Abstract 633P
Background
Prostate cancer (Pca) is the second common cancer among male worldwide. In recent years, the incidence and mortality in China have gradually increased. Most tumours profiled in these studies were obtained from patients from Caucasians population, while conditions in other races remain unclear.
Methods
Somatic and germline mutations were identified via targeted next generation sequencing with Acornmed panel including 808 genes associated with tumor development. Sequencing data were analyzed to call tumor specific single nucleotide variants (SNV), small insertions and deletions (InDels), copy number alterations (CNA) and chromosomal rearrangements.
Results
A total 3158 genomic alterations (GA) were identified in 429 Pca patients, including missense mutations(61%), followed by frameshift indel (22%), inframeshift indel (2%),stop gain (6%) , copy number loss (6%) copy number gain (2%) and splicing (2%) stop loss (0.1%) mutations. Germline pathogenic or likely pathogenic mutations occurred in DNA damage repair genes 13%. The median age of patients with Pca was 55 (range 31-59) in the patients who were <60 and 70 (range 60-91) in the patients who were ≥60. The GA/sample in patients who were ≥60 were higher (3.8 in <60 vs. 7.8 in ≥60). P/LP mutations in DDR genes were more common in early-onset Pca < 60 (23% in <60 vs. 12% in ≥60, p=0.024). In addition, the somatic spectrum was different between patients who were <60 and ≥60 years of age. The most common mutations detected in patients with early-onset Pca < 60 were TP53 (25%), AR (17%), CDK12 (9%), FOXA1 (9%) and PTEN (9%) vs. FOXA1 (16%), AR (14%), TP53 (14%), CDK12 (11%) and SPOP (9%) in patients who were ≥60 years of age. Frequency of TP53 mutations were significantly higher in patients < 60 years of age (p=0.04), while FOXA1 mutations were higher in patients ≥60 years of age.
Conclusions
To our knowledge, this is a first systematic comparison study in Pca patients in the patients who were < 60 and ≥60 years of age. At a population level, there were notable differences observed in germline and somatic variants in two cohorts. Those molecular profiling may predict the benefit of targeted therapy and immunotherapy in patients with Pca and that could potentially be used in clinical trials.
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
Y. Niu.
Funding
Has not received any funding.
Disclosure
All authors have declared no conflicts of interest.