Questions related to Urologic Oncology
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?
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?
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.
Ana Filipa Semedo
What are the most prevalent genes which mutated in prostate cancer ?
What are the genes polymorphisms that show obviously in prostate cancer ?
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);
9. Formate (highest in presence of Gram-);
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+);
18. L-fucose (may have an influence to virulence of some E. coli strains producing verotoxin);
25. Mandelic acid (antibacterial properties);
27. N-acetylneuraminic acid (found in cell membranes, may make a sense in diagnosing intracellular E. coli?);
28. Nicotinic acid (P. aeruginosa);
30. Succinate (highest in presence of Gram-);
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.
What is your opinion on the relevance of Prostate specific antigen density in screening patients with indeterminate PSA?
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.
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.
Looking for a bilingual urologist (French and English) to collaborate in a writing scientific paper in the urology area
If you have the answers, I hope you also tell me the titles of articles your answers are from.
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?
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!
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?
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!
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.
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.
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.
Satellite urethral melanoma has been reported. Does anyone have experience with followup/surveillance of primary urethral melanoma?
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?