Wnioski z Genitourinary Cancers Symposium luty 2019

Wnioski z Genitourinary Cancers Symposium luty 2019

Nieprzeczytany postautor: wiatger » 24 lut 2019, 14:10

W dniach 14 - 16 lutego 2019 roku w San Francisco odbyło się międzynarodowe sympozjum poświęcone nowotworom ukladu moczowego:

Genitourinary Cancers Symposium

Oto program i obserwacje poczynione przez Dr. Jeffrey Tosoian z University of Michigan Department of Urology, USA.

The 2019 Genitourinary Cancers Symposium is being held this week in San Francisco, California.
This conference features multidisciplinary sessions covering prostate, renal, urothelial, penile, testicular, and adrenal cancers.
I have found it to be one of the most informative, high-yield conferences in the field. Here, I have attempted to summarize presentations from several world-renowned faculty in the briefest way possible. Obviously, this approach cannot do justice to the wealth of insight and information provided in these presentations, but rather it is intended to capture only the broadest ideas conveyed by each. It is possible that my own interests have impacted the points I found most pertinent. For additional information and commentary from others, I would encourage you to explore Twitter, where the hashtag #GU19 has been particularly active.
The official symposium website can be viewed via https://gucasym.org/.

General Session 1:
Optimizing Diagnosis and Treatment of Clinically Significant Nonmetastatic Prostate Cancer.
Chairs: JA Efstathiou, H Beltran

=> PSA Screening: Towards a Harm-Reduction Approach. A Vickers
PSA screening is not about personal preference. It is about how we can reduce harms.
Some very simple changes to the PSA screening approach can drastically reduce harms:
Do not screen men >70 years.
Stop screening most men at age 60.
Practice selective use of biopsy.
Provide active surveillance for all Gleason score 6 prostate cancer.

=> Role of MRI in Targeted Biopsy. S Taneja
Prebiopsy MRI and MRI targeting lead to improved detection of high-grade cancer.
The intention of prebiopsy MRI is to reduce detection of indolent cancers.
A critical question for practitioners is how to properly balance detection of high-grade disease and avoid low-grade cancers.

=> Advanced Imaging and Biomarkers for Clinical Decision Making: Where Are We Now? FY Feng
Advanced imaging improves disease detection and has led to a “new” disease state, oligometastatic prostate cancer. But does this yield clinical benefit?
We need to do a better job incorporating molecular biomarkers into clinical trials; these biomarkers have the potential to guide therapy.

=> Intensification Versus Deintensification in High-Risk Prostate Cancer. SS Sridhar, A Briganti, HA Payne
There are an abundance of data exploring a surgical versus radiation approach in a high-risk setting, all of which have severe limitations: retrospective, population-based, unknown confounders, etc.
Evolution of radiation therapy has yielded benefits in treatment outcomes without increased toxicity.
High-risk disease should be considered within a multidisciplinary paradigm; however, surgery as monotherapy may be an option in approximately one-third of men.

General Session 2:
Quality, Value, and Science for Optimizing Advanced Prostate Cancer Treatment.
Chairs: KE Knudsen, CJ Ryan

=> Quality of Life–Focused Decision-Making for Castrate-Sensitive Prostate Cancer. AK Morgans
Quality of life is not represented by adverse events alone, but rather includes adverse events, patient-reported outcomes, and additional factors.
Patient-related outcomes are critical in assessing quality of life but remain difficult to interpret in light of no standardized methodology.

=> Value-Based Decision-Making for Castrate-Sensitive Prostate Cancer. RC Chen
Value-based decision-making is anchored in understanding effectiveness, but effectiveness alone is not sufficient.
It is necessary to consider cost from a societal perspective given finite resources.

=> Biologic Basis for Sequencing Novel Treatments for Metastatic Prostate Cancer. H Beltran
Precision medicine approaches to prostate cancer remain challenged by tumor evolution, heterogeneity, and other nongenomic and clinical factors.
There is a need for more biomarkers to inform treatment choice and sequence; the future is likely to combine patient and molecular features to define subgroups for specific management approaches.

=> Practical Application of Genomic Assays in Clinical Decision-Making. MA Rubin
There are several “actionable” assays that require prospective validation: blood/biopsy/cfDNA DNA repair, CTCs for ARV7, AR gain in metastatic biopsy, cfDNA for DNA fraction.
Dr. Rubin has made his presentation available online:

ur. 1943. Od 2011 (PSA 1,87 ng/ml) leczenie BPH (Omnic Ocas).
02.2015 – PSA 4,12 ng/ml; MRI miednicy: podejrzenie zmiany npl gruczołu krokowego.
10.2016 – tPSA 6,19 ng/ml; fPSA 0,54 ng/ml; DRE: wyczuwalny guzek.
12.2016 – PSA 7,71 ng/ml; mpMRI: ognisko hipointensywne, cechy infiltracji lewych pęcherzyków nasiennych; miednica bez adenopatii- wysokie podejrzenie naciekającego raka stercza, PI-RADS 5. 02.01.2017 biopsja : płat prawy - w jednym z bioptatów mikroognisko raka gruczołowego ; płat lewy - rak gruczołowy, Gleason 8 (4+4). Naciekanie nerwów niewidoczne. Scyntygrafia b. z.,
Od 18.01.17 Flutamid 3x250mg; 02.17 PSA 2,44 ng/ml; 31.01.17 Eligard 22,5 mg;14.02.17 Flutamid stop. 20.03.17 PSA 0,786 ng/ml. 29.03.17 rozpoczęcie TomoTherapy. 05.2017 Eligard 45 mg. 25.05.17 zakończenie RT, PSA 0,184 ng/ml, T 34 ng/dl; 10.17 tPSA 0,02 ng/ml, T 8,5 ng/dl; 11.17 Eligard 22,5; 02.18 PSA <0,01, Diphereline 11,25; 05.18 PSA <0,006, T 5,0 ng/dl, Diphereline 11,25; 08.18 PSA <0,01, T 28 ng/dl (inne lab.), HT STOP!
po 3 m bez HT (11.18) – PSA 0,035 ; T 127; po 6 m bez HT (02.19) – PSA 0,828 ; T 255;
po 7 m bez HT (03.19) – PSA 0,911; T n.b.; po 8 m bez HT (04.19) – PSA 0,873; T 197;
po 9 m bez HT (05.19) - PSA 0,782; T – 189 ; 06.19 - scyntygrafia i SPECT/CT - bez zmian ogniskowych.
Po 11 m bez HT (07.19) - PSA 0,711; T - 216; po 14 m bez HT (10.19) - PSA 0,467; T - 238;
po 17 mieś. bez HT (02.20): PSA – 0,625; T - 250; po 20 mieś. bez HT (05.20): PSA - 1,62; T - 298;
08.06. - PET/CT PSMA z 18F - ogniska w Th3 i Th6, nie jasna sprawa prostaty. 03.08.20: PSA – 3,077.
06.08.20 - mpMRI prostaty: naciek npl. 21-27.08.20 - 3 frakcje po 8 Gy na zmianę na kręgosłup (Th3 iTh6) met. CK. 24.08.20 - biopsja prostaty - w dwóch (na 14) bioptatach wznowa Gl 8 (4+4 ). 07.10.20: PSA 4,296. 07-16.10.20 - 5 frakcji po 6,75 Gy na prostatę met. CK. Styczeń 2021 - covid. 02.21 PSA 5,58; 03.21 PSA 4,17; 04.21 PSA 6,01. 03.21 bad. genetyczne - mutacja c.444+1G>A w genie CHEK2. 04.21-PET 68Ga PSMA - podejrzany pęcherzyk. 05.21 PSA 8,13; Diphereline 11,25.
Posty: 245
Rejestracja: 11 lis 2016, 12:00
Lokalizacja: okolice Łodzi
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