Abstract 1638P
Background
FOLFIRINOX and gemcitabine-nabpaclitaxel (GnP) are both standard first-line treatment regimens for advanced pancreatic ductal adenocarcinoma (PDAC), however, predictive biomarkers are currently lacking to guide treatment selection. We aimed to investigate the prognostic and predictive value of class III β-Tubulin (TUBB3) and human equilibrative nucleoside transporter 1 (hENT1) expression, which have previously been shown to be associated with taxane and gemcitabine resistance in advanced PDAC.
Methods
We conducted a retrospective analysis of 106 patients with advanced PDAC at Hacettepe University Cancer Institute. TUBB3 and hENT1 immunohistochemical staining were analyzed in tumor specimens and scored jointly according to the intensity of expression: high score (TUBB3low/hENT1high) and low score (TUBB3high/hENT1high, TUBB3low/hENT1low or TUBB3high/hENT1low). Response rates and progression-free survival (PFS) rates were compared based on TUBB3 and hENT1 expression.
Results
The median age was 60 years (range; 38-80 years) and 65% were male patients. The median progression-free survival (PFS) and overall survival (OS) of patients were 6.83 and 12.06 months, respectively. In patients who received the GnP regimen (n=68), a high combined score (TUBB3low/hENT1high) was associated with a higher disease control rate (DCR) (84.2% vs. 39.6%, p=0.001) and longer PFS (8.76 months vs. 3.1 months, p<0.001) compared to those with low score. In the multivariate analysis, a high combined score was an independent predictor of higher DCR (OR: 11.96; 95% CI: 2.61-54.82; p=0.001) and longer PFS (HR: 0.33; 95%CI: 0.18–0.60; p<0.001). However, there was no difference in response rates or PFS based on TUBB3 and hENT1 expression among patients receiving FOLFIRINOX regimen.
Conclusions
Our findings suggest that tumor TUBB3 and hENT1 expression may predict the efficacy of GnP regimen, and low TUBB3 and high hENT1 expression are associated with a higher DCR and longer PFS in patients with advanced PDAC.
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
The authors.
Funding
Has not received any funding.
Disclosure
All authors have declared no conflicts of interest.
Resources from the same session
1655P - Nampt inhibitors re-sensitize MAP17 expressing pancreas tumors
Presenter: Julia Martinez Perez
Session: Poster session 22
1656P - Targeting NPC1L1 rescues anti-tumor immunity and improves immunotherapeutic efficacy in pancreatic cancer
Presenter: Houjie Liang
Session: Poster session 22
1657P - Understanding the role of SAGA and mediator in the resistance to Pdk1 deletion in PDAC
Presenter: Katarina Ondrejkova
Session: Poster session 22
1658P - Molecular subtyping of familial pancreatic ductal adenocarcinoma identifies novel pathogenic germline variants
Presenter: Julie Earl
Session: Poster session 22
1659P - The use of liquid biopsy in patients with advanced pancreatic cancer (PDAC) to guide enrollment in phase I clinical trials
Presenter: Octave Letissier
Session: Poster session 22
1660P - Squalene epoxidase promotes pancreatic cancer growth by attenuating ER stress and activating lipid rafts-regulated Src/PI3K/Akt signalling pathway
Presenter: Ruiyuan Xu
Session: Poster session 22
1661P - Precision medicine for pancreatic cancer: A clinical study validating EUS biopsies
Presenter: Joanne Lundy
Session: Poster session 22
1662P - Targeting stress granule formation as a synthetic lethality strategy for kras-induced pancreatic cancer initiation
Presenter: Patricia Santofimia
Session: Poster session 22
1663P - Role of next-generation sequencing somatic assays in patients with advanced pancreatic cancer
Presenter: Rafaela Naves
Session: Poster session 22
1664P - Italian Association for Medical Oncology (AIOM) guideline application in real-world: Multi-institutional based survey of adjuvant and first-line pancreatic ductal adenocarcinoma treatment in Italy (GARIBALDI) - survival analyses in the metastatic cohort
Presenter: Michele Reni
Session: Poster session 22