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  2. pauldhodson

    New radioactive Lutetium trial in the USA

    Thanks Jim, This trial is also happening here in Oz. (See: https://www.anzup.org.au/content.aspx?page=lutetiumprostatecancertrial) I asked my MO if I could participate and I was put forward, but assessed to be ineligible as I'm responding well to Enzalutamide and my PSA in not over 20 Ug/L. I intend to get the infusions privately in any case. Cheers Paul (from Perth).
  3. Yesterday
  4. Jim - was this the trial in which Paul Hobson GRHS participated? O&U, rd
  5. Last week
  6. Jim Marshall (not a doctor) said ... The problem Prostate cancer patients last much longer than most other cancer patients. This bonus has a darker side. Men with prostate cancer have had to wait years longer to see the results of treatments tests (called clinical trials). To take a local example, researchers led by Damien Bolton followed Victorian men who had had a radical prostatectomy between 1995 and 2000, and followed them up for about 10 years. Their report was published in 2014 (PMID: 23824175). Nineteen years! Some of the men studied can be expected to last more than 20 years - a total of twenty-nine years to see that result is anyone continues the study. The problem has been that men and their doctors have been interested in survival - will men live longer on a treatment. And to see how many men survive and how many die, you have to wait a long time. First solution The first solution to the problem was to try the drugs first on men who had tried everything else first. On average they should die soon-ish and you get results in only a few years. New solution - look at scans Rathkopf and others did some research to help speed up the process. They looked at the data from a trial that had gone the full length - the PREVAIL trial. This trial had started accepting men in 2010, and published its results in 2016. Then, for each man in the study, they looked at: how long it took for each man's scans to get worse; and how long they survived. There was a pretty good match - on average, if a man took a long time before the cancer seen on his scans got worse, he lasted a longer time. So, this research has given us much shorter clinical study times. We don't have to wait to count heads in years to come. We just have to see if, on average, a new treatment keeps scans from getting worse longer than the best existing treatment. Statistics - not a rule It's important to note that this works on statistics - on the average of the men's times. As usual, the group giving the average will be well spread out. So, some men with shorter times to scan worsening will actually live longer than the average. And vice versa, some unlucky men with long times to scan worsening may not live as long. Results for all prostate cancer treatments are highly individual. New trials are happening based on this new knowledge. Decisions will be made on how well the treatment affects what show up on the men's scans. Using this new information Two trials have looked at men whose primary hormone therapy is not holding the cancer, and their PSA is rising, but there is no sign of metastases (mets, new cancers growing away from the prostate). The PROSPER trial is looking at treating these men with Xtandi (Enzalutamide). The SPARTAN trial is looking at treating these men with Erleada (apalutamide). Both trials are looking mainly at how long a man takes to have his scans get worse. This has already led to the FDA in the USA approving the use of Erleada (apalutamide) for men in this position, and similar approval is expected for Xtandi (Enzalutamide). Newish guidelines for the Pharmaceutical Benefits Advisory Committee (PBAC) should make approval in Australia happen in a reasonable time. ... end Jim ============================= JAMA Oncol. 2018 May 1;4(5):694-701. doi: 10.1001/jamaoncol.2017.5808. Radiographic Progression-Free Survival as a Clinically Meaningful End Point in Metastatic Castration-Resistant Prostate Cancer: The PREVAIL Randomized Clinical Trial. Rathkopf DE1, Beer TM2, Loriot Y3, Higano CS4, Armstrong AJ5, Sternberg CN6, de Bono JS7, Tombal B8, Parli T9, Bhattacharya S10, Phung11, Krivoshik A12, Scher HI1, Morris MJ1. Author information In Library Abstract IMPORTANCE: Drug development for metastatic castration-resistant prostate cancer has been limited by a lack of clinically relevant trial end points short of overall survival (OS). Radiographic progression-free survival (rPFS) as defined by the Prostate Cancer Clinical Trials Working Group 2 (PCWG2) is a candidate end point that represents a clinically meaningful benefit to patients. OBJECTIVE: To demonstrate the robustness of the PCWG2 definition and to examine the relationship between rPFS and OS. DESIGN, SETTING, AND PARTICIPANTS: PREVAIL was a phase 3, randomized, double-blind, placebo-controlled multinational study that enrolled 1717 chemotherapy-naive men with metastatic castration-resistant prostate cancer from September 2010 through September 2012. The data were analyzed in November 2016. INTERVENTIONS: Patients were randomized 1:1 to enzalutamide 160 mg or placebo until confirmed radiographic disease progression or a skeletal-related event and initiation of either cytotoxic chemotherapy or an investigational agent for prostate cancer treatment. MAIN OUTCOMES AND MEASURES: Sensitivity analyses (SAs) of investigator-assessed rPFS were performed using the final rPFS data cutoff (May 6, 2012; 439 events; SA1) and the interim OS data cutoff (September 16, 2013; 540 events; SA2). Additional SAs using investigator-assessed rPFS from the final rPFS data cutoff assessed the impact of skeletal-related events (SA3), clinical progression (SA4), a confirmatory scan for soft-tissue disease progression (SA5), and all deaths regardless of time after study drug discontinuation (SA6). Correlations between investigator-assessed rPFS (SA2) and OS were calculated using Spearman ρ and Kendall τ via Clayton copula. RESULTS: In the 1717 men (mean age, 72.0 [range, 43.0-93.0] years in enzalutamide arm and 71.0 [range, 42.0-93.0] years in placebo arm), enzalutamide significantly reduced risk of radiographic progression or death in all SAs, with hazard ratios of 0.22 (SA1; 95% CI, 0.18-0.27), 0.31 (SA2; 95% CI, 0.27-0.35), 0.21 (SA3; 95% CI, 0.18-0.26), 0.21 (SA4; 95% CI, 0.17-0.26), 0.23 (SA5; 95% CI, 0.19-0.30), and 0.23 (SA6; 95% CI, 0.19-0.30) (P < .001 for all). Correlations of rPFS and OS in enzalutamide-treated patients were 0.89 (95% CI, 0.86-0.92) by Spearman ρ and 0.72 (95% CI, 0.68-0.77) by Kendall τ. CONCLUSIONS AND RELEVANCE: Sensitivity analyses in PREVAIL demonstrated the robustness of the PCWG2 rPFS definition using additional measures of progression. There was concordance between central and investigator review and a positive correlation between rPFS and OS among enzalutamide-treated patients. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT01212991. PMID: 29522174 PMCID: PMC5885186 DOI: 10.1001/jamaoncol.2017.5808 Free PMC Article
  7. Claude

    lutetium 177 treatment any experience

    My husband had 2 infusions with no results at all. The PSA went from 85 to 200 after the 1st one . We were told it is a flare up ( PSA climbing because the cancer cells died) then to 400 after the 2sd infusion, , the bone scan showing an increase activity of the Mets, the traitment was stopped. He is now on Xtandy and the P.sa had gone down to 373 new blood test in about 2 weeks. Pain wise the traitment did very little for my husband
  8. Jim Marshall (not a doctor) said ... Radioactive Lutetium is being trialled in a few places around the world as a treatment for end-stage, progressive, metastatic, castrate resistant prostate cancer. The current best treatment for end-stage, progressive, metastatic, castrate resistant prostate cancer is a chemotherapy drug Jevtana (Cabazitaxel). Phase I and II trials look to see if a treatment is safe. Phase III trials test it against the best current treatment. A new trial of Lutetium-177 has started in the USA. The trial is called PROter. Phoenix Molecular Imaging Center is the only listed location on ClinicalTrials.gov so far. The trial is phase I/II, looking at safety and best dose for later phase III trials. PSMA is a compound found on the surface of many prostate cells. Prostate cancer cells often have more than 10 times as much PSMA on their surfaces than ordinary prostate cells. All radioactive Lutetium treatments consist of: a PSMA grabber; a joiner; and radioactive Lutetium. The PSMA grabber grabs on to PSMA on the cell surface, bringing the radioactive Lutetium close enough to damage the cell. It seems from the press release that the joiner in the PROter trial is called R2. PSMA = Prostate Specific Membrane Antigen Thanks to Alan Barlee for bringing this to our attention ... end Jim
  9. susan horn

    lutetium 177 treatment any experience

    Hi my husband is considering a trial in New York with Lu-PSMA wondering how everyone who has tried this is doing a year later and if you can repeat the dose there are two trials one just gives one large dose I think 8 and the other is a trial that is opening soon thank you Susan Horn wondering of it helps with bone Mets and pain
  10. The results have now been published of the recent Lutetium-177 trial. Lutetium is a metal. Lutetium-177 is a manufactured form of Lutetium which is radioactive. Its half-life is 6.5 days. This means it is active for long enough to kill cancer cells, but is then cleared from the body. This 30 man trial was to test for safety, effectiveness, and quality of life. The treatment is still experimental until a trial compares Lutetium-177 for the best treatment available now. Such a trial is now open, comparing Lutetium-177 to the chemotherapy Jevtana (Cabazitaxel), the best proven treatment we have now. From PubMed: [177Lu]-PSMA-617 radionuclide treatment in patients with metastatic castration-resistant prostate cancer (LuPSMA trial): a single-centre, single-arm, phase 2 study. Hofman MS1, Violet J2, Hicks RJ3, Ferdinandus J4, Thang SP4, Akhurst T3, Iravani A4, Kong G4, Ravi Kumar A4, Murphy DG5, Eu P4, Jackson P4, Scalzo M4, Williams SG2, Sandhu S6. Author information In Library Abstract BACKGROUND: Progressive metastatic castration-resistant prostate cancer is a highly lethal disorder and new effective therapeutic agents that improve patient outcomes are urgently needed. Lutetium-177 [177Lu]-PSMA-617, a radiolabelled small molecule, binds with high affinity to prostate-specific membrane antigen (PSMA) enabling beta particle therapy targeted to metastatic castration-resistant prostate cancer. We aimed to investigate the safety, efficacy, and effect on quality of life of [177Lu]-PSMA-617 in men with metastatic castration-resistant prostate cancer who progressed after standard treatments. METHODS: In this single-arm, single-centre, phase 2 trial, we recruited men (aged 18 years and older) with metastatic castration-resistant prostate cancer and progressive disease after standard treatments, including taxane-based chemotherapy and second-generation anti-androgens, from the Peter MacCallum Cancer Centre, Melbourne, VIC, Australia. Patients underwent a screening PSMA and FDG-PET/CT to confirm high PSMA-expression. Eligible patients had progressive disease defined by imaging (according to Response Evaluation Criteria In Solid Tumours [RECIST] or bone scan) or new pain in an area of radiographically evident disease, and were required to have an Eastern Cooperative Oncology Group (ECOG) performance status score of 2 or lower. Eligible patients received up to four cycles of intravenous [177Lu]-PSMA-617, at six weekly intervals. The primary endpoint was PSA response according to Prostate Cancer Clinical Trial Working Group criteria defined as a greater than 50% PSA decline from baseline and toxicity according to CTCAE. Additional primary endpoints were imaging responses (as measured by bone scan, CT, PSMA, and FDG PET/CT) and quality of life (assessed with the EORTC-Q30 and Brief Pain Inventory-Short Form questionnaires), all measured up to 3 months post completion of treatment. This trial is registered with the Australian New Zealand Clinical Trials Registry, number 12615000912583. FINDINGS: Between Aug 26, 2015, and Dec 8, 2016, 43 men were screened to identify 30 patients eligible for treatment. 26 (87%) had received at least one line of previous chemotherapy (80% docetaxel and 47% cabazitaxel) and 25 (83%) received prior abiraterone acetate, enzalutamide, or both. The mean administered radioactivity was 7·5 GBq per cycle. 17 (57%) of 30 patients (95% CI 37-75) achieved a PSA decline of 50% or more. There were no treatment-related deaths. The most common toxic effects related to [177Lu]-PSMA-617 were grade 1 dry mouth recorded in 26 (87%) patients, grade 1 and 2 transient nausea in 15 (50%), and G1-2 fatigue in 15 (50%). Grade 3 or 4 thrombocytopenia possibly attributed to [177Lu]-PSMA-617 occurred in four (13%) patients. Objective response in nodal or visceral disease was reported in 14 (82%) of 17 patients with measurable disease. Clinically meaningful improvements in pain severity and interference scores were recorded at all timepoints. 11 (37%) patients experienced a ten point or more improvement in global health score by the second cycle of treatment. INTERPRETATION: Our findings show that radionuclide treatment with [177Lu]-PSMA-617 has high response rates, low toxic effects, and reduction of pain in men with metastatic castration-resistant prostate cancer who have progressed after conventional treatments. This evidence supports the need for randomised controlled trials to further assess efficacy compared with current standards of care. FUNDING: None. Copyright © 2018 Elsevier Ltd. All rights reserved. PMID: 29752180
  11. Agenda Friday 22 June 2018 You must dial in - we do NOT dial you. Landline - Anywhere in Australia - 25 cents Phone numbers only in email. Problem? Contact Jim Apologies From Jim Marshall who may need to exit quickly to visit N&S. Late starters Maybe you haven't had access to the agenda or you have late breaking news you would like to share. Tell the chairman here at the beginning of the meeting that you would like to speak, and he will fit you in - probably later, perhaps right now if that suits. Getting the most from standard drugs Convenor Jim Marshall was one of a number of our members who attended the 2017 PCRI Annual Conference in Los Angeles. The PCRI conference is the largest prostate cancer patient conference in the world. One of the speakers at the conference was Dr Luke Nordquist. Part of his presentation was about getting the most out of standard treatments for prostate cancer. Jim was impressed with this will attempt to tell members the gist of his approach. Roundtable - new stories, updates, questions Any man who wishes is welcome to contribute here. We will start with an update from member Noel Preston from Redland Bay in Queensland. Noel needs to choose his next treatment. He recently withdrew from a clinical trial before it started because he was not happy with the treatment option he was selected for. His current choices include a new clinical trial or to resume a former treatment. Formal end The Chair will declare the formal part of the teleconference closed at his discretion, perhaps around 11am. The teleconference lines will be kept open until at least 11:30 for anyone who wishes to continue discussions, update his health, or just chat. Informal chat Any topic you like - topics we didn't reach, something discussed earlier you wish to comment on, an update on your health, how your new boat is going, moaning about the weather, anything that you wish to say. Disclaimer This Community does not give medical advice. No members are authorised to give medical advice. Ask your doctor if you hear anything here that you think may be related to your treatment. Time 9:30am - 11:00am Eastern Standard Time (Queensland) The formal phone-in meeting ends after 90 minutes. The lines are kept open for up to an hour after that for members to informally chat. Daylight savings times Brisbane 9:30am Sydney, Melbourne, Hobart: 10:30am Adelaide, 10:00am Perth 7:30am Winter times Brisbane 9:30am Sydney, Melbourne, Hobart9:30am Adelaide 9:00am Perth7:30am Daylight saving ends first Sunday in April Daylight saving starts first Sunday in October Mobile phone warning The costs of mobile calls are nothing to do with the Advanced Prostate Cancer Support Group or with PCFA. They are between you and your phone provider (Optus, Telstra, Virgin, Vodafone, etc). If you dial one of the capital city numbers given above from a mobile phone, the cost to you will be the cost on your mobile phone plan. If your plan gives you free, or low cost local calls, and you are in one of these cities, it should be free, or a local call. If your plan gives you free, or local cost national calls that should work too. Be sure - call your provider, give the number you might be calling, and check the cost for you to call that number. Speaking time We want many voices to be heard. If you are a member listed to speak below, the chair will probably expect you to take no more than about 5 minutes on presentation so there is plenty of time for others to respond. Special Guest Speakers are invited to speak for 10-15 minutes, then field questions. Guidelines No noise House - radio, TV, computer, pets, other phones, conversation Yourself - mute button, or mouthpiece away from mouth Phone - call waiting off (#43#), Mute button or hang up to leave the room. No mute button? ##4 to mute, ##5 to unmute. Cordless phone - don't carry, put on folded handkerchief to limit reverberation Other calls - Please do NOT use call waiting or another line on the same phone to take another call - members around Australia are left listening to your 'hold' music until you return. Speaker phone Please do NOT use a speaker phone, unless you are very good at keeping it Mute, and at lifting and using the hand piece when you wish to join in the conversation. Mobile phone You will need enough charge for the length of the call, or take the call with your charger plugged in. Speaking Speak clearly into mouthpiece in ordinary voice. Say who you are when signing in, and each time you speak. Listen for the gavel. The Chair may need to interrupt. It's a meeting of 20 people, not a simple phone conversation. If you are not one of the two people in the particular conversation at the time, keep your mute button down and let others contribute. Help the secretary by later emailing details for the minutes.Restarting You may hang up and sign in again as many times as necessary. Sometimes we may have to restart the meeting - dial in again. With everyone calling at once you may need to try more than once. Future phone-in support group meetings Fourth Friday of each month, except: January (one week late for Australia Day, making 2 meetings in February), and December (one week early for Christmas). Phone-in support group meeting dates 2018 June 22 (not the last Friday) July 27 August 24 (not the last Friday) September 28 October 26 November 23 (not the last Friday) December 14 (one week early for Christmas) Changes or questions If you wish to update us about any changes in your health or treatment, or have a question you would like answered or discussed, or you would like to talk about joining a teleconference group, let us know. Then we can put it high on the agenda so it doesn't get lost - just reply to this email, or use Contact Jim on JimJimJimJim.com. This message has been sent to you because you are a member of the Australian Advanced Prostate Cancer Support Group. Visit JimJimJimJim.com and click on Contact Jim if this is a problem.
  12. Earlier
  13. Cam

    43 with stage 4 prostate cancer

    Plenty to digest as usual, feedback is so very much appreciated.
  14. Barree

    43 with stage 4 prostate cancer

    Hi Cam, Chuck has really summed up all the relevant information very concisely and the might helps are in my opinion certainly very worthy of consideration and discussion with your MO. Just a couple of points – Casodex when initially taken can on occasions cause a spike in PSA levels rather than a reduction - so if and when you commencing taking Casodex it is necessary to monitor your PSA regularly and often. The other consideration relates to Avodart ( Dutasteride). When you take Avodart and other 5-ARIs after 6–12 months of treatment they can reduce serum PSA levels by up to 50%, even if cancer is still present at the existing level. . It is important to measure serum PSA levels 6–12 months after starting Avodart or combination treatment - to establish a new PSA baseline (Nadir). After 6 months on Avodart to compare treatment levels with normal (untreated) ranges, for comparison purposes it is necessary to multiply the measured serum PSA value by 2.
  15. Cam

    43 with stage 4 prostate cancer

    Thanks Chuck, just 15 months into this nightmare and following a robotic RP, ADT, multiple mop up surgeries, 6 rounds of docetaxel, 3 rounds of SBRT, and a bilateral orchiectomy..... I was just hoping for some good news for once (seems that's not coming). I will digest you valuable information and discuss with my Oncologist. Cam.
  16. Charles (Chuck) Maack

    43 with stage 4 prostate cancer

    Dear Cam, The level 1.7 if nmol/L is equivalent to 50ng/dl, and 50ng/dl used to be considered castrate level but no longer so. 20ng/dl (0.68nmol/L) is the level considered castration level that has been achieved with androgen deprivation medications to reduce the testosterone level of active testicular/Leydig Cell production. With bilateral orchiectomy, testosterone, on average, falls to 15 ng/dL (0.5 nmol/L). Using the explanation as to androgen (testosterone) produced from other sources, your orchiectomy has not sufficiently lowered testosterone to suppress PSA elevation. An antiandrogen such as bicalutamide/generic of Casodex might suppress adrenal gland produced androgen from accessing cancer cell androgen receptors (AR). Adding dutasteride/Avodart, a 5Alpha Reductase (5AR) inhibitor prescribed to inhibit androgen/testosterone from conversion to the stronger stimulant to cancer cell growth, dihydrotestosterone/DHT, might serve to inhibit any androgen not suppressed by the antiandrogen while enroute to 5AR and bring PSA down and manageable. If these are not found effective, then either abiraterone/Zytiga to totally shut down testosterone production from all sources (testicular, adrenal glands, and that produced within cancer cells) or enzalutamide/Xtandi to block androgen access to cancer cell androgen receptors, may be alternatives – since these last two are extremely expensive medications, it would be important that they are covered under your government or private health insurance plan. Please note that I am only expressing considerations to discuss with your treating physician (Medical Oncologist?). Testosterone from other sources than testicular: Despite testicular shut down of testosterone production either by LHRH agonists/GnRH antagonist, the adrenal glands still secretes precursors to androgens such as testosterone and advanced androgen independent prostate cancer cells acquire complete steroidogenic ability to synthesize androgens and underline the fact that castration and inhibition of testosterone production in the testes may not achieve androgen deficiency in prostate cancer cells in advanced stages of the disease. (MY NOTE: Though the below reference goes into detail as to how androgen can be produced from other sources (adrenal glands, and cancer cells can produce androgen within themselves which, I believe, is derived from cholesterol) to fuel androgen “independent” cancer cells, the same can occur to continue to fuel androgen “dependent” cancer cells.) FROM: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2802176/ (I have emphasized in bold lettering that of interest) "Results and Discussion The results described in this study show for the first time that androgen-independent human prostate cancer cells are able to acquire complete steroidogenic potential and are capable of synthesizing testosterone from cholesterol, indicating an intracrine regulation of AR in advanced stages of prostate cancer. Several studies have shown the expression of key steroidogenic enzymes in prostate cancer cells indicating that these cells are able to synthesize androgens from adrenal precursors (El-Alfy, et. al., 1999,Nakamura, et. al., 2005,Stanbrough, et. al., 2006). The presence of functional AR in advanced stages of the disease and the presence of testosterone and DHT, sufficient to activate the AR, in cancer tissues under androgen ablation therapy, also support this notion (Gelmann, 2002,Mohler, et. al., 2004,Titus, et. al., 2005). The purpose of our studies was to determine whether prostate cancer cells in advanced stages of the disease can synthesize testosterone from cholesterol hence making them completely independent of serum testosterone and/or adrenal steroid precursors. In conclusion, our results clearly show for the first time that advanced androgen independent prostate cancer cells acquire complete steroidogenic ability to synthesize androgens and underline the fact that castration and inhibition of testosterone production in the testes may not achieve androgen deficiency in prostate cancer cells in advanced stages of the disease. Our results also explain the essential role of AR in survival and proliferation of androgen- independent prostate cancers under androgen-ablation therapy and suggest that inhibitors of steroid biosynthesis in prostate cancer cells may be required to completely abolish the androgens in these tumors for its therapy." DISCLAIMER: Please recognize that I am not a Medical Doctor. Rather, I do consider myself a medical detective. I have been an avid student researching and studying prostate cancer as a survivor and continuing patient since 1992. I have dedicated my retirement years to continued deep research and study in order to serve as an advocate for prostate cancer awareness, and, from an activist patient’s viewpoint, as a mentor to voluntarily help patients, caregivers, and others interested develop an understanding of this insidious men’s disease, its treatment options, and the treatment of the side effects that often accompany treatment. There is absolutely no charge for my mentoring – I provide this free service as one who has been there and hoping to make their journey one with better understanding and knowledge than was available to me when I was diagnosed so many years ago. IMPORTANTLY, readers of medical information I may provide are provided this “disclaimer” to make certain they understand that the comments or recommendations I make are not intended to be the procedure to blindly follow; rather, they are to be reviewed as MY OPINION, then used for further personal research, study, and subsequent discussion with the medical professional/physician providing their prostate cancer care. Charles (Chuck) Maack - Prostate Cancer Patient/Activist/Mentor (A mentor should be someone who offers courtesy, professionalism, respect, wisdom, knowledge, and support to help you achieve your goals; would that I succeed) Website: www.theprostateadvocate.com
  17. Maffy

    43 with stage 4 prostate cancer

    Dear Cam, I really feel your frustrations and your pain. I can wish you well but I know it does nothing. I can even say my thoughts are with you but that would be a lie and even my thoughts does nothing to comfort. The only thing can truly offer is my prayers for you and your family at this time. I know that my God, the God of the Bible, can heal and can comfort. Blessings Maffy
  18. stevecavill

    43 with stage 4 prostate cancer

    Given you have actually been castrated, seems odd to say you aren’t castrate resistant ! Testosterone is also made outside the testes. Have you looked at an anti androgen such as bicalutamide ? That blocks the androgen receptors on the prostate cells. 1.7 is still pretty low, you probably need another test in a few weeks to check the trajectory of the psa. I cant recall from previous posts. Have you had a PSMA scan to look for metastases? Steve
  19. Cam

    43 with stage 4 prostate cancer

    Thanks Jim, In an endeavour to maintain some sanity and get a few hours sleep tonight, I’ll go with the optimistic side and use Hotte’s 2.2.1 ”Castrate-resistant pca is usually suspected in patients with new symptoms on adt, with a rising psa, or with new evidence of disease on bone scans or computed tomography scans. To determine the castrate-resistant state and to properly assign a clinical state, it is imperative that patients have a testosterone level drawn. If patients are non-castrate, androgen ablation therapy should be instituted or maximized. If patients have testosterone levels in the castrate range, the diagnosis of crpc can be made.
  20. Admin

    43 with stage 4 prostate cancer

    Far be it from me to challenge your MO, but at least by this definition: Castrate-resistant pca (crpc) is defined by disease progression despite androgen-deprivation therapy (adt) and may present as one or any combination of a continuous rise in serum levels of prostate-specific antigen (psa), progression of pre-existing disease, or appearance of new metastases. does not need the actual achievement of castrate levels. Ref: Hotte, 2010: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2935714/
  21. Cam

    43 with stage 4 prostate cancer

    Hi Team, My prostate cancer journey continues to be anything but ordinary: had blood test results today and my testosterone has actually risen from 1.1 to 1.7 following the orchiectomy 5 weeks ago. My GU Oncologist said he has never seen it before but says I’m not mCRPC because we have never achieved castration levels of testosterone. Testorone rise has unfortunately fueled a rise in PSA from 0.034 to 0.248. Looking at cutting out all vitamins and supplements, and seeing a hormone therapist.... then regrouping. Are we (and my Onc) just kidding ourselves and should we just accept that this is an indication that I’ve moved to castration resistance? Would welcome any opinions. Cam
  22. Patrick Turner

    LU psma targeted therapy

    Hi Barree, and to all readers. My Psa is now about 5.5, and the last test showed it rose from 3.2 to 5.2 in 2 months, and rate of rise is increasing. Abiraterone is unable to now keep Psa low, after 10 months. The latest PsMa gallium Pet and CT scan is becoming more like a picture of a Dalmatian dog; there spots everywhere, but all are in bones, and nothing is in organs. The salvation RT I had to PG at Epworth in mid 2016 seems to have worked because the report scan says there's no cancer activity there. Symptoms of frequent nightly get-ups are no worse than 6 years ago, about 4 on average. No incontinence and bowels work OK. So in that area I am doing OK, but the bone mets in cervical spine are just starting to give discomfort at night, because they are presently small. So the storm clouds gather, pain is on the way. I an still OK to cycle 40km to-from the hospital to see my docs, and do the occasional 60km ride across town for a cuppa and read of newspapers. But I fear pain will shove me off the bike. Then I have the horrible thought that a decent 4 hour cycle ride for 90km may be very good for cardio health but the high rate of circulation could spread the cancer. I think my days of doing 330km a week sometimes is gone, and maybe its time to join the more normal human race who'd never ride more than 100km a week. Meanwhile, the onco fellows at Canberra Hospital ( public) are eager to get me to go to a Sydney specialist for maybe DNA test to see what chemo would work best because the CT part of the last PsMa scan report spoke of some spots which are not generating PsMa and to Lu117 would not do anything with them. Fortunately, I am able to afford whatever the bills may be for the DNA testing and the $40g for Dr Lenzo and all the other bits and pieces, and I don't need insurance, because I saved up a decent fighting fund. As the complexity of my situation grows, its very hard to know exactly what is best because there comes a time where only the docs know enough, and that isn't everything that could be known, and you just have to go with them not against them, so part of the cancer situation is not having any control over anything much at all. I am most grateful for what Canberra Hospital and Calvary Hospitals have done for me, and continue to do completely for free, and thank heavens I don't live in the USA where my costs without Australia's Medicare system would have been horrendous. My docs here said they would not send referrals to the Sydney specialists unless I got a mobile phone, something I loathe because like my mum who died in 2015 at 98, she found life was quite OK without a mobile. But I was told the docs in Sydney may need to phone so I need a mobile. But Dr Lenzo's office said I'd get a letter, and if there was a conference it would never be by mobile phone, and only face to face or by Skype. But the doctor's office staff may need to contact me. I am waiting for a nano simcard in the mail. I downloaded Skype to my laptop for Dr Lenzo - if he agrees to treat me which I guess will depend on whether he thinks it would be of benefit. Trials of Lu117 have found some blokes did not get a benefit with it. It is all so easy to be in the group for whom Lu117 is a waste of time and dough. BTW, sound quality using a laptop inbuilt camera, mic, and speakers is horrible. I got a set of headphones with a mic and with USB plug, and although the video picture quality is not marvellous, its good enough in daylight. I now have to make sure the data speed is fast enough from my ISP, and see what amount I'd use for say a 20 minute call. I think I might be begging my oncologist for docetaxel if there is pain soon; something has to be done sooner rather than later, and although I might have tried enzalutamide my docs suggest that may have kept the Psa down, but not stopped my disease progress. I have a Melbourne friend on his 10th docetaxel and he is playing competition tennis, and doing lots of stuff. But his Psa went from 40 to 2, and now shows sign of slight rise, all in 5 months, so his battle is far from over. Its now about 3 years since his diagnosis, and Pca continued after RP, and then ADT worked for only 3 months, and Cosadex made Psa rise even faster, so hormone manipulation does not always work for everyone. I ain't afraid of this chemo, but carboplatin might be horrible I have heard. The PBS scheme does not allow a switch to enzal after abira unless I had severe side effects; one doc said I would be able to provide a list, the other said that if an audit of records was done, they could get cooked by authorities, so no enzal, and it would not do me much good because the cancer has now become differentiated and gone to many bones and some does not respond testosterone starvation or blocking. This is just what old Pca tumours do, and its why they are so dangerous, and mine probably began in 2004, and it didn't make much Psa for the amount of Pca found. 95% of men will pass away within 5 years of a CT scan that shows the first bone lesions. Lu117 has median life extension of 13 months, and its a gamble at to how long anyone gets, I may need Radium223, also doable in Sydney, but side effects could be quite bad, and so I have no idea exactly how I would fare if I bought whatever is on offer. I am lucky to not have other co-morbidities, and that I am fit and BMI < 25, resting HR 50, but the cancer ignores this, and I think maybe if a man is real healthy then so is his cancer, but I do not suggest anyone neglect their fitness, so I'll try to keep cycling, pain permitting. Being fit ( apart from cancer ), probably means side my effects are less than for those who are not fit. The radiation doc at CH told me I could get local EBRT to cervical spine for pain if needed, but said I'd have a sore throat afterwards, and from what I have seen in a friend here, that's not all, maybe dry mouth and no taste. One by one the things that make a simple life tolerable and enjoyable just leave us as treatments go on. But the friend here is now 79, and Psa = 0.01, and he didn't get any Pca spread to distant sites, although be did need 70Gy to site of operation for robotic RP he'd had 7 years earlier when Psa had gone to 0.01 for 3 years, then back up slowly to 0.5. 2 years Before Pca got him, he had a small neck cancer and he had a small op, RT, chemo, and appears OK now. His treating doctor got a similar thing which killed him. I must now away, to collect a dear sister at a railway station to spend the rest of today with her, galivanting in art galleries and having a decent lunch. Patrick Turner.
  23. Barree

    LU psma targeted therapy

    Hi Patrick, If your Medical Oncologist is considering treating you with Docetaxel, it would as Ardee has suggested be wise to have Docetaxel first and then - if and when its needed check out the availability of Lu177 treatment via the TheraP trial. This is a randomised controlled trial. Randomisation means that trial participants are put randomly into one group or the other, so that the only major difference between the two groups is the type of treatment they receive. They then compare the outcomes of the two groups to see if one treatment is better than the other. In this trial, half of the participants will receive Lu-PSMA and half will receive cabazitaxel. The trial is not “blinded,” which means that you and your treating team will know which treatment you receive, but you do not get to choose which treatment you will get but both are appropriate for advanced metastatic PCa. As you probably know Patrick, treatment with Docetaxel ( is in most cases in Australia) a necessary prerequisite to qualify for treatment with some of the more exotic treatments that are subsidized by the PBS. I understand there might still some be some vacancies on the TheraP Lu177 trial (Royal North Shore Hospital and Liverpool Hospital in Sydney) After treatment with docetaxel if you are are suitable for treatment with Lu177, if you qualify for the trial - treatment will be provided whereas treatment with Lu177 by Dr Lenzo at Theranostics is I understand somewhere in the region of $9800.00 per treatment and you may need up to 4 treatments. Cheers, Barree
  24. ardee

    LU psma targeted therapy

    Hello Patrick ..... the most significant comorbidity from Lu177 I have observed to date involves myelosuppression i.e. the bone marrow is suppressed and unable to produce healthy blood cells as efficiently. Since this can also be a side effect of chemo, it is unwise to combine chemo with Lu177. Trials have also observed this with other radionuclides like Radium223 (Xofigo). Ironically one of the men I know well who tried Lu177 also did well on chemo, and actually won a tennis tourney after his 5th chemo infusion! He stopped his Lu177 after 3 blood transfusions. If timing allows, please feel free to join our virtual group - Nev Black was on yesterday's session. You can also listen to recordings of the groups here ... or on our YouTube Channel Onward & upwards, rd
  25. Patrick Turner

    LU psma targeted therapy

    Hi Susan, Ardee and to all others, I'm in Canberra, Australia. My scans looks worse than last year and the abiraterone is failing, but Psa was only 5.2. My doc says I should continue abi for a month while they arrange the best they can with me with DNA test, and Lu117 infusions from a Dr Lenzo from a clinic in Sydney. I have yet to confer with Dr Lenzo, and probably he may want me to be on docetaxel which a friend here says is fine to take because he's had 10 shots now and is still playing competition tennis at age 59. Some chemo is worse than others, but DNA profile may show what will or won't work. So how are the guys who have had LU117 now? what are side effects? Meanwhile, I'll try to keep going forwards while delaying to the upwards trip for as long as possible 🙂 Patrick Turner.
  26. ardee

    LU psma targeted therapy

    Not sure what your question is, but I do see you are in the US. Please feel free to join our Advanced PCa virtual support group that meets weekly. The next meeting is today, Tuesday, May 29 @ 6 pm EDT; participation is free and drop-in. For joining instructions please visit https://www.ancan.org/joining-instructions or send an e-mail to info@ancan.org to be added to the advanced notice distribution. We have a couple of participants who have recently experienced or are about to start Lu-177 stateside. Onward & upwards, rd
  27. Some members of the Australian Advanced Prostate Cancer Support Group attended the recent PCFA Community Conversations event in Melbourne. David Abrahams was a star of the show when he was presented with the PCFA Max Gardner 2017 "in recognition of distinguished service and outstanding contribution in the Australian community." Pictured with David (left) are Alan Barlee, Lorraine and Barry Elderfield, Nev Black and Steve Cavill.
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