Khodabandehloo, Mazaher;Hosseini, Weria;Rahmani, Mohammad-Reza;Rezaee, Mohammad-Ali;Hakhamaneshi, Mohammad-Saied;Nikkhoo, Bahram;Jalili, Ali
Asian Pacific Journal of Cancer Prevention
/
제14권11호
/
pp.6929-6933
/
2013
Background: Multiple etiologies have been hypothesized for prostate cancer, including genetic defects and infectious agents. A recently reported gamaretrovirus, xenotropic murine leukemia virus-related virus (XMRV) has been reported to be detected in prostate cancer. However, this virus has not been detected in similar groups of patients in other studies. Herein, we sought to detect XMRV in prostate cancers and benign controls in Sanandaj, west of Iran. Materials and Methods: In a case-control study, genomic DNA was extracted from formalin fixed and paraffin embedded prostate tissues from a total of 163 Iranian patients. We developed a conventional and a nested PCR assay using primers targeting to an env specific sequence of XMRV. PCR assays were carried out on 63 prostate cancers and 100 benign prostate hyperplasias. Results: Beta-actin sequences were successfully detected in the DNA extracts from all prostate tissues, confirming DNA extraction integrity. We did not detect XMRV in samples either from prostate cancers or benign prostate hyperplasias using XMRV specific primers. Conclusions: We conclude that in our population XMRV does not play a role in genesis of prostate cancer.
Lalitha, Krishnappa;Suman, Gadicherla;Pruthvish, Sreekantaiah;Mathew, Aleyamma;Murthy, Nandagudi S.
Asian Pacific Journal of Cancer Prevention
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제13권12호
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pp.6245-6250
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2012
Background: With increase in life expectancy, adoption of newer lifestyles and screening using prostate specific antigen (PSA), the incidence of prostate cancer is on rise. Globally prostate cancer is the second most frequently diagnosed cancer and sixth leading cause of cancer death in men. The present communication makes an attempt to analyze the time trends in incidence for different age groups of the Indian population reported in different Indian registries using relative difference and regression approaches. Materials and Methods: The data published in Cancer Incidence in Five Continents for various Indian registries for different periods and/or publications by the individual registries served as the source materials. Trends were estimated by computing the mean annual percentage change (MAPC) in the incidence rates using the relative difference between two time periods (latest and oldest) and also by estimation of annual percentage change (EAPC) by the Poisson regression model. Results: Age adjusted incidence rates (AAR) of prostate cancer for the period 2005-2008 ranged from 0.8 (Manipur state excluding Imphal west) to 10.9 (Delhi) per $10^5$ person-years. Age specific incidence rates (ASIR) increased in all PBCRs especially after 55 years showing a peak incidence at +65 years clearly indicating that prostate cancer is a cancer of the elderly. MAPC in crude incidence rate(CR) ranged from 0.14 (Ahmedabad) to 8.6 (Chennai). Chennai also recorded the highest MAPC of 5.66 in ASIR in the age group of 65+. Estimated annual percentage change (EAPC) in the AAR ranged from 0.8 to 5.8 among the three registries. Increase in trend was seen in the 55-64 year age group cohort in many registries and in the 35-44 age group in Metropolitan cities such as Delhi and Mumbai. Conclusions: Several Indian registries have revealed an increasing trend in the incidence of prostate cancer and the mean annual percentage change has ranged from 0.14-8.6.
Human prostate cancer is the second most frequently diagnosed cancer worldwide, and its incidence rate continues to increase. Advanced prostate cancer is more difficult to treat than early forms due to its chemotherapy resistance. There is need for more effective agents that can inhibit the progression of advanced prostate cancer. Demethoxyfumitremorgin C (DMFTC) was isolated from the fermentation extract of the marine fungus Aspergillus fumigatus. Antiproliferative activity of DMFTC against human prostate cancer PC3 cells was examined through cell cycle analysis by flow cytometry, the fluorescent nuclear imaging analysis with propidium iodide (PI), and proteins expression related to cell cycle arrest and apoptosis were investigated via Western blotting. DMFTC inhibited PC3 cells growth through G1 phase cell cycle arrest and apoptosis induction. It activated the tumor suppressor p53 and the Cdk inhibitor p21, which regulate the cell progression into the G1 phase. Additionally, PI-positive late apoptotic non-viable cells were increased and the expression levels of the G1-positive downstream regulators cyclin D, cyclin E, Cdk2, and Cdk4 were decreased by DMFTC treatment. These results suggest that DMFTC induces G1 arrest and apoptosis induction through regulation of p53/p21-dependent cyclin-Cdk complexes, and it may be a useful therapeutic agent for the treatment of human advanced prostate cancer.
We report a case of a patient with locally advanced prostate cancer who had only lymph node involvement without bone metastasis on F-18 FDG PET/CT. A 62-year-old Korean male was admitted to our hospital due to dysuria. His PSA level on admission was 79.35 ng/mL. A transrectal ultrasound-guided prostate biopsy confirmed prostate cancer and his Gleason score was 10 (5+5). F-18 FDG PET/CT demonstrated a hypermetabolic mass lesion with SUVmax 7.0 in the prostate and hypermetabolism with SUVmax 4.7 of the abdominal and pelvic lymph nodes. Tc-99m HDP bone scan showed no significant bone metastasis. The patient underwent hormonal therapy for 9 months. Follow-up F-18 FDG PET/CT showed significantly reduced size and FDG uptake in the prostate and abdominal and pelvic lymph nodes. In this case, treatment monitoring with F-18 FDG PET/CT showed decreased mass size and FDG uptake in the prostate and abdominal and pelvic lymph nodes.
Background: Alpha-methylacyl-CoA racemase(AMACR) is thought to play key roles in diagnosis and prognosis of prostate cancer. However, studies of associations between AMACR gene polymorphisms and prostate cancer risk reported inconsistent results. Therefore, we conducted the present meta-analysis to clarify the link between AMACR gene polymorphisms and prostate cancer risk. Materials and Methods: A literature search was performed in PubMed, Embase, China National Knowledge Infrastructure (CNKI), Wanfang and Weipu databases. Odds ratios (ORs) and 95% confidence intervals (95%CIs) were calculated to assess the strength of any association between AMACR polymorphisms and prostate cancer risk. Subgroup analyses by ethnicity, source of controls, quality control and sample size were also conducted. Results: Five studies covering 3,313 cases and 3,676 controls on five polymorphisms (D175G, M9V, S201L, K277E and Q239H) were included in this meta-analysis. Significant associations were detected between prostate cancer and D175G (dominant model: OR=0.89, 95%CI=0.80-0.99, P=0.04) and M9V (dominant model: OR=0.87, 95%CI=0.78-0.97, P=0.01) polymorphisms as well as that in subgroup analyses. We also observed significant decreased prostate cancer risk in the dominant model (OR=0.90, 95%CI=0.81-0.99, P=0.04) for the S201L polymorphism. However, K277E and Q239H polymorphisms did not appear to be related to prostate cancer risk. Conclusions: The current meta-analysis indicated that D175G and M9V polymorphisms of the AMACR gene are related to prostate cancer. The S201L polymorphism might also be linked with prostate cancer risk to some extent. However, no association was observed between K277E or Q239H polymorphisms and susceptibility to prostate cancer.
Purpose: The purpose of this study was to identify relationship of urinary symptom, urinary discomfort and quality of life among the bladder cancer patients and benign prostate hypertrophy patients, and to contribute health promotion of such patients and nursing intervention development based on this results. Method: Study sample recruited bladder cancer patents(n=49) and benign prostate hypertrophy patients who admitted Seoul National University Hospital from June, 2002 to June, 2003. Both group patients were operated, and prostate hypertrophy patients group (mean 67.8 years old) were older than bladder cancer patients group(60.82 years old). Instruments was composed of general characteristics, urinary symptom scale(19 items), urinary discomfort scale(19 items) and quality of life scale(21 items). Data was analysed SPSS PC + 10. using mean, standard deviation, pearson correlation coefficient. Result as follows: 1. There was a statistically significant difference in occupation between two groups (p=.027). Hypertrophy patients group's age was more older than bladder cancer patients group. 2. The prostate hypertrophy patients group had the significantly higher score in urinary symptom (p=000) and nighttime urination frequency. However, there was no significant difference in incontinence symptoms and the symptoms associated bladder cancer between two groups. 3. The prostate hypertrophy patients group had significantly higher score in urinary discomfort (p=000) than the bladder cancer patients group. However, there was no significant difference incontinence discomfort and the discomfort associated bladder cancer between two groups. 4. The prostate hypertrophy patients group suffered more urinary discomfort than the bladder cancer patients group did. The quality of life the prostate hypertrophy patients group was lower than the quality of life the bladder cancer patients group. Quality of life was no statistically significant difference between two groups (p=000). 5. There was a positive correlation between urinary symptoms and urinary discomfort. However, there was a negative correlation between the quality of life and urination symptoms and discomfort. Conclusions: The prostate hypertrophy patients group had significantly higher score in urinary symptom and urinary discomfort (p=000) than the bladder cancer patients group. The quality of life the prostate hypertrophy patients group was lower than the quality of life the bladder cancer patients group. This means that urinary symptom and urinary discomfort in prostate hypertrophy patient group is more important problem. So, prostate hypertrophy patient group need to control the symptom. Therefore, nurses will be provide the intervention program to improve the bladder function after prostate hypertrophy surgery.
Prostate cancer is one of the most common cancers in men. Choline PET or PET/CT has been used to visualize prostate cancer, and high levels of choline accumulation have been observed in tumors. However, the uptake system for choline and the functional expression of choline transporters in prostate cancer are not completely understood. In this study, the molecular and functional aspects of choline uptake were investigated in the LNCaP prostate cancer cell line along with the correlations between choline uptake and cell viability in drug-treated cells. Choline transporter-like protein 1 (CTL1) and CTL2 mRNA were highly expressed in LNCaP cells. CTL1 and CTL2 were located in the plasma membrane and mitochondria, respectively. [3H]Choline uptake was mediated by a single Na+-independent, intermediate-affinity transport system in the LNCaP cells. The anticancer drugs, flutamide and bicalutamide, inhibited cell viability and [3H]choline uptake in a concentration-dependent manner. The correlations between the effects of these drugs on cell viability and [3H]choline uptake were significant. Caspase-3/7 activity was significantly increased by both flutamide and bicalutamide. Furthermore, these drugs decreased CTL1 expression in the prostate cancer cell line. These results suggest that CTL1 is functionally expressed in prostate cancer cells and are also involved in abnormal proliferation. Identification of this CTL1-mediated choline transport system in prostate cancer cells provides a potential new therapeutic target for the treatment of this disease.
Purpose: To determine the utility of secondary circulating prostate cells for predicting early biochemical failure after radical prostatectomy for prostate cancer and compare the results with the Walz nomagram. Materials and Methods: A single centre, prospective study of men with prostate cancer treated with radical prostatectomy between 2004 and 2014 was conducted, with registration of clinical-pathological details, total serum PSA pre-surgery, Gleason score, extracapsular extension, positive surgical margins, infiltration of lymph nodes, seminal vesicles and pathological stage. Secondary circulating prostate cells were obtained using differential gel centrifugation and assessed using standard immunocytochemistry with anti-PSA. Biochemical failure was defined as a PSA >0.2ng/ml, predictive values werecalculated using the Walz nomagram and CPC detection. Results: A total of 326 men participated, with a median follow up of 5 years; 64 had biochemical failure within two years. Extracapsular extension, positive surgical margins, pathological stage, Gleason score ${\geq}8$, infiltration of seminal vesicles and lymph nodes were all associated with higher risk of biochemical failure. The discriminative value for the nomogram and circulating prostate cells was high (AUC >0.80), predictive values were higher for circulating prostate cell detection, with a negative predictive value of 99%, sensitivity of 96% and specificity of 75%. Conclusions: The nomagram had good predictive power to identify men with a high risk of biochemical failure within two years. The presence of circulating prostate cells had the same predictive power, with a higher sensitivity and negative predictive value. The presence of secondary circulating prostate cells identifies a group of men with a high risk of early biochemical failure. Those negative for secondary CPCs have a very low risk of early biochemical failure.
Introduction: Prostate cancer in Indonesia is the $3^{rd}$ ranking cancer among males and the $5^{th}$ rank for their cancer mortality. Prognostic markers that can identify aggressive prostate cancer in early stages and help select appropriate therapy to finally reduce the mortality are therefore urgently needed. It has been suggested that stem cells in the prostate gland have a role in initiation, progression, and metastasis of cancer, although controversy continues to exist. Maintenance of normal stem cell or reserve cell populations in several epithelia including prostate has been shown to be regulated by p63 and alteration of p63 expression is considered to have an oncogenic role in prostate cancer. We hypothesize that the expression of cytoplasmic aberrance of p63 is associated with high ALDH1A1 expression as a cancer stem cell marker, thus leading to progression of prostate cancer. Methods: Using a cross-sectional study during two years (2009-2010), a total of 79 paraffin embedded tissues of benign prostatic hyperplasia, PIN prostatic intraepithelial neoplasia, low and high Gleason score prostate cancer were investigated using immunohistochemistry. Associations between cytoplasmic p63 and ALDH1A1, as well as with pathological diagnosis, were analyzed by Chi-Square test using SPSS 15.0. Links of both markers with cell proliferation rate (KI-67) and apoptotic rate (cleaved caspase 3) were also analyzed by Kruskal-Wallis test. Results: The mean age of patient at the diagnosis is 70.0 years. Cytoplasmic aberrance of p63 was associated with ALDH1A1 expression (p<0.001) and both were found to have significant relationships with pathological diagnosis (including Gleason score), (p=0.006 and p<0.001 respectively). Moreover, it was also found that higher levels of cytoplasmic p63 were significantly associated with the frequency of proliferating cells and cells undergoing apoptosis in prostate cancers (p=0.001 and p=0.016 respectively). Conclusion: p63 cytoplasmic aberrance is associated with high ALDH1A1 expression. These components are suggested to have an important role in prostate cancer progression and may be used as molecular markers.
Inhibition of cancer-associated fibroblasts (CAFs) may improve the efficacy of cancer therapy. Polysaccharide extracted from polygonatum can selectively inhibit the growth of prostate-CAFs (p<0.001) without inhibiting the growth of normal fibroblasts (NAFs). Polysaccharides from polygonatum stimulate autophagy of prostate-CAFs. 3-methyl-adenine(3-MA) is an autophagy inhibitor. 3-MA was added to prostate-CAFs with polysaccharide from polygonatum to determine whether autophagy plays an important role in the restrained effect. Finally, polysaccharide from polygonatum treatment significantly increased the activation of Beclin-1 and LC3, key autophagy proteins. Polysaccharide from polygonatum stimulates autophagy of prostate-CAFs and inhibits prostate-CAF growth, indicating that a novel anti-cancer strategy involves inhibiting the growth of prostate-CAFs.
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