Top Tweets for #USPCC26
đ§Ź Capivasertib + abiraterone offers a precision-medicine alternative to chemotherapy-based triplet therapy in PTEN-deficient metastatic APMN/S prostate cancer.
At #USPCC26, Dr. Russell Szmulewitz @UChicagoMed highlighted CAPItello-281: in 1,012 patients with PTEN-deficient de novo metastatic disease, capivasertib improved median rPFS from 25.7 to 33.2 months, with the largest apparent benefit in complete PTEN loss. OS is still immature, while toxicityâincluding diarrhea, hyperglycemia, rash, and anemiaâwas manageable but led to discontinuation in ~18%.
Bottom line: For high-volume, de novo PTEN-deficient disease, capivasertib + abiraterone targets a poor-prognosis biology at the earliest opportunityâwithout requiring docetaxel.
Written coverage by @zklaassen_md on UroToday > https://t.co/LEiVlqqq17

Should PSMA PETâdefined MFS count as a legitimate, actionable trial endpoint?
Dr. Steve Cho @UTMDAnderson at #USPCC26 says YES.
â
PSMA PET outperforms CT/bone scan for nodal, bone, and visceral metastases
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In an EMBARK-eligible cohort with negative conventional imaging, 84% were PSMA PET+, 46% had M1 disease
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Bone scans are becoming obsoleteâmore sensitive molecular imaging should define progression
â ď¸ Use rigorous PROMISE/PSMA-RADS criteria, expert central reads, and confirm equivocal lesions
Bottom line: A new PSMA PETâdetected metastasis is real progressionânot âmetastasis-freeâ simply because CT/bone scan is negative.
Written coverage by @zklaassen_md @GACancerCenter > https://t.co/jyV3N4bVW6 @PCFnews

Should PSMA PET be used for treatment response assessment today?
Dr. Steven Rowe @UTSWMedCenter at #USPCC26 says NOT YET.
Key cautions:
â ď¸ PSMA expression is dynamically regulated by the androgen axisâADT/ARPIs can alter uptake independent of true tumor burden (flare, downregulation)
â ď¸ Quantitative metrics (SUVmax/mean/total, volume) show meaningful testâretest variability; lesion identification/segmentation remains inconsistent
â ď¸ RECIP is promising for radioligand therapy but needs broader validation; AI-assisted standardization is still evolving
Bottom line: PSMA PET has clear staging value, but biologic modulation, reproducibility issues, and immature criteria mean it has no routine role for response assessment yetâfocus on understanding PSMA kinetics and improving AI-based quantification.
Written coverage by @zklaassen_md @GACancerCenter on UroToday > https://t.co/RBonFyL2QY @PCFnews

đ Docetaxel in metastatic androgen pathwayânaĂŻve (APMN) #ProstateCancerâwho benefits most?
@CaPsurvivorship @DanaFarber at #USPCC26: Yes, for the right patients.
Key points:
â
Greatest OS benefit in de novo high-volume disease (CHAARTED/STAMPEDE); early > late chemo
â
Biomarker signals: high Decipher and PTEN-inactive tumors derive more benefit; BRCA2 alterations favor PARP inhibitors over docetaxel (TRITON3)
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PLUDO: rPFS similar to 177Lu-PSMA-617; OS numerically favored docetaxel but confounded by crossover; QoL comparable
â
Practical wins: rapid start, widely available, finite 6 cycles, no radiation safety precautions
Best candidates: chemo-fit, high-volume/de novo, aggressive biology (high Decipher, PTEN-inactive), limited access to Lu-PSMA, or wish to avoid radiation logistics.
Written coverage by @zklaassen_md @GACancerCenter > https://t.co/ORBZdsKKEb @PCFnews

đŹ 177Lu-PSMA-617 in metastatic androgen pathwayânaĂŻve #APMN #ProstateCancer?
@sandysrimd at #USPCC26: Reasonable for selected patients.
Key data (PSMAddition, n=1,144):
â
rPFS HR 0.72; ORR 85% (CR 57% vs 42%); PSA progression HR 0.42; time to CRPC HR 0.70
â
OS immature; HRQoL/pain similar to control
â ď¸ More xerostomia, cytopenias, dry eye; logistics/cost > docetaxel; needs PSMA PET+
Best candidates: de novo high-risk/high-volume, frail/poor chemo candidates, high PSMA uptake, no visceral disease, no adverse genomic profile.
Written coverage by @zklaassen_md on UroToday > https://t.co/l0yBbzAEt5

Should a PSMA PETâonly lesion count as an MFS event by conventional imaging standards?
Dr. Michael Carducci at #USPCC26 says NO.
Key points:
â
MFS is validated as an OS surrogate using CT/bone scanânot PSMA PET. PSMA-defined progression lacks prospective OS validation (ongoing: ARASTEP)
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PSMA finds disease earlier, but earlier â more aggressive; PSMA-only lesions often asymptomatic with variable growth
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NCI Consensus: PSMA+/conventional imagingânegative BCR is a distinct stateânot automatically "metastatic"
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Risk: labeling PSMA-only findings as progression can trigger premature therapy changes without proven benefit
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PCWG4: PSMA PET remains investigational for response/progression; continue to use CT/bone scan criteria; consider "No Longer Clinically Benefiting"
â
Caveats: PSMA flare on ARPI start; PSMA downregulation on 177Lu-PSMA-617 can confound serial reads
Record PSMA-only events for research, but don't call progression or switch therapy solely on PSMA PET unless protocol-defined.
Written coverage by @zklaassen_md on UroToday > https://t.co/AJnuv1aLS2 @PCFnews

đ¸ Should PSMA PET be used to assess treatment effects in routine #ProstateCancer care?
@Daniel_J_George @DukeCancer at #USPCC26 argues YES.
Key points:
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PSMA PET >> conventional imaging for sensitivity/specificity across disease states
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ORIOLE: treating all PSMA-visible lesions improved composite PFS and DMFS
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RECIP 1.0 provides standardized response criteria on serial PSMA PET (tumor volume + new lesions); predicts OS independent of PSA
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Early PSMA response (â3 months) prognostic in mCRPC: RECIP PD vs non-PD HR 2.6 for OS
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Practical uses: guide consolidative RT in PSA-complete responders, target oligoprogression with SBRT, decide continue/stop/switch in mCRPC
â
PSMA-RADS improves interpretive consistency across readers
PSMA PET refines burden classification, targets therapy, and offers earlier, more biologic response assessment than PSA or CT/bone scan alone.
Written coverage by @zklaassen_md @GACancerCenter > https://t.co/2Qi5EkXJRj @PCFnews

Point-Counterpoint: BCR PSA less than 0.5 patients benefit from ADT intensification with radiation (RTOG 0534).
@AarmstrongDuke at #USPCC26 says YESâfor the right biology.
Key evidence:
â
RTOG 9601: HT benefit concentrated in Decipher >0.45; no benefit (possible harm) in low genomic risk, especially at PSA <0.6
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DADSPORT/POSEIDON meta-analyses: modest but real OS/MFS gains with HT + SRT; NNT ~21â43 in selected subgroups
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BALANCE (NRG-GU006): In luminal B tumors, apalutamide + SRT improved bPFS and MFS; no benefit in nonâluminal B
â
MMAI digital pathology: high-risk patients saw larger DM reduction with intensification
Bottom line: ~60% of early salvage patients may not need HT, but ~40% with luminal B or MMAI High-Risk profiles do. Use biomarkers to personalizeânot blanket intensify.
Written coverage by @zklaassen_md @GACancerCenter > https://t.co/yspTQxhB56 @PCFnews

Point-Counterpoint đ§Ź Do molecular biomarkers justify encouraging active surveillance (AS) in localized #ProstateCancer?
Dr. @zklaassen_md @GACancerCenter at #USPCC26: They informâbut shouldn't independently driveâAS decisions yet.
Key points:
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AS is already SOC for low-risk disease with excellent long-term MFS/CSS
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Biomarkers (Decipher, Oncotype GPS, Prolaris, ArteraAI) show clinical validity (prognosis) but lack prospective clinical utility (changing management â better outcomes)
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PASS study: adding GPS to clinical models gave minimal incremental value; association attenuated after adjusting for PSA density
â ď¸ Tumor heterogeneity complicates interpretation (targeted vs systematic cores can disagree)
đŻ What's needed: prospective, MRI-era, biomarker-guided RCT showing reduced overtreatment without compromising safety
Written coverage by @RKSayyid @UAUrology on UroToday > https://t.co/yrBeceCrqw @PCFnews

Point-Counterpoint: đ§Ź Should molecular biomarkers encourage active surveillance in intermediate-risk prostate cancer?
@dr_coops @UCSFCancer at #USPCC26 says YESâfor the right patients.
Key points:
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AS is already SOC for low-risk (GG1) disease; GG1 is an "incidentaloma" that rarely, if ever, metastasizes
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Practice variation persistsâclinician preference still drives AS use despite guideline support
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Intermediate-risk is heterogeneous: CAPRA (c-index ~0.76) + histologic features (cribriform, IDC, pattern 5) better stratify risk than NCCN buckets alone
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Biomarkers add most value in borderline GG2/selected GG3 to support AS discussions; strongest data to date for Decipher GC
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Emerging tools: Prolaris, @arteraAI, MPS2-AS urine assay, AI-pathology, liquid biopsies
Bottom line: AS decisions should be granular, individualized, and dynamic. Use biomarkers to reassure and select for AS in intermediate-riskânot to overtreat GG1.
Written coverage by @zklaassen_md @GACancerCenter. #ReadMore on UroToday > https://t.co/yZ7VsrfRFw @PCFnews @neerajaiims

Point-Counterpoint: Neoadjuvant intensified ADT-radical prostatectomy needs more validation.
Key cautions from Dr. Evan Yu @fredhutch at #USPCC26 on #PROTEUS:
â ď¸ Primary MFS benefit relied heavily on PSMA PET (53% of events); conventional imaging MFS was NOT significant
â ď¸ ICECaP validated MFSâOS using conventional imagingânot PSMA PET. PSMA-detected progression may behave more like BCR, not true metastatic disease
â ď¸ Control arm included ~1 year of ADT; current surgical SOC is RP alone. True toxicity burden (metabolic, CV, sexual, QoL) is underestimated
â ď¸ Mature SOC exists for many: RT + long-term ADT (EORTC) and RT + ADT + abiraterone (STAMPEDE) with proven OS benefit
âł Await PROTEUS substudy (APA + RP vs RP alone) and longer follow-up before adopting widely
Bottom line: Discuss with patients, but don't declare a new standard yetâmore validation needed.
Written coverage by @zklaassen_md @GACancerCenter > https://t.co/XCZRxF414C @PCFnews @neerajaiims

Point-Counterpoint: When considering capivasertib for #mAPMN disease, IHC for PTEN loss is necessary.
Key points from @aaparicioMD @UTMDAnderson at #USPCC26:
â
CAPItello-281 used ONLY the VENTANA PTEN (SP218) RxDx IHC assay (âĽ90% tumor cells with no cytoplasmic staining) for patient selection
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IHC measures functional protein lossâcapturing epigenetic/post-transcriptional mechanisms NGS can miss
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IHC & NGS are NOT interchangeable (IPATential150 & other studies show discordance)
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Practical wins: IHC is faster, cheaper, widely available, and avoids ctDNA/NGS pitfalls (low tumor fraction, PTENP1 pseudogene, variable CNV calling)
Bottom line: To treat per the registration trial, use the companion diagnostic IHCânot NGS or ctDNA alone.
Written coverage by @zklaassen_md @GACancerCenter > https://t.co/cpLV2tW4jS @PCFnews @neerajaiims

Point-Counterpoint: Does #PROTEUS represents a new standard of care?
Dr. David Morris @UA_Nashville at #USPCC26 says YESâfor carefully selected patients planning RP.
Key arguments:
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PSMA PET is now routine practiceâMFS by PSMA PET reflects real-world staging
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Perioperative apalutamide delayed next therapy by ~3 years (NNT ~10 at 5 yrs)
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~3Ă higher odds of organ-confined disease; pCR may convert some to surgical candidates
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77â80% recover testosterone >150 ng/dL by 1 year with proactive AE management
Bottom line: For high-risk/node+ patients accepting upfront toxicity to delay progression, PROTEUS supports perioperative intensified therapy as "a" new SOC.
Written coverage by @zklaassen_md @GACancerCenter > https://t.co/agXcd2Kw3N

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