Displaying publications 1 - 20 of 86 in total

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  1. Sathasivam HP, Casement J, Bates T, Sloan P, Thomson P, Robinson M, et al.
    J Oral Pathol Med, 2021 Jan;50(1):60-67.
    PMID: 32740996 DOI: 10.1111/jop.13090
    BACKGROUND: A large number of oral squamous cell carcinomas (OSCCs) are believed to be preceded by oral potentially malignant disorders (OPMD) that have an increased likelihood of malignant transformation compared to clinically normal mucosa. This study was performed to identify differentially expressed genes between OPMDs that underwent malignant transformation (MT) and those that did not, termed "non-transforming" (NT) cases.

    METHODS: Total RNA was extracted from formalin-fixed paraffin-embedded tissue biopsies of 20 OPMD cases with known clinical outcomes (10 MT vs. 10 NT). Samples were assessed for quantity, quality and integrity of RNA prior to sequencing. Analysis for differential gene expression between MT and NT was performed using statistical packages in R. Genes were considered to be significantly differentially expressed if the False Discovery Rate corrected P-value was  1.90). Analysis of RNA-Sequencing outputs revealed 41 genes (34 protein-coding; 7 non-coding) that were significantly differentially expressed between MT and NT cases. The log2 fold change for the statistically significant differentially expressed genes ranged from -2.63 to 2.48, with 23 protein-coding genes being downregulated and 11 protein-coding genes being upregulated in MT cases compared to NT cases.

    CONCLUSION: Several candidate genes that may play a role in malignant transformation of OPMD have been identified. Experiments to validate these candidates are underway. It is anticipated that this work will contribute to better understanding of the etiopathogenesis of OPMD and development of novel biomarkers.

    Matched MeSH terms: Cell Transformation, Neoplastic/genetics
  2. Gan CP, Lee BKB, Lau SH, Kallarakkal TG, Zaini ZM, Lye BKW, et al.
    Front Immunol, 2022;13:954567.
    PMID: 36119104 DOI: 10.3389/fimmu.2022.954567
    Oral potentially malignant disorders (OPMD) are precursors of oral squamous cell carcinoma (OSCC), and the presence of oral epithelial dysplasia (OED) in OPMD confers an increased risk of malignant transformation. Emerging evidence has indicated a role for the immune system in OPMD disease progression; however, the underlying immune mechanisms remain elusive. In this study, we used immune signatures established from cancer to delineate the immune profiles of moderate and severe OED, which are considered high-risk OPMD. We demonstrated that moderate and severe OEDs exhibit high lymphocyte infiltration and upregulation of genes involved in both immune surveillance (major histocompatibility complex-I, T cells, B cells and cytolytic activity) and immune suppression (immune checkpoints, T regulatory cells, and tumor-associated macrophages). Notably, we identified three distinct subtypes of moderate and severe OED: immune cytotoxic, non-cytotoxic and non-immune reactive. Active immune surveillance is present in the immune cytotoxic subtype, whereas the non-cytotoxic subtype lacks CD8 immune cytotoxic response. The non-immune reactive subtype showed upregulation of genes involved in the stromal microenvironment and cell cycle. The lack of T cell infiltration and activation in the non-immune reactive subtype is due to the dysregulation of CTNNB1, PTEN and JAK2. This work suggests that moderate and severe OED that harbor the non-cytotoxic or non-immune reactive subtype are likely to progress to cancer. Overall, we showed that distinct immune responses are present in high-risk OPMD, and revealed targetable pathways that could lead to potential new approaches for non-surgical management of OED.
    Matched MeSH terms: Cell Transformation, Neoplastic/genetics
  3. Lee JY, Bhandare RR, Boddu SHS, Shaik AB, Saktivel LP, Gupta G, et al.
    Biomed Pharmacother, 2024 Apr;173:116275.
    PMID: 38394846 DOI: 10.1016/j.biopha.2024.116275
    Tumour suppressor genes play a cardinal role in the development of a large array of human cancers, including lung cancer, which is one of the most frequently diagnosed cancers worldwide. Therefore, extensive studies have been committed to deciphering the underlying mechanisms of alterations of tumour suppressor genes in governing tumourigenesis, as well as resistance to cancer therapies. In spite of the encouraging clinical outcomes demonstrated by lung cancer patients on initial treatment, the subsequent unresponsiveness to first-line treatments manifested by virtually all the patients is inherently a contentious issue. In light of the aforementioned concerns, this review compiles the current knowledge on the molecular mechanisms of some of the tumour suppressor genes implicated in lung cancer that are either frequently mutated and/or are located on the chromosomal arms having high LOH rates (1p, 3p, 9p, 10q, 13q, and 17p). Our study identifies specific genomic loci prone to LOH, revealing a recurrent pattern in lung cancer cases. These loci, including 3p14.2 (FHIT), 9p21.3 (p16INK4a), 10q23 (PTEN), 17p13 (TP53), exhibit a higher susceptibility to LOH due to environmental factors such as exposure to DNA-damaging agents (carcinogens in cigarette smoke) and genetic factors such as chromosomal instability, genetic mutations, DNA replication errors, and genetic predisposition. Furthermore, this review summarizes the current treatment landscape and advancements for lung cancers, including the challenges and endeavours to overcome it. This review envisages inspired researchers to embark on a journey of discovery to add to the list of what was known in hopes of prompting the development of effective therapeutic strategies for lung cancer.
    Matched MeSH terms: Cell Transformation, Neoplastic/genetics
  4. 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*
  5. 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: Cell Transformation, Neoplastic
  6. Zainina S, Cheong SK
    Clin Lab Haematol, 2006 Aug;28(4):282-3.
    PMID: 16898972
    Myelodysplastic syndrome (MDS) is recognized as a preleukaemic disorder with a variable risk of transformation to acute myeloid leukaemia. Usually the blast cells in leukaemia are transformed after MDS displays a myeloid phenotype. Even though lymphoid progression had been reported previously, most displayed myeloid-lymphoid hybrid or early B phenotype. We report a case of an elderly man who had MDS transformed into Acute Lymphoblastic Leukaemia (ALL:L3) which is a rare lymphoid transformation.
    Matched MeSH terms: Cell Transformation, Neoplastic/pathology*
  7. Misron NA, Looi LM, Nik Mustapha NR
    Asian Pac J Cancer Prev, 2015;16(4):1553-8.
    PMID: 25743830
    BACKGROUND: COX-2 has been shown to play an important role in the development of breast cancer and increased expression has been mooted as a poor prognostic factor. The purpose of this study was to investigate the relationship between COX-2 immunohistochemical expression and known predictive and prognostic factors in breast cancer in a routine diagnostic histopathology setting.

    MATERIALS AND METHODS: Formalin-fixed paraffin- embedded tumour tissue of 144 no special type (NST) invasive breast carcinomas histologically diagnosed between January 2009 and December 2012 in Hospital Sultanah Bahiyah, Alor Setar, Kedah were immunostained with COX-2 antibody. COX-2 overexpression was analysed against demographic data, hormone receptor status, HER2- neu overexpression, histological grade, tumour size and lymph node status.

    RESULTS: COX-2 was overexpressed in 108/144 (75%) tumours and was significantly more prevalent (87%) in hormone receptor-positive tumours. There was no correlation between COX-2 overexpression and HER2/neu status. Triple negative cancers had the lowest prevalence (46%) (p<0.05). A rising trend of COX-2 overexpression with increasing age was observed. There was a significant inverse relationship with tumour grade (p<0.05), prevalences being 94%, 83% and 66% in grades 1, 2 and 3 tumours, respectively. A higher prevalence of COX-2 overexpression in smaller size tumours was observed but this did not reach statistical significance. There was no relationship between COX-2 expression and lymph node status.

    CONCLUSIONS: This study did not support the generally held notion that COX-2 overexpression is linked to poor prognosis, rather supporting a role in tumorigenesis. Larger scale studies with outcome data and basic studies on cancer pathogenetic pathways will be required to cast further light on whether COX-2 inhibitors would have clinical utility in cancer prevention or blockage of cancer progression. In either setting, the pathological assessment for COX-2 overexpression in breast cancers would have an important role in the selection of cancer patients for personalized therapy with COX-2 inhibitors.

    Matched MeSH terms: Cell Transformation, Neoplastic/metabolism; Cell Transformation, Neoplastic/pathology*
  8. Kumar SK, Zain RB, Ismail SM, Cheong SC
    J Exp Clin Cancer Res, 2005 Dec;24(4):639-46.
    PMID: 16471328
    Human telomerase reverse transcriptase (hTERT), the catalytic subunit of telomerase, is strongly associated with telomerase activity implicated in cellular immortalization and tumorigenesis. In situ detection of hTERT will aid in determining the localization of telomerase positive cells. The aim of this study was to detect hTERT protein expression in multistep oral carcinogenesis using paraffin embedded tissue samples, and to study the relationship of hTERT expression with different histological stages in oral carcinogenesis. Normal (n = 4), hyperplastic (n = 4), dysplastic (n = 4) and neoplastic (n = 10) oral epithelia representing different histological stages in oral carcinogenesis were included in the study. hTERT protein detection was done by immunohistochemistry (IHC) technique. Nuclear staining intensities were noted and the hTERT-labelling index was determined. Dysplastic and neoplastic oral epithelia showed an increased percentage of hTERT positive cells (Grade 4: > 50% positive staining nuclei) with intense staining in the basal, parabasal and superficial layers of the epithelia, unlike normal oral mucosa which showed intense staining only in the basal and parabasal cell layers, which are the normal proliferative progenitor compartments. hTERT protein expression was elevated with the corresponding advancement of the histological stages of oral carcinogenesis, from normal to hyperplasia to dysplasia to carcinoma. There seems to be an upregulation of hTERT protein expression during the progression of oral cancer, therefore, this may indicate the feasibility of IHC detection of hTERT protein in oral carcinogenesis as a potential diagnostic or prognostic marker.
    Matched MeSH terms: Cell Transformation, Neoplastic/metabolism*; Cell Transformation, Neoplastic/pathology
  9. Sathasivam HP, Kist R, Sloan P, Thomson P, Nugent M, Alexander J, et al.
    Br J Cancer, 2021 Aug;125(3):413-421.
    PMID: 33972745 DOI: 10.1038/s41416-021-01411-z
    BACKGROUND: This study was undertaken to develop and validate a gene expression signature that characterises oral potentially malignant disorders (OPMD) with a high risk of undergoing malignant transformation.

    METHODS: Patients with oral epithelial dysplasia at one hospital were selected as the 'training set' (n = 56) whilst those at another hospital were selected for the 'test set' (n = 66). RNA was extracted from formalin-fixed paraffin-embedded (FFPE) diagnostic biopsies and analysed using the NanoString nCounter platform. A targeted panel of 42 genes selected on their association with oral carcinogenesis was used to develop a prognostic gene signature. Following data normalisation, uni- and multivariable analysis, as well as prognostic modelling, were employed to develop and validate the gene signature.

    RESULTS: A prognostic classifier composed of 11 genes was developed using the training set. The multivariable prognostic model was used to predict patient risk scores in the test set. The prognostic gene signature was an independent predictor of malignant transformation when assessed in the test set, with the high-risk group showing worse prognosis [Hazard ratio = 12.65, p = 0.0003].

    CONCLUSIONS: This study demonstrates proof of principle that RNA extracted from FFPE diagnostic biopsies of OPMD, when analysed on the NanoString nCounter platform, can be used to generate a molecular classifier that stratifies the risk of malignant transformation with promising clinical utility.

    Matched MeSH terms: Cell Transformation, Neoplastic/genetics; Cell Transformation, Neoplastic/pathology*
  10. Wynn, Aye Aye, Myint, Ohnmar, Mya, Nang Khin
    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: Cell Transformation, Neoplastic
  11. 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: Cell Transformation, Neoplastic
  12. 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
  13. 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
  14. 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
  15. Muhammad Fauzi HG, Mohan Singh AS, Abdul Rahim S, Chooi LL, Ramasamy V, Mohamad Pakarul Razy NH, et al.
    Gulf J Oncolog, 2021 May;1(36):79-81.
    PMID: 35017141
    Malignant transformation of recurrent respiratory papillomatosis (RRP) is a rare entity occurring in only less than 5% of patients with RRP. The risk of transformation can arise even in the absence of risk factors such as smoking and radiation. We describe a patient with juvenile RRP diagnosed since childhood, who suffered malignant transformation into a squamous cell carcinoma after 29 years. Keywords: Recurrent respiratory papillomatosis; laryngeal neoplasms; squamous cell carcinoma; human papilloma-virus.
    Matched MeSH terms: Cell Transformation, Neoplastic
  16. 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: Cell Transformation, Neoplastic
  17. Akhir MKAM, Choy CS, Abdullah MA, Ghani FA, Veerakumarasivam A, Hussin H
    Malays J Med Sci, 2020 Feb;27(1):37-45.
    PMID: 32158343 MyJurnal DOI: 10.21315/mjms2020.27.1.4
    Introduction: Lin-11, Isl-1 and Mec-3 domains (LIM) homeobox genes are among the most important sub-families of homeobox genes. These genes are thought to play an important role in cancer. In this study, the protein expression of these genes was examined in urothelial carcinoma of the bladder. The expression pattern of Islet-1 (ISL1) and LIM homeobox 5 (LHX5) across different cancer stages and grades, as well as the association between the protein expression of these genes and patient demographics and clinicopathological features, were examined.

    Methods: A total of 100 formalin-fixed paraffin-embedded urothelial carcinoma tissues were selected from the Department of Pathology, Hospital Kuala Lumpur and the protein expression of ISL1 and LHX5 was determined using immunohistochemistry.

    Results: Positive expression of ISL1 and LHX5 was detected in 94% and 98% of the samples, respectively. There were no distinct LHX5 expression patterns associated with different cancer stages, but the proportion of high-expressing tumours was higher in high-grade tumours. In addition, there was a significant association between the expression of LHX5 and tumour grade. The proportion of tumours expressing high levels of ISL1 was found to be highest in later stage tumours.

    Conclusion: The high percentage of tumours expressing both these genes suggests that ISL1 and LHX5 play an important role in bladder tumourigenesis across multiple stages.

    Matched MeSH terms: Cell Transformation, Neoplastic
  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. Chong LA, Josephine P, Ariffin H
    Med J Malaysia, 2006 Jun;61(2):236-8.
    PMID: 16898320 MyJurnal
    We report a case of a child with severe congenital neutropenia (Kostmann's syndrome) who was treated with daily prophylactic subcutaneous granulocyte colony-stimulating factor (G-CSF) from the age of eight to sixteen years before being discontinued for poor haematological and clinical response. She did not have a HLA-matched sibling to enable bone marrow transplantation. She subsequently developed acute megakaryoblastic leukemia at the age of 17 years and succumbed during induction chemotherapy. The role of G-CSF in the pathogenesis of her malignant transformation to AML is complicated as this disorder has a propensity for myelodysplasia or AML as part of its natural history.
    Matched MeSH terms: Cell Transformation, Neoplastic/pathology*
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