Abstract 3166
Background
Aberrations in fibroblast growth factor receptors (FGFR) are common in multiple cancers, making them highly promising therapeutic targets. Optimal application of FGFR inhibitors requires a comprehensive understanding of the prevalence and types of FGFR mutations, which may vary significantly among ethnicities. Such analysis has not been conducted in Chinese pan-cancer. This study investigated the prevalence and the distribution of FGFR aberrations in Chinese cancer patients.
Methods
We screened genomic profiling results of plasma or tissue samples from 10,582 patients spanning 16 cancer types: lung, breast, gastric, hepatobiliary, pancreatic, soft tissue sarcoma, esophageal, ovarian, colorectal, head and neck, renal, endometrial, osteogenic sarcoma, cervical, melanoma and lymphoma.
Results
Of the 10,582 patients screened, we observed 745 patients with FGFR aberrations, revealing an overall prevalence of 7.03%. Approximately, 3.78% harbored FGFR amplification, 2.73% had other mutations and 0.53% had fusions. A majority (56.78%) of patients had FGFR1 aberrations, followed by 17.72%, 14.43% and 2.82% with FGFR3, FGFR2 and FGFR4 aberrations, respectively. Furthermore, 8.46% of patients with aberrations in more than 1 FGFR gene. The most common type of aberrations was amplification (53.69%), followed by other mutations (38.79%) and fusions (5.64%). Concurrent FGFR fusion and amplification occurred in 1.88% patients. Of the 16 cancer types, except for head and neck cancer, osteogenic sarcoma, renal carcinoma, and lymphoma, all other cancer types had FGFR aberrations detected with colorectal cancer (31.03%) having the highest prevalence. Other relatively commonly affected cancers included: gastric cancer (16.78%), breast cancer (14.27%) and esophageal cancer (12.68%). FGFR1 amplification was the most common genetic alteration in CRC, breast cancer and lung cancer. FGFR2 amplification was more commonly seen in gastric cancer. Of the patients with FGFR aberrations, 57 patients, spanning 9 cancer types, had fusions. Among them, breast cancer patients are more likely to have concurrent FGFR amplification than other cancer types (p < 0.001).
Conclusions
Our study provides a comprehensive view of FGFR aberrations in Chinese cancer patients.
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
Yang Gao.
Funding
Key Research and Development Program of Hunan province (2016JC2039).
Disclosure
All authors have declared no conflicts of interest.
Resources from the same session
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
3839 - Fenofibrate impairs pro-tumorigenic potential of cancer stem cell-like cells within drug-resistant prostate cancer cell populations.
Presenter: Tomasz Wróbel
Session: Poster Display session 3
Resources:
Abstract