National Cancer Institute®
Last Modified: July 1, 2002
UI - 11598447
AU - Lopez Cubillana P; Martinez Barba E; Prieto A; Server Pastor G; Sola J;
TI - Nicolas JA; Garcia Hernandez JA; Gomez G; Martinez Pertusa P; Perez Albacete M; Banon V; Valdelvira P; Guardiola A; Castillo D; Cao E; Alonso JD Oat-cell carcinoma of the prostate. Diagnosis, prognosis and therapeutic implications.
SO - Urol Int 2001;67(3):209-12
AD - Service of Urology, Virgen de la Arrixaca Hospital, E-30009 Murcia, Spain. email@example.com
BACKGROUND: Any carcinoma of prostatic origin which is not an acinary adenocarcinoma of the prostate is considered to be an atypical carcinoma. One member of this group of atypical prostatic tumors is the oat-cell carcinoma, or small cell carcinoma (SCC) of the prostate. This variety of carcinoma constitutes the histologic basis of <1% of all prostatic neoplasms. METHODS: Between 1992 and 1997, four patients were diagnosed with SCC of the prostate at our hospital. In 3 of the 4 cases, the histopathological diagnosis was pure SCC, and in the 4th case there was a component of prostatic adenocarcinoma associated with the SCC. At the time of diagnosis, extracapsular extension of the tumor was present in all 4 cases, with T3 or higher stages in all of them (T(3A)N(0)M(1), T(3A)N(0)M(0), T(3B)N(0)M(1), and T(4)N(0)M(0)). Because of the presence of extracapsular extension, radiotherapy and radical surgery were ruled out for all 4 patients. They were all offered systemic chemotherapy with cyclophosphamide (1 g/m(2)), doxorubicin (50 mg/m(2)) and vincristine (1.2 mg/m(2)). This therapeutic protocol was carried out in only 2 cases. RESULTS: Survival was <1 year in the 3 patients with pure SCC, and the patient with a mixed tumor is alive with detectable disease 9 months after diagnosis. CONCLUSIONS: This poor vital prognosis in SCC stresses the need for early diagnosis a timely and appropriate therapeutic intervention in this condition. Copyright 2001 S. Karger AG, Basel
UI - 11598448
AU - Borchers H; Brehmer B; van Poppel H; Jakse G
TI - Radical prostatectomy in patients with previous groin hernia repair using synthetic nonabsorbable mesh.
SO - Urol Int 2001;67(3):213-5
AD - Urologic Clinic, University Clinic of RWTH Aachen, Pauwelsstrasse 30, D-52057 Aachen, Germany.
OBJECTIVE: Identification of patients in whom the perineal route is the optimal approach to perform radical prostatectomy. MATERIAL AND METHODS: During 1992-1999, 376 patients with prostate cancer underwent radical perineal prostatectomy. Four patients were identified in whom the perineal approach was indicated because of previous bilateral groin hernia repair using synthetic meshes. In addition, 1 patient underwent perineal prostatectomy elsewhere for similar reasons. RESULTS: The perineal approach offered an uneventful surgical solution for an adequate and straightforward radical perineal prostatectomy without complications and without biochemical recurrence during the follow-up. CONCLUSION: Radical perineal prostatectomy is suggested to be the optimal approach in patients with previous bilateral groin hernia repair using synthetic, nonabsorbable meshes. Copyright 2001 S. Karger AG, Basel
UI - 11598449
AU - Suzuki S; Tadakuma T; Kunitomi M; Takayama E; Sato M; Asano T; Nakamura
TI - H; Hayakawa M Liposome-mediated gene therapy using HSV-TK/ganciclovir under the control of human PSA promoter in prostate cancer cells.
SO - Urol Int 2001;67(3):216-23
AD - Department of Urology, National Defense Medical College, 302 Namiki, Tokorozawa, Saitama 359-8513, Japan. firstname.lastname@example.org
To more accurately determine the tissue-specific expression of the target gene in prostate cancer cells, we introduced the enhancer element (-4,777 to -3,934; PSAR) and the promoter region (PSAP) of the prostate-specific antigen (PSA) gene. Furthermore, to elucidate the advantages of using liposomes as a gene carrier, we screened more than 20 liposome preparations in this study. The 5' upstream region of PSA gene (PSARPSAP) was conjugated to either the chloramphenicol acetyltransferase (CAT) gene or herpes simplex virus thymidine kinase (TK) gene, and the transfection of these plasmids was carried out using cationic liposomes, DMRIE-C (Gibco) or LipoTAXI (Stratagene). The expression of CAT activity was clearly observed when PSARPSAP-CAT plasmid was transfected into PSA-positive LNCaP cells, whereas no CAT activity was detected in PSA-negative DU145 cells or bladder carcinoma T24 cells. The CAT activity increased after the addition of testosterone. We then evaluated the therapeutic effect of the PSARPSAP-TK plasmid in vitro. When PSARPSAP-TK plasmid was transfected and ganciclovir was added to the medium, the growth of LNCaP cells was inhibited, while no growth inhibition was observed in DU145 cells. Furthermore, this inhibitory effect was observable even when the cells were cultured in a medium supplemented with dialyzed fetal bovine serum. These results suggest that the liposome-mediated transfection of PSARPSAP-TK appears to be a potentially effective approach for selecting the optimal treatment for tumor cells producing PSA even with the low androgen levels seen in patients treated by anti-androgen therapy. Copyright 2001 S. Karger AG, Basel
UI - 9622059
AU - Segawa T; Takebayashi H; Kakehi Y; Yoshida O; Narumiya S; Kakizuka A
TI - Prostate-specific amplification of expanded polyglutamine expression: a novel approach for cancer gene therapy.
SO - Cancer Res 1998 Jun 1;58(11):2282-7
AD - The 4th Department, Osaka Bioscience Institute, Suita, Japan.
For cancer gene therapy, it is of primary importance to develop a system to sufficiently and selectively express therapeutic genes in cancer cells. In this study, we showed that an approximately 5.3-kb promoter region of the prostate-specific antigen (PSA) gene can replicate the endogenous expression pattern, although its expression is very weak. We then developed a novel two-step transcriptional activation system in which the PSA promoter drives an artificial transcriptional activator, GAL4-VP16 fusion protein, and it in turn activates transgene expressions under the control of GAL4-responsive elements. By using this system, transgene expressions can be greatly augmented while maintaining prostate-specific expression. Finally, we applied this system to drive an expanded polyglutamine, a potent proapoptotic molecule, to induce apoptosis selectively in PSA-positive prostate cancer cells. This novel system would provide an ideal approach for cancer gene therapy applicable not only to prostate cancer but to other cancers as well.
UI - 11173145
AU - Sanchez-Nieto B; Nahum AE; Dearnaley DP
TI - Individualization of dose prescription based on normal-tissue dose-volume and radiosensitivity data.
SO - Int J Radiat Oncol Biol Phys 2001 Feb 1;49(2):487-99
AD - Joint Department of Physics, Institute of Cancer Research and the Royal Marsden NHS Trust, Sutton, Surrey, UK. email@example.com
PURPOSE: The aim of this paper is to illustrate the potential gain in tumor control probability (TCP) of prostate cancer patients by individualizing the prescription dose according to both normal-tissue (N-T) dose-volume and radiosensitivity data. METHODS AND MATERIALS: Two exercises have been carried out. Firstly, patients' dose prescriptions were individualised on the basis of N-T dose-volume histograms (DVHs) alone and secondly modeling potential differences in N-T sensitivity as well. In both cases, the change in tumor control that may be achieved by individualizing patients' dose was estimated assuming that after the dose adjustments, every patient had (1) the same value of normal tissue complication probability (NTCP) (5%) and (2) NTCP equal to the average NTCP before individualization (i.e., without increasing the average NTCP). The Lyman-Kutcher-Burman NTCP model was used to predict the N-T response curves with two different sets of parameters. The first exercise, based only on individual NT DVHs (i.e., assuming all patient equally radiosensitive), was over a real population of 50 prostate cancer patients. The second exercise modeled a 10,000-prostate-cancer patient population with varying NT dose-volume distributions and radiosensitivity (through allowing TD(50) to vary). RESULTS: A gain of more than 9% in TCP was predicted when doses were individualized based only on DVHs so that every patient had 5% NTCP after dose adjustments. By adding the estimate of radiosensitivity, the gain increased to more than 15%. When the individualisation was performed without increasing the mean NTCP, then the potential gain in TCP was almost 5% (for adjustment based on DVH distribution solely) increasing to 7% with the additional consideration of radiosensitivity. CONCLUSIONS: There is a potential gain (increase in local tumor control) from dose individualisation strategies based on both N-T dose-volume data and radiosensitivity (assuming that this is available). Dose prescription individualization based only on dose-volume data can be exploited provided that reliable N-T response models are available. There will be additional gains if some estimate of N-T radiosensitivity is available to allow further patient stratification, identification of patients with high radiosensitivity being particularly important.
UI - 11458056
AU - Walsh PC; DeWeese TL; Eisenberger MA
TI - A structured debate: immediate versus deferred androgen suppression in prostate cancer-evidence for deferred treatment.
SO - J Urol 2001 Aug;166(2):508-15; discussion 515-6
AD - James Buchanan Brady Urological Institute and Departments of Urology and Oncology, The Johns Hopkins Medical Institutions, Baltimore, Maryland, USA.
PURPOSE: We present a structured debate supporting the premise that immediate hormonal intervention has not been conclusively shown to provide a survival advantage in the management of advanced prostate cancer. MATERIALS AND METHODS: The literature emphasizing randomized trials was reviewed. Recommendations are based solely on a demonstrated advantage in survival. RESULTS: In patients with stage Tx Nx Mo or MI disease who did not receive other primary therapy there is no demonstrated survival advantage to immediate hormonal therapy. In men with positive lymph nodes who underwent radical prostatectomy a relatively small study showed a survival advantage in favor of immediate hormonal treatment compared to deferred treatment. This study did not reach the projected accrual of 240 patients and results have not been supported by other trials. In men with stages T2-4 Nx Mx disease who underwent primary treatment with radiotherapy a survival advantage for early hormonal therapy is primarily limited to high risk subgroups. In patients with biochemical relapse following primary treatment there are no trials. CONCLUSIONS: Because hormonal therapy is associated with the development of irreversible resistance in virtually all patients, it does not cure, there is usually a long interval from first prostate specific antigen elevation to the development of metastatic disease, and hormonal therapy has profound side effects and is expensive, delayed treatment is recommended in men with biochemical relapse following surgery or radiotherapy. Patients should be strongly encouraged to enter clinical trials to answer this question.
UI - 11506741
AU - Kramer G; Steiner GE; Sokol P; Handisurya A; Klingler HC; Maier U; Foldy
TI - M; Marberger M Local intratumoral tumor necrosis factor-alpha and systemic IFN-alpha 2b in patients with locally advanced prostate cancer.
SO - J Interferon Cytokine Res 2001 Jul;21(7):475-84
AD - Department of Urology, University of Vienna, Austria. firstname.lastname@example.org
To examine tolerability and activity of local, intratumoral tumor necrosis factor-alpha (TNF-alpha) and systemic interferon-alpha2b (IFN-alpha2b) in locally advanced, hormone-resistant prostate cancer (LA-HRPC), 10 patients with LA-HRPC (T4N x M0, n = 3, T4N x M1, n = 5; T4N1M1, n = 2) were treated with recombinant TNF-alpha injected locally into prostate tumor tissue at 4-week intervals (maximum of four cycles) combined with intermittent subcutaneous (s.c.) administration of 5 x 10(6) IU IFN-alpha2b. Twenty-nine TNF-alpha cycles were administered. Despite significant TNF-alpha leakage into the systemic circulation 2 h after intraprostatic application (from a mean of 9 to a mean of 416 pg/ml; p = 0.0034), TNF-alpha (and IFN-alpha2b) was well tolerated (WHO grade 1-2 toxicity), possibly because of its rapid neutralization by increasing soluble 55-kDa and 75-kDa TNF receptor levels in the serum (mean increase 268% and 91%, respectively) at the same time. TNF-alpha induced prostate tumor cell necrosis in all patients, leading to a significant reduction of prostate volume in 9 of 10 cases (mean 38%; p = 0.0025). The significant short-term increase of prostate-specific antigen (PSA) (mean 65%; p < 0.001), tissue polypeptide-specific antigen (TPS) (mean 85%; p = 0.001), and possibly interleukin-8 (IL-8) (mean 2687%; p < 0.009) serum levels within 4 h after TNF-alpha confirmed the cytotoxic effect in vivo. In the long term, serum PSA levels dropped by 18%-87%, reaching the nadir value 7 weeks after baseline. Objective responses of metastases were not seen. Intraprostatic administration of TNF-alpha is feasible at a tolerable toxicity in patients with LA-HRPC and, thus, may be a new treatment option for these patients.
UI - 11728705
AU - Amer A; MacKay R
TI - In regard to Sanchez-Nieto et al. IJROBP 2001;49:487-499.
SO - Int J Radiat Oncol Biol Phys 2001 Dec 1;51(5):1437
UI - 11790277
AU - Porter C; O'Donnell C; Crawford ED; Gamito EJ; Errejon A; Genega E;
TI - Sotelo T; Tewari A Artificial neural network model to predict biochemical failure after radical prostatectomy.
SO - Mol Urol 2001 Winter;5(4):159-62
AD - Department of Urology, Veterans Affairs Medical Center, Washington, DC, USA.
BACKGROUND: Biochemical failure, defined here as a rise in the serum prostate specific antigen (PSA) concentration to >0.3 ng/mL or the initiation of adjuvant therapy, is thought to be an adverse prognostic factor for men who undergo radical prostatectomy (RP) as definitive treatment for clinically localized cancer of the prostate (CAP). We have developed an artificial neural network (ANN) to predict biochemical failure that may benefit clinicians and patients choosing among the definitive treatment options for CAP. MATERIALS AND METHODS: Clinical and pathologic data from 196 patients who had undergone RP at one institution between 1988 and 1999 were utilized. Twenty-one records were deleted because of missing outcome, Gleason sum, PSA, or clinical stage data. The variables from the 175 remaining records were analyzed for input variable selection using principal component analysis, decision tree analysis, and stepped logistic regression. The selected variables were age, PSA, primary and secondary Gleason grade, and Gleason sum. The records were randomized and split into three bootstrap training and validation sets of 140 records (80%) and 35 records (20%), respectively. RESULTS: Forty-four percent of the patients suffered biochemical failure. The average duration of follow up was 2.5 years (range 0-11.5 years). Forty-two percent of the patients had pathologic evidence of non-organ-confined disease. The average area under the receiver operator characteristic (ROC) curve for the validation sets was 0.75 +/- 0.07. The ANN with the highest area under the ROC curve (0.80) was used for prediction and had a sensitivity of 0.74, a specificity of 0.78, a positive predictive value of 0.71, and a negative predictive value of 0.81. CONCLUSION: These results suggest that ANN models can predict PSA failure using readily available preoperative variables. Such predictive models may offer assistance to patients and physicians deciding on definitive therapy for CaP.
UI - 11790278
AU - Tewari A; Issa M; El-Galley R; Stricker H; Peabody J; Pow-Sang J; Shukla
TI - A; Wajsman Z; Rubin M; Wei J; Montie J; Demers R; Johnson CC; Lamerato L; Divine GW; Crawford ED; Gamito EJ; Farah R; Narayan P; Carlson G; Menon M Genetic adaptive neural network to predict biochemical failure after radical prostatectomy: a multi-institutional study.
SO - Mol Urol 2001 Winter;5(4):163-9
AD - Josephine Ford Cancer Center and Department of Urology, Henry Ford Medical Center, Detroit, Michigan 48202, USA. Atiwari1@hfhs.org
BACKGROUND AND PURPOSE: Despite many new procedures, radical prostatectomy remains one of the commonest methods of treating clinically localized prostate cancer. Both from the physician's and the patient's point of view, it is important to have objective estimation of the likelihood of recurrence, which forms the foundation for treatment selection for an individual patient. Currently, it is difficult to predict the probability of biochemical recurrence (rising serum prostate specific antigen [PSA] concentration) in an individual patient, and approximately 30% of the patients do experience recurrence. Tools predicting the recurrence will be of immense practical utility in the treatment selection and planning follow up. We have utilized preoperative parameters through a computer based genetic adaptive neural network model to predict recurrence in such patients, which can help primary care physicians and urologists in making management recommendations. PATIENTS AND METHODS: Fourteen hundred patients who underwent radical prostatectomy at participating institutions form the subjects of this study. Demographic data such as age, race, preoperative PSA, systemic biopsy based staging and Gleason scores were used to construct a neural network model. This model simulated the functioning of a trained human mind and learned from the database. Once trained, it was used to predict the outcomes in new patients. RESULTS: The patients in this comprehensive database were representative of the average prostate cancer patients as seen in USA. Their mean age was 68.4 years, the mean PSA concentration before surgery was 11.6 ng/mL, and 67% patients had a Gleason sum of 5 to 7. The mean length of follow-up was 41.5 months. Eighty percent of the cancers were clinical stage T2 and 5% T3. In our series, 64% of patients had pathologically organ-confined cancer, 33% positive margins, and 14% had seminal vesicle invasion. Lymph node positive patients were not included in this series. Progression as judged by serum PSA was noted in 30.6%. With entry of a few routinely used parameters, the model could correctly predict recurrence in 76% of the patients in the validation set. The area under the curve was 0.831. The sensitivity was 85%, the specificity 74%, the positive predictive value 77%, and the negative predictive value of 83%. CONCLUSION: It was possible to predict PSA recurrence with a high accuracy (76%). Physicians desiring objective treatment counseling can use this model, and significant cost savings are anticipated because of appropriate treatment selection and patient-specific follow-up protocols. This technology can be extended to other treatments such as watchful waiting, external-beam radiation, and brachytherapy.
UI - 11792945
AU - Fourcade RO
TI - Re: A structured debate: immediate versus deferred androgen suppression in prostate cancer--evidence for deferred treatment.
SO - J Urol 2002 Feb;167(2 Pt 1):651-2; discussion 653
UI - 11799972
AU - Kirk D
TI - Re: A structured debate: immediate versus deferred androgen suppression in prostate cancer--evidence for deferred treatment.
SO - J Urol 2002 Feb;167(2 Pt 1):652, discussion 653
UI - 11829051
AU - Anonymous
TI - New drug for prostate cancer.
SO - Eur J Cancer Care (Engl) 2001 Jun;10(2):79-80
UI - 12050502
AU - Freedland SJ; Wieder JA; Jack GS; Dorey F; deKernion JB; Aronson WJ
TI - Improved risk stratification for biochemical recurrence after radical prostatectomy using a novel risk group system based on prostate specific antigen density and biopsy Gleason score.
SO - J Urol 2002 Jul;168(1):110-5
AD - Department of Urology, University of California Los Angeles School of Medicine and Veterans Administration Greater Los Angeles Healthcare System, 90095-1738, USA.
PURPOSE: Previous studies have suggested that prostate specific antigen (PSA) density is a significant independent predictor of biochemical failure after primary therapy. We determined whether pathological PSA density using surgical weight of the radical prostatectomy specimen was an independent predictor of adverse pathological features or biochemical recurrence after radical prostatectomy. We also examined whether combining pathological PSA density with biopsy Gleason score improved risk stratification compared with serum PSA and biopsy Gleason score for predicting PSA recurrence after prostatectomy. MATERIALS AND METHODS: Multivariate analysis was used to determine whether pathological PSA density was an independent predictor of adverse pathology or PSA recurrence after radical prostatectomy in 325 patients treated at a Veterans Affairs medical center. Cutoff points of pathological PSA density were generated to identify patients at various risks for biochemical recurrence. These cutoffs were combined with biopsy Gleason cutoff points 2 to 6, 7 and 8 to 10 to generate a risk stratification system that was compared with a previous risk stratification system using PSA and biopsy Gleason score cutoff points. The validity of the risk stratification system using pathological PSA density and biopsy Gleason score was evaluated in another cohort of 490 patients treated with radical prostatectomy at a tertiary care medical center. RESULTS: Pathological PSA density was an independent predictor of positive surgical margins (p <0.001), nonorgan confined disease (p <0.001), seminal vesicle invasion (p = 0.003) and biochemical recurrence after radical prostatectomy (p <0.001). The cutoff points for pathological PSA density of less than 0.3, 0.3 to 0.7 and greater than 0.7 ng./ml./gm. separated patients into 3 distinct groups at increasing risk for biochemical failure after radical prostatectomy (p <0.001). Pathological PSA density cutoffs combined with biopsy Gleason score cutoffs 2 to 6, 7 and 8 to 10 provided better risk stratification for biochemical failure than cutoffs based on a combination of PSA and biopsy Gleason score in patients treated at the Veterans Affairs (hazards ratio 3.04, confidence interval 2.25 to 4.11, p <0.001) and tertiary care (hazards ratio 2.38, confidence interval 1.78 to 3.18, p <0.001) medical centers. CONCLUSIONS: Pathological PSA density was a strong predictor of advanced pathology and biochemical failure after radical prostatectomy. Pathological PSA density combined with biopsy Gleason score defined a novel risk group system that improved risk stratification compared with a combination of PSA and biopsy Gleason score. These results were validated in another cohort of patients treated with radical prostatectomy at a tertiary care medical center. Further studies are required using PSA density values calculated from preoperative transrectal ultrasound measurements to determine whether a combination of PSA density and biopsy Gleason score provides significant pretreatment risk stratification.
UI - 12050525
AU - Curry EA 3rd; Sweeney CJ
TI - Resistance to luteinizing hormone releasing hormone agonist therapy for metastatic prostate cancer.
SO - J Urol 2002 Jul;168(1):193
AD - Purdue University School of Pharmacy and Pharmacal Sciences, West Lafayette and Indiana University School of Medicine, Indianapolis, Indiana, USA.
UI - 12065563
AU - Cross CK; Shultz D; Malkowicz SB; Huang WC; Whittington R; Tomaszewski
TI - JE; Renshaw AA; Richie JP; D'Amico AV Impact of race on prostate-specific antigen outcome after radical prostatectomy for clinically localized adenocarcinoma of the prostate.
SO - J Clin Oncol 2002 Jun 15;20(12):2863-8
AD - Department of Radiation Oncology, Brigham and Women's Hospital and Dana-Farber Cancer Institute, Boston, MA 02115, USA. email@example.com
PURPOSE: To compare prostate-specific antigen (PSA) outcome after radical prostatectomy (RP) for prostate cancer in African-American and white men using previously established risk groups. PATIENTS AND METHODS: Between 1989 and 2000, 2,036 men (n = 162 African-American men, n = 1,874 white men) underwent RP for clinically localized prostate cancer. Using pretreatment PSA, Gleason score, clinical T stage, and percentage of positive biopsy specimens, patients were stratified into low- and high-risk groups. For each risk group, PSA outcome was estimated using the actuarial method of Kaplan and Meier. Comparisons of PSA outcome between African-American and white men were made using the log-rank test. RESULTS: The median age and PSA level for African-American and white men were 60 and 62 years old and 8.8 and 7.0 ng/mL, respectively. African-Americans had a statistically significant increase in PSA (P =.002), Gleason score (P =.003), clinical T stage (P =.004), and percentage of positive biopsy specimens (P =.04) at presentation. However, there was no statistical difference in the distribution of PSA, clinical T stage, or Gleason score between racial groups in the low- and high-risk groups. The 5-year estimate of PSA outcome was 87% in the low-risk group for all patients (P =.70) and 28% versus 32% in African-American and white patients in the high-risk group (P =.28), respectively. Longer follow-up is required to confirm if these results are maintained at 10 years. CONCLUSION: Even though African-American men presented at a younger age and with more advanced disease compared with white men with prostate cancer, PSA outcome after RP when controlled for known clinical predictive factors was not statistically different. This study supports earlier screening in African-American men.
UI - 12065564
AU - Burkhardt JH; Litwin MS; Rose CM; Correa RJ; Sunshine JH; Hogan C;
TI - Hayman JA Comparing the costs of radiation therapy and radical prostatectomy for the initial treatment of early-stage prostate cancer.
SO - J Clin Oncol 2002 Jun 15;20(12):2869-75
AD - Research Department, American College of Radiology, Reston, VA, USA. firstname.lastname@example.org
PURPOSE: Radical prostatectomy and external-beam radiation are the most common treatments for localized prostate cancer. Given the absence of clinical consensus in favor of one treatment or the other, relative costs may be a significant factor. This study compares the direct medical costs during the month before and 9 months after diagnosis for patients treated primarily with external-beam radiation or radical prostatectomy for early-stage prostate cancer. METHODS: Patients age 65 or older and coded by the Surveillance, Epidemiology, and End Results (SEER) registry as having been diagnosed with adenocarcinoma of the prostate treated primarily with external-beam radiation or radical prostatectomy during 1992 and 1993 were identified. The initial treatment costs, as measured by Medicare-approved payment amounts, for each strategy were analyzed using linked SEER-Medicare claims data after adjusting for differences in comorbidity and age. An intent-to-treat analysis was also performed to adjust for differences in staging between the two groups. RESULTS: For patients in the treatment-received analysis, the average costs were significantly different; $14,048 (95% confidence interval [CI], $13,765 to $14,330) for radiation therapy and $17,226 (95% CI, $16,891 to $17,560) for radical prostatectomy (P <.001). The average costs for patients in the intent-to-treat analysis were also significantly less for radiation therapy patients ($14,048; 95% CI, $13,765 to $14,330) than for those who underwent radical prostatectomy ($17,516; 95% CI, $17,195 to $17,837; P <.001). CONCLUSION: For patients with early-stage prostate cancer, average costs during the initial treatment interval were at least 23% greater for radical prostatectomy than for external-beam radiation. Major limitations of the research include not studying costs after the initial treatment interval and questionable current applicability, given changes in management of early prostate cancer.
UI - 12086406
AU - Moran EM
TI - Epidemiological and clinical aspects of nonsteroidal anti-inflammatory drugs and cancer risks.
SO - J Environ Pathol Toxicol Oncol 2002;21(2):193-201
AD - Department of Medicine, University of California, Irvine, USA. email@example.com
It is well known that about 70% of cancer cases are due to environmental, dietary, or lifestyle factors. Accordingly, these cases maybe avoided by appropriate modifications. In addition, active chemoprevention has become a major interventional approach following the epidemiological observation of a beneficial effect of nonsteroidal anti-inflammatory drugs (NSAIDs) in colon cancer prevention. This is chiefly due to the inhibition of the cyclooxygenase (COX) enzymes. The COX enzymatic system includes two isoenzymes, COX-1 and COX-2, that convert arachidonic acid to prostaglandins. COX-1 is constitutively expressed and synthesizes cytoprotective prostaglandins in the gastrointestinal tract. COX-2 is inducible by the oncogenes ras and scr and other cytokines; it is overexpressed in human cancer cells in which it stimulates cellular division and angiogenesis and inhibits apoptosis. NSAIDs restore apoptosis and decrease tumor mitogenesis and angiogenesis. Most cancer cells have been found to exhibit overexpression of COX-2. Epidemiological studies showed a lower risk of developing cancer of the colon, breast, esophagus, and stomach following the ingestion of NSAIDs. The use of NSAIDs in low dose was associated with a statistically significant decrease in the risk of adenomatous polyps and of overt colon cancer. The regressive effects of sulindac on foci of aberrant crypts in the colon (considered to be precursors of adenoma), and on adenocarcinoma of the colon, are of particular interest because this NSAID does not have an inhibitory effect on COX. This may support the view that the antineoplastic effect of NSAIDs may also be due to a mechanism other than COX-2 inhibition. In breast cancer, large cohort studies reported a 40 to 50% reduced risk of developing cancer, a smaller size of the primary tumor, and a reduction in the number of involved axillary lymph nodes. Similar findings have been reported in the esophagus and stomach, but not in gastric cardia adenocarcinoma. The recent development of selective COX-2 inhibitors resulted in better clinical tolerance than that associated with NSAIDs in general, with the absence of gastrointestinal side effects known to occur after the inhibition of COX-1. Encouraging results have been obtained with these new agents in familial adenomatous polyposis, colon, breast, and prostate cancer.
UI - 11887621
AU - Witjes JA
TI - [Guidelines for follow-up of patients with prostate carcinoma]
SO - Ned Tijdschr Geneeskd 2002 Feb 23;146(8):360-2
AD - Universitair Medisch Centrum St Radboud, afd. Urologie, Postbus 9101, 6500 HB Nijmegen. firstname.lastname@example.org
The follow-up investigation of patients with prostate cancer is mainly conducted on the basis of complaints, serum prostate-specific antigen and digital rectal examination. Other investigations, such as bone scintigraphy, are only performed on indication. The frequency and duration of the follow-up investigation, as well as the consequences of the findings during this, depend on the stage of the disease, the patient's wishes and the possibilities of additional treatment.
UI - 12027414
AU - Kaminski JM; Nguyen K; Buyyounouski M; Pollack A
TI - Prostate cancer gene therapy and the role of radiation.
SO - Cancer Treat Rev 2002 Feb;28(1):49-64
AD - Department of Radiation Oncology, Fox Chase Cancer Center, 7701 Burolme Avenue, Philadelphia, PA 19111, USA. JM_Kaminski@FCCC.edu
Even though prostate cancer is detected earlier than in the pre-PSA era, prostate cancer is the second leading cause of cancer mortality in the American male. Prostate cancer therapy is not ideal, especially for high-risk localized and metastatic cancer; therefore, investigators have sought new therapeutic modalities such as angiogenesis inhibitors, inhibitors of the cell signaling pathway, vaccines, and gene therapy. Gene therapy has emerged as potential therapy for both localized and systemic prostate cancer. Gene therapy has been shown to work supra-additively with radiation in controlling prostate cancer in vivo. With further technological advances in radiation therapy, gene therapy, and the understanding of prostate cancer biology, gene therapy will potentially have an important role in prostate cancer therapy. Copyright 2002 Elsevier Science Ltd. All rights reserved.
UI - 11482451
AU - Serafin AM; Binder AB; Bohm L
TI - Chemosensitivity of prostatic tumour cell lines under conditions of G2 block abrogation.
SO - Urol Res 2001 Jun;29(3):221-7
AD - Department of Radiation Oncology, University of Stellenbosch Medical Faculty, Tygerberg, South Africa.
Conventional chemotherapy has had very limited success in the control of hormone-refractory prostate cancer. Methylxanthine derivatives, such as pentoxifylline (PTX), are known to abrogate the G2 block and enhance the toxicity of ionising irradiation and chemotherapeutic agents. It is now also established that late addition of the cytotoxic drug after irradiation under conditions of G2 block abrogation sensitises human tumour cells for cytotoxins. Here we assess whether the chemosensitivity of prostate tumour cell lines can be enhanced by the application of a low dose of drug in conjunction with a G2 block abrogator. Prostate cell lines DU145, BM1604 and LNCaP were irradiated with 7 Gy 60Co gamma-irradiation. A sub-toxic (2 mM) dose of pentoxifylline and a cytotoxic drug were added at maximum expression of the G2 cell cycle block and cell survival was determined by colony assay. Cisplatin, etoposide and vinblastine were tested at a toxic dose of 10% (TD10). In the TP53 mutant cell lines, DU145 and BM1604, dose enhancement factors (EFs) were found to be in the region of 4.20 for cisplatin, 3.70 for vinblastine, and 3.20 for etoposide. In the TP53 wild-type cell line, LNCaP, the enhancement factors were low and in the region of 1.20 for cisplatin, vinblastine and etoposide. It is clear, therefore, that toxicity enhancement factors (EFs) are greater in the TP53 mutant cell lines, DU145 and BM1604, than in the TP53 wild-type cell line, LNCaP. The results indicate that a significant enhancement of drug toxicity can be obtained if the cytotoxic drug is given under conditions of G2 block abrogation. The sensitisation of prostate cancer cells to cytotoxic drugs is particularly high in radiation-resistant TP53 mutant tumour cells. Drugs which abrogate G2 block have the potential to enhance the therapeutic index and therefore reduce the toxicity of chemotherapy drugs.
UI - 11770521
AU - Cella L; Lomax A; Miralbell R
TI - New techniques in hadrontherapy: intensity modulated proton beams.
SO - Phys Med 2001;17 Suppl 1():100-2
AD - Dipartimento di Scienze Fisiche, Universita di Napoli, Napoli, Italy.
Inverse planning and intensity modulated (IM) X-ray beam treatment techniques can achieve significant improvements in dose distributions comparable to those obtained with forward planned proton beams. However, intensity modulation can also be applied to proton beams and further optimization in dose distribution can reasonably be expected. A comparative planning exercise between IM X-rays and IM proton beams was carried out on two different tumor cases: a pediatric rhabdomyosarcoma and a prostate cancer. Both IM X-rays and IM protons achieved equally homogenous coverage of the target volume in the two tumor sites. Predicted NTCPs were equally low for both treatment techniques. Nevertheless, a reduced low-to-medium dose to the organs at risk and a lesser integral non-target mean dose for IM protons in the two cases favored the use of IM proton beams.
UI - 11785860
AU - Yong VT
TI - Interviewing men on sensitive issues.
SO - Contemp Nurse 2001 Sep;11(1):18-27
AD - Department of Psychological Medicine, Monash Medical Centre, Monash University, Clayton, Melbourne.
The body alterations of men with prostate cancer affect their sexual functioning and raise common issues for men with this disease. This study examines these issues with the use of in-depth interviewing to collect sensitive data. The intention here is not to report the findings of the main study but to discuss broad methodological and practical issues raised by the research method of in-depth interviewing. Interviews were conducted with 30 men with prostate cancer and it was found that access, sensitivity of the research topic, the environment and a number of psychological factors profoundly affected the interview process. The researcher's position in the study is that of the interviewer but she is also a nurse by profession. The findings will have implications for future studies which utilise in-depth interviewing as a research method to collect sensitive data.
UI - 11824894
AU - Henry AM; Ash DV
TI - Prostate cancer treated with brachytherapy in a group of patients who previously underwent pelvic radiotherapy for testicular cancer.
SO - Clin Oncol (R Coll Radiol) 2001;13(6):490
UI - 11876163
AU - Meyer-Siegler K
TI - COX-2 specific inhibitor, NS-398, increases macrophage migration inhibitory factor expression and induces neuroendocrine differentiation in C4-2b prostate cancer cells.
SO - Mol Med 2001 Dec;7(12):850-60
AD - Department of Research and Development, Bay Pines Veteran's Administration Medical Center, FL 33744, USA. email@example.com
BACKGROUND: Cyclooxygenase-2 (COX-2) is an inducible enzyme involved in the conversion of arachadonic acid to prostaglandins and other eicosaniods. Persistent COX-2 expression is associated with multiple forms of cancer.Therefore, there is much interest in COX-2 specific, non-steroidal anti-inflammatory drug use for cancer chemotherapy. The mechanism by which these drugs inhibit tumor growth and progression is unclear, and our knowledge about their potential to prevent or treat prostate cancer is inadequate. MATERIALS AND METHODS: The effects of NS-398, a selective COX-2 inhibitor, on human prostate carcinoma cell line LNCaP and the LNCaP subline C4-2b were investigated in this study. NS-398 effects on apoptosis were examined by caspase-3 activity increase, as well as internucleosomal cleavage. ELISA and PCR were used to determine inhibitor effects on macrophage migration inhibitory factor (MIF) and COX-2 production. RESULTS: At 10 microM, NS-398 treatment resulted in increased production of COX-2 and the pro-inflammatory cytokine, MIF by the C4-2b LNCaP subline. NS-398 (10 microM) induces apoptosis in LNCaP cells, but not in the more aggressive, androgen-unresponsive C4-2b cells. The C4-2b cells were observed to continue to proliferate when treated with NS-398 and continued to retain malignant phenotype characteristics. NS-398 treatment resulted in C4-2b cell differentiation into an unusual neuroendocrine-like cell. These neuroendocrine-like cells produced both epithelial (cytokeratin 18 and prostate specific antigen) and neuronal (neuron-specific enolase and chromogranin A) proteins. Furthermore, this C4-2b cellular response to NS-398