Abstract 5637
Background
Due to improved outcome in mCRPC, most prognostic models may not reflect the current treatment landscape. Recently, Armstrong et al (Ann Oncol 2018) published a prognostic model based on the phase III PREVAIL trial.
Methods
We applied the Armstrong prognostic model to patients (pts) treated in the COU-AA-302 trial. Variables included in the model: albumin, ALP, Hb, LDH, NLR, number of bone metastases, pain, pattern of spread, PSA, time from diagnosis. Pts were categorized into low ( < =3), intermediate (4-6) or high (7-10 risk factors) risk. A continuous score was calculated. Association with overall survival (OS), radiographic progression-free survival (rPFS) and time to PSA progression (TTPSAP) was calculated with Cox-regression models, with Kaplan Meier estimates for median values. C-indices were used to assess the performance of the continuous risk score.
Results
918 pts (84,4%) had data on all variables. Risk score (continuous) was associated with OS (HR 2.19; p < 0.001) with a c-index of 0.68 (se = 0.011). 483 (52.6%), 403 (43.9%) and 32 (3.5%) pts were classified as low-, intermediate- and high-risk. OS was longer in low- than in intermediate- (HR: 0.4; p < 0.001) and high-risk (HR: 0.24; p < 0.001) pts. rPFS was prolonged in low risk versus intermediate (HR: 0.57; p < 0.001) and high-risk (HR: 0.41; p < 0.001) pts. TTPSAP was also improved in low-risk vs intermediate (HR: 0.6; p < 0.001) and high-risk (HR: 0.41; p < 0.001) pts. The association of risk group with OS, rPFS and TTPSAP was independent of treatment arm (Table). KM estimates of median (95%CI) OS, rPFS and TTPSAP.Table:
864P
OS | rPFS | TTPSAP | |
---|---|---|---|
Low | 41.7m (38.7-46.8) | 16.4m (13.8-19.1) | 11.1m (8.3-11.2) |
Intermediate | 24.6m (23.1-26.8) | 8.3m (8-11) | 5.6m (5.5-8.2) |
High | 16.7m (11.7-30.2) | 3.9m (3.6-4.1) | 5.3m (3.7-8.3) |
Conclusions
The Armstrong model is valid for mCRPC pts treated with first-line abiraterone. Less pts with high-risk features were included in COU-AA-302 than PREVAIL. These results may improve individual prognostic estimation and patient stratification in clinical trials. Study carried out under YODA Project #2018-3813.
Clinical trial identification
NCT00887198.
Editorial acknowledgement
Legal entity responsible for the study
The authors.
Funding
Has not received any funding.
Disclosure
D. Lorente: Advisory / Consultancy, Speaker Bureau / Expert testimony, Travel / Accommodation / Expenses: Sanofi; Advisory / Consultancy, Speaker Bureau / Expert testimony, Travel / Accommodation / Expenses: Janssen; Speaker Bureau / Expert testimony, Travel / Accommodation / Expenses: Astellas; Advisory / Consultancy, Speaker Bureau / Expert testimony, Travel / Accommodation / Expenses: Bayer. All other authors have declared no conflicts of interest.
Resources from the same session
2316 - A 3D co-culture platform of breast cancer and patient derived immune cells to analyse the response to chemotherapy and immunotherapies
Presenter: Diana Saraiva
Session: Poster Display session 3
Resources:
Abstract
4290 - Characterization of the mechanism of action and efficacy of MEN1611 (PA799), a novel PI3K inhibitor, in breast cancer preclinical models.
Presenter: Alessio Fiascarelli
Session: Poster Display session 3
Resources:
Abstract
2167 - Neat-1: culprit lnRNA tying PIG-C, MSLN, CD80 in TNBC
Presenter: Nada Hussein
Session: Poster Display session 3
Resources:
Abstract
1829 - A novel RAF/MEK inhibitor CH5126766 in phase 1 clinical trial has an effectiveness in the combination with eribulin for the treatment of triple negative breast cancer
Presenter: Hisako Ono
Session: Poster Display session 3
Resources:
Abstract
4357 - Identification of a stemness-related gene panel associated with BET inhibition in triple negative breast cancer
Presenter: Eva Galan-Moya
Session: Poster Display session 3
Resources:
Abstract
5163 - Preclinical Evaluation targeting both IGF1R and IR in Triple Negative Breast Cancer
Presenter: Alex Eustace
Session: Poster Display session 3
Resources:
Abstract
832 - Monospecific antibody targeting of CDH11 inhibits epithelial-to-mesenchymal transition and represses cancer stem cell-like phenotype by up-regulating miR-335 in metastatic breast cancer, in vitro and in vivo.
Presenter: Jia-Hong Chen
Session: Poster Display session 3
Resources:
Abstract
3781 - Pharmacological screening with Chk1 inhibitors identify synergistic agents to overcome resistance to platinums in basal breast and ovarian cancer
Presenter: Ana Lucia Sanabria
Session: Poster Display session 3
Resources:
Abstract
3275 - Comparison of 11 circulating miRNAs and CA125 kinetics in ovarian cancer during first line treatment: data from the randomized CHIVA trial (a GINECO-GCIG study)
Presenter: Patrick Robelin
Session: Poster Display session 3
Resources:
Abstract
3391 - Inhibiting Ehmt2 and Ezh2 histone methyltransferases alters the immune microenvironment in a Trp53-/- murine ovarian cancer model
Presenter: Pavlina Spiliopoulou
Session: Poster Display session 3
Resources:
Abstract