Abstract 343P
Background
PDAC is a common cancer with poor survival. Real-world biomarker testing/prevalence and treatment patterns are not well understood. This retrospective cohort study describes biomarker prevalence and treatment patterns in patients with PDAC.
Methods
The study used multimodal (MM) and clinical only or clinical-genomic (CO/CG) data from the Tempus Clinicogenomic Database in the US. Adults with a confirmed diagnosis of PDAC between 1 January 2015 – 31 March 2023, who received ≥ 1 systemic anticancer therapy, and who had at least one outcome for the treatment were included. MM data included patients with a biopsy and DNA/RNA sequencing at a Tempus laboratory, and because use of a biomarker test may not be fully captured in CO/CG data, biomarker prevalence was estimated only in the MM data.
Results
A total of 2995 patients (2240 from MM data; 755 from CO/CG data) were identified in the database (median age: 65 years; 46.3% female). Biomarker prevalence in the MM data is in the table. Metastatic (m) PDAC was observed in 2350/2995 (78.5%) patients at or after primary PDAC diagnosis. Among them, 1831/2350 (77.9%) received first-line (1L) systemic therapy; of these, 774/1831 (42.3%) received second-line (2L) systemic therapy. The most common 1L therapies for mPDAC were FOLFIRINOX and gemcitabine + nab-paclitaxel-containing regimens (741/1831 [40.5%] and 729/1831 [39.8%], respectively). The most common 2L therapies for mPDAC were gemcitabine + nab-paclitaxel-containing regimens (318/774 [41.1%]). Table: 343P
| Biomarker | Prevalence (%) |
| Germline BRCA1/2 mutation | 1.6 |
| Somatic BRCA1/2 mutation | 6.5 |
| PALB2 mutation | 1.1 |
| NTRK1/2/3 gene fusion | 0.6 |
| BRAFV600E mutation | 0.4 |
| KRAS codon 12 mutation (all) | 83.2 |
| KRASG12D mutation | 38.8 |
| KRASG12V mutation | 27.9 |
| KRASG12R mutation | 14.7 |
| KRASG12C mutation | 1.3 |
| Other KRAS codon 12 mutations | 0.9 |
| KRAS amplification | 1.5 |
| NGR1 gene fusion | 1.6 |
| Deficient mismatch repair (dMMR) | 0.7 |
| High microsatellite instability (MSI-H) | 0.7 |
| High tumor mutational burden (TMB-H) | 1.7 |
Conclusions
The prevalence of most prespecified genetic biomarkers was low in patients with PDAC. The identification of additional biomarkers, increased biomarker testing, and matching of patients with novel targeted therapies may improve survival in these patients.
Editorial acknowledgement
Medical writing support was provided by Ann Ferguson, PhD, of Oxford PharmaGenesis Inc., and was funded by Astellas Pharma Inc.
Legal entity responsible for the study
Astellas Pharma Inc.
Funding
Astellas Pharma Inc.
Disclosure
M.A. Lewis: Financial Interests, Personal, Other, All support for the present abstract (e.g., funding, provision of study materials, medical writing, article processing charges, etc.) - Paid for consultancy: Astellas; Financial Interests, Personal, Other, Consulting fees - Paid for consultancy: Astellas. T. Kimura, C. Young, G. Gurumoorthy: Financial Interests, Personal and Institutional, Full or part-time Employment, Employee: Astellas Pharma US. R. Fuldeore: Financial Interests, Personal and Institutional, Full or part-time Employment, Employee: Astellas.