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Urologic Oncology - Science topic

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BPH is a innocent bystander in later stages of male life in humans. Normally Benign Prostatic hyperplasia is curable by using the various avaliable treatments and medications like 5alpha reductase inhibitors and antiandrogenic therapies. TURP, TUIP and prostatectomy are also advised very often. But what is the indication of the progression of the problem which is not curable from the avaliable measures. Is it a cancerous situation then? Is herbal therapy the probable answer of the problem in complicated cases?
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Prostatic abscess is a rare urological disease. Patients with prostatic abscess and those with PCa can have similar presentation, such as LUTS, lymphadenopathy and abnormal PSA values.
USG-guided needle aspiration maybe an option of treatment for prostatic abscess, but TURP should be considered in patients with complicated abscess or suspected prostatic carcinoma.
If the histopathology result shows PCa, staging and risk stratification should be done for the treatment decision… “Shared-decision making” for PCa mgt
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Do you think that a Side-effect questionnaire - Intravesical instillation of Bacillus Calmette-Guèrin (BCG) for nonmuscle invasive bladder cancer’ improves the recognition and reporting of potential side effects of BCG treatment by patients?
Dear all,
My name is Ana Filipa Semedo, I am doing the Master in Leadership in Cancer, End life and Palliative Care in Southampton University specific Dissertation(MSc) module.
I am a Clinical Nurse Specialist Urological - Oncology in the United Kingdom in Royal Marsden Hospital (Oncology Hospital) in London.    
My thesis question is: "Simplified terminology of the EAUN (European Association of Urology Nurses) Side-effect questionnaire - Intravesical instillation of Bacillus Calmette-Guèrin (BCG) for nonmuscle invasive bladder cancer’ improves the recognition and reporting of potential side effects of BCG treatment by patients".
I would appreciate if could share your opinions and answers to the question of this discussion group.
Could you please also share any assessment tool/ questionnaire to identify the side-effects provoke by the Intravesical BCG therapy for non-invasive muscle bladder cancer.
Thank you very much for your help in this matter.
Regards,
Ana Filipa Semedo 
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In Sweden, most urology departments have questionnaires, which is documented at each visit before the next instillation. If any persistent side effects occur, the nurse consult the doctor, before the next instillation is given. I think it is very important to be aware of the side effects, to stop treatment in case of severe side effects!
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The urine were obtained from pre-operation and post-operation respectively.
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As many as 30 to 50% of children with proteinuria may have transient, non-repetitive proteinuria. Transient proteinuria can occur after abdominal surgery and with strenuous exercise, emotional stress, exposure to extreme cold, epinephrine administration,  or congestive heart failure, as well. In all of these circumstances, proteinuria resolves spontaneously after the cessation of the causal factor, and an extensive work-up is usually not recommended.
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What are the most prevalent genes which mutated in prostate cancer ?
What are the genes polymorphisms that show obviously in prostate cancer ?
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Thanks for all 
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Dear colleagues,
I am Jakhongir F. Alidjanov, urologist from Uzbekistan, working on Research Project at the Justus-Liebig University of Giessen.
The main aim of the project is to investigate changes in metabolomic profile of the urine due to causative pathogens of urinary tract infections. Since being clinician, I am not so familiar with advanced microbiology. Therefore I would really appreciate if you could help me to clarify some advanced issues.
What pathogenic bacteria (E. coli, P. aeruginosa, E, faecalis, K. pneumoniae, S. saprophiticus etc.) do usually use as a nutrient source for living and multiplication in the urine? Below, I am posting some metabolites present in the urine which in my humble opinion could be appropriate to be investigated.
1. 1.3-propanediol (K. pneumoniae);
2. 4-Pyridoxic acid;
3. 6-hydroxylnicotinic acid (P. aeruginosa);
4. Acetate (highest in presence of Gram+);
5. Androsterone (may be reduced in stress urinary incontinence);
6. Citrate;
7. Creatinine;
8. Ethanol;
9. Formate (highest in presence of Gram-);
10. Glucose;
11. Glycerol (K. pneumoniae);
12. Glycolic acid;
13. Hippurate (highest in presence of Gram-);
14. Indoxyl sulphate (may be converted by uropathogens into indirubin and indigo – “purple bag syndrome”);
15. Lactate (highest in presence of Gram+);
16. L-alanine;
17. L-cysteine;
18. L-fucose (may have an influence to virulence of some E. coli strains producing verotoxin);
19. L-glutamine;
20. L-histidine;
21. L-lysine;
22. L-serine;
23. L-theronine;
24. L-tyrosine;
25. Mandelic acid (antibacterial properties);
26. Methanol;
27. N-acetylneuraminic acid (found in cell membranes, may make a sense in diagnosing intracellular E. coli?);
28. Nicotinic acid (P. aeruginosa);
29. Nitrite;
30. Succinate (highest in presence of Gram-);
31. Taurine;
32. Trimethylamine (E. coli);
33. Trimethylamine N-oxide (E. coli);
34. Urea (highest in presence of Gram-);
35. α-Aminoadipic acid;
Could you please look on them and give your suggestions regarding this issue? What else should we investigate?
Thank you all in advance for your responses.
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Dear Jakhongir,
It is a very interesting project. I suggest that you take a look on the recent advances in this field. For example, H-NMR has been utilized for profiling of urinary tract infection.
Ekaterina Nevedomskaya et al. have published an article entitled " 1H NMR-based metabolic profiling of urinary tract infection: combining multiple statistical models and clinical data" and the conclusions emerged from their study:
"In the current paper we used a metabolomics approach to profile UTI, which is on the one hand one of the most common infectious diseases among the adults, and on the other hand a disease that still lacks markers of morbidity. Using 1H NMR profiles of urine we generated various statistical models: (a) discriminating UTI patients and control subjects, (b) following the recovery process of UTI patients and (c) associating urine metabolic content with bacterial contamination. The discriminative model was able to classify most of the independent samples correctly according to their diagnosis, which indicates its high predictive ability. Comparing the sets of molecules derived from different analyses, we concluded that some of the compounds (e.g. trimethylamine and acetate) can be attributed to the effect of bacterial contamination of urine; others (e.g. para-aminohippuric acid, scyllo-inositol) can be considered markers of morbidity."
On the other hand, Haitao Lv et al. have used LC-MS as an Integrated Metabolomic Profiling Approach for Infectious Diseases Research. The following is the publication abstract for quick view:
Metabolomic profiling offers direct insights into the chemical environment and metabolic pathway activities at sites of human disease. During infection, this environment may receive important contributions from both host and pathogen. Here we apply untargeted metabolomics approach to identify compounds associated with an E. coli urinary tract infection population. Correlative and structural data from minimally processed samples were obtained using an optimized LC-MS platform capable of resolving ∼2300 molecular features. Principal components analysis readily distinguished patient groups and multiple supervised chemometric analyses resolved robust metabolomic shifts between groups. These analyses revealed nine compounds whose provisional structures suggest candidate infection-associated endocrine, catabolic, and lipid pathways. Several of these metabolite signatures may derive from microbial processing of host metabolites. Overall, this study highlights the ability of metabolomic approaches to directly identify compounds encountered by, and produced from, bacterial pathogens within human hosts.
Other important publications which may be helpful are contained in the following links:
Hoping this will be helpful,
Rafik
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What is your opinion on the relevance of Prostate specific antigen density in screening patients with indeterminate PSA?
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You should try diffusion MRI. DOI: 10.1002/mrm.26340 and many other references.
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Dear colleagues, 
I think this question is more related to biochemists ans microbiologists. We would like to produce "home-made" artificial urine for investigating pathogen-pathogen relations by simulation. We have produced the artificial urine proposed by Griffith et al. containing calcium chloride - 0.46g/L, magnesium chloride hexahydrate - 0.65 g/L, sodium chloride - 4.60 g/L, sodium sulfate - 2.30 g/L, trisodium citrate dihydrate - 0.65 g/L, disodium oxalate - 0.02 g/L, potassium dihydrogen phosphate - 2.80 g/L, potassium chloride -1.60 g/L, ammonium chloride - 1.0 g/L, urea - 25.0 g/L, We decided to not adding gelatin and have added tryptic soy broth instead. It was very good for UPEC strains and for E.coli UTI89, but Lactobacilli and some other microbiota did not demonstrate a growth in this solution. We would like to perform simulation as close to nature as possible. Reason for not using human urine is attempt to avoid "individual" characteristics such as dietary habits, alcohol abuse, antibiotics etc. As well, we would like to know what may happen exactly in the urine with the exclusion of local defence mechanisms of the bladder uroepithelium. Separate uroepithelilal cell culture studies are planned to be performed later.  
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It's a multifaceted problem (see attached file). For Lactobacilli, you must add a monosaccharide and for other bacteria the suitable substrate for each one. Two hocus-pocus solutions:
1. Why do you use -as basis- comercial urine controls, without antibacterial products, of course? http://quantimetrix.com/
2. Why do you use a pool of urines obtained from nuns (good option to control many variables? If they say ok, naturally.
"¿Local defence mechanisms?" is not the question. Why some bacteria are permitted while others do not? This is the question. Remember that the principal mechanism is uromodulin (see attached file).
I hope I have been able to help you.
Best regards
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 Why the peripheral zone of the prostate gland is said to more affected by prostate cancer than the other zones such as central and transitional zones.
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Due to the glandular tissue.
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In a castrated patient is really necessary to use analog LHRH?
We could use Abiraterone and prednisone Alone
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Hormonal treatment should be continued with chemotherapy as still there are some cells that respond to androgen deprivation. I believe the story is different with Abiraterone as it is a sort of an alternative hormonal treatment and I believe whenever we prescribe Abiraterone for CRPC, there is no need to continue LHRH analogues.
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Looking for a bilingual urologist (French and English) to collaborate in a writing scientific paper in the urology area
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Well Dr Hani, I am still willing having a collaborative work with you.I am lecturer in urology in my faculty and it will be interesting for me to work with you.I will join you in box and I transmitt you my email : adamsouat1@hotmail.com.
Hoping having news from you and your email.Thank you.
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If you have the answers, I hope you also tell me the titles of articles your answers are from.
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Try this one it might help you.
Here I am posting few suggestions given by one of RG member that will help you in protocol optimization.
I thing forming single cell suspension will vary....but I am sure you need to check it
Best wishes
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hormone blockade is generally followed by a sharp decrease of PSA to unmeasurable levels. This can mean that the cell population secreting PSA is destroyed or that the cell's ability to secrete PSA is blocked. Does anyone know a study showing the response of a prostate cancer cell culture to hormone blockade?
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Several clinical studies showed histopathogic chenges induced by androgen deprivation: regressive effect and apoptosis sere more pronunced in low grade disease rather thai in high grade. However chenges were reversibile. You can find a recent pubblication on Future Oncology. A medline Search including neo adiuvante  hormonal treatment is helpful.
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Dear colleagues,
I need some reliable information on treatment patterns in prostate cancer patients with regard to the two questions mentioned below.
Thank you for your help and all the best!
Sabine
1. Are patients in your country/region/center treated with hormonal treatment (LHRH) when they have rising PSA despite no metastasis on imaging?
2. Is adjuvant treatment after surgery or radiotherapy done and if yes, how long?
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a recent study presented at ASCO showed there was no benefit in early ADT for PSA relapse,until the occurence of clinical metastatic disease
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I’d like to set up collaboration with those who have an access to human and/or canine prostates with cancer and might be interested in 1) exploring interstitial optical studies of prostates with cancer for diagnostic purposes and 2) using gold nanoparticles as contrast agents for prostate cancer detection. The goal is two-fold.
First, we want to establish a correlation between concentrations of major chromophores like Hb, HbO2 and H2O and a presence of PC, as well as measure optical absorption and scattering parameters of the organ on ex vivo excised prostates. Since those prostates will be excised anyway we’d like to perform optical measurements on them after excision before they go for some other destructive tests etc. Once this stage is completed and data make sense, we can proceed to a development of an endoscope for performing such measurements in vivo (illumination via rectum, detection via urethra). The approach would be similar to cystoscopy and will utilize a side-firing fiber (or its variation) as a detector and a cylindrical diffuser as the light source.
Second, we would like to target PC biomarkers (like PSMA) in the gland, functionalize gold nanoparticles with appropriate surface agents, deliver Au NPs to the prostate with cancer and detect them with the same technique (illumination via rectum, detection via urethra). This project is more challenging on a number of reasons: 1) preparing Au NPs for targeting PMSA and still protected from RES that can be efficiently accumulated in the gland has never been done (most studies in vitro); 2) since such studies would require working with Au NPs and patients, FDA approval can be an issue. Doing these experiments in dogs would be almost ideal. However, there are conflicting reports on PSMA as a biomarker in canine prostate cancer (see below). Thus, if PSMA can indeed be used and targeted in canine PC, no human prostates would be involved and entire experiments can be performed on canine prostates.
Why not going with rats, for example? Because of the size of the prostate. We really want to go through cm’s of prostate tissue, and dog’s prostate is almost an ideal substitute for a human prostate (sizewise). On the other hand, we’d like to target realistic Au NPs concentrations in the prostate that can be achieved in such studies. So, I’d really like to get your thoughts and possibly practical suggestions on this aspect. I do believe that such molecular imaging of PC via optical detection of Au NPs may not only improve the early cancer detection but pave the way for Au NPs-mediated thermal therapies for focal cancer ablation (but this is a scientist talking:) The nature of this project would require a multidisciplinary team of oncology urologists, molecular biologists, chemists.
We can detect Au NPs in the prostate via urethra using optical radiance technique. Moreover, the sensitivity is much better than the sensitivity of the clinical CT (see the comparison in the publication and relevant references). We can see <=10^10 Au nanorods in the prostate. It means that with saturating of 1-10% of existing PSMA copies per cell ( close to 10^6 sites per cell), detecting 10^10 Au NPs would correspond to seeing ~10^5 malignant cells in the prostate. This number corresponds to the so-called angiogenic switch indicating very promising potential for early cancer detection.
More details on the method are provided in our recent publication (below). I encourage you to read it, and I’d be happy to discuss logistics and answer questions on this topic because there is no way to address all relevant issues in this posting.
Really looking forward for the feedback!
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Let converse.
Best,
Dragan
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LESS is still technically difficult and in urology we have already our own limitations. Therefore, do you think that LESS will survive?
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Dear Aly,
if in fact the surgical quality is identical and the scar invisible there is no doubt that LESS will be the future: However, my personal experience teaches me - at least valid for myself - there are complex procedures I can do better by multiarm robotics compared to classical laparoscopy and particularly single site surgery. A lot of procedures in fact can be done by all of the thechniques in same quality. However there are also surgeons who do it best open - either due to their training or capability.
So, we agree that the quality of surgery is most important and not how to come there. So, there is no best access generally, but only individually: each surgeon has to decide how to access (with minimized injury) to guarantuee best surgical qualitiy and minimized morbiditiy of access, but with clear priority. Although surgical qualitiy is extremely difficult to measure we shold not confuse it with feasability.
Happy and Healthy New Year Aly
Yours Rainer
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In clinical management of the disease, there is a question of when and to which extent Androgen Deprivation and/or Radiotherapy would make sense. However, I did not find a clear definition especially of high-risk localized prostate cancer.
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This appears to be more complex then though at first sight. Thank you both !!! I think I do understand it by now (:-))).
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At least since 2008 IAD has been considered an option that may be offered to men with metastatic prostate cancer but I have no idea about actual application of this strategy. Any feedback or publications would be welcomed.
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Also are there androgen receptor mutations, which confer agonistic activity to enzalutamide or abiraterone, like we’ve previously seen with flutamide?
I’m interested whether the androgen receptor pathway still plays a role at this advanced stage of disease (after enzalutamide / abiraterone treatment) or whether these tumors may have become indeed androgen-insensitive. In this case I would expect that this tumors look very undifferentiated in histology, with cytoplasmic AR staining (if any). I can’t find much literature on histology and androgen receptor staining of enzalutamide/abiraterone-resistant patient material. I’m just not sure whether growth of these tumors is mainly stimulated by constitutively active androgen receptor variants, like some claim. It could also be that these tumors have bypassed the androgen receptor by activation of alternative growth pathways.
What are your thoughts about this issue? If possible, support with literature references.
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Biopsies of patients progressing on abiraterone or enzalutamide show nuclear staining for AR indicating continued AR activation. Also, enzalutamide has activity after abiraterone and the reverse is also true, although the response rates are lower indicating some degree of cross-resistance but also contiued sensitivty to AR targeting agents in other patients (see also publications Loriot Annals of Oncology 2013, Bianchini EJC 2013, Noonan Annals of Oncology 2013, Schrader Eur Urol 2013).
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Satellite urethral melanoma has been reported. Does anyone have experience with followup/surveillance of primary urethral melanoma?
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Urethral cancer has varying lymphatic drainage in males/females depending on whether proximal or distal urethra is involved. In general urethral melanoma is a very rare and aggressive disease with high mortality and recurrence rates. In males, the prostate is often involved.
While for distal disease partial urethrectomy may be considered and total urethrectomy/diversion may provide better long-term control (?); for proximal disease total urethrectomy with cystectomy/pelvic exenteration and urinary diversion as well as regional lymphadenectomy is usually the treatment of choice
In terms of follow up - there are no established protocols; published retrospective reports show poor outcomes. I would base follow up on what we know on urethral carcinoma in general - serial pelvic imaging with CT; if urethra/bladder have not been removed then cystoscopy - probably more frequent than for urothelial carcinoma which is every 3 months for the first 2 years.
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LNcap cell might be unsuitable to be a cell model for androgen deprivation to watch cell death for its mutant AR. AR-expressing prostate cancer cells derived from castrated patients (e.g., LNCaP, LAPC-4 etc), the cells have developed castration resistance mechanisms (i.e., mutation, gene amplification, protein over-expression) to activate AR signaling for their continued growth even in the presence of castrate levels of androgen. What kind of cell line would be suitable?
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LNCaP cells will not die in the absence of androgen, they will merely stop dividing. PC3 or DU145 cells will not die as a result of androgen deprivation either, as they are androgen independent. In fact, these 2 cell lines will continue to proliferate in the absence of androgens.
RWPE1 (American Type Culture Collection) cells are non-tumorigenic and immortalised, but may be useful for your studies.
Are you looking to induce cell death by androgen deprivation alone, or by also treating with a drug?