Abstract 1643P
Background
Compound alterations in TP53, RB1, and/or PTEN have been correlated with poor outcomes in pts with mPC; however, there is limited data regarding whether PTEN alterations(alt) by next generation sequencing (NGS) are prognostic in isolation. PTEN -null de novo mPC is currently being investigated in CAPItello-281 and may represent a clinically actionable subtype. As such, we sought to characterize outcomes of this genomically defined subgroup.
Methods
PROMISE is a multi-institutional database including mPC pts (N=2027) with NGS. Using PROMISE, we analyzed outcomes based on PTEN status in de novo mPC pts.
Results
Among 1036 pts with de novo mPC, 212 (20%) had PTEN alt by NGS. Median age at diagnosis was 64 yrs, 21% were Black, 53% had high volume (HV) disease. Compared to the PTEN-wildtype (wt) group, PTEN-altered mPC had higher co-occurrence of TP53 and/or RB1 mutations (57% vs 37%); lower median PSA (38 vs 63 ng/ml); and more visceral disease (18 vs 11%). Groups were otherwise similar. The table shows univariate (UVA) outcomes based on PTEN status. Outcomes were similar in men with high volume disease on UVA. On multivariable analysis controlling for clinical prognostic features and TP53/RB1 alterations, PTEN status remained independently associated with overall survival (OS) [HR 1.27, 95% CI (0.99, 1.63) p=0.05]. Table: 1643P
PTEN -alt | PTEN -wt | P value | HR (95% CI) | |
Median OS, mo (95% CI) | ||||
Entire cohort | 48.7 (45.3 - 57.5) | 65.4 (60.0 - 72.6) | 0.003 | 0.73 (0.59 - 0.90) |
LV (n=418) | 52.5 (45.3 - 81.5) | 79.1 (72.1 - 95.8) | 0.002 | 0.60 (0.44 - 0.83) |
TP53/RB1 null * | 46.1 (34.5 - 56.1) | 56.1(44.7-65.5) | 0.063 | 0.70 (0.48 - 1.02) |
wt * | 51.6 (47.0 - 79.8) | 72.6 (64.0 − 80.6) | ConclusionsPTEN status correlated with poor outcomes in de novo mPC independent of other clinical and genomic factors. Clinical trial identificationEditorial acknowledgementLegal entity responsible for the studyThe authors. FundingAstraZeneca. DisclosureD. Kilari: Financial Interests, Personal, Invited Speaker: Janssen, Pfizer, Aveo oncology, Seagen, MJH - Life Sciences, Binaytara Foundation; Financial Interests, Personal, Advisory Board: Exelixis, Eisai; Financial Interests, Institutional, Coordinating PI: Exelixis, Genentech. All other authors have declared no conflicts of interest. Resources from the same session1627P - Long survivors after androgen deprivation therapy (ADT) with or without docetaxel for metastatic castration-sensitive prostate cancer (mCSPC): Long-term follow-up of GETUG-15Presenter: Sarah Blanchet-Deverly Session: Poster session 11 1628P - Factors influencing clinical and biological response in patients treated with [177Lu]Lu-PSMA-617 under France's early access programPresenter: Vincent Habouzit Session: Poster session 11 1629P - Lutetium-177–prostate-specific membrane antigen (177Lu-PSMA) therapy in patients (pts) with prior Radium-223 (223Ra)Presenter: Kambiz Rahbar Session: Poster session 11 1630P - A multicenter retrospective study on the efficacy of anti-PD-(L)1 in microsatellite unstable (MSI-H) metastatic castrate-resistant prostate cancer (mCRPC)Presenter: Sandra Van Wilpe Session: Poster session 11 1632P - Impact of androgen pathway inhibitors on cognitive function in elderly patients with metastatic prostate cancer: Results from the COG-PRO trialPresenter: Antoine Boué Session: Poster session 11 1634P - Does lower serum testosterone predict metastases-free survival in nmCRPC patients treated with novel antiandrogens? A post-hoc analysis of SPARTAN and ARAMISPresenter: Xudong Ni Session: Poster session 11 1635P - Validation of automated bone scan index as a progression endpoint in two phase III studies of metastatic castration resistant prostate cancer (mCRPC) patientsPresenter: Andrea Knezevic Session: Poster session 11 This site uses cookies. Some of these cookies are essential, while others help us improve your experience by providing insights into how the site is being used. For more detailed information on the cookies we use, please check our Privacy Policy.
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