Tag Archive for: prostate

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Have the days of ADT Monotherapy for Hormone Sensitive Prostate Cancer Come to an End? STAMPEDE in the June #urojc

The much awaited results of the STAMPEDE study of abiraterone for hormone naive prostate cancer was simultataneously presented at #ASCO17 and published ‘on line ahead of print’ in the NEJM. The formal title of the study was “Abiraterone for Prostate Cancer Not Previously Treated with Hormone Therapy”.

Briefly, the study randomised 1917 men with locally advanced or metastatic hormone naive prostate cancer  to receive either ADT alone or ADT in combination with abiraterone and prednisolone.  significantly higher rates of overall and failure-free survival than ADT alone.We were privileged to have the lead author Professor Nick James join us for the June #urojc.  He posted the following video which is a lovely summary about STAMPEDE.  All of us could benefit from watching this and it is a useful link for our patients.

The data from the study is clear and it was not surprising that the majority of the discussion surrounding this paper was not going to be a dissection of the methodology or dataset and its analysis but rather how these results might impact upon urological practice.

There was a somewhat provocative start to the discussion with:-

To turn the question around, we saw the following tweet:-

But @urogeek came out swinging

But he was not alone in these thoughts.

But lets be fair, these responses are from urologists immersed in clinical trials experience and highly academic centers.  The following tweet perhaps brought out what many were thinking.

But perhaps the onus is upon us to make that extra effort to learn. As has been mentioned, we manage one of the most toxic agents competently in the form of intravesical BCG for bladder cancer.

Naturally, there was bound to be some discussion about cost of treatment.

For a bit of light hearted banter, there was the following exchange which we hope nobody took too seriously.

The twitter account of the journal Prostate Cancer and Prostatic Diseases posted a poll which was responded to by 117 participants with only 10% choosing the ADT alone option.  Whilst far from scientific, does this represent a significant change in thinking?  It was not long ago where we could have predicted that almost all respondents would have chosen the ADT alone option.

And to finish up, a question answered by Nick James as follows:-

A big thanks to all who participated in the June #urojc discussion. A special thanks to lead author Nick James for his insightful comments that really added to the discussion.  We will be back for another installment of the #urojc in July.  See you then.

Henry Woo (@drhwoo) is the Director of Uro-Oncology and Professor of Robotic Cancer Surgery at the Chris O’Brien Lifehouse in Sydney, Australia. He is also Professor Surgery at the Sydney Adventist Hospital Clinical School of the University of Sydney.

 

Article of the Week: Evaluation of Sig24, a 24-gene signature

Every week the Editor-in-Chief selects an Article of the Week from the current issue of BJUI. The abstract is reproduced below and you can click on the button to read the full article, which is freely available to all readers for at least 30 days from the time of this post.

In addition to the article itself, there is an accompanying editorial written by a prominent member of the urological community. This blog is intended to provoke comment and discussion and we invite you to use the comment tools at the bottom of each post to join the conversation.

Finally, the third post under the Article of the Week heading on the homepage will consist of additional material or media. This week we feature a video discussing the paper.

If you only have time to read one article this week, it should be this one.

Evaluation of a 24-gene signature for prognosis of metastatic events and prostate cancer-specific mortality

Kathryn L. Pellegrini*, Martin G. Sanda*, Dattatraya Patil*, Qi Long†‡§, MarıSantiago-Jimenez, Mandeep Takhar, Nicholas Erho, Kasra Youse, Elai DavicioniEric A. Klein**, Robert B. Jenkins††, R. Jeffrey Karnes‡‡ and Carlos S. Moreno§§§

 

*Department of Urology, Emory University School of Medicine, Winship Cancer Institute, Atlanta, GA‡ Department of Biostatistics and Epidemiology and Abramson Cancer Center, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, §Department of Biomedical Informatics, Emory University School of Medicine, Atlanta, GA, USA, GenomeDx Biosciences, Vancouver, BC, Canada, **Glickman Urological and Kidney Institute, Cleveland Clinic, Cleveland, OH, ††Department of Pathology and Laboratory Medicine, ‡‡Department of Urology, Mayo Clinic, Rochester, MN, and §§Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA
Read the full article

How to Cite

Pellegrini, K. L., Sanda, M. G., Patil, D., Long, Q., Santiago-Jiménez, M., Takhar, M., Erho, N., Yousefi, K., Davicioni, E., Klein, E. A., Jenkins, R. B., Karnes, R. J. and Moreno, C. S. (2017), Evaluation of a 24-gene signature for prognosis of metastatic events and prostate cancer-specific mortality. BJU International, 119: 961–967. doi: 10.1111/bju.13779

Abstract

Objectives

To determine the prognostic potential of a 24-gene signature, Sig24, for identifying patients with prostate cancer who are at risk of developing metastases or of prostate cancer-specific mortality (PCSM) after radical prostatectomy (RP).

Patients and Methods

Sig24 scores were calculated from previously collected gene expression microarray data from the Cleveland Clinic and Mayo Clinic (I and II). The performance of Sig24 was determined using time-dependent c-index analysis, Cox proportional hazards regression and Kaplan–Meier survival analysis.

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Results

Higher Sig24 scores were significantly associated with higher pathological Gleason scores in all three cohorts. Analysis of the Mayo Clinic II cohort, which included time-to-event information, indicated that patients with high Sig24 scores also had a higher risk of developing metastasis (hazard ratio [HR] 3.78, 95% confidence interval [CI]: 1.96–7.29; P < 0.001) or of PCSM (HR 6.54, 95% CI: 2.16–19.83; P < 0.001).

Conclusions

The findings of the present study show the applicability of Sig24 for the prognosis of metastasis or PCSM after RP. Future studies investigating the combination of Sig24 with available prognostic tests may provide new approaches to improve risk stratification for patients with prostate cancer.

Read more articles of the week

Changing the LATITUDE of Treatment for High-Risk Hormone-Naïve Prostate Cancer: STAMPEDE-ing Towards Androgen Biosynthesis Inhibition

zach-klaassenEarlier this month at the annual American Society of Clinical Oncology (ASCO) meeting in Chicago, IL, Dr. Karim Fizazi and Dr. Nicholas James (@Prof_Nick_James) presented results from the LATITUDE and STAMPEDE trials, respectively. These randomized controlled trials (RCTs) assessed the utility of adding abiraterone acetate (AA) + prednisone to conventional androgen deprivation therapy (ADT) among men with high-risk, hormone-naïve prostate cancer. Since Dr. Charles Huggins’ 1941 Nobel prize winning finding that ADT is highly effective in controlling metastatic prostate cancer, nearly 70 years passed before CHAARTED and STAMPEDE demonstrated in 2015 that the addition of docetaxel to ADT prolongs survival in men with high volume metastatic prostate cancer. The de novo metastatic prostate cancer global incidence is striking: 3% in the US and rising, 6% across Europe, 4-10% in Latin America, and nearly 60% in Asia-Pacific. Historically, ADT has been standard of care, however most men with metastases progress to metastatic castration-resistant prostate cancer (mCRPC) driven by the reactivation of androgen receptor (AR) signaling. The rationale for adding AA + prednisone to ADT for metastatic hormone-naïve prostate cancer patients is threefold: (i) the mechanism of resistance to ADT may develop early, (ii) ADT alone does not inhibit androgen synthesis by the adrenal glands or prostate cancer cells, and (iii) AA + prednisone improves overall survival (OS) in mCRPC patients and reduces tumor burden in high-risk, localized prostate cancer.

LATITUDE

LATITUDE was conducted at 235 sites in 34 countries in Europe, Asia-Pacific, Latin America, and Canada. The objectives of the study were to evaluate the addition of AA + prednisone to ADT on clinical benefit in men with newly diagnosed, high-risk, metastatic hormone-naïve prostate cancer. Patients were stratified by the presence of visceral disease (yes/no) and ECOG performance status (0, 1 vs 2) and then randomized 1:1 to either ADT + AA (1000 mg daily) + prednisone (5 mg) (n=597) or ADT + placebo (n=602). The co-primary endpoints were OS and radiographic progression-free survival (rPFS). Secondary endpoints included time to: (i) pain progression, (ii) PSA progression, (iii) next symptomatic skeletal event, (iv) chemotherapy, and (v) subsequent prostate cancer therapy. The study was powered to detect an HR of 0.67 and 0.81 in favor of AA for rPFS and OS, respectively.
Over a median follow-up of 30.4 months, patients treated with ADT + AA + prednisone had a 38% risk reduction of death (HR 0.62, 95%CI 0.51-0.76) compared to ADT + placebo.

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Median OS was not yet reached in the ADT + AA + prednisone arm compared to 34.7 months in the ADT + placebo arm. OS rates at 3 years for the ADT + AA + prednisone arm was 66%, compared to 49% in the ADT + placebo arm. This OS benefit was consistently favorable across all subgroups including ECOG 0 and 1-2, visceral metastases, Gleason ≥8 disease, and bone lesions >10.

There was also 53% risk of reduction of radiographic progression or death for patients treated with ADT + AA + prednisone (median 33.0 months; HR 0.47, 95%CI 0.39-0.55) compared to ADT + placebo (14.8 months).

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Secondary endpoints showed statistically significant improvement for ADT + AA + prednisone, including time to PSA progression (HR 0.30, 95%CI 0.26-0.35), time to pain progression (HR 0.70, 95%CI 0.58-0.83), time to next symptomatic skeletal event (HR 0.70, 95%CI 0.54-0.92), time to chemotherapy (HR 0.44, 95%CI 0.35-0.56), and time to subsequent prostate cancer therapy (HR 0.42, 95%CI 0.35-0.50).

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Secondary to the results presented at ASCO, the study was discontinued after the first interim analysis. Adverse events were comparable in the two groups. Hypertension only rarely required treatment discontinuation, and only two patients discontinued treatment due to hypokalemia (no hypokalemia-related deaths). Two patients in each arm died of cerebrovascular events, and 10 patients treated with ADT + AA + prednisone compared to 6 patients treated with ADT + placebo died of cardiac disorders.

STAMPEDE

STAMPEDE is a large multi-stage, multi-arm, RCT being conducted in the United Kingdom to assess the utility of novel therapeutic agents in conjunction with ADT. Currently being tested are AA, enzalutamide, zoledronic acid, docetaxol, celecoxib and radiotherapy (RT). The AA arm of the study was presented at ASCO as a late-breaking abstract. Inclusion criteria included men with locally advanced or metastatic prostate cancer, including newly diagnosed with N1 or M1 disease, or any two of the following: stage T3/4, PSA ≥ 40 ng/mL, or Gleason score 8-10. Patients undergoing prior radical prostatectomy or RT were eligible if they had more than one of the following: PSA ≥ 4 ng/mL and PSADT < 6 months, PSA ≥ 20 ng/mL, N1, or M1 disease. Patients were then randomized 1:1 to standard of care (SOC; ADT for ≥2 years, n=957) vs SOC + AA (1000 mg) + prednisone 5 mg daily (n=960). Treatment with RT was mandated in patients with N0M0 disease, while strongly encouraged for N1M0 patients. Primary outcomes were OS and failure-free survival (FFS), where failure was defined as PSA failure, local failure, lymph node failure, distant metastases or prostate cancer death. Secondary outcome included toxicity and skeletal-related events (SREs). The study was powered to detect a 25% improvement in OS for the treatment group (requiring 267 control arm mortalities).
Both groups were balanced and patients were predominantly metastatic (52% M1, 20% N+M0, 28% N0M0), median was PSA 53 ng/mL, and 99% were treated with LHRH analogues. Over a median follow-up of 40 months, there were 262 control arm deaths, of which 82% were prostate cancer-related; there were 184 deaths in the SOC + AA + prednisone arm. There was a 37% relative improvement in overall survival (HR 0.63, 95%CI 0.52-0.76) favoring SOC + AA + prednisone.

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A Forrest plot split on stratification factors demonstrated no evidence of heterogeneity based on any of the factors, including M0/M1 status (p=0.37). Second, SOC+AA + prednisone demonstrated a 71% improvement in FFS (HR 0.29, 95%CI 0.25-0.34), with an early split in the KM curves.

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SOC + AA + prednisone also significantly decreased SREs among the entire cohort (HR 0.46, 95%CI 0.37-0.58), as well as specifically in the M1 cohort (HR 0.45, 95%CI 0.37-0.58). This resulted in a 55% reduction in SREs in the M1 subset analysis.

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When looking at treatment progression, 89% of the SOC arm went on to next line of therapy, whereas 79% of the SOC + AA + prednisone arm received additional therapy, most commonly docetaxel. As expected, the rate of Grade 3-5 adverse events was higher in the SOC + AA prednisone arm (47% vs. 33%), and were primarily cardiovascular (HTN, MI, cardiac dysrhythmias) or hepatic (transaminitis) in nature.

REACTION, INTERPRETATION & FUTURE DIRECTIONS

As has become the norm during academic conferences, there was significant buzz on Twitter over the course of the two days these results were presented:

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This also included the New England Journal of Medicine immediately tweeting after the presentations that LATITUDE and STAMPEDE were published instantaneously:

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Furthermore, immediately following Dr. Fizazi’s presentation of LATITUDE, Dr. Eric Small from @UCSF presented a discussion of LATITUDE. A number of important points were raised. First, although this was a well-designed, placebo controlled, randomized phase III study, early unblinding (although appropriate) resulting in an HR of 0.62 for OS is based on only 50% of the targeted total deaths. Making conclusions based on interim analyses must be made with caution. However, with every endpoint reaching statistical significance and conditional probability modeling, if the study had remained blinded, the probability of reaching the same conclusions is high. Second, since twice as many patients in the ADT + placebo arm received life-prolonging therapy than compared to the ADT + AA + placebo arm, the benefit of AA is not explained by more secondary life-prolonging therapy, strengthening the cause for AA + ADT.

Perhaps the most interesting and pertinent clinical comparison is assessing outcomes of the LATITUDE and CHAARTED (high-volume disease) treatment arms (AA vs docetaxel). With similar median OS outcomes between the ADT control arms of the two trials (suggesting similar populations), the HRs for OS based on treatment are nearly identical:

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Similarly, the rPFS outcomes were comparable between the two trials:

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With nearly identical OS and rPFS outcomes for men receiving ADT + AA or ADT + docetaxel, the question becomes whether the impact of adding AA to ADT is volume or risk dependent. Results from the STAMPEDE trial would suggest remarkably similar outcomes support the use of AA + ADT in patients with less burden of disease. Arguably the most important slide of the meeting was captured and tweeting by Dr. Agarwal (@neerajaiims):

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Dr. Small eloquently summarized future directions into two groups. Unanswered questions regarding efficacy include: (i) Can a genomic classifier be used to select patients more likely to benefit from AA or docetaxel? (ii) Can AA be added in even earlier settings (with radiation? Increasing PSAs?) (iii) Should AA and docetaxel be combined or used sequentially? Additionally, there are also unanswered questions regarding AA resistance, including (i) Will the mechanisms of resistance to AA be the same when used in the non-mCRPC setting? (ii) Will androgen receptor amplification still be observed? (iii) Will there be an increased risk of treatment-associated small cell/neuroendocrine prostate cancer? (iv) Does adding chemotherapy or AA to ADT result in more aggressive disease at the time of resistance? (v) What is the optimal therapy for a patient who progresses on ADT + AA, compared to a patient who progresses on ADT + docetaxel? Given the avoidance of potential chemotherapy related side effects (ie. neutropenic complications) for an oral, long-term treatment, AA + ADT should be considered standard of care for untreated, high-risk metastatic prostate cancer.

But what is the long-term economic landscape like when practice changing trials such as LATITUE and STAMPEDE suddenly thrust an expensive medication such as AA + prednisone directly to the forefront of hormone-naïve disease? Following these presentations, urologic oncologist, Twitter veteran, and Forbes correspondent Dr. Ben Davies (@daviesbj) wrote a provocative piece highlighting the potential ‘financial toxicity’ (particularly in the United States) that may result downstream of these trials:

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A conservative estimate is a wholesale cost of $115,000 per year per patient for AA + prednisone, resulting in a crude estimate of a $2.8 billion annual expenditure for the drug in the United States alone if used in the hormone-naïve setting, according to Dr. Davies. As Dr. Davies also points outs, although the patent for AA expired in 2016 and there are currently 13 applications to make generic AA, the patent for prednisone lasts until 2027, with $30 billion riding on the lawsuit. Dr. David Penson (@urogeek) succinctly summarized via Twitter:

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Strictly academically speaking, LATITUDE and STAMPEDE, in addition to the docetaxel benefits of CHAARTED, have provided clinicians with exciting Level 1 evidence for improving patient care in the high-risk/metastatic setting. The investigators and more importantly the thousands of patients and families are to be thanked and congratulated for their perseverance, hard-work, and willingness to participate in these practice-changing clinical trials. It is our job as clinicians to continue advocating the best treatment for our patients, whether this be through economic barriers in the United States, or access to appropriate care on a global scale.

 

Zach Klaassen, MD

Urologic Oncology Fellow

University of Toronto/Princess Margaret Cancer Centre

Toronto, Ontario, Canada

@zklaassen_md

 

Tagore’s Last Days: the little Prostate ends a big Legend

tagoreKabiguru Rabindranath Tagore is perpetually present in the Bengali memory and is a part and parcel of the Indian cultural fabric even after 75 years of his demise. The Bard of Bengal has retained his greatness through his songs, poetry, stories, progressive world view and love for his country.

The first Nobel Prize winner of Asia (1913), Tagore was knighted in 1915 and had the courage to return it as a mark of protest after the Jalianawala Bagh massacre in 1919. He is compared to the likes of William Shakespeare and Johann Wolfgang Goethe for his extraordinarily rich literature and sensitive understanding of human nature.

Rabindranath has been a hero, an idol and a father figure for the Bengali. That is why when it comes to his death there is a self-imposed oblivion among his followers because there is an aversion to accept that he too was human, he too had suffered in his last days.

The way the city cried and the huge congregation of people that came to pay him their last respects go on to show the place Tagore had in the heart of the Kolkatan. But very few people actually know that Kabiguru Rabindranath Tagore did not allow his deteriorating health to affect his spirit.

Seventy-five years after his death this is the first time Tagore’s illness has been revealed and his last days talked about. At an exhibition organised at Tagore’s home ‘Jorsanko Thakur Bari’ on his death anniversary on August 7, 2016 with the official approval of the Rabindra Bharati University Museum, the verandah of his home came alive with photographs and exposition of his last days when Tagore smiled through extreme pain and was surrounded by family and friends. The exhibition showed that despite his failing health he remained positive and at his creative best, and how doctors did their best to make him feel better. Rabindra Bharati University, that is housed in the premises of Tagore’s home, and Kolkata Prostate Cancer Foundation led by the author of this blog, organized this exhibition. It is evident that Tagore died from the complications of an enlarged prostate gland.

Tagore was a handsome man blessed with a good physique and an impressive personality. For the sake of building his body, he even learnt how to wrestle and lived a disciplined life. He learnt horse riding and had commendable stamina, which enabled him to swim across the Padma River. Despite this his health deteriorated at the age of 76 and unfortunately on 10th September, 1937 he lost consciousness and remained that way for two days. Kidney and prostate problems were diagnosed simultaneously. His health demanded immediate attention, which was duly given to him in Shantiniketan by a team of doctors headed by Dr Nilratan Sarkar from Kolkata.

He was also suffering from ailments like fever, headache, chest pains and a lack of appetite. Tagore strongly believed that his life had a meaning beyond these mortal diseases. That’s why the moment he could sit upright on his bed he took to his ink and paper. His love for nature was not only restricted to the stories he wrote, indeed he profoundly believed that he would feel much better if he spent his time in the lap of nature.  That is why he kept visiting the hills of North-Eastern India.

He also ensured that his creativity did not suffer. Even in such trying times he wrote ‘Sejuti’, ‘Naba Jatak’ and ‘Shyama’. He also composed numerous songs and painted to his heart’s content. Tagore cared deeply for his country and despite his ill health he continued to have political discussions with Jawaharlal Nehru and Subhash Chandra Bose. He played host to Mahatma Gandhi and his wife Kasturba when they visited Shantiniketan. It seemed that his deteriorating health was the least of his worries.

On 15th September, 1940 when Tagore was in Kalimpong, due to a pain in his urinary bladder he lost consciousness again. He was unable to pass urine either. Despite the evident symptoms of uraemia, his grand-daughter, Pratima Debi wasn’t ready to accept that Tagore needed an operation. On 29th September, he was brought back to his Jorasanko House on the advice of Dr Prasanto Chandra Mohalanobis.

With the help of Dr Satyasabha Mitra, Dr Amiya Basu and Dr Mahalanobis he was moved to the marble room on the first floor where he spent most of his time. In the presence of his near and dear ones along with dutiful attendants and under the supervision of Sir Nilratan Sarkar and Dr Bidhan Chandra Roy he seemed to be on the path of recovery.

A considerable amount of attention was given to his diet, medicines and cleanliness in order to ensure complete recovery. The poet continued to have his biochemic medicines, which he felt would also give him relief. Dr Dakhshinaranjan Roy visited him regularly and advised him.

On his return to Shantiniketan it seemed, Tagore had come to terms with his failing health and was determined to win this battle without dampening his spirits. He narrated a sea of stories every now and then and his imagination took on the colour of his palette. What emerged were timeless paintings. Around this time he also welcomed the Chinese missionary Tai-Chi-Tao with open arms.

It was the Poush Utsav in December that year, actually the last one that Tagore witnessed, when it dawned on him that time plays the most crucial role in one’s life. The harder he tried to hold on to time, it slipped away from him. Despite the mental and physical struggle, he managed to stand by his beliefs and played an active part in some major protests demanding independence for India. His works ‘Golpo Solpo’ and ‘Teen Sangee’ reflected these precise thoughts in his last days.

Despite this positivity his illness persisted. Because of the constant persuasion of doctors, both, allopathic and ayurvedic treatments were started in a desperate attempt to revive him. On 16th July, 1941, his doctors advised him to undergo surgery.

The operation was scheduled for 30th July. But he was not informed about it for fear that he would not accept it. On the day of the operation after making all arrangements, Dr Lalit Bandopadhyay finally broke the news to Tagore that he would be operated upon. The poet was shocked and not very happy; however, he was taken to the verandah of his house where a special operation theatre had been created for him. A Suprapubic Cystotomy was performed where the doctors aimed to insert a tube into his bladder to relieve his urinary retention. The operation was done by Dr Lalit Bandopadhyay, assisted by Dr Satysakha Maitra and Dr Amiya Sen.

After the operation, he often complained of a burning sensation but thankfully remained unconscious most of the time. To everyone’s dismay, his condition worsened and his pain was evident even while he was unconscious. On 4th August his kidneys stopped working and uremia had set in. Saline was administered to him and oxygen was kept handy. On the night of 6th August, his condition had hit rock bottom and people started gathering in the premises of Jorasanko.

Slowly oxygen tubes were removed and Tagore’s spirit freed itself from the shackles of a human body, at 12.10 pm. The news spread like wildfire and thousands of people rushed to Jorasanko to pay their last respects. The deafening silence of the crowd was broken by the blowing of conch shells. Flowers carpeted his path to the crematorium on the banks of the Ganges.

The echo of his words from “The Postmaster” keep coming to my mind. He said: “So, the traveller, borne on the breast of the swift-flowing river, consoled himself with philosophical reflections on the numerous meetings and partings going on in the world – on death, the great parting, from which none returns.”

A line from his famous song sums up his last days:

Exists Sorrows, Exists Death, Separation Chars,

Yet Exists Peace, Yet Exists Happiness, Yet The Infinite Stirs.

 

Dr. Amit Ghose, Kolkata, India

 

IN THE MEDIA:

“Finally, when his condition worsened and he had almost stopped passing urine, doctors diagnosed him with severe uremia and other complications. It was then decided that surgery could not be postponed any further and the poet was brought back to Jorasanko. It was here that a sterilized OT was created for the surgery conducted by Lalit Bandyopadhyay and overseen by BC Roy and Nil Ratan Sircar. They did not operate on the enlarged prostrate, but did a bypass surgery to take out accumulated urine. The prostate had to be left untouched,” said urologist Amit Ghose, who has been supervising the installation of the exhibition – Published in the Times Of India, August 7, 2016

“Not many people know that Kabiguru Rabindranath Tagore suffered from a disease of the Prostate Gland (not cancer). At that time he was given the best medical treatment possible. With the advancement of technology in India we are well-equipped to detect and handle diseases related to the prostate. Also, we wanted to create an awareness through this initiative that with regular check-ups it is possible to have an early detection of prostate-related issues and prostate cancer as well,” said the person behind this initiative, Dr. Amit Ghose, Director, Prostrate Cancer Foundation. – Published in BusinessWire India, August 9, 2016

The kind of love and care Rabindranath Tagore had got from everyone around him also is something to talk about. The doctors treating him tried their level best and they often sat by his bedside holding his hand hoping the pain and the discomfort would subside,” said Dr Ghose. – Published in Asia Times, August 21, 2016

 

 

Article of the Week: Prevalence of the HOXB13 G84E mutation in Danish men undergoing radical prostatectomy and its correlations with prostate cancer risk and aggressiveness

Every Week the Editor-in-Chief selects an Article of the Week from the current issue of BJUI. The abstract is reproduced below and you can click on the button to read the full article, which is freely available to all readers for at least 30 days from the time of this post.

In addition to the article itself, there is an accompanying editorial written by a prominent member of the urological community. This blog is intended to provoke comment and discussion and we invite you to use the comment tools at the bottom of each post to join the conversation.

If you only have time to read one article this week, it should be this one.

Prevalence of the HOXB13 G84E mutation in Danish men undergoing radical prostatectomy and its correlations with prostate cancer risk and aggressiveness

Tine M. Storebjerg*,,, Søren Høyer, Pia Kirkegaard§, Flemming Bro§, the LuCamp Study Group, Torben F. Ørntoft, Michael Borre* and Karina D. Sørensen

 

Departments of*Urology Pathology, Aarhus University Hospital, Department of Molecular Medicine, Aarhus University Hospital, §Research Unit for General Practice and Research Centre for Cancer Diagnosis in Primary Care, Aarhus University, Aarhus, and Lundbeck Foundation Centre for Applied Medical Genomics in Personalized Disease Prediction, Prevention and Care, Copenhagen, Denmark

 

Read the full article

Objectives

To determine the prevalence of the HOXB13 G84E mutation (rs138213197) in Danish men with or without prostate cancer (PCa) and to investigate possible correlations between HOXB13 mutation status and clinicopathological characteristics associated with tumour aggressiveness.

Materials and Methods

We conducted a case–control study including 995 men with PCa (cases) who underwent radical prostatectomy (RP) between 1997 and 2011 at the Department of Urology, Aarhus University Hospital, Denmark. As controls, we used 1622 healthy men with a normal prostate specific antigen (PSA) level.

Results

The HOXB13 G84E mutation was identified in 0.49% of controls and in 2.51% of PCa cases. The mutation was associated with a 5.12-fold increased relative risk (RR) of PCa (95% confidence interval [CI] 2.26–13.38; P = 13 × 10−6). Furthermore, carriers of the risk allele were significantly more likely to have a higher PSA level at diagnosis (mean PSA 19.9 vs 13.6 ng/mL; P = 0.032), a pathological Gleason score ≥7 (83.3 vs 60.9%; P = 0.032), and positive surgical margins (56.0 vs 28.5%; P = 0.006) than non-carriers. Risk allele carriers were also more likely to have aggressive disease (54.2 vs 28.6%; P = 0.011), as defined by a preoperative PSA ≥20 ng/mL, pathological Gleason score ≥ (4+3) and/or presence of regional/distant disease. At a mean follow-up of 7 months, we found no significant association between HOXB13mutation status and biochemical recurrence in this cohort of men who underwent RP.

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Conclusions

This is the first study to investigate the HOXB13 G84E mutation in Danish men. The mutation was detected in 0.49% of controls and in 2.51% of cases, and was associated with 5.12-fold increased RR of being diagnosed with PCa. In our RP cohort, HOXB13 mutation carriers were more likely to develop aggressive PCa. Further studies are needed to assess the potential of HOXB13 for future targeted screening approaches.

Read more articles of the week

Editorial: HOXB13 mutations and prostate cancer risk

For the first time, Storebjerg et al. [1] describe the prevalence of the HOXB13 G84E mutation in a Danish population and its association with prostate cancer risk and features indicative of clinically aggressive disease in a cohort of men undergoing radical prostatectomy. In this study, the prostate cancer risk mutation was seen in 0.49% of controls with an ~5-fold increase in risk of prostate cancer among carriers. The homeobox transcription factor gene HOXB13, is located on the long arm of chromosome 17 (17q21), and belongs to a superfamily of genes considered critical to animal embryonic development, characterised by a highly-conserved DNA-binding domain. In 2012, our research team described the association of a rare recurrent HOXB13 mutation, substituting adenine for guanine in the second position of codon 84 resulting in the replacement of glycine by glutamic acid, with prostate cancer and found that the carrier frequency was ~20-times higher among men with early onset disease and multiple affected close relatives compared with men presumed without disease [2]. Since then, numerous studies have confirmed this association with estimates of risk overall varying from ~3 to 9-fold, and generally a greater risk seen among men diagnosed before the age of 60 years and among those with a positive family history of disease among first-degree relatives [3]. The G84E mutation is almost exclusively found in men of Northern European descent with evidence suggesting that it is a relatively recent (circa 1790s) founder mutation in the population, and considered to be of moderate penetrance (estimated lifetime risk among carriers 35–65%) [4]. The same germline mutation has also been preliminarily reported to be associated with cancers of the breast, colon, bladder, and leukaemia, but requires further investigation [5, 6].

The findings from this study [1], both for the prevalence of the mutation, as well as its magnitude of association with prostate cancer, are comparable to prior reports in Northern European populations. Furthermore, among the 995 cases, the mutation frequency was significantly associated with features predictive of progression after surgery (high PSA level, positive surgical margins, higher pathological Gleason score, and non-organ confined disease) suggesting that genetic evaluation of men with a strong family history would identify a subset of men that would benefit from early screening and intervention in the same manner as are male carriers of known founder mutations in BRCA2[7]. The observation between HOXB13 and clinical features indicative of aggressive disease has been less consistent compared with studies of risk overall and the exact mechanism whereby the gene contributes to malignant progression in the prostate is not well-understood. There is some suggestion that the gene may operate both as a tumour suppressor, as early studies reported its suppression of androgen receptor activity, and as an oncogene as HOXB13 overexpression has been seen in androgen-independent tumours [8].

Currently, most countries (including the USA) do not recommend use of PSA screening for men at average risk for prostate cancer. However, given the significant risk of prostate cancer in men carrying a single copy of the HOXB13 G84E allele, should these male mutation carriers be screened for prostate cancer with PSA testing and DRE? If so, how do we identify these men and at what age should testing commence? Unfortunately, many G84E carriers may not be identified by family history, which raises the question about when is the risk of disease significant enough to warrant population level testing? As Nordic countries, including Denmark, have a higher frequency of HOXB13 G84E allele in the general population, research directed toward understanding the benefit of genetic testing followed by prostate cancer early detection strategies should be considered.

Read the full article
Kathleen A. Cooney* and Jennifer L. Beebe-Dimmer

 

*Departments of Internal Medicine and Urology, The University of Michigan, Comprehensive Cancer Center, Ann Arbor, and Department of Oncology, Wayne State University School of Medicine, Karmanos Cancer Institute, Detro it, MI, USA

 

References

 

 

2 Ewing CM, Ray AM, Lange EM et al. Germline mutations in HOXB13 and prostate-cancer risk. N Engl J Med 2012; 366: 1419

 

3 Beebe-Dimmer JL, Isaacs WB, Zuhlke KA et al. Prevalence of the HOXB13 G84E prostate cancer risk allele in men treated with radical prostatectomy. BJU Int 2014; 113: 8305

 

 

5 Alanee S, Couch F, OftK. Association of a HOXB13 variant with breast cancer. N Engl J Med 2012; 367: 4801

 

6 Beebe-Dimmer JL, Hathcock M, Yee C et al. The HOXB13 G84E mutation is associated with an increased risk for prostate cancer and other malignancies. Cancer Epidemiol Biomarkers Prev 2015; 24: 136672

 

7 National Comprehensive Cancer Network (NCCN), NCCN Clinical Practice Guidelines in Oncology. Genetic/Familial High-risk Assessment: Breast and Ovarian (Version 2.2015). Available at: https://www.nccn.org/professionals/physician_gls/f_guidelines.asp. Accessed 12-27-2015

 

8 Shah N, Sukumar S. The Hox genes and their roles in oncogenesis. Nat Rev Cancer 2010; 10: 36171

 

Article of the Month: Recent advances in immuno-oncology and its application to urological cancers

Every Month the Editor-in-Chief selects an Article of the Month from the current issue of BJUI. The abstract is reproduced below and you can click on the button to read the full article, which is freely available to all readers for at least 30 days from the time of this post.

In addition to the article itself, there is an accompanying comment written by a prominent member of the urological community. This blog is intended to provoke comment and discussion and we invite you to use the comment tools at the bottom of each post to join the conversation.

If you only have time to read one article this week, it should be this one.

Recent advances in immuno-oncology and its application to urological cancers

Jennifer M. Mataraza and Philip Gotwals

 

Exploratory Immuno-Oncology, Novartis Institutes for BioMedical Research, Cambridge, MA, USA

 

Read the full article

Abstract

Recent advances in immuno-oncology have the potential to transform the practice of medical oncology. Antibodies directed against negative regulators of T-cell function (checkpoint inhibitors), engineered cell therapies and innate immune stimulators, such as oncolytic viruses, are effective in a wide range of cancers. Immune‘based therapies have had a clinically meaningful impact on the treatment of advanced melanoma, and the lessons regarding use of single agents and combinations in melanoma may be applicable to the treatment of urological cancers. Checkpoint inhibitors, cytokine therapy and therapeutic vaccines are already showing promise in urothelial bladder cancer, renal cell carcinoma and prostate cancer. Critical areas of future immuno-oncology research include the prospective identification of patients who will respond to current immune-based cancer therapies and the identification of new therapeutic agents that promote immune priming in tumours, and increase the rate of durable clinical responses.

oct-aotm-results

Read more articles of the week

Comment: Immune checkpoint blockade – a treatment for urological cancers?

Introduction

In the last few years there have been concerted attempts at using the power of the immune system as an effective treatment option for cancer. This has become possible as our understanding of the workings of the immune system has improved. Tumours form because of failure of the organism to destroy a rogue, mutated cell in an appropriate way. Once the tumour is formed it can further develop when the immune system fails to contain and control it and certain equilibrium is lost in favour of the tumour. This is referred to as the immune editing theory. At this point of failure of the immune system, tumour growth and progression become possible and tumours develop various mechanisms to evade the immune systems surveillance. Therefore, a mechanism to restore the lost equilibrium or to tip it in favour of the immune system would be a new modality in anti-cancer treatment. The initial approach was to use stimulators of the immune system systemically such as interleukin 2 and interferon γ i.v. in patients with metastatic cancers including melanoma and renal cancers [1]. A sustained response was shown in 22% of patients with metastatic kidney cancer, lasting for over a year. Although this treatment was not a resounding success, it did highlight an approach that could yield a durable tumour regression in a minority of cases. As our understanding of the immune system–tumour interaction further developed, new research focused on a specific mechanism in the immune system that seems to be exploited by tumours. This is an activation-inhibition mechanism, which controls the extent of adaptive immune response to invading organisms or to mutated cancer cells. In healthy individuals, this mechanism is a ‘safety’ feature allowing cessation of the immune response once it has performed its task. This is controlled by ‘receptor’ molecules at the T-cell surface and their corresponding ‘ligands’ at the surface of the cells interacting with the T-cell, which can be an antigen presenting cell or a tumour cell surface. This mechanism is called the immune checkpoint [2] (Fig. 1). Cytotoxic T lymphocyte antigen 4 (CTLA-4) and programmed death 1 (PD-1) are the most well-known checkpoints but there are up to 20 others (and counting) [2]. Their main role is to inhibit an immune response by blocking the activation of T-cells when those cells are presented with a foreign antigen or cancer proteins. This inhibition leads to immune ‘tolerance’ of the presence of cancer cells. So the policeman (T cell) is oblivious to the robbery in front of him. Thus an anti-tumour treatment strategy to disrupt the immune checkpoints seems to be a valid one (Table 1).

image

Figure 1. Blocking checkpoint inhibitors with antibodies is the new immunotherapy strategy to unlock T-cell activation and improve anti-tumour immune response. MHC, major histocompatibility complex; PD-L1, programmed death ligand 1; TCR, T-cell antigen receptor.

Table 1. A selected group of trials of immune checkpoint inhibitors in urological cancers
Tumour Phase Treatment N Results Trial.gov identifier
  1. mCRPC, metastatic castrate-resistant prostate cancer; PD-L1, programmed death ligand 1. The total number of current trials of immune checkpoint inhibitors is 46 for lung, breast, ovarian, rectal, prostate, pancreatic, bladder, renal cancers and melanoma.

mCRPC 1 Dendritic cell therapy and ipilimumab 20 Recruiting NCT02423928
All advanced solid tumours 1 Various combinations of ipilimumab, nivolumab and pembrolizumab 122 Recruiting NCT02467361
RCC 3 Nivolumab vs everolimus 822 Recruiting NCT01668784
RCC 3 Atezolizumab (anti PD-L1) 70 Good safety profile with antitumour activity NCT01375842
mCRPC 3 Ipilimumab vs placebo 799 No improvement of survival in treatment group NCT00861614
Urothelial 2 Gemcitabine, cisplatin and ipilimumab combinations 36 Recruiting NCT01524991

In recent years, a plethora of various inhibitors in the form of monoclonal antibodies to the checkpoint molecules were developed and to date three at least have been approved by the USA Food and Drug Administration (FDA) – ipilimumab (Yervoy), nivolumab (Opdivo), and pembrolizumab (Keytruda). They are anti-CTLA4 and anti-PD-1 antibodies. At least another eight checkpoint inhibitors are being developed. These agents have been shown to have survival benefit in some malignancies and limited benefit in others. However, the breakthrough seems to be happening in the treatment of metastatic malignant melanomas where immune checkpoint inhibitors treatment may become the standard of care. Patients with metastatic malignant melanoma who were treated with ipilimumab had a median survival of ~11 months; however, 22% of patients survived for ≥3 years with a plateau in the survival curve and in a subset of patients up to 10 years [3]. This success has not yet been replicated in prostate cancer [4]. In a more recent clinical trial involving patients with melanoma who progressed, nivolumab showed survival benefit of 72% at 1 year as compared with 42% with dacarbazine [5]. The latest approach is to combine anti-CTLA-4 and anti-PD-1 in one treatment regime as they are expected to act synergistically to remove the inhibition to the immune response, and clinical results seem to show survival benefit for combined therapy [6]. Combination of different treatment methods may potentiate the ‘abscopal effect’, which is seen when local radiation therapy can cause regression of tumour distant to the radiation site. This seems to be mediated by the immune system and potentiated by checkpoint inhibitors. Until now checkpoint inhibitors were used in patients with end-stage metastatic cancer, but recently anti-CTLA-4 has been trialled in pre-radical cystectomy patients not as a neoadjuvant therapy but rather to monitor immune response and surgical safety [2]. It is likely that checkpoint inhibitors will have a place in cancer treatment including urological cancers. However, this new class of anti-cancer treatment comes with a price. The emerging risks and side-effect profile of checkpoint inhibitors are completely different from those seen with the conventional chemotherapy and radiotherapy. Those side-effects are related to the activation of the immune system. Although most are not uncommon, they can occasionally have devastating effect on the patients. These side-effects include autoimmune conditions like dermatitis, mild colitis, and occasionally hepatitis. A severe form of colitis resulting in perforation has been reported. Unfortunately, the rate of adverse effects seems to correlate with positive clinical response. A list of some of the side-effects is summarised in Table 2. Treatment is usually with steroids, and clinicians are starting to develop strategies to minimise those risks.

Table 2. Autoimmune-based adverse effects that are associated with immune checkpoint inhibitors treatment. Most are tolerated. Severe ones are rare but can be devastating. Treatment is usually with steroids [2, 5, 6]
Adverse effects
Common Rare
Diarrhoea Severe colitis – colonic perforation
Pruritus/dermatitis Adrenal insufficiency
Rash Panhypopituitarism
Colitis Hepatitis
Fatigue Uveitis
Decreased appetite Temporal arteritis

The cost of checkpoint inhibitors remains relatively high and a full treatment course of ipilimumab costs >£18 000. One dose of pembrolizumab can cost >£3 500. However, the National Institute for Health and Care excellence (NICE) in the UK deemed this to be cost-effective and approved it for patients with metastatic melanoma that has progressed despite ipilimumab treatment.

Will the 21st century be the era for immunotherapy? It is still too early to tell. At present it remains rather expensive and beyond the means of many patients with cancer.

Read the full article
Oussama Elhage*, Christine Galustian* and Prokar Dasgupta*,

 

*Medical Research Council (MRC) Centre for Transplantation, and National Institute for Health Research (NIHR) Biomedical Research Centre, Kings Health Partners, Kings College London and Guys Hospital, London, UK

 

References
1 Rosenberg SA, Lotze MT, Yang JC et al. Experience with the use of high-dose interleukin-2 in the treatment of 652 cancer patients. Ann Surg 1989; 210: 47485

 

2 Allison JP, Freeman GJ, Gotwals P. Targeting cancer pathways: understanding immune checkpoints. Science Webinar Series. Science 2016; 351: 303

 

 

4 Mataraza J, Gotwals P. Recent advances in immuno-oncology and its application to urological cancers. BJU Int 2016; 118: 50614

 

5 Robert C, Long GV, Brady B et al. Nivolumab in previously untreated melanoma without BRAF mutation. N Engl J Med 2015; 372: 32030

 

6 Larkin J, Chiarion-Sileni V, Gonzalez R et al. Combined nivolumab and ipilimumab or monotherapy in untreated melanoma. N Engl J Med 2015; 373: 2334

 

Asia-Pacific Prostate Cancer Conference 2016 Highlights

JSAfter briefly venturing to tropical Cairns in 2015, the Asia-Pacific Prostate Cancer Conference returned to its traditional home in Melbourne for its 17th edition in 2016 (#APCC16). The meeting has previously featured the who’s who of prostate cancer and this year was no different with an all-star multidisciplinary faculty consisting of 18 international members in addition to our local experts. The meeting was well attended by over the 750 delegates from all parts of the globe and remains one of the largest prostate cancer educational events worldwide.

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Conference president Professor Tony Costello opened the conference with the famous Whitmore aphorisms and outlined the impressive progress and discoveries we have made in the field over the last century. The first case of prostate cancer was described in 1853 in the London Hospital and was noted by the surgeon to be a “very rare disease” whereas now it is known to be the most commonly diagnosed malignancy amongst men. Pleasingly, research and emphasis on men’s health has grown with the disease highlighted by the newly completed, world-class Parkville Biomedical precinct in Melbourne, which includes “The Royal Men’s Hospital” (@APCR). Melbourne’s Lord Mayor (@LordMayorMelb) also dropped-by to reiterate his support for the meeting and the advancements made in men’s health.

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In what is becoming an annual tradition, honourary Melbournian and Australian, Dr Stacy Loeb (@LoebStacy) once again got the sessions off to a flying start by delivering the ‘prostate cancer year in review’ which was an excellent overview of the abstracts produced over the last 12 months. The male attendees in particular were excited by the recent paper suggesting that more than 21 ejaculations per month acted as a protective factor for the development of prostate cancer. Although confounding factors may have played a role in the association seen, these were easily over-looked and its results were accepted as gospel and promoted as a public health message. The abstract featured the following day on the home page of The Australian Financial Review (https://www.afr.com/lifestyle/health/mens-health/tell-your-partner-frequency-counts-even-against-cancer-20160831-gr5fs4) – who knew that the answer to the world economic problems was so simple!

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The meeting did however become more scientific as we heard from a range of international and local experts on the challenges of trying to find the balance of precision oncology in a time of tumour heterogeneity. It was clear that the future has arrived with recent advances in the field of genomics and biomarkers. These discoveries appear to be only the tip of the iceberg and further research holds the key in understanding tumour behavior in order to tailor treatment on a patient-to-patient level. Having witnessed a variety of experts from all parts of the globe present their finding there is little doubt that a major breakthrough is just around the corner. A special mention to Dr Niall Corcoran whose research was of such high quality that A/Prof Henry Woo (@DrHWoo) raised the white flag early in the Melbourne vs. Sydney inter-city rivalry.

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The named lectures of #APCC16 were highlights of the conference. Keeping with the theme of the first morning, Dr Martin Gleave delivered the 4th Patrick C Walsh lecture titled ‘Two Tales of Precision Oncology.” Prof Peter Wiklund gave the inaugural ERUS lecture on the role of surgery for high risk and metastatic prostate cancer.

It wouldn’t have been a prostate cancer conference without the age-old debate of surgery vs. radiotherapy being revisited. Over three days Dr Robert Nam presented a series of talks on Canadian long-term outcomes and meta-analysis showing favourable results for team surgery. He also predicted that the highly anticipated ProtecT randomised trial due in the NEJM would show no difference ensuring the debate prolongs into the future and vowed to “eat my shorts” if the trial demonstrated a result favouring either modality. Dr John Violet flew the flag strongly for radiation oncologists in presenting the promising outcomes for 177Lu-PSMA in the mCRPC setting. Similarly, Dr Andrew Kneebone presented a compelling case for stereotactic radiation for oligometastatic disease.

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Imaging of the prostate was a hot topic throughout the conference. The excitement around PSMA-PET was at a climax following The Victorian Comprehensive Cancer Centre’s (@VCCC) experience that was presented by Associate Professors Michael Hofman (@DrMHofman) and Nathan Lawrentschuk (@lawrentschuk). The proceeding panel discussion focused on how to best utilise the technology and the role it currently plays in the prostate cancer landscape.  Despite not being FDA approved, its role in evaluating recurrence appears to be entrenched with data to support its superiority over other modalities but it was also proposed that it might have a place in initial staging of high-risk cancer.  The advancement of PSMA over conventional imaging also raised the question of how we now interpret previous trials such as CHAARTED and STAMPEDE whose results are based on superseded technology.

The hype surrounding PSMA-PET only just eclipsed that of mpMRI in the imaging landscape. Professor Philip Stricker presented a nomogram, which integrated MRI in determining who to biopsy and Dr Rob Reiter reported a terrific novel study of using 3D modeling to compare MRI results to final histopathology to determine correlation but did caution us with performing targeted biopsies alone which risks missing clinically significant cancers. Dr Nam also chimed in with a pilot study of using MRI as a screening test.

Suspense was built until Friday for the highly anticipated session on open vs. robotic surgery featuring the first presentation of the Brisbane RCT. The results of the trial have been already widely debated in the urological community and a discussion similar to the recent BJUI blog (https://www.bjuinternational.com/bjui-blog/its-not-about-the-machine-stupid/) ensued. Regardless of individual opinions on the trial, there is no dispute about the volume of work required to conduct a surgical randomised trial and there was wide praise for the efforts of the Brisbane team. Prof Peter Wiklund and Dr Homi Zargar (@hzargar) also reported the Swedish and Victorian experience respectively. The overall consensus was that robotic surgery offers the benefit of minimally invasive surgery but it is the surgeon rather than the modality, which has the most significant impact on outcomes.

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There was a strong multi-disciplinary theme throughout the conference. The Nursing & Allied Health and Translational Science streams both had strong contingents attending. The quality of research presented and engagement amongst attendee was of the highest standard. This was exemplified by the session ‘MDT 2020’, which was a case-centred discussion by a panel of experts from a variety of professions and highlighted the value of a multidisciplinary approach in patient care.

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The social program of #APCC16 was not overshadowed by its academic counterpart. The conference dinner was held at The Glasshouse where the food was exquisite and entertainment was provided by three waiters come tenors. Their classical renditions were received by guests with napkin twirling and swinging wine glasses. The frivolities were thoroughly enjoyed by all.

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The final day of the conference was highlighted by the masterclasses. The 6th da Vinci© Prostatectomy Masterclass was convened by Drs Daniel Moon (@DrDanielMoon) and Geoff Coughlin and featured international faculty involvement by Dr John Davis (@jhdavis) and Professors Thalman and Wiklund. Considering the hype surrounding MRI it was no surprise that the 3rd Prostate MRI Imaging and Biopsy masterclass reached capacity many months ago. It should also be mentioned that the sponsored satellite meetings and breakfast sessions in the previous days which starred Dr Stacy Loeb, Dr Tia Higano (@thigano), Dr Jaspreet Sandhu, Prof Bertrand Tombal (@BertrandTOMBAL) and Genevieve Muir-Smith drew large numbers of attendees.

We would like to congratulate all attendees and their teams on the abstracts presented throughout the conference. The BJUI once again proudly supported the meeting with all accepted abstracts published in a special supplements issue and BJUI Associate Editors Declan Murphy (@declanmurphy), John Davis, and Nathan Lawrentschuk being prominent figures throughout the conference. A special mention to the poster prize winners from this year:

  • Clinical Urology: Jonathan Kam – Do multi-parametric MRI guided biopsies add value to the standard systematic prostate needle biopsy? – early experience in an Australian regional centre
  • Nursing & Allied Health: Thea Richardson – An Androgen Deprivation Therapy Clinic: An integrative approach to treatment
  • Translational Science: Natalie Kurganovs – Identifying the origins and drivers of castration resistant prostate cancer

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On behalf of all the delegates, we thank the entire international and local faculty who shared their knowledge over the conference and devote their time to improving men’s health. Furthermore, meetings such as this would not occur without the unheralded behind the scenes work. We extend our thanks to president Prof Costello, the convenors of the streams (A/Prof Declan Murphy, Dr Niall Corcoran, A/Prof Chris Hovens, Ms Helen Crowe (@helenrcrowe) & Mr Dave Gray (@DavidGrayAust)) and the APCC committee. We also graciously thank our sponsors without whom none of this would be possible and are vital to further advancements in men’s health.

Last but not least, given the rich history of social media seen at this conference, it would be remiss not to acknowledge another #SoMe landmark. Melbourne has previously been responsible in welcoming urology SoMe royalty, Dr Stacy Loeb, to the twitter world and this year the twitterati were introduced to Dr Peter Carroll (@pcarroll_). He managed to send out 4 tweets and eclipse 100 followers before the end of the conference.

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#APCC17 will return to Melbourne on 30th of August 2017 – we hope to see you there!

Dr Niranjan Sathianathen (@NiranjanJS) is a researcher at Peter MacCallum Cancer Centre, Melbourne.

 

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