Rac1 is a member of the Rho GTPases involved in the regulation of the cell migration and cell-cycle progression. Rac1 knockdown leads to significant inhibition of viral replication. In this work, we demonstrated that NDV treatment led to significant reduction of tumour tissue viability of freshly isolated heterogeneous human brain tumour slice, known as an ex vivo glioma acute slice (EGAS). Analysis of gene expression indicated that reduced tissue viability was associated with downregulation of Rac1. However, the viability reduction was not persistent. We conclude that NDV treatment induced EGAS viability suppression, but subsequent downregulation of Rac1 gene may reduce the NDV replication and lead to regrowth of EGAS tissue.
    Matched MeSH terms: Cell Transformation, Neoplastic
  18. Siar CH, Mah MC, Gill PP
    Eur Arch Otorhinolaryngol, 2012 Mar;269(3):999-1004.
    PMID: 21789676 DOI: 10.1007/s00405-011-1712-x
    Early detection of oral potentially malignant epithelial lesions (PMELs) is aimed at improving survival rates as carcinogenesis is a multistep process and prevention is possible if these lesions are detected at an early and reversible stage of the disease. A prospective clinical study aimed at determining the prevalence of bilateral 'mirror-image' oral PMELs was carried out. Sample consisted of 32 (53.3%) Indians, 23 (38.3%) Chinese, 4 (6.7%) Malays and one (1.7%) Nepalese. All had histopathological confirmation of their primary existing PMEL as inclusion criteria. A total of 70 primary lesions were detected. The most common PMEL found was oral lichen planus. Of these, 28 (46.7%) patients exhibited bilateral 'mirror-image' lesions (n = 42) either synchronously (n = 32/42) or metachronously (n = 10/42). The remaining 32 (53.3%) patients had normal-looking contralateral mucosa. Present findings suggest that patients presenting with oral PMELs are at greater risk of developing a second lesion, most probably in the contralateral 'mirror-image' site.
    Matched MeSH terms: Cell Transformation, Neoplastic
  19. Yaacob HB, Tan PL, Ngeow WC
    J Oral Sci, 2002 Jun;44(2):65-71.
    PMID: 12227497
    The objective of this study was to determine the socio-demography (age, race and gender) of a group of Malaysian patients who were diagnosed as suffering from oral lichen planus (OLP). The occurrence of malignancy was also investigated. A total of 77 clinical and biopsy records of patients with OLP were studied. Females were affected more than males, with the female to male ratio being 2:1. Middle-aged Indian and Chinese females tend to be affected by OLP when compared with the rest of the population. Only 19 patients returned for further follow-up. One adult Indian female with a six-year history of lichenoid reaction showed the presence of malignancy.
    Matched MeSH terms: Cell Transformation, Neoplastic
  20. Jayaram G, Looi LM
    Malays J Pathol, 1994 Jun;16(1):83-7.
    PMID: 16329582
    A five-month-old male baby presented with an abdominal mass which was found on computerised tomography (CT) to be involving the left kidney. Nephrectomy and histopathological study showed morphological featues of a malignant rhabdoid tumour. The tumour cells stained strongly for cytokeratin and epithelial membrane antigen and less intensely for vimentin. Electron microscopy revealed concentric whorled arrays of intermediate filaments within the tumour cell cytoplasm. The child was put on post-operative chemotherapy and radiotherapy but developed bilateral lung metastases and died three months after surgery.
    Matched MeSH terms: Cell Transformation, Neoplastic
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