Cancer Treatment Today » Prostate Cancer

Bone scan in staging prostate cancer- pro

M Levin, MD — Wed, 02 Oct 2013 16:20:23 +0000

Staging of any cancer requires an assessment of distant metasases. At the same time, for most cancer types, groups that have too low of a chance of having metastatic diseae can be defined, and generally these groups can be spared the cost and discomfort of imaging to look for them.

The American Urological Association (AUA) and the European Association of Urology (EAU) and NCCN provide guideliens that have a bearing on this question in prostate cancer. The AUA guideline provides no specific indications concerning imaging for patients undergoing radical prostatectomy. However, the PSA best practice statement of the AUA guidelines reports that routine imaging staging and bone scans are not necessary in every case of diagnosed prostate cancer. In particular, imaging is thought unnecessary if the PSA is <25 ng/mL and bone scans are not recommended when PSA is <20 ng/mL.

The EAU guidelines on prostate cancer were first published in 2001 and recently ( and frequently) updated. The latest version in 2011 says that a bone scan to rule out skeletal metastases may not be appropriate in asymptomatic patients if the serum PSA level is less than 20 ng/mL in the presence of well or moderately differentiated tumors. TThe NCCN on p. PROS-1 defiens the appropriate group for bone scanning to be T1 and PSA >20,T2 and PSA >10,Gleason score 8,T3, T4, symptomatic disease.

Guidelines for the management of clinically localized prostate cancer: 2007 update,” http://www.auanet.org/content/guidelines-and-quality-care/clinical-guidelines/main-reports/proscan07/content.pdf.

“Prostate-specific antigen best practice statement: 2009 update,” http://www.auanet.org/content/media/psa09.pdf.

A Heidenreich, M Bolla, S Joniau, et al., “EAU guidelines on prostate cancer,” European Association of Urology, 2011.

nccn, Prostate 2013

A. Simonato et al, Adherence to Guidelines among Italian Urologists on Imaging Preoperative Staging of Low-Risk Prostate Cancer: Results from the MIRROR (Multicenter Italian Report on Radical Prostatectomy Outcomes and Research) Study, Advances in Urology
Volume 2012 (2012), Article ID 651061, 6 pages

Xtandi in prostate cancer patients not treated with docetaxel – pro

M Levin, MD — Fri, 16 Nov 2012 16:12:34 +0000

Enzalutamide (Xtandi, MDV3100) is an androgen receptor antagonist drug reported to cause an up to an 89% decrease in PSA levels after a month of use. It is more potent than Casodex. Enzalutamide has approximately fivefold higher binding affinity for the androgen receptor (AR). It also does not promote translocation of AR to the nucleus and it prevents binding of AR to DNA and AR to coactivator proteins.

In August of 2012, the U.S. Food and Drug Administration approved enzalutamide for the treatment of castration-resistant prostate cancer in patients who failed docetaxel. This was based on the AFFIRM study results. AFFIRM showed that Enzalutamide significantly prolonged the survival of men with metastatic castration-resistant prostate cancer after chemotherapy(Scher et al). The PREVAIL study that is directly investigating Xtandi before docetaxel is still ongoing: A Multinational Phase 3, Randomized, Double-Blind, Placebo-Controlled Efficacy and Safety Study of Oral MDV3100 in Chemotherapy-Naive Patients With Progressive Metastatic Prostate Cancer Who Have Failed Androgen Deprivation Therapy.

There is current evidence to support the use of Xtandi for patients who had not or cannot receive docetaxel. Median time to radiographic progression in one phase II study by Scher, 2010, was 56 weeks for chemo-naive patients and 25 weeks for patients previously treated with chemotherapy. There are several studies, however, that have been initiated. There is a phase II trial began in March 2011 comparing MDV3100 with Casodex in patients patients who have progressed while on LHRH analogue therapy (e,g., leuprorelin) or surgical castration. This ASPIRE trial is an an open-label study intended to evaluate the effects of enzalutamide in about 150 men who are theoretically eligible to receive chemotherapy but have chosen not to do this. Another phase II study, STRIVE trial is a randomized, double-blind, multi-center clinical study of the efficacy and safety study of enzalutamide (160 mg/day) compared to bicalutamide (50 mg/day) in men with recurrent prostate cancer who have serologic and/or radiographic disease progression subsequent to primary androgen deprivation therapy (ADT). The TERRAIN trial, is a randomized, double-blind, multi-center, Phase II trial designed to test the efficacy and safety of enzalutamide compared to bicalutamide (Casodex) in men with metastatic prostate cancer already controlled by either bilateral orchiectomy (surgical castration) or ongoing androgen deprivation therapy with an LHRH agonist or an LHRH antagonist at a stable dose. There are also combination trials.

Recently, results were released of the large phase III PREVAIL trial evaluating enzalutamide against placebo in chemotherapy-naive men with metastatic castration-resistant prostate cancer (mCRPC) amount to another big win for the rationally designed “super-antiandrogen” . An interim analysis uncovered such dramatic improvements with enzalutamide in overall survival and radiographic progression-free survival—the co-primary endpoints of the study—that the investigators stopped the trial early in October 2013 at the behest of the Independent Data Monitoring Committee and offered enzalutamide to the patients who were originally assigned the placebo.
Recenlty FDA approved Xtandi without preceding docetaxel: “XTANDI is indicated for the treatment of patients with metastatic castration-resistant prostate cancer (CRPC).”.

Tran C, Ouk S, Clegg NJ, Chen Y, Watson PA, Arora V, Wongvipat J, Smith-Jones PM, Yoo D, Kwon A, Wasielewska T, Welsbie D, Chen CD, Higano CS, Beer TM, Hung DT, Scher HI, Jung ME, Sawyers CL (May 2009). “Development of a second-generation antiandrogen for treatment of advanced prostate cancer”. Science 324 (5928): 787–90.

Howard I Scher MD,Tomasz M Beer MD,Celestia S Higano MD,Aseem Anand MA,Mary-Ellen Taplin MD,Eleni Efstathiou MD,Dana Rathkopf MD,Julia Shelkey BS,Evan Y Yu MD,Joshi Alumkal MD,David Hung MD,Mohammad Hirmand MD,Lynn Seely MD,Michael J Morris MD,Daniel C Danila MD,John Humm PhD,Steve Larson MD,Martin Fleisher PhD,Charles L Sawyers MD,the Prostate Cancer Foundation/Department of Defense Prostate Cancer Clinical Trials Consortium Antitumour activity of MDV3100 in castration-resistant prostate cancer: a phase 1–2 study The Lancet – 24 April 2010 ( Vol. 375, Issue 9724, Pages 1437-1446 ), see also Scher HI, Fizazi K, Saad F, et al. N Engl J Med. 2012;367:1187-1197

William L Dahut,Ravi A Mada Revisiting the ultimate target of treatment for prostate cancer The Lancet – 24 April 2010 ( Vol. 375, Issue 9724, Pages 1409-1410 )

Scher HI, Beer TM, Higano CS, Anand A, Taplin ME, Efstathiou E, Rathkopf D, Shelkey J, Yu EY, Alumkal J, Hung D, Hirmand M, Seely L, Morris MJ, Danila DC, Humm J, Larson S, Fleisher M, Sawyers CL; Prostate Cancer Foundation/Department of Defense Prostate Cancer Clinical Trials Consortium Antitumour activity of MDV3100 in castration-resistant prostate cancer: a phase 1-2 study.
.Lancet. 2010 Apr 24;375(9724):1437-46.

Mukherji D, Pezaro CJ, De-Bono JS. MDV3100 for the treatment of prostate cancer.Expert Opin Investig Drugs. 2012 Feb;21(2):227-33.

For Lay version see here

IMRT for prostate cancer – pro

M Levin, MD — Sun, 23 Sep 2012 16:52:15 +0000

IMRT is a rapidly evolving technique, which affords a more precise radiation dose delivery of escalated doses, in appropriate cases, to targeted tumors, while sparing nearby healthy tissue structures. The FDA clearance of numerous devices for the technical delivery of IMRT is based on the capability of this technology to incorporate accurate dose calculation algorithms, associated with a verifiable dose distribution, as managed by the treating physician, (i.e., radiation oncologist). Although, to date, no randomized trials have matured to document long-term outcomes data and efficacy for IMRT, the scientific evidence currently available indicates that IMRT permits better treatment planning and sparing of surrounding tissues, which is of particular usefulness with “Radiosensitive” tumors of the head/neck, prostate and CNS lesions where the target volume is in close proximity to critical healthy structures that must be protected. These results may be extrapolated to the treatment of other cancers at other anatomic sites; however, a number of technical issues need to be resolved before IMRT can be recommended routinely for lung cancer use, particularly the issue of tumor mobility must be addressed, (e.g., a lung tumor moving with respiration)” . CCited from: htttp://atc.wustl.edu/home/NCI/NCI_IMRT_Guidelines_2006.pdf

Currently, there are no randomized controlled trials of IMRT compared with other radiation techniques for treatment of prostate cancer. Non-randomized studies consistently demonstrate reduced rates of toxicity in IMRT-treated patients. The 2010 Agency for Healthcare Research and Quality (AHRQ) comparative evaluation of radiation treatments for clinically localized prostate cancer concluded that data on comparative effectiveness between different forms of radiation treatments are inconclusive with respect to overall or disease-specific survival. In addition, the AHRQ technology assessment states that more studies of better quality are needed to confirm or refute the suggested findings in the studies that compared outcomes in patients treated with different forms of radiation therapy.

Sheets NC, Goldin GH, Meyer AM, et al. Intensity-modulated radiation therapy, proton therapy, or conformal radiation therapy and morbidity and disease control in localized prostate cancer. JAMA 2012; 307:1611.

Alongi F, Fiorino C, Cozzarini C, et al. IMRT significantly reduces acute toxicity of whole-pelvis irradiation in patients treated with post-operative adjuvant or salvage radiotherapy after radical prostatectomy. Radiother Oncol 2009; 93:207.

Zelefsky MJ, Levin EJ, Hunt M, et al. Incidence of late rectal and urinary toxicities after three-dimensional conformal radiotherapy and intensity-modulated radiotherapy for localized prostate cancer. Int J Radiat Oncol Biol Phys 2008; 70:1124

Blue Cross Blue Shield Association. Special Report: Intensity Modulation Radiation Therapy for Cancer of the Breast or Lung. TEC Assessment. Chicago, IL. December 2005; 20 (13)

Das, I., Cheng, C., Chopra, K., et al. Intensity modulated radiation therapy dose prescription, recording, and delivery: patterns of variability among institutions and treatment planning systems. Journal of the National Cancer Institute. 2008.National Cancer Institute (NCI). National Cancer Institute Guidelines for the use of Intensity Modulated Radiation Therapy in Clinical Trials. Bethesda, MD: NCI; January 14, 2005

Agency for Healthcare Research and Quality (AHRQ) Technology Assessments. Comparative evaluation of radiation treatments for clinically locazlized prostate cancer: an update. Available from: http://www.cms.gov/coveragegeninfo/downloads/id69ta.pdf

Wilt TJ, Shamliyan T, Taylor B et al. Comparative effectiveness of therapies for clinically localized prostate cancer. Comparative Effectiveness Review No. 13. Agency for Healthcare Research and Quality. February 2008.

Pearson SD, Ladapo, Prosser L. Intensity modulated radiation therapy (IMRT) for localized prostate cancer. Institute for Clinical and Economic Review. 2007.

Staffurth, J. A review of the clinical evidence for intensity-modulated radiotherapy. Clin Oncol (R Coll Radiol). 2010 Oct;22(8):643-57.

Zelefsky, MJ, Levin, EJ, Hunt, M, et al. Incidence of late rectal and urinary toxicities after three-dimensional conformal radiotherapy and intensity-modulated radiotherapy for localized prostate cancer. Int J Radiat Oncol Biol Phys. 2008 Mar 15;70(4):1124-9.

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Taxotere and Xeloda for prostate cancer – pro

M Levin, MD — Thu, 13 Sep 2012 15:11:34 +0000

The Xeloda and Taxotere regimen is supported by several phase II studies and is also in a clinical study, NCT00258284: Capecitabine and Docetaxel in Treating Patients With Metastatic Prostate Cancer. This study is ongoing, but not recruiting participants.

The available studies in metastatic or neaodjuvant setting show some responses but the most recent study of 2008 was dissapointing. “A total of 15 patients were treated, of whom 6 (40%) experienced a 50% or greater decrease in prostate specific antigen with infrequent diarrhea or hand-foot syndrome. Eleven patients underwent radical prostatectomy. There were no pathological complete responses and 4 patients demonstrated mild histological changes, including focal necrosis and vacuolated cytoplasm. While there was no discernable pattern of increased thymidine phosphorylase expression, 4 specimens showed decreased survivin expression, suggesting a possible mechanism for chemotherapy induced apoptosis. There was no correlation of prostate specific antigen response and survivin expression, and no increase in serum CK18Asp396. ”

Friedman J, Dunn RL, Wood D, Vaishampayan U, Wu A, Bradley D, Montie J, Sarkar FH, Shah RB, Hussain M.Neoadjuvant docetaxel and capecitabine in patients with high risk prostate cancer J Urol. 2008 Mar;179(3):911-5; discussion 915-6.

C. Soto, S. Reyes, F. Delgadillo, M. Ramirez, L. Torrecillas, L. Perez, H. Benitez, G. Cervantes, R. Zamora, A. Silva Capecitabine (X) plus docetaxel (T) vs capecitabine plus paclitaxel (P) vs sequential capecitabine then taxane in anthracycline pretreated patients (pts) with metastatic Proc Am Soc Clin Oncol 22: 2003 (abstr 28)

Jean-Marc Ferrero et al, Phase II trial evaluating a docetaxel-capecitabine combination as treatment for hormone-refractory prostate cancer Cancer Cytopathology
Volume 107 Issue 4, Pages 738 – 745

CIalis for erectile dysfuncton after prostate cancer – pro

M Levin, MD — Thu, 13 Sep 2012 15:07:32 +0000

Erectile dysfunction is common among patients treated for prostate cancer. It is greatest among those treated with prostatectomy; More than half of men who undergo radical prostatectomy for prostate cancer experience erectile dysfunction. It also occurrs among those treated iwth radiation and seed implants. More than 80% of prostate cancer patients develop erectile dysfunction (ED) as a result of treatment, regardless of whether they have surgery or external beam radiation therapy. Less clear is how it can be surmounted. One study shoed that Sildenafil is well tolerated and effective in improving erectile function of patients with ED after 3D-CRT for prostate cancer. Another study is ongoing:
Sildenafil in Treating Erectile Dysfunction in Patients With Prostate Cancer, NCT00057759. Cialis appears to imprve erectile dysfunctoni in two randomized European trials. I consider it supported by medical llterature.

David C. Miller, John T. Wei, Rodney L. Dunn, James E. Montie, Hector Pimentel, Howard M. Sandler, P. William McLaughlin and Martin G. Sanda. Use of medications or devices for erectile dysfunction among long-term prostate cancer treatment survivors: Potential influence of sexual motivation and/or indifference Urology, Volume 68, Issue 1 , July 2006, Pages 166-171

RISK OF ERECTILE DYSFUNCTION SIMILAR FOR DIFFERENT PROSTATE CANCER TREATMENTS
CA Cancer J Clin 2001 51: 148-149

Incrocci L, Slob AK, Hop WC. Tadalafil (Cialis) and erectile dysfunction after radiotherapy for prostate cancer: an open-label extension of a blinded trial.Urology. 2007 Dec;70(6):1190-3.

Eardley I, Gentile V, Austoni E, Hackett G, Lembo D, Wang C, Beardsworth A.
Efficacy and safety of tadalafil in a Western European population of men with erectile dysfunction.BJU Int. 2004 Oct;94(6):871-7.

Proton Beam Radiotherapy and prostate cancer – pro

M Levin, MD — Thu, 13 Sep 2012 15:05:47 +0000

Charged-particle beams consisting of protons or helium ions are a type of particulate radiation therapy that contrast with conventional electromagnetic (i.e., photon) radiation therapy due to the unique properties of minimal scatter as the particulate beams pass through the tissue, and deposition of the ionizing energy at a precise depth (i.e., the Bragg Peak). Thus radiation exposure to surrounding normal tissues is minimized. The theoretical advantages of protons and other charged-particle beams may improve outcomes but this has not been proven. At the same time proton beam radiotherapy is significantly more expensive than other modalities.1

A recent review concluded: “While there is growing enthusiasm for the use of protons in the treatment of prostate cancer, a review of the literature suggests that there is so far no clear evidence to show that proton therapy would be superior to highly conformal photon treatments. As the use of protons in prostate cancer will no doubt become more widespread in the coming years, there is urgent need for a randomized trial of IMRT vs protons to provide us with concrete clinical data about the relative merits and potential risks of each type of therapy. The possibility of launching such a trial is currently being explored by the RTOG.” 2

Until results from such a trial are available, we continue to view protons in prostate cancer as a modality with tremendous promise. As it comes with a relatively high price tag, however, proton therapy must remain under scrutiny until it has proven itself against the best possible alternative.”

Y. Lievens, W. den BogaertProton beam therapy: Too expensive to become true?. Radiotherapy and Oncology, Volume 75, Issue 2, Pages 131-133 2005Beyer DC, Reed DR, Roach III M, Merrick G, Michalski JM, Moran BJ, Rosenthal SA, Rossi CJ, Carroll PR, Higano CS, Expert Panel on Radiation Oncology-Prostate. ACR Appropriateness Criteria® definitive external beam irradiation in stage T1 and T2 prostate cancer. [online publication]. Reston (VA): American College of Radiology (ACR); 2007. 20 p. [103 references]

PAUL L. NGUYEN, Which Is Best for Treating Prostate Cancer? Proton-Beam vs Intensity-Modulated Radiation Therapy June 1, 2008 Oncology. Vol. 22 No. 7

NCCN Prostate Cancer 2016

S. Patel et al, Recommendations for the referral of patients for proton-beam therapy, an Alberta Health Services report: a model for Canada?
Curr Oncol. 2014 Oct; 21(5): 251–262.

Leukine for prostate cancer – pro

M Levin, MD — Thu, 13 Sep 2012 15:04:15 +0000

Granulocyte macrophage colony-stimulating factor is a pleiotropic cytokine capable of inducing systemic immune responses against experimental and human tumors. GM-CSF stimulates the differentiation of hematopoietic progenitors to monocytes and neutrophils, and reduces the risk for febrile neutropenia in cancer patients. GM-CSF also has been shown to induce the differentiation of myeloid dendritic cells (DCs) that promote the development of T-helper type 1 (cellular) immune responses in cognate T cells. This review summarizes some of the immunological effects of GM-CSF relevant to antitumor immunity in cancer patients. GM-CSF has been used to augment the activity of rituximab in patients with follicular lymphoma and to induce autologous antitumor immunity in patients with hormone-refractory prostate cancer. A number of studies and reports focus on its activity, alone or in combination, for prostate cancer. It has been used with thalidomide, revlimid, provenge and a variety of other drugs and vaccines as an immunolodulator. It remains in active investigation, and clinicaltrials.gov lists 43 trials of various kinds with Leukine in prostate cancer. It is not recommended by any guideline or consensus statement.
J. A. Garcia, P. Triozzi, S. Smith, B. I. Rini, T. Gilligan, D. Peereboom, P. Elson, E. Klein, R. Dreicer Abstract Phase I/II study of lenalidomide and GM-CSF in hormone refractory prostate cancer (HRPC). No: 229 2007 Prostate Cancer Symposium

Prostate Cancer Immunology: Biology, Therapeutics, and Challenges
W. S. Webster, E. J. Small, B. I. Rini, and E. D. Kwon
JCO November 10, 2005 23:8262-8269

Immunotherapeutics in Development for Prostate Cancer
A. L. Harzstark andE. J. Small
The Oncologist April 1, 2009 14:391-398

Testosterone replacement after prostatectomy for prostate cancer – pro

M Levin, MD — Thu, 13 Sep 2012 15:02:54 +0000

Little evidence exists on the safety of TRT initiation after treatment for primary prostate cancer. Agarwal et al. treated 10 hypogonadal men, treated for organ-confined prostate cancer, with TRT for a median of 18 months. They reported no PSA recurrence in all men with associated significant symptomatic improvement in quality of life indices. However, there are no documented large and long-term studies proving that the risk of recurrence is not affected by TRT in men treated with definitive therapy. A known risk of recurrence or biochemical failure after radical prostatectomy is estimated to be 10-20% within 15 years indicating that the possibility of micrometastasis at the time of diagnosis is real and substantial. On the other hand, there are strong indications that normal testosterone levels play a protective role in the natural history of prostate cancer. Many studies have demonstrated that a low testosterone level prior to treatment is an independent predictor of a more aggressive, high-grade cancer, an increased likelihood of extraprostatic disease at the time of diagnosis, and a decreased likelihood of a favorable treatment response.This group reported no PSA recurrence in all men with associated significant symptomatic improvement in quality of life indices. However, there are no documented large and long-term studies proving that the risk of recurrence is not affected by TRT in men treated with definitive therapy. A known risk of recurrence or biochemical failure after radical prostatectomy is estimated to be 10-20% within 15 years indicating that the possibility of micrometastases at the time of diagnosis is real and substantialIt is generally thought that prostate cancer is an absolute contraindication for testosterone therapy, as recommended by the WHO from the Third International Consensus Consultation on Prostate Cancer in 2002. Recommendations of The International Society for The Study of the Aging Male (ISSAM) say that ‘Androgen administration is absolutely contraindicated in men suspected of having carcinoma of the prostate or breast Cancer. However, increasing numbers of men who are hypogonadal and whose cancer were at a very early stage, has led to increasing use of testosterone. Most information is in patients treated with prostatectomy as opposed to radiation, for early prostate cancer. More recent data suggest that this recommendation can be modified in select cases, that is, when cancer is undetectable and the patient has documented hypogonadism. In men aged over 40 years without prostate cancer, DRE and PSA levels must be shown to be normal before testosterone replacement therapy is started. Follow-up monitoring at 3-6 months for the first year, then yearly thereafter has been recommended

Morales A, Lunenfeld B. Investigation, treatment and monitoring of late-onset hypogonadism in males. Official recommendations of ISSAM. Aging Male 2002; 5: 74-86.

Agarwal PK, Oefelein MG. Testosterone replacement therapy after primary treatment for prostate cancer. J Urol 2005; 173: 533-536.

Brawer MK. Testosterone replacement therapy for a man with prostate cancer. Rev Urol 2004; 6(Suppl 6): S35-37.

Rhoden EL, Morgentaler A. Risks of testosterone-replacement therapy and recommendations for monitoring. N Engl J Med 2004; 350: 482-492.

Prostate Px – pro

M Levin, MD — Thu, 13 Sep 2012 14:25:43 +0000

Risk assessment can be useful to clinicians because it allows assessment of risk versus benefit of partcular treatments. Risk assessment methods currently used for newly diagnosed prostate cancer patients have disadvantages. THey include: D’Amico risk categories, Partin probability tables, University of California, San Francisco-Cancer of the Prostate Risk Assessment risk score, and Kattan nomograms; all rely heavily on traditional clinical variables (eg, serum prostate-specific antigen level, Gleason score, and clinical stage) to estimate risk of various outcomes. Using nomograms maximizes the predictive ability of each factor, allowing for an individualized characterization of risk compared with risk categories or probability tables.

Another approach relies of characterization and analysis of the cancer tissue obtained from a patient. Clinical data is integrated with an analysis of each patient’s cancer using spatial analysis of tissue histology and examining molecular biomarkers, such as androgen receptor, associated with disease progression. This approach represents a cutting edge of diagnostic science, sometimes termed, “Personalized Medciine”. The concept that one can individualize cancer therpay based on specific tumor characteristics is attractive but needs to be proven before being widely adapted. As of now, there is little evidence to support it and no guidelines or professional bodies recommending it.

Prostate Dx is one such test. It uses its own method of data analysis derived from a large patient cohort to generate a personalized report that is sent to the physician for discussion with the patient. This processand information remains proprietary and not peer-reviewed. This testing has not been cleared (or reviewed) by the U.S. Food and Drug Administration (FDA) becasue the company has indicated that Prostate Px does not require FDA approval. The test is considered a laboratory developed test (LDT) and is performed in Aureon’s Clinical Laboratory Improvement Act (CLIA)-certified, College of American Pathologists (CAP)-accredited, New York State-regulated laboratory.

Studies are ongoing to improve standardization and to determine whether this test can enhance prediction of prostate cancer recurrence and risk compared with current standard methods. Memorial Sloan-Kettering Cancer Center is currently recruiting candidates for a prospective study to determine if there is a small peptide mass protein pattern in blood that can distinguish men with clinically latent prostate cancer from men with more a more advanced disease state.

William T Lowrance, and Peter T Scardino,Predictive Models for Newly Diagnosed Prostate Cancer Patients

Rev Urol. 2009 Summer; 11(3): 117–126.

Donovan, Michael J., PhD, MD, et al., “Systems Pathology: A Paradigm Shift in the Practice of Diagnostic and Predictive Pathology, Cancer, Vol. 115, No. 13, July 1, 2009, pp. 3078–3084.

Eggener, Scott E., MD, et al., “Comparison of Models to Predict Clinical Failure after Radical Prostatectomy, Cancer, Vol. 115, January 15, 2009, pp. 303-310.

HAYES Update Search, “Prostate Px® (Aureon Laboratories Inc.) for Prediction of Recurrence of Prostate Cancer,” Lansdale, PA: HAYES, Inc., January 6, 2012.

Triptorelin in prostate cancer – pro

M Levin, MD — Thu, 13 Sep 2012 14:24:20 +0000

Triptorelin is a gonadotropin-releasing hormone agonist. By causing constant stimulation of the pituitary, it decreases pituitary secretion of gonadotropins luteinizing hormone (LH) and follicle stimulating hormone (FSH). Like other GnRH agonists, triptorelin may be used in the treatment of hormone-responsive cancers such as prostate cancer. TRELSTAR DEPOT is indicated in the palliative treatment of advanced prostate cancer. It offers an alternative treatment for prostate cancer when orchiectomy or estrogen administration are either not indicated or unacceptable to the patient.

Watson Pharma. Trelstar LA 11.25 mg (triptorelin pamoate for injectable suspension) prescribing information. Corona, CA: 2006 Aug.

Heyns, Chris F Triptorelin in the Treatment of Prostate Cancer: Clinical Efficacy and Tolerability, American Journal of Cancer:
2005 – Volume 4 – Issue 3 – pp 169-183