Displaying publications 61 - 80 of 197 in total

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  1. Lim J, Bhoo-Pathy N, Sothilingam S, Malek R, Sundram M, Hisham Bahadzor B, et al.
    PLoS One, 2014;9(8):e104917.
    PMID: 25111507 DOI: 10.1371/journal.pone.0104917
    OBJECTIVES: To study the baseline PSA profile and determine the factors influencing the PSA levels within a multiethnic Asian setting.
    MATERIALS AND METHODS: We conducted a cross-sectional study of 1054 men with no clinical evidence of prostate cancer, prostate surgery or 5α-reductase inhibitor treatment of known prostate conditions. The serum PSA concentration of each subject was assayed. Potential factors associated with PSA level including age, ethnicity, height, weight, family history of prostate cancer, lower urinary tract voiding symptoms (LUTS), prostate volume and digital rectal examination (DRE) were evaluated using univariable and multivariable analysis.
    RESULTS: There were 38 men (3.6%) found to have a PSA level above 4 ng/ml and 1016 (96.4%) with a healthy PSA (≤4 ng/ml). The median PSA level of Malay, Chinese and Indian men was 1.00 ng/ml, 1.16 ng/ml and 0.83 ng/ml, respectively. Indians had a relatively lower median PSA level and prostate volume than Malays and Chinese, who shared a comparable median PSA value across all 10-years age groups. The PSA density was fairly similar amongst all ethnicities. Further analysis showed that ethnicity, weight and prostate volume were independent factors associated with age specific PSA level in the multivariable analysis (p<0.05).
    CONCLUSION: These findings support the concept that the baseline PSA level varies between different ethnicities across all age groups. In addition to age and prostate volume, ethnicity may also need to be taken into account when investigating serum PSA concentrations in the multiethnic Asian population.
    Matched MeSH terms: Prostatic Neoplasms/blood; Prostatic Neoplasms/diagnosis
  2. Guo W, Wu X, Li Y, Gao J, Wang F, Jin Y, et al.
    J Drug Target, 2020 01;28(1):41-45.
    PMID: 30943812 DOI: 10.1080/1061186X.2019.1601199
    Purpose: The present study evaluated biochemical as well as biophysical mechanisms behind the synergistic effects of curcumin and resveratrol during prostate carcinogenesis.Methods: The rats were segregated into five groups that included normal control, 3,2'-dimethyl-4-aminobiphenyl (DMAB)treated, DMAB + curcumin treated, DMAB + resveratrol-treated and DMAB + curcumin + resveratrol-treated.Results: The DMAB treatment resulted in a significant increase in the levels of lipid peroxidation (LPO) in DMAB treated rats. Also, significant changes were recorded in the enzyme activities of both drug metabolising enzyme and antioxidant enzymes after DMAB treatment. Further, radiorespirometric studies showed a significant increase in the 14C-glucose turnover as well as 14C-glucose uptake in the prostate slices of DMAB treated rats. Moreover, a significant rise in cell proliferation was confirmed indirectly by enhanced uptake of 3H-thymidine in the prostate slices of DMAB treated rats. Interestingly, combined treatment of curcumin and resveratrol to DMAB treated animals resulted in a significant decrease in lipid peroxidation, 14C glucose uptakes/turnover and 3H-thymidine uptake in the DMAB treated rats. Besides this, curcumin and resveratrol in combination significantly modulated biochemical indices including drug-metabolising enzymes; antioxidant enzymes in DMBA treated rats.Conclusion: The study, therefore, concludes that the combination of curcumin and resveratrol holds strong modulatory potential against prostate carcinogenesis.
    Matched MeSH terms: Prostatic Neoplasms/drug therapy*
  3. Ho CC, Khor TW, Singam P, Goh EH, Tan GH, Bahadzor B, et al.
    Clin Ter, 2012;163(3):211-4.
    PMID: 22964693
    OBJECTIVE: To evaluate power doppler ultrasonography (PDU)-directed prostate biopsy in patients with elevated serum prostate specific antigen (PSA) levels.
    MATERIALS AND METHODS: Men with serum total PSA levels of more than 4 ng/ml undergoing biopsy for the first time were included. Grey-scale transrectal ultrasound (TRUS) and PDU were performed. PDU signal on vascularity accumulation and perfusion characteristics were recorded and graded as normal or abnormal in the peripheral zone of the prostate. Abnormalities were defined on transverse image as radial or arc hypervascularities. A biopsy regime based on Vienna-normogram was performed in all patients.
    RESULTS: Overall, prostate adenocarcinoma detection rate was 21.4% and abnormal accumulation on PDU signal was identified in 96.7% of those patients (p = 0.01). PDU directed prostate biopsies were positive in 66.7% of the patients with prostate cancer. The sensitivity, specificity, positive predictive value and negative predictive value of PDU signal alone for prostate cancer detection was 96.7%, 24.5% and 96.4% respectively, and PDU guided biopsies were 66.7%, 24.5%, 19.4% and 73% respectively.
    CONCLUSIONS: The high sensitivity and negative predictive value of PDU makes it useful as an aid for TRUS biopsy in selected patient with previous negative biopsies at risk of harbouring prostate cancer.
    Matched MeSH terms: Prostatic Neoplasms/blood*; Prostatic Neoplasms/diagnosis*
  4. Heidari MH, Movafagh A, Abdollahifar MA, Abdi S, Barez MM, Azimi H, et al.
    Anat Cell Biol, 2017 Mar;50(1):69-72.
    PMID: 28417057 DOI: 10.5115/acb.2017.50.1.69
    Prostate cancer is the most common cancer type in men and is the second cause of death, due to cancer, in patients over 50, after lung cancer. Prostate specific antigen (PSA) is a widely used tumor marker for prostate cancer. Recently, PSA is discovered in non-prostatic cancer tissues in men and women raising doubts about its specificity for prostatic tissues. PSA exists in low serum level in healthy men and in higher levels in many prostate disorders, including prostatitis and prostate cancer. Thus, a supplementary tumor marker is needed to accurately diagnose the cancer and to observe the patient after treatment. Recently, soluble human leukocyte antigen-G (sHLA-G) has been introduced as a new tumor marker for different cancer types, including colorectal, breast, lung, and ovary. The present descriptive-experimental study was carried out including patients with malignant prostate tumor, patients with benign prostate tumor, and a group of health men as the control group, as judged by an oncologist as well as a pathologist. After sterile blood sampling, sHLA-G was measured by enzyme-linked immunosorbent assay in each group. The data was then analyzed using one-way ANOVA. P≤0.05 was considered as statistically significant. The results showed that the mean of sHLA-G level was high in patients. Also, it was found that there was a significant difference in sHLA serum level between the three groups. The data revealed that sHLA-G can be a novel supplementary tumor marker in addition to PSA to diagnose prostate cancer.
    Matched MeSH terms: Prostatic Neoplasms
  5. Ma B, Khazali A, Shao H, Jiang Y, Wells A
    Cell Commun Signal, 2019 12 12;17(1):164.
    PMID: 31831069 DOI: 10.1186/s12964-019-0489-1
    BACKGROUND: Carcinoma cells shift between epithelial and mesenchymal phenotypes during cancer progression, as defined by surface presentation of the cell-cell cohesion molecule E-cadherin, affecting dissemination, progression and therapy responsiveness. Concomitant with the loss of E-cadherin during the mesenchymal transition, the predominant receptor isoform for ELR-negative CXC ligands shifts from CXCR3-B to CXCR3-A which turns this classical G-protein coupled receptor from an inhibitor to an activator of cell migration, thus promoting tumor cell invasiveness. We proposed that CXCR3 was not just a coordinately changed receptor but actually a regulator of the cell phenotype.

    METHODS: Immunoblotting, immunofluorescence, quantitative real-time PCR and flow cytometry assays investigated the expression of E-cadherin and CXCR3 isoforms. Intrasplenic inoculation of human prostate cancer (PCa) cells with spontaneous metastasis to the liver analyzed E-cadherin and CXCR3-B expression during cancer progression in vivo.

    RESULTS: We found reciprocal regulation of E-cadherin and CXCR3 isoforms. E-cadherin surface expression promoted CXCR3-B presentation on the cell membrane, and to a lesser extent increased its mRNA and total protein levels. In turn, forced expression of CXCR3-A reduced E-cadherin expression level, whereas CXCR3-B increased E-cadherin in PCa. Meanwhile, a positive correlation of E-cadherin and CXCR3-B expression was found both in experimental PCa liver micro-metastases and patients' tissue.

    CONCLUSIONS: CXCR3-B and E-cadherin positively correlated in vitro and in vivo in PCa cells and liver metastases, whereas CXCR3-A negatively regulated E-cadherin expression. These results suggest that CXCR3 isoforms may play important roles in cancer progression and dissemination via diametrically regulating tumor's phenotype.

    Matched MeSH terms: Prostatic Neoplasms/genetics*; Prostatic Neoplasms/metabolism; Prostatic Neoplasms/pathology
  6. Suriani Ismail, Huda Zainuddin, Titi Rahmawati Hamedon, Muhammad Hanafiah Juni, Nor Afiah Mohd. Zulkefli, Suhainizam bin Muhamad Saliluddin
    MyJurnal
    Background: Lack of awareness, poor knowledge and attitude regarding cancer have been identified as possible reasons accounting for the late presentation which lead to the poor survival of cancer patients in Malaysia. Method: A cross sectional study was conducted in three traditional Malay villages in Negeri Sembilan among adult males. Those who were already diagnosed with prostate cancer or Non malaysians were excluded from the study. Data was collected using self-administered questionnaires which consist of several sections namely socio-demographic, awareness about prostate cancer, sources of information, family history of prostate cancer, lifestyle associated with risk of cancer, knowledge and attitude towards prostate cancer. Data was analysed using SPSS version 22.0. Chisquare test was used to determine associations. Level of significance was set at p
    Matched MeSH terms: Prostatic Neoplasms
  7. Ting CY, Teh GC, Yu KL, Alias H, Tan HM, Wong LP
    Support Care Cancer, 2020 Apr;28(4):1703-1715.
    PMID: 31292755 DOI: 10.1007/s00520-019-04975-y
    PURPOSE: This study examined the prevalence of financial toxicity (FT) and associated factors among urologic cancer patients. The association between FT and health-related quality of life (HRQoL) was also investigated.

    METHODS: A total of 429 respondents diagnosed with urologic cancers (prostate cancer, bladder and renal cancer) from Sarawak General Hospital and Subang Jaya Medical Centre in Malaysia were interviewed using a structured questionnaire. Objective and subjective FT were measured by catastrophic health expenditure (healthcare-cost-to-income ratio greater than 40%) and the Personal Financial Well-being Scale, respectively. HRQoL was measured with the Functional Assessment of Cancer Therapy - General 7 Items scale.

    RESULTS: Objective and subjective FT were experienced by 16.1 and 47.3% of the respondents, respectively. Respondents who sought treatment at a private hospital and had out-of-pocket health expenditures were more likely to experience objective FT, after adjustment for covariates. Respondents who were female and had a monthly household income less than MYR 5000 were more likely to experience average to high subjective FT. Greater objective FT (OR = 2.75, 95% CI 1.09-6.95) and subjective FT (OR = 4.68, 95% CI 2.63-8.30) were associated with poor HRQoL.

    CONCLUSIONS: The significant association between both objective and subjective FT and HRQoL highlights the importance of reducing FT among urologic cancer patients. Subjective FT was found to have a greater negative impact on HRQoL.

    Matched MeSH terms: Prostatic Neoplasms/drug therapy; Prostatic Neoplasms/economics*
  8. Dadaev T, Saunders EJ, Newcombe PJ, Anokian E, Leongamornlert DA, Brook MN, et al.
    Nat Commun, 2018 06 11;9(1):2256.
    PMID: 29892050 DOI: 10.1038/s41467-018-04109-8
    Prostate cancer is a polygenic disease with a large heritable component. A number of common, low-penetrance prostate cancer risk loci have been identified through GWAS. Here we apply the Bayesian multivariate variable selection algorithm JAM to fine-map 84 prostate cancer susceptibility loci, using summary data from a large European ancestry meta-analysis. We observe evidence for multiple independent signals at 12 regions and 99 risk signals overall. Only 15 original GWAS tag SNPs remain among the catalogue of candidate variants identified; the remainder are replaced by more likely candidates. Biological annotation of our credible set of variants indicates significant enrichment within promoter and enhancer elements, and transcription factor-binding sites, including AR, ERG and FOXA1. In 40 regions at least one variant is colocalised with an eQTL in prostate cancer tissue. The refined set of candidate variants substantially increase the proportion of familial relative risk explained by these known susceptibility regions, which highlights the importance of fine-mapping studies and has implications for clinical risk profiling.
    Matched MeSH terms: Prostatic Neoplasms/genetics*
  9. Perez-Cornago A, Travis RC, Appleby PN, Tsilidis KK, Tjønneland A, Olsen A, et al.
    Int J Cancer, 2017 Jul 15;141(2):287-297.
    PMID: 28419475 DOI: 10.1002/ijc.30741
    Several dietary factors have been studied in relation to prostate cancer; however, most studies have not reported on subtypes of fruit and vegetables or tumor characteristics, and results obtained so far are inconclusive. This study aimed to examine the prospective association of total and subtypes of fruit and vegetable intake with the incidence of prostate cancer overall, by grade and stage of disease, and prostate cancer death. Lifestyle information for 142,239 men participating in the European Prospective Investigation into Cancer and Nutrition from 8 European countries was collected at baseline. Multivariable Cox regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). After an average follow-up time of 13.9 years, 7,036 prostate cancer cases were identified. Compared with the lowest fifth, those in the highest fifth of total fruit intake had a significantly reduced prostate cancer risk (HR = 0.91; 95% CI = 0.83-0.99; p-trend = 0.01). No associations between fruit subtypes and prostate cancer risk were observed, except for citrus fruits, where a significant trend was found (HR = 0.94; 95% CI = 0.86-1.02; p-trend = 0.01). No associations between total and subtypes of vegetables and prostate cancer risk were observed. We found no evidence of heterogeneity in these associations by tumor grade and stage, with the exception of significant heterogeneity by tumor grade (pheterogeneity <0.001) for leafy vegetables. No significant associations with prostate cancer death were observed. The main finding of this prospective study was that a higher fruit intake was associated with a small reduction in prostate cancer risk. Whether this association is causal remains unclear.
    Matched MeSH terms: Prostatic Neoplasms/epidemiology*; Prostatic Neoplasms/pathology*; Prostatic Neoplasms/prevention & control
  10. Isa MR, Ming MF, Abdul Razack AH, Zainuddin ZM, Zainal NZ
    Asian Pac J Cancer Prev, 2012;13(12):5999-6004.
    PMID: 23464393
    Measurement of quality of life among prostate cancer patients helps the health care providers to understand the impact of the disease in the patients' own perspective. The main aim of this study is to measure the quality of life among prostate cancer patients at University Malaya Medical Center (UMMC) and Universiti Kebangsaan Malaysia Medical Centre (UKMMC) and to ascertain the association factors for physical coefficient summary (PCS) and mental coefficient summary (MCS). A hospital based, cross sectional study using the Short Form-36 (SF-36) questionnaire was conducted over a period of 6 months. A total of 193 respondents were recruited. Their total quality of life score was 70.1± 14.7 and the PCS score was lower compared to MCS. The factors associated for PCS were: age, living partner, renal problem, urinary problem of intermittency, dysuria and hematuria. Factors associated for MCS were: age, living partner, renal problem, presenting prostatic specific antigen and urinary problem of intermittency and dysuria. Our prostate cancer patients had moderate quality of life in the physical health components but their mental health was less affected.
    Matched MeSH terms: Prostatic Neoplasms
  11. Jalil MA, Abdolkarim A, Saktioto T, Ong CT, Yupapin PP
    Int J Nanomedicine, 2012;7:773-9.
    PMID: 22359455 DOI: 10.2147/IJN.S27625
    In this study, we have generated terahertz (THz) frequency by a novel design of microring resonators for medical applications. The dense wavelength-division multiplexing can be generated and obtained by using a Gaussian pulse propagating within a modified PANDA ring resonator and an add/drop filter system. Our results show that the THz frequency region can be obtained between 40-50 THz. This area of frequency provides a reliable frequency band for THz pulsed imaging.
    Matched MeSH terms: Prostatic Neoplasms/chemistry
  12. Kar SP, Beesley J, Amin Al Olama A, Michailidou K, Tyrer J, Kote-Jarai Z, et al.
    Cancer Discov, 2016 Sep;6(9):1052-67.
    PMID: 27432226 DOI: 10.1158/2159-8290.CD-15-1227
    Breast, ovarian, and prostate cancers are hormone-related and may have a shared genetic basis, but this has not been investigated systematically by genome-wide association (GWA) studies. Meta-analyses combining the largest GWA meta-analysis data sets for these cancers totaling 112,349 cases and 116,421 controls of European ancestry, all together and in pairs, identified at P < 10(-8) seven new cross-cancer loci: three associated with susceptibility to all three cancers (rs17041869/2q13/BCL2L11; rs7937840/11q12/INCENP; rs1469713/19p13/GATAD2A), two breast and ovarian cancer risk loci (rs200182588/9q31/SMC2; rs8037137/15q26/RCCD1), and two breast and prostate cancer risk loci (rs5013329/1p34/NSUN4; rs9375701/6q23/L3MBTL3). Index variants in five additional regions previously associated with only one cancer also showed clear association with a second cancer type. Cell-type-specific expression quantitative trait locus and enhancer-gene interaction annotations suggested target genes with potential cross-cancer roles at the new loci. Pathway analysis revealed significant enrichment of death receptor signaling genes near loci with P < 10(-5) in the three-cancer meta-analysis.

    SIGNIFICANCE: We demonstrate that combining large-scale GWA meta-analysis findings across cancer types can identify completely new risk loci common to breast, ovarian, and prostate cancers. We show that the identification of such cross-cancer risk loci has the potential to shed new light on the shared biology underlying these hormone-related cancers. Cancer Discov; 6(9); 1052-67. ©2016 AACR.This article is highlighted in the In This Issue feature, p. 932.

    Matched MeSH terms: Prostatic Neoplasms/genetics*; Prostatic Neoplasms/metabolism
  13. Szulkin R, Karlsson R, Whitington T, Aly M, Gronberg H, Eeles RA, et al.
    Cancer Epidemiol Biomarkers Prev, 2015 Nov;24(11):1796-800.
    PMID: 26307654 DOI: 10.1158/1055-9965.EPI-15-0543
    BACKGROUND: Unnecessary intervention and overtreatment of indolent disease are common challenges in clinical management of prostate cancer. Improved tools to distinguish lethal from indolent disease are critical.

    METHODS: We performed a genome-wide survival analysis of cause-specific death in 24,023 prostate cancer patients (3,513 disease-specific deaths) from the PRACTICAL and BPC3 consortia. Top findings were assessed for replication in a Norwegian cohort (CONOR).

    RESULTS: We observed no significant association between genetic variants and prostate cancer survival.

    CONCLUSIONS: Common genetic variants with large impact on prostate cancer survival were not observed in this study.

    IMPACT: Future studies should be designed for identification of rare variants with large effect sizes or common variants with small effect sizes.

    Matched MeSH terms: Prostatic Neoplasms/genetics; Prostatic Neoplasms/mortality*
  14. Poniah P, Mohd Zain S, Abdul Razack AH, Kuppusamy S, Karuppayah S, Sian Eng H, et al.
    Urol Oncol, 2017 09;35(9):545.e1-545.e11.
    PMID: 28527622 DOI: 10.1016/j.urolonc.2017.04.017
    BACKGROUND: Two key issues in prostate cancer (PCa) that demand attention currently are the need for a more precise and minimally invasive screening test owing to the inaccuracy of prostate-specific antigen and differential diagnosis to distinguish advanced vs. indolent cancers. This continues to pose a tremendous challenge in diagnosis and prognosis of PCa and could potentially lead to overdiagnosis and overtreatment complications. Copy number variations (CNVs) in the human genome have been linked to various carcinomas including PCa. Detection of these variants may improve clinical treatment as well as an understanding of the pathobiology underlying this complex disease.

    METHODS: To this end, we undertook a pilot genome-wide CNV analysis approach in 36 subjects (18 patients with high-grade PCa and 18 controls that were matched by age and ethnicity) in search of more accurate biomarkers that could potentially explain susceptibility toward high-grade PCa. We conducted this study using the array comparative genomic hybridization technique. Array results were validated in 92 independent samples (46 high-grade PCa, 23 benign prostatic hyperplasia, and 23 healthy controls) using polymerase chain reaction-based copy number counting method.

    RESULTS: A total of 314 CNV regions were found to be unique to PCa subjects in this cohort (P<0.05). A log2 ratio-based copy number analysis revealed 5 putative rare or novel CNV loci or both associated with susceptibility to PCa. The CNV gain regions were 1q21.3, 15q15, 7p12.1, and a novel CNV in PCa 12q23.1, harboring ARNT, THBS1, SLC5A8, and DDC genes that are crucial in the p53 and cancer pathways. A CNV loss and deletion event was observed at 8p11.21, which contains the SFRP1 gene from the Wnt signaling pathway. Cross-comparison analysis with genes associated to PCa revealed significant CNVs involved in biological processes that elicit cancer pathogenesis via cytokine production and endothelial cell proliferation.

    CONCLUSION: In conclusion, we postulated that the CNVs identified in this study could provide an insight into the development of advanced PCa.

    Matched MeSH terms: Prostatic Neoplasms/genetics*; Prostatic Neoplasms/pathology
  15. Suparji NS, Chan G, Sapili H, Arshad NM, In LL, Awang K, et al.
    PLoS One, 2016;11(3):e0151472.
    PMID: 26974436 DOI: 10.1371/journal.pone.0151472
    Geranylated 4-phenylcoumarins, DMDP-1 & -2 isolated from Mesua elegans were investigated for anticancer potential against human prostate cancer cells. Treatment with DMDP-1 & -2 resulted in cell death in a time and dose dependent manner in an MTT assay on all cancer cell lines tested with the exception of lung adenocarcinoma cells. DMDP-1 showed highest cytotoxic efficacy in PC-3 cells while DMDP-2 was most potent in DU 145 cells. Flow cytometry indicated that both coumarins were successful to induce programmed cell death after 24 h treatment. Elucidation on the mode-of-action via protein arrays and western blotting demonstrated death induced without any significant expressions of caspases, Bcl-2 family proteins and cleaved PARP, thus suggesting the involvement of caspase-independent pathways. In identifying autophagy, analysis of GFP-LC3 showed increased punctate in PC-3 cells pre-treated with CQ and treated with DMDP-1. In these cells decreased expression of autophagosome protein, p62 and cathepsin B further confirmed autophagy. In contrary, the DU 145 cells pre-treated with CQ and treated with DMDP-2 has reduced GFP-LC3 punctate although the number of cells with obvious GFP-LC3 puncta was significantly increased in the inhibitor-treated cells. The increase level of p62 suggested leakage of cathepsin B into the cytosol to trigger potential downstream death mediators. This correlated with increased expression of cathepsin B and reduced expression after treatment with its inhibitor, CA074. Also auto-degradation of calpain-2 upon treatment with DMDP-1 &-2 and its inhibitor alone, calpeptin compared with the combination treatment, further confirmed involvement of calpain-2 in PC-3 and DU 145 cells. Treatment with DMDP-1 & -2 also showed up-regulation of total and phosphorylated p53 levels in a time dependent manner. Hence, DMDP-1 & -2 showed ability to activate multiple death pathways involving autophagy, lysosomal and endoplasmic reticulum death proteins which could potentially be manipulated to develop anti-cancer therapy in apoptosis resistant cells.
    Matched MeSH terms: Prostatic Neoplasms/enzymology*; Prostatic Neoplasms/pathology*
  16. Sapili H, Ho CS, Malagobadan S, Arshad NM, Nagoor NH
    Sci Rep, 2020 01 22;10(1):986.
    PMID: 31969640 DOI: 10.1038/s41598-020-57781-6
    Geranylated 4-phenylcoumarins DMDP-1 and DMDP-2 isolated from Mesua elegans were elucidated for their role in inducing caspase-independent programmed cell death (CI-PCD) in prostate cancer cell lines, PC-3 and DU 145, respectively. Cell homeostasis disruption was demonstrated upon treatment, as shown by the increase in calcium ion through colourimetric assay and endoplasmic reticulum (ER) stress markers GRP 78 and p-eIF2α through western blot. Subsequently, cytoplasmic death protease calpain-2 also showed increased activity during DMDP-1 & -2 treatments, while lysosomic death protease cathepsin B activity was significantly increased in PC-3 treated with DMDP-1. Flow cytometry showed a reduction in mitochondrial membrane potential in both cell lines, while western blotting showed translocation of mitochondrial death protease AIF into the cytoplasm in its truncated form. Furthermore, DMDP-1 & -2 treatments caused significant increase in superoxide level and oxidative DNA damage. Concurrent inhibition of calpain-2 and cathepsin B during the treatment showed an attenuation of cell death in both cell lines. Hence, DMDP-1 & -2 induce CI-PCD in prostate cancer cell lines through calpain-2 and cathepsin B.
    Matched MeSH terms: Prostatic Neoplasms/metabolism; Prostatic Neoplasms/pathology
  17. Matejcic M, Saunders EJ, Dadaev T, Brook MN, Wang K, Sheng X, et al.
    Nat Commun, 2018 Nov 05;9(1):4616.
    PMID: 30397198 DOI: 10.1038/s41467-018-06863-1
    Chromosome 8q24 is a susceptibility locus for multiple cancers, including prostate cancer. Here we combine genetic data across the 8q24 susceptibility region from 71,535 prostate cancer cases and 52,935 controls of European ancestry to define the overall contribution of germline variation at 8q24 to prostate cancer risk. We identify 12 independent risk signals for prostate cancer (p 
    Matched MeSH terms: Prostatic Neoplasms/genetics*; Prostatic Neoplasms/epidemiology; Prostatic Neoplasms/pathology
  18. Awang A, Md Isa N, Yunus R, Azhar Shah S, Md Pauzi SH
    Malays J Pathol, 2019 Dec;41(3):253-257.
    PMID: 31901909
    INTRODUCTION: Gleason scoring (GS) categorised prostatic adenocarcinoma into five prognostic grade groups (PGGs); associated with different prognosis and treatment. This study aims to correlate between Gleason scores of needle biopsies with the corresponding total prostatectomy specimens, and to assess the relationship between the percentage of Gleason 4 tumour pattern (GP4) within Gleason score 7 (GS7) needle biopsy groups with the pathological staging.

    MATERIALS AND METHODS: Seventy-eight specimens of needle prostate biopsy and its subsequent radical prostatectomy were retrospectively studied. The GSs of the needle biopsy were compared with the corresponding prostatectomy specimens. The percentage of GP4 in GS7 needle biopsy groups was calculated and correlated with the pathological staging.

    RESULTS: More than half (60%) of GS 6 needle biopsy cases (PGG 1) were upgraded in the prostatectomy specimen, while the majority (80%) of the GS7 needle biopsy groups (PGG 2 and 3) remain unchanged. Cohen's Kappa shows fair agreement in the Gleason scoring between needle biopsies and prostatectomy specimens, K = 0.324 (95% CI, 6.94 to 7.29), p <0.0005 and in the percentage of GP4 in GS7 needle biopsy groups and their corresponding radical prostatectomy specimens, K = 0.399 (95% CI 34.2 - 49.2), p<0.0005. A significant relationship was seen between the percentage of GP4 in GS7 needle biopsy with the pT and pN stage of its radical prostatectomy (p = 0.008 and p=0.001 respectively).

    CONCLUSION: A higher percentage of GP4 in GS7 tumour is associated with worse tumour behaviour, therefore it is crucial for clinicians to realise this in deciding the optimal treatment.

    Matched MeSH terms: Prostatic Neoplasms/diagnosis; Prostatic Neoplasms/pathology*
  19. Nurdin A, Hoshi Y, Yoneyama T, Miyauchi E, Tachikawa M, Watanabe M, et al.
    J Pharm Sci, 2016 Nov;105(11):3440-3452.
    PMID: 27665127 DOI: 10.1016/j.xphs.2016.08.013
    Prostate-specific antigen is currently the only protein biomarker routinely used as a diagnostic tool for early detection and treatment monitoring of prostate cancer. However, it remains questionable whether prostate-specific antigen-based screening can sensitively and selectively identify the presence and progression status of primary and metastatic prostate cancers. Hence, the purpose of this study was to identify potential biomarker candidates in the secretome of primary and metastatic prostate cancer cells by using a combination of global and targeted proteomics. Quantitative comparisons among secretome proteins derived from androgen-responsive primary cancer cells (P-22Rv1), androgen-irresponsive bone metastatic cancer cells (M-PC-3), and noncancerous prostate cells (N-PNT2) were performed using 2-dimensional image-converted analysis of liquid chromatography and mass spectrometry followed by in silico selection selected reaction monitoring analysis. Mediator of RNA polymerase II transcription subunit 13-like, insulin-like growth factor-binding protein 2, and hepatocyte growth factor were identified as highly secreted proteins from P-22Rv1 cells compared with N-PNT2 cells. Prostate-associated microseminoprotein, proactivator polypeptide, collagen-α-1 (VI) chain, and neuropilin-1 were identified as predominantly secreted proteins in M-PC-3 cells compared with N-PNT2 cells. These proteins in biological fluids are considered to be candidate biomarkers of primary and/or metastatic prostate cancer.
    Matched MeSH terms: Prostatic Neoplasms/genetics*; Prostatic Neoplasms/pathology
  20. Abd Rahman SF, Md Arshad MK, Gopinath SCB, Fathil MFM, Sarry F, Ibau C
    Chem Commun (Camb), 2021 Sep 23;57(76):9640-9655.
    PMID: 34473143 DOI: 10.1039/d1cc03080a
    Prostate cancer is currently diagnosed using the conventional gold standard methods using prostate-specific antigen (PSA) as the selective biomarker. However, lack of precision in PSA screening has resulted in needless biopsies and delays the treatment of potentially fatal prostate cancer. Thus, identification of glycans as novel biomarkers for the early detection of prostate cancer has attracted considerable attention due to their reliable diagnostic platform compared with the current PSA systems. Therefore, biosensing technologies that provide point-of-care diagnostics have demonstrated the ability to detect various analytes, including glycosylated micro- and macro-molecules, thereby enabling versatile detection methodologies. This highlight article discusses recent advances in the biosensor-based detection of prostate cancer glycan biomarkers and the innovative strategies for the conjugation of nanomaterials adapted to biosensing platforms. Finally, the article is concluded with prospects and challenges of prostate cancer biosensors and recommendations to overcome the issues associated with prostate cancer diagnosis.
    Matched MeSH terms: Prostatic Neoplasms/diagnosis*
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