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PubMed2003

Early diagnosis and surgical management of prostate cancer.

Prostate cancer is a significant cause of morbidity and mortality in the United States and Europe. The natural ageing of the population as well as the continued and widespread use of diagnostic tests such as prostate specific antigen (PSA), has led to an increase in the numbers of men diagnosed with localised prostate cancer. Screening to identify organ-confined disease has provoked much public and scientific attention, but remains controversial. Radical prostatectomy is one of the most challenging urological procedures performed. Improvements in technique due to better understanding of pelvic anatomy have reduced complications, with acceptable standards and excellent results in high-volume institutions. Continual refinements in technique and the recent introduction of laparoscopic radical prostatectomy are likely to improve functional outcome further. However the effectiveness of surgery in improving survival and quality of life, in men with early prostate cancer remains to be determined. The results from large randomised controlled trials are eagerly awaited.

Biomarkers, Tumor↗

PubMed2005

The use of genetic markers to determine risk for prostate cancer at prostate biopsy.

PURPOSE: We examined a panel of 13 polymorphisms in 13 different genes to determine whether specific genotypes can help predict prostate cancer at the time of biopsy among men prescreened with prostate-specific antigen and digital rectal exam. EXPERIMENTAL DESIGN: We examined 2,088 consecutive men who were referred for prostate biopsy from 1997 to 2003. Thirteen genes were examined, including TNF308, GSTT1, KLK2, endostatin, MCRA, MCRV, tyrosinase, MSR1, CHK2, RNasel, HOGG1-326, HOGG1-11657, and HRAS1. Odds ratio for detection of prostate cancer were adjusted for age, race, prostate-specific antigen, digital rectal exam, family history of prostate cancer, and urinary symptoms. RESULTS: Of the 2,088 men, 996 (47.7%) had cancer detected. Four genes (TNF308, GSTT1, KLK2, and HOGG1-326) were significantly associated with prostate cancer. The adjusted odds ratios (OR) for prostate cancer for patients with the AA genotype of the TNF308 gene was 1.92 [95% confidence interval (95% CI), 1.0-1.5, P = 0.05], compared with those with the GG genotype, and for patients with the TT genotype of the KLK2 gene, the OR was 1.5 (95% confidence interval, 1.0-2.2, P = 0.04), compared with the CC genotype. The OR for patients with a homozygous deletion of the GSTT1 gene was 0.81 (95% CI, 0.6-1.0, P = 0.06) compared with those with the deletion, and the OR for patients with the GG genotype of the HOGG1-326 gene was 0.68 (95% CI, 0.5-1.0, P = 0.05) compared with the CC genotype. Patients who had all four alleles that were positively associated with prostate cancer had an OR of 9.33 (95% CI, 2.4-35.8, P = 0.0005) for prostate cancer compared with patients with alleles that were negatively associated with prostate cancer. CONCLUSIONS: Of the 13 polymorphisms, two were found to be positively associated with prostate cancer (TNF308 and KLK2) and two were negatively associated with prostate cancer (GSTT1 and HOGG1-326). Future studies are required to confirm these results.

Adenocarcinoma↗

PubMed1993

Growth factors and their receptors as determinants in the proliferation and metastasis of human prostate cancer.

Prostate adenocarcinoma, the most common tumor occurring among North American men, preferentially metastasizes to bone, where it characteristically forms osteoblastic lesions. The following growth regulatory factors are expressed in some human prostate cancers and/or established cell lines: epidermal growth factor (EGF), transforming growth factor alpha, transforming growth factor beta, basic fibroblast growth factor (bFGF), and insulin-like growth factor. Some of these, especially EGF, bFGF, and TGF-beta, are also implicated in growth regulation in normal and benign hyperplastic prostates. Although evidence from in vitro study of the small number of prostate cell lines available demonstrates that these growth regulatory pathways are exploited by some of these cells, direct in vivo evidence is limited. The development of human prostate cancer cell lines which grow and metastasize in immune-deficient rodents is an advance which now permits experimental analysis of the role of these growth factors in prostatic metastasis, particularly to bone. The progression and metastasis of human prostate cancer results from the complex interactions of multiple growth factors, androgens, and cellular communication, which form a dynamic network. Continued progress in the study and treatment of this disease will require new conceptual frameworks as well as successful application of the techniques of molecular and cellular biology.

Animals↗

PubMed2004

Mitochondrial mutagenesis and oxidative stress in human prostate cancer.

Prostate cancer is the most common cancer diagnosed in men in the United States, but the primary cause and the molecular events leading to prostate carcinogenesis are poorly understood. Using the approach of laser capture microdissection, we revealed extensive somatic mitochondrial DNA (mtDNA) mutations in prostatic neoplastic lesions. Inspection of the lesion associated mutations not only provided new insights into the genetics of prostate cancer, but also revealed new patterns of mtDNA mutation in prostate carcinogenesis. Further analysis on a high frequency of multiple mutational events observed in the same neoplastic lesion revealed an unusually rapid process in mitochondrial mutagenesis, suggesting a new process of mitochondrial hyper-mutagenesis in cancer cells, likely mediated by cellular oxidative stress. Thus, active mitochondrial mutagenesis in prostate cancer suggests a prominent role of increased cellular oxidative stress in neoplastic transformation and the increased susceptibility of neoplastic cells to oxidative damage.

DNA, Mitochondrial↗

PubMed1996

Recent advances in the medical management of prostate cancer.

Prostate cancer is a 20th century seedling which, because of its attendant morbidity and mortality and the increased longevity of the population, is set to germinate into a substantial economic burden in the next millennium. Most patients with prostatic cancer present with either locally advanced or metastatic disease, for which palliative endocrine therapies are the first-line treatment. The increasingly sophisticated and selective hormonal methods available today, such as the longer-acting formulations of luteinizing hormone-releasing hormone (LH-RH) analogues and newer, better-tolerated, once-daily, non-steroidal anti-androgens, have increased the therapeutic options and improved patient quality of life. Maximum androgen blockade, combining medical or surgical castration with an anti-androgen, is an increasingly accepted therapy, and offers the greatest efficacy, particularly for patients with a lesser disease burden. The development of hormone-refractory tumours is still a problem in advanced prostate cancer, although elucidation of the mechanisms involved should offer many potentially fruitful avenues for new therapies.

Adrenergic Antagonists↗

PubMed1993

The effect of advanced age on the efficacy of radiation therapy for early breast cancer, local prostate cancer and grade III-IV gliomas.

PURPOSE: This study was undertaken to determine the effect of advanced age on radiation therapy outcomes for early breast cancer, local prostate cancer and Grade 3-4 gliomas of the brain. METHODS AND MATERIALS: Radiation therapy outcomes for three malignancies (N = 1,401) were determined for a geriatric cancer population defined as 70 years of age or older and compared to a non-geriatric cancer population defined as less than 70 years of age. The three patient groups studied were: (a) primary breast cancer patients with clinical Stage I or II disease treated with lumpectomy and radiation therapy (N = 994), (b) local prostate cancer patients with Stage A2, B, or C disease treated with radical radiation therapy (N = 294), and (c) patients with Grade 3-4 gliomas of the brain treated with high dose radiation therapy (N = 113). RESULTS: For Stage I and II breast cancer, there was no statistically significant difference in the overall 10-year survival rates (63% vs. 73%), 10-year cause-specific disease-free survival rates (70% vs. 63%), and 10-year local breast recurrence free survival rates (76% vs. 79%) comparing the geriatric cancer population to the non-geriatric cancer population. For local prostate cancer, there was no statistically significant difference in the 10-year survival rates (38% vs. 41%) or in the 10-year cause-specific disease-free survival rates (58% vs. 52%) in the geriatric population compared with the non-geriatric population. On the other hand, the use of high dose radiation therapy for malignant gliomas resulted in statistically significant inferior 1-year (18% vs. 38%) and 2-year (0% vs. 10%) survival rates for the geriatric population versus the non-geriatric population. CONCLUSION: This study strongly supports the use of standard radiation therapy programs for early breast and prostate cancer patients age 70 years or more. However, our study raises questions about the efficacy of radiation therapy in patients over the age of 70 years with Grade 3-4 gliomas.

Age Factors↗

PubMedDate not supplied

Biopsychosocial aspects of prostate cancer.

Prostate cancer early detection choices and treatment options are fraught with controversy. To update the consultation-liaison psychiatrist who works with at-risk men, the authors reviewed all pertinent citations in the medicine database from 1966 to 1998 and in other relevant publications. Though watchful waiting for early-stage prostate cancer has no side effects, men must cope psychologically with issues of long-term cancer survivorship. Men can choose between different treatment options (e.g., radiation vs. radical prostatectomy) with early detection. Urinary incontinence, sexual dysfunction, and fatigue are major emotional and physical stressors for this population. Consultation-liaison psychiatrists and physicians need to be aware of the psychosocial sequelae of both prostate cancer and treatment-related side effects.

Adaptation, Psychological↗

PubMed1984

Comparison of immunologic and enzymatic assay of prostatic acid phosphatase for follow-up and assessment of clinical status of stage D prostate cancer.

Prostatic acid phosphatase (PAP) was measured in 70 patients with stage D prostate cancer under different modalities of treatment. PAP was determined by radioimmunoassay (RIA), counter immunoelectrophoresis (CIEP), and enzymatic method using alpha-naphthyl phosphate to compare the usefulness of the three methods in follow-up and assessing the clinical status of stage D prostate cancer. In the regressive state (29 patients), RIA and enzymatic methods correlated well; both gave 17% of abnormal results with a mean value of 4.7 +/- 4.6 and 3 +/- 1.7. Also, in the progressive state (17 patients) the two methods showed similar percentages of abnormal results with a mean value of 40 +/- 38 and 19 +/- 17 for RIA and enzymatic method, respectively. There was greater variability in the stable group owing to the difference in the tumour load. Again the two methods correlated well regarding their diagnostic sensitivity and specificity as a parameter for assessing the clinical response. CIEP, used as a qualitative method, showed more positive than negative results and did not correlate with the clinical state. We feel that the conventional enzymatic method is adequate for follow-up and assessing clinical state of stage D prostate cancer.

Acid Phosphatase↗

PubMed2003

Role of PI3K/AKT/mTOR signaling in the cell cycle progression of human prostate cancer.

Prostate cancer is one of the most common cancers among men. Recent studies demonstrated that PI3K signaling is an important intracellular mediator which is involved in multiple cellular functions including proliferation, differentiation, anti-apoptosis, tumorigenesis, and angiogenesis. In the present study, we demonstrate that the inhibition of PI3K activity by LY294002, inhibited prostate cancer cell proliferation and induced the G(1) cell cycle arrest. This effect was accompanied by the decreased expression of G(1)-associated proteins including cyclin D1, CDK4, and Rb phosphorylation at Ser780, Ser795, and Ser807/811, whereas expression of CDK6 and beta-actin was not affected by LY294002. The expression of cyclin kinase inhibitor, p21(CIP1/WAF1), was induced by LY294002, while levels of p16(INK4) were decreased in the same experiment. The inhibition of PI3K activity also inhibited the phosphorylation and p70(S6K), but not MAPK. PI3K regulates cell cycle through AKT, mTOR to p70(S6K). The mTOR inhibitor rapamycin has similar inhibitory effects on G(1) cell cycle progression and expression of cyclin D1, CDK4, and Rb phosphorylation. These results suggest that PI3K mediates G(1) cell cycle progression and cyclin expression through the activation of AKT/mTOR/p70(S6K) signaling pathway in the prostate cancer cells.

Cell Cycle↗

PubMed1999

Genetic predisposition to prostate cancer.

Prostate cancer has been known to run in families for about 40 years and epidemiological studies have demonstrated an increased risk to close relatives of cases. This risk rises markedly when the closeness and number of cases in a cluster increases. There has been considerable debate about the genetic model, in particular whether there is a commoner lower penetrance (moderately increased risk of the disease due to the gene(s)) in addition to contribution from high risk genes. For the first time, molecular results are starting to emerge, indicating the location of high risk genes. These have shown that there is evidence for more than one site of a high risk, gene two sites on chromosome 1 and one on chromosome X. These do not account for all clusters of prostate cancer cases and further genes remain to be discovered. This article also outlines the contribution of the numerous collaborators in the British Prostate Group to the UK Familial Prostate Cancer Study.

Journal Article↗

PubMed1989

Bone scintigraphy in patients with breast cancer, pulmonary cancer, uterine cervix cancer, and prostatic cancer. Statistical study of spinal accumulation cases.

This is a review of bone scintigraphy performed in patients with breast cancer, pulmonary cancer, uterine cervix cancer, and prostatic cancer from 1980 to 1985. The incidence of accumulation in the spine was 25.0% in breast cancer, 29.5% in lung cancer, 24.3% in cervical cancer, and 47.0% in prostatic cancer. The predominant location of the accumulation was the lumbar vertebra (68.9%), followed by the thoracic vertebra (45.0%), sacral vertebra (37.5%), and cervical vertebra (23.6%). The survivability after spinal accumulation was determined by the Kaplan-Meyer survival curve. The 1-year survival rate of breast cancer, pulmonary cancer, cervical cancer, and prostatic cancer was 88%, 19%, 74%, and 90%, respectively, the record of pulmonary cancer being significantly lower. Hence, in the treatment of patients with metastatic spinal tumors, the therapeutic method should be selected according to the underlying disease.

Adult↗

PubMed1993

Determining Local-Regional Extension of Prostate Cancer.

Prostate cancer evaluation and staging are based on the findings of clinical, radiological, and pathological studies. There has been a significant change in the type and availability of evaluative procedures in recent years. To summarize the current status of staging procedures, the role of computed tomography (CT), magnetic resonance imaging (MR), transrectal ultrasound (TRUS), lymph node dissection, and lymphangiogram in determining the extent of local and regional prostate cancer will be reviewed. CT has little utility in the assessment of local extension and is hampered in evaluating lymphatic metastasis because of a low sensitivity. However, CT is useful for radiotherapeutic treatment planning MR may provide better local disease assessment than TRUS, but TRUS is conducive to directed biospy of abnormalities. The role of laparoscopic lymph node dissection is expanding and early data seems to indicate that the procedure is similar to the more traditional procedure regarding the extent of anatomic dissection and number of lymph nodes removed for pathological examination. Stage migration occurs as staging procedures evolve and the proper role of staging procedures for prostate cancer must be considered to be a dynamic process, continually open for discussion and re-evaluation.

Journal Article↗

PubMed2005

Small-interfering RNA-induced androgen receptor silencing leads to apoptotic cell death in prostate cancer.

Prostate cancer is the second leading cause of cancer death in the United States and, thus far, there has been no effective therapy for the treatment of hormone-refractory disease. Recently, the androgen receptor (AR) has been shown to play a critical role in the development and progression of the disease. In this report, we showed that knocking down the AR protein level by a small interfering RNA (siRNA) approach resulted in a significant apoptotic cell death as evidenced by an increased annexin V binding, reduced mitochondrial potential, caspase-3/6 activation, and DFF45 and poly(ADP-ribose) polymerase cleavage. The apoptotic response was specifically observed in those siRNA-transfected cells that harbor a native AR gene. No cell death was found in the AR-null prostate cancer cell PC-3 or its subline that has been reconstituted with an exogenous AR gene, as well as two breast cancer cell lines that are AR positive. Moreover, in parallel with the siRNA-induced AR silencing, the antiapoptotic protein Bcl-xL was significantly reduced, which might account for the apoptotic cell death because ectopic enforced expression of Bcl-xL protein partially inhibited apoptosis after AR silencing. Taken together, our data showed that knocking down the AR protein level in prostate cancer cells leads to apoptosis by disrupting the Bcl-xL-mediated survival signal downstream of AR-dependent survival pathway.

Annexin A5↗

PubMed2006

[The treatment options for localized prostate cancer].

Prostate cancer is a very common tumor in men. Today the disease is very often diagnosed early because of an elevated PSA without symptoms and the disease is localized to the prostate. Patients with prostate cancer can be divided into 3 subgroups for the carcinoma: favorable, moderate, and poorly. The grouping depends mainly on the Gleason score of the prostate biopsy. According to the Gleason score, favorable cancer is up to score 6 (3 + 3), moderate score 7, and poor--Gleason score 8-10. The other favorable clinical factors are PSA < 10 ng/ml, and clinical stage by DRE of T1C or T2 (no nodule or palpable nodule not extending beyond the prostatic capsule). The treatment options for cure when the prostate cancer is localized are either radical prostatectomy or radiotherapy (external or brachytherapy or combination). Each of these therapies has side effects and each has advantages and disadvantages. Sometimes the treatment choice is not for cure and the options are hormonal treatment or watchful waiting. Twenty to 30% of the patients treated for cure may fail the treatment and have elevation of PSA without any clinical symptoms, or signs of local recurrence or distant spread. Some of these patients with biochemical failure may be cured by salvage treatment: radiotherapy after radical prostatectomy and salvage radical prostatectomy or cryotherapy following failure of radiotherapy.

Humans↗

PubMed1998

Linkage analysis of chromosome 1q markers in 136 prostate cancer families. The Cancer Research Campaign/British Prostate Group U.K. Familial Prostate Cancer Study Collaborators.

Prostate cancer shows evidence of familial aggregation, particularly at young ages at diagnosis, but the inherited basis of familial prostate cancer is poorly understood. Smith et al. recently found evidence of linkage to markers on 1q, at a locus designated "HPC1," in 91 families with multiple cases of early-onset prostate cancer. Using both parametric and nonparametric methods, we attempted to confirm this finding, in 60 affected related pairs and in 76 families with three or more cases of prostate cancer, but we found no significant evidence of linkage. The estimated proportion of linked families, under a standard autosomal dominant model, was 4%, with an upper 95% confidence limit of 31%. We conclude that the HPC1 locus is responsible for only a minority of familial prostate cancer cases and that it is likely to be most important in families with at least four cases of the disease.

Chromosomes, Human, Pair 1↗

PubMed2000

The role of candidate genetic polymorphisms in the etiology of prostate cancer.

Prostate cancer appears to result from complex interactions among genetic, endocrine and environmental factors. Identification of risk factors for development and progression of prostate cancer is needed. This will allow researchers to design strategies to reduce the morbidity and mortality from this cancer and to identify individuals at increased risk of developing the disease. It is probable that common genetic polymorphisms (variants) in genes directly and indirectly involved in androgen biosynthesis, metabolism and regulation are important. Other important genes are likely to be those directly involved in regulation of prostate cell proliferation and apoptosis.Prostate Cancer and Prostatic Diseases (2000) 3, 236-240

Journal Article↗

PubMed1992

Prostate-specific antigen levels in 1695 men without evidence of prostate cancer. Findings of the American Cancer Society National Prostate Cancer Detection Project.

The American Cancer Society National Prostate Cancer Detection Project is a prospective, multidisciplinary, and multicenter trial to assess the potential for early detection of prostate cancer by transrectal ultrasonography (TRUS), digital rectal examination (DRE), and serum prostate-specific antigen assay (PSA). By November 1990, 2805 men between the ages of 55 and 70 years with no known signs or symptoms of prostate cancer were enrolled in the study, which is planned to run for 5 years. Annual TRUS, DRE, and PSA tests were done on these subjects, and biopsies were recommended for suspicious lesions when detected. To study the performance of PSA testing in presumed normal subjects, all men were eliminated who had (1) prostate cancer detected on their initial examinations and proven by biopsy or (2) cancer detected during the year or subsequent examinations. Additionally, all men with TRUS or DRE findings that were interpreted as suspicious for cancer but who are being followed and have not yet had biopsies done were removed from this series. This left a unique, extensively screened group of 1695 men who were free of prostate cancer, as far as could be determined. Analyses of the PSA levels in this large population in the appropriate age range for increasing risk of prostate cancer revealed several important findings. First, there was a direct relationship between serum PSA levels and estimated prostate volume for both the currently available monoclonal and polyclonal PSA assays. Individuals with benign prostatic hyperplasia and larger gland volume have a higher normal limit of PSA than men with normal gland volume. Second, analyses showed no relationship between age and PSA levels or between symptoms of prostatism and PSA levels independent of gland enlargement. It was concluded that volume-adjusted upper limits of normal PSA can be determined for different levels of specificity desired. This information may be applicable to the use of PSA in men not already suspected of having prostate cancer and may increase its effectiveness as a tool for early detection.

Age Factors↗

PubMed1998

Prostate cancer and prostate bed SPECT imaging with ProstaScint: semiquantitative correlation with prostatic biopsy results.

BACKGROUND: ProstaScint (Cytogen Corporation, Princeton, NJ) murine monoclonal antibody imaging is FDA-approved for imaging of prostate cancer patients at high risk for metastatic disease and patients postprostatectomy with a rising serum prostate-specific antigen (PSA) level. ProstaScint is a murine monoclonal antibody which targets prostate-specific membrane antigen (PSMA). PSMA expression is upregulated in primary and metastatic prostate cancer. FDA Cytogen (Princeton, NJ) protocol studies using 111indium-labeled ProstaScint revealed correlation between areas of increased concentration in the prostate and biopsy-proven tumors in patients imaged pretherapy. METHODS: In our study, four transverse, single-photon emission tomography (SPECT) images were isolated and regions of interest were selected and correlated with pretherapy prostate biopsy results. Prostate cancer and normal tissue prostate/muscle background (P/M) ratios were derived, so that postprostatectomy/radiation therapy patients could be evaluated for the presence of residual prostate cancer. Twenty-three pretherapy prostate cancer patients with quadrant/sextant biopsies had SPECT 96-hr 111indium ProstaScint pelvic images. The four transverse 1-cm slices above the midline penile blood pool were chosen, and four to six 27-30-pixel regions of interest were placed over the prostate bed. The background muscle region of interest was placed over the external obturator muscle region. The P/M ratio was calculated and compared to the quadrant/sextant prostatic biopsy result. The same procedure was applied to 17 posttherapy prostate cancer patients with rising PSA. RESULTS: In the 23 pretherapy prostate cancer patients, there was a correlation between the P/M ratio of at least 3.0 in 32 of 35 prostatic cancer biopsy regions, and there was correlation with P/M ratios less than 3.0 in 82 of 89 negative biopsy regions. Seventeen posttherapy patients underwent ProstaScint studies. Six underwent biopsy, with typically one biopsy site per patient. All 6 had P/M ratios greater than 3.0 in the biopsied region. Five out of six biopsies revealed residual prostate cancer. CONCLUSIONS: A prostate/muscle ratio was developed from 111indium ProstaScint regions of interest obtained on 1-cm SPECT transverse slices through the prostate bed in 23 patients preprostatic cancer therapy. A P/M ratio above 3.0 correlated in the majority of positive cases, and a P/M ratio below 3.0 was demonstrated in negative prostatic biopsy cases. The P/M ratio of above 3.0 or below 3.0 also separated those posttherapy prostate cancer patients with rising PSA who had residual prostate carcinoma in the prostate bed.

Aged↗