Displaying publications 1 - 20 of 66 in total

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  1. Looi LM, Azura WW, Cheah PL, Ng MH
    Pathology, 2001 Aug;33(3):283-6.
    PMID: 11523925
    This investigation was carried out to gain insight into the prevalence of pS2 expression in invasive ductal breast carcinoma in the Malaysian population and its correlation with oestrogen receptor (ER) protein expression and tumour aggressiveness. Seventy consecutive infiltrating ductal breast carcinomas treated with mastectomy and axillary lymph node clearance were investigated, using the standard avidin-biotin complex immunoperoxidase method with microwave antigen retrieval and commercial monoclonal antibodies (Dako), for expression of pS2 and human ER. This was correlated against histological grade (modified Bloom and Richardson) and the presence of axillary lymph node metastasis of these carcinomas. Four (5.7%) were grade 1, 40 (57.1%) grade 2 and 26 (37.1%) grade 3 tumours. A total of 45 (64%) showed histological evidence of axillary lymph node metastasis. Forty (57%) were ER-positive, while 31 (44%) were pS2-positive. There was a statistically significant correlation between pS2 and ER expressions (chi2-test with Yates correction: P<0.005). There was no correlation between pS2 expression and histological grade (P>0.1) and the presence of lymph node metastasis (P>0.1). Our findings support the views that pS2 may be a co-marker of endocrine responsiveness in invasive breast cancer and that it does not influence breast cancer biology in terms of potential for metastatic spread.
    Matched MeSH terms: Breast Neoplasms/pathology; Lymph Nodes/pathology
  2. Hoe SL, Lee ES, Khoo AS, Peh SC
    Pathology, 2009;41(6):561-5.
    PMID: 19900105
    AIMS: Nasopharyngeal carcinoma (NPC) is a common malignancy among men in Malaysia. To determine the role of p53 in NPC, we screened for p53 mutations and evaluated the protein expression levels in samples from local patients with NPC.

    METHODS: Fifty-three formalin-fixed, paraffin-embedded nasopharyngeal carcinoma tissue blocks were chosen for this study. The presence of Epstein-Barr virus (EBV) was determined by in situ hybridisation using an EBER probe. p53 protein expression was detected using immunohistochemistry. Simultaneously, amplifications by PCR were performed for p53 exons 5 to 8, followed by mutation screening via single strand conformation polymorphism (SSCP). Sequencing of all the four exons was performed in five samples with mobility shift. To rule out false negative results by SSCP, 13 samples with p53 overexpression and five samples with low p53 expression were randomly selected and sequenced.

    RESULTS: There was no mutation found in exons 5 to 8 in all the samples despite 46 (87%) of them having high p53 levels. EBV was detected in 51 (96%) out of 53 samples. There was no statistically significant association between p53 expression level and EBV presence.

    CONCLUSIONS: High-intensity staining for p53 by immunohistochemistry was common in our series of NPC tissue samples but was not associated with 'hot spot' mutations of exons 5-8 of the gene. We did not find a significant relationship between the expression level of p53 and presence of EBV. Our study confirms that mutation of the DNA-binding domain of p53 is rare in NPC.

    Matched MeSH terms: Adenocarcinoma/pathology; Nasopharyngeal Neoplasms/pathology; Epstein-Barr Virus Infections/pathology
  3. Shaminie J, Peh SC, Tan J
    Pathology, 2005 Feb;37(1):39-44.
    PMID: 15875732
    AIM: Tumour suppressor gene p53 is a common target in carcinogenesis, reported to be altered and functionally inactive in 70% of human cancers. Although p53 mutations are less commonly present in haematological malignancies when compared with other solid tumours, they have been reported in histological transformation of follicular lymphoma. We aimed to investigate the frequency of p53 gene alterations in paraffin-embedded tissue using commercially available PCR-SSCP, and to correlate the results with P53 protein expression by immunohistochemistry.

    METHODS: Surgical samples from seven patients with a total of 17 sequential biopsies were retrieved for the study of p53 gene expression using immunohistochemical stain, and gene status by PCR-SSCP for exons 5-8. The tumours were graded according to the WHO classification criteria. P53 was distinctly over-expressed in five transformed higher grade biopsies, and all except one showed electrophoretic mobility shift in PCR-SSCP analysis. Sequencing analysis revealed single nucleotide substitutions in three of four of these high-grade transformed cases with band shift (75%), whereas some other studies reported a lower frequency of 25-30%, and mobility shift result was found to correlate with P53 expression. Lower grade tumours without P53 over-expression did not demonstrate band shift, and sequencing analysis did not reveal mutations.

    CONCLUSIONS: We demonstrated the feasibility of adopting PCR-SSCP for screening of p53 mutations in archival tissue samples in this study, and there is a strong correlation of p53 gene over-expression and mutation events in high-grade transformed tumours.

  4. Masir N, Jones M, Abdul-Rahman F, Florence CS, Mason DY
    Pathology, 2012 Apr;44(3):228-33.
    PMID: 22406486 DOI: 10.1097/PAT.0b013e3283513fb2
    The hallmark of follicular lymphoma is the t(14;18)(q32;q21) chromosomal translocations that lead to deregulation of BCL2 expression in tumour cells. However, not all cases of follicular lymphoma express BCL2, nor is the t(14;18) translocation always present. Follicular lymphomas lacking the BCL2 rearrangement are less well studied with regards to their immunohistochemical and molecular features. This study aims to investigate the BCL2 protein expression pattern in t(14;18) negative follicular lymphomas.
    Matched MeSH terms: Lymphoma, Follicular/pathology; Trisomy/pathology
  5. Rajandram R, Yap NY, Pailoor J, Razack AH, Ng KL, Ong TA, et al.
    Pathology, 2014 Oct;46(6):518-22.
    PMID: 25158810 DOI: 10.1097/PAT.0000000000000145
    Renal cell carcinoma (RCC) generally has a poor prognosis because of late diagnosis and metastasis. We have previously described decreased tumour necrosis factor receptor-associated factor-1 (TRAF-1) in RCC compared with paired normal kidney in a patient cohort in Australia. In the present study, TRAF-1 expression in clear cell RCC (ccRCC) and normal kidney was again compared, but in a cohort from University Malaya Medical Centre. Serum TRAF-1 was also evaluated in RCC and normal samples.Immunohistochemistry with automated batch staining and Aperio ImageScope morphometry was used to compare TRAF-1 in 61 ccRCC with paired normal kidney tissue. Serum from 15 newly diagnosed and untreated ccRCC and 15 healthy people was tested for TRAF-1 using ELISA.In this cohort, TRAF-1 was highly expressed in proximal tubular epithelium of normal kidney, and significantly decreased in ccRCC tissue (p 
  6. Wong SF, Lai LC
    Pathology, 2001 Feb;33(1):85-92.
    PMID: 11280615
    Transforming growth factor beta (TGFbeta) is secreted as a large latent precursor from both normal and transformed cells which needs to be activated for biological activity. The active TGFbeta binds either directly to TbetaR-II or indirectly by binding to beta-glycan which then presents the TGFbeta to TbetaR-II. Formation of the TGFbeta-TbetaR-II complex rapidly leads to phosphorylation of TbetaR-I. TbetaR-I, in turn, phosphorylates receptor-specific Smads and induces their translocation into the nucleus. TGFbeta is able to act as a growth stimulator or inhibitor and elicits a broad spectrum of biological effects on various cell types. However, these cells may lose their sensitivity and responsiveness to TGFbeta. Down-regulation or loss of functional receptors, aberrant signal transduction pathways due to Smad mutations, loss of the cell's ability to activate latent TGFbeta, loss of the peptide itself or functional genes that control the transcription and translation of TGFbeta may contribute to development of cancer.
  7. Kim LH, Eow GI, Peh SC, Poppema S
    Pathology, 2003 Oct;35(5):428-35.
    PMID: 14555388
    AIMS: CD30, CD40 and CD95 are members of the tumour necrosis factor receptor superfamily. Ligation to their respective ligands (CD30L, CD40L, CD95L) will generate a diverse set of signalling cascades. We aim to study the expression pattern of CD30, CD40 and CD95 in classical Hodgkin's lymphoma (cHL) and to correlate the expressions with proliferation and apoptosis in the Hodgkin/Reed-Sternberg (H/RS) cells of cHL with or without associated Epstein-Barr virus (EBV) infection.

    METHODS: A total of 66 cHL cases were retrieved from the archives. Expressions of CD30, CD40, CD95 and proliferation by Ki-67 expression were detected with an immunohistochemical staining method. Apoptosis index was assessed by in situ TUNEL staining technique on 30 randomly selected cases and the presence of EBV was determined by EBER in situ hybridisation.

    RESULTS: Expression of CD30, CD40 and CD95 in the H/RS cells was observed in a high proportion of the cases (100, 93.9, 90.5%, respectively). There was no significant association or correlation of the expression of these molecules with the presence of EBV. Expression of CD40 was associated with expression of the proliferation marker Ki-67 (P=0.044), whereas strong (intermediate and high) expression of CD30 showed a significant correlation with proliferation in the EBV-negative cases only (P=0.025). No correlation was observed for the expression of CD30 and CD40 with apoptosis of the H/RS cells. The childhood cases showed weaker CD95 expression in the H/RS cells than the adult cases, and the expression of CD95 was weaker than that of CD40 in the childhood group.

    CONCLUSIONS: Our results showed that CD30, CD40 and CD95 are highly expressed in the H/RS cells of the majority of cases of cHL. The expression patterns seem to be independent of EBV and do not correlate with apoptosis of the H/RS cells.

    Matched MeSH terms: Hodgkin Disease/pathology; Reed-Sternberg Cells/pathology; Pseudolymphoma/pathology
  8. Premasiri MK, Lee YS
    Pathology, 2003 Oct;35(5):409-13.
    PMID: 14555385
    AIMS: This study attempts to determine the type and relative frequency of muscle diseases contributing to floppy and hypotonic infants in Singapore.

    METHODS: Eighty consecutive muscle biopsies in the Department of Pathology, National University of Singapore, in the period 1978-2000, in which a clinical diagnosis of floppy or hypotonic infant was made, were reviewed.

    RESULTS: The commonest cause of severe hypotonia in infancy was spinal muscular atrophy, which accounted for 33% of cases followed by congenital muscular dystrophy (13%). Eight cases (10%) of infantile type II glycogenosis (Pompe's disease) were encountered. There were seven cases of congenital myopathy, of which four were centronuclear myopathy, and one each of central core myopathy, nemaline myopathy and congenital fibre type disproportion. One case of centronuclear myopathy was associated with type I fibre smallness. Type II atrophy, which is generally considered a non-specific change, was encountered in five cases. Of interest is the relatively large number of muscle biopsies (29%) in which no significant pathological features were encountered at the light microscopic, histochemical as well as ultra-structural level.

    CONCLUSIONS: The study has revealed a great variety of pathology affecting the muscle of children presenting as floppy infants or with hypotonia. The muscle diseases included spinal muscular atrophy, congenital muscular dystrophies, congenital myopathies and metabolic myopathies. However, 23 (29%) cases showed no significant pathology. For this group of floppy and hypotonic infants further studies are needed.

    Matched MeSH terms: Muscle Hypotonia/pathology*; Muscular Diseases/pathology*; Spinal Muscular Atrophies of Childhood/pathology; Muscle, Skeletal/pathology*
  9. Denize T, Irtan S, Tabone MD, Coulomb A, Gharbi S, Ducou Le Pointe H, et al.
    Pathology, 2023 Oct;55(6):890-892.
    PMID: 37393145 DOI: 10.1016/j.pathol.2023.03.015
    Matched MeSH terms: Abdomen/pathology; Pancreas/pathology
  10. Jayaranee S, Sthaneshwar P, Sokkalingam S
    Pathology, 2009 Feb;41(2):178-82.
    PMID: 18972320 DOI: 10.1080/00313020802436840
    AIM: Hepcidin, a recently identified peptide, acts as a central regulator of iron metabolism. It is regarded as a factor regulating the uptake of dietary iron and its mobilisation from macrophages and hepatic stores. It is considered as a mediator of anaemia of inflammation. The aim of this study was to assess whether serum prohepcidin concentration is able to distinguish iron deficiency from anaemia of inflammation in patients with rheumatoid arthritis (RA).

    METHOD: Blood samples were obtained from 20 healthy blood donors, 30 RA patients who presented with anaemia and 30 patients who had pure iron deficiency anaemia (IDA). The samples were analysed for full blood count, iron, ferritin, transferrin, soluble transferrin receptor and prohepcidin.

    RESULTS: The mean prohepcidin level in the control subjects was 256 microg/L. The prohepcidin level was significantly lower in IDA patients (100 microg/L; p < 0.0001) but not significantly different from that of control in RA patients (250 microg/L; p > 0.05). Higher serum soluble transferrin receptor (sTfR) levels were observed in IDA (p < 0.0001) but not in RA compared with that of control (p > 0.05). RA patients were divided into iron depleted and iron repleted subgroups based on the ferritin level. Prohepcidin in the iron depleted group was significantly lower than the iron repleted group and the control (p < 0.0001) and higher levels were observed in the iron repleted group (p < 0.01). sTfR levels in the iron depleted group were significantly higher than the control and the iron repleted patients (p < 0.001). In the iron repleted group, sTfR level was not statistically different from that of control (p > 0.05).

    CONCLUSION: Serum prohepcidin is clearly reduced in uncomplicated iron deficiency anaemia. The reduced prohepcidin levels in the iron depleted RA patients suggests that there may be conflicting signals regulating hepcidin production in RA patients. In RA patients who have reduced hepcidin in the iron depleted group (ferritin <60 microg/L) where sTfR levels are increased suggests that these patients are iron deficient. Further studies with a larger cohort of patients are required to substantiate this point.

  11. Wong MS, Chew WL, Aw TC
    Pathology, 1999 Aug;31(3):225-9.
    PMID: 10503268
    Lipoprotein(a) [Lp(a)] is formed when apolipoprotein(a) is linked to low density lipoprotein (LDL)-cholesterol via a single disulfide bond. It is an independent risk factor for myocardial infarction and raised concentrations are associated with an increased risk of developing coronary artery disease. Singapore has a multi-racial population of 77% Chinese, 14% Malays and 7% Indians. Studies have shown that the Indians have significantly higher standardised mortality ratios (SMR) compared to the Chinese and the Malays. We measured serum Lp(a) concentrations in 803 healthy individuals recruited from the Multiphasic Health Screening Programme, using the Macra Lp(a) sandwich enzyme immunoassay kit (Strategics Diagnostics, Delaware, USA). Lp(a) concentrations were skewed in all three groups. Our population mean was 9.0 mg/dl, with 50th, 75th and 95th percentile values of 10.2, 19.8 and 43.1 mg/dl, respectively, which are lower than values reported from Caucasian populations (15.0, 29.0 and 60.0 mg/dl, respectively). Males had lower Lp(a) concentrations than females (P < 0.05). The Indian group had significantly higher concentrations (median 12.3 mg/dl) compared to their Chinese (median 9.6 mg/dl) and Malay (median 8.4 mg/dl) counterparts (P < 0.05). This could partly account for the higher SMR seen in the Indian population in Singapore. As serum Lp(a) concentrations are method- and population-dependent, we recommend that laboratories determine their own reference ranges by their method to avoid misclassification of the coronary heart disease (CHD) risk of patients.
  12. Mohamad Zaki FH, Nik Hussain NH, Ismail P, Wan Yusoff WZ, Othman NH
    Pathology, 2016 Feb;48 Suppl 1:S148.
    PMID: 27772923 DOI: 10.1016/j.pathol.2015.12.402
    Background: The major problem with cervical cancer screening in countries which have no organized national screening program for cervical cancer is sub-optimal participation. Implementation of self-sampling method may increase the participation of women to screen for cervical cancer.
    Aims: To determine the agreement of cytological diagnoses made on samples collected by women themselves (self-sampling) versus cytological diagnoses made on samples collected
    by physicians (Physician sampling)
    Methods: We invited women volunteers to undergo two procedures; cervical self-sampling using the Evalyn brush and physician scraping using Cervex brush. They women were
    shown a video presentation on how to take their own cervical samples before the procedure. The samples taken by physicians were taken as per routine testing (Gold Standard). All
    samples were subjected to Thin Prep monolayer smears. The diagnoses made were according to the Bethesda classification. The results from the two sampling methods were analysed and compared.
    Results: A total of 367 women were recruited into the study. Thin Prep smears by physicians were better in terms of volume and variety of the cells seen. There is significant good agreement of the cytological diagnoses made on the samples from the two sampling methods with the Kappa value of 0.568 (p=0.040). The Thin Prep smears by self-sampling method were better in detecting microorganisms.
    Conclusion: This study shows that samples taken by women themselves (self-sampling) and physicians sampling had good cytology agreement. Self-sampling could be the method of
    choice in countries in which the coverage of women attending clinics for screening for cervical cancer is poor.
  13. Salman IM, Ameer OZ, Sattar MA, Abdullah NA, Yam MF, Najim HS, et al.
    Pathology, 2010 Apr;42(3):259-66.
    PMID: 20350220 DOI: 10.3109/00313021003631304
    We investigated the role of renal sympathetic innervation in the deterioration of renal haemodynamic and excretory functions during the early post-ischaemic phase of renal ischaemia/reperfusion injury.
  14. Sthaneshwar P, Jamaluddin FA, Fan YS
    Pathology, 2010;42(5):454-6.
    PMID: 20632822 DOI: 10.3109/00313025.2010.493861
    The aim of this study was to evaluate the distribution of cardiac troponin I (cTnI) values, measured by the ADVIA TnI-Ultra method in a multi-ethnic group and to determine the imprecision of the assay.
  15. Masir N, Campbell LJ, Jones M, Mason DY
    Pathology, 2010 Apr;42(3):212-6.
    PMID: 20350212 DOI: 10.3109/00313021003631296
    The t(14;18)(q32;q21) chromosomal translocation induces BCL2 protein expression in most follicular lymphomas. However, a small number of cases lack BCL2 expression despite carrying the t(14;18)(q32;q21) translocation. This study aims to explore the mechanism accounting for the lack of BCL2 protein expression when the t(14;18) translocation is present.
  16. Wong KK, Prepageran N, Peh SC
    Pathology, 2009 Feb;41(2):133-9.
    PMID: 18972319 DOI: 10.1080/00313020802436790
    AIMS: To stratify upper aerodigestive tract (UAT) diffuse large B-cell lymphoma (DLBCL) into prognostic subgroups by immunohistochemical staining (IHC) method, and to evaluate the association rate of UAT DLBCL with Epstein-Barr virus (EBV).

    METHODS: Using a panel of antibodies to CD10, Bcl-6, MUM1 and CD138, consecutive cases of primary UAT DLBCL were stratified into subgroups of germinal centre B-cell-like (GCB) and non-GCB, phenotype profile patterns A, B and C, as proposed by Hans et al. and Chang et al., respectively. EBER in situ hybridisation technique was applied for the detection of EBV in the tumours.

    RESULTS: In this series of 32 cases of UAT DLBCL, 34% (11/32) were GCB, and 66% (21/32) were non-GCB types; 59% (19/32) had combined patterns A and B, and 41% (13/32) had pattern C. Statistical analysis revealed no significant difference in the occurrence of these prognostic subgroups in the UAT when compared with series of de novo DLBCL from all sites. There was also no site difference in phenotype protein expressions, with the exception of MUM1. EBER in situ hybridisation stain demonstrated only one EBV infected case.

    CONCLUSIONS: Prognostic subgroup distribution of UAT DLBCL is similar to de novo DLBCL from all sites, and EBV association is very infrequent.

    Matched MeSH terms: Otorhinolaryngologic Neoplasms/pathology; Lymphoma, Large B-Cell, Diffuse/pathology
  17. Cheah PL, Looi LM
    Pathology, 2002 Aug;34(4):326-31.
    PMID: 12190289
    AIMS: The pattern of p53 expression was studied in pre-invasive and invasive cervical carcinoma in an attempt to clarify its role in cervical carcinogenesis.

    METHODS: A total of 234 invasive cervical carcinomas (152 squamous cell carcinomas, 61 adenocarcinomas and 21 adenosquamous carcinomas) and 16 cervical intraepithelial neoplasia (CIN) I, six CIN II and 25 CIN III were immunohistochemically studied for p53.

    RESULTS: p53 was detected more frequently in CIN and invasive carcinoma (100% of CIN I, 74.2% CIN II + III and 70.1% invasive carcinoma) compared with benign cervices (P< 0.001); however, only three squamous cell carcinomas, 11 adenocarcinomas and two adenosquamous carcinomas exhibited p53 expression in >75% of tumour nuclei. Six of the 11 adenocarcinomas and both adenosquamous carcinomas were poorly differentiated compared with one of the three squamous carcinomas. p53 immunoreactive cells were randomly distributed in invasive carcinoma, confined to the lower third of the epithelium in CIN I, reached the middle third in 20% of CIN II and upper third in 16.6% of CIN III.

    CONCLUSIONS: Assuming that p53 immunoreactivity indicates gene mutation when the majority (> 75%) of neoplastic cells express p53, p53 mutations would seem uncommon in cervical carcinogenesis. Nonetheless, glandular malignancies, in particular poorly differentiated variants, may show a higher frequency of mutation. p53 was detected more frequently in CIN I compared with CIN II/III and invasive carcinoma which may be due to p53 protein degradation following interaction with high risk human papillomavirus E6 protein in CIN II/III and invasive carcinoma.

    Matched MeSH terms: Uterine Cervical Neoplasms/pathology; Cervical Intraepithelial Neoplasia/pathology
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