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Poster Display session

69P - Circulating tumor DNA (ctDNA) dynamics in response to hepatic artery infusion pump therapy

Date

27 Jun 2024

Session

Poster Display session

Presenters

Michelle Chung

Citation

Annals of Oncology (2024) 35 (suppl_1): S1-S74. 10.1016/annonc/annonc1477

Authors

M. Chung1, H. Stitzel2, M. Lumish3, A. Mohamed2, D. Bajor3, S. Chakrabarti4, M.L. Conces3, A. Mahipal1, S. Tirumani1, L. Ocuin1, J..E.E. Selfridge4

Author affiliations

  • 1 University Hospitals Cleveland Medical Center, Cleveland/US
  • 2 Case Western Reserve University / University Hospitals, Cleveland/US
  • 3 University Hospitals Seidman Cancer Center, Case Western Reserve University, Cleveland/US
  • 4 University Hospitals Seidman Cancer Center, Cleveland/US

Resources

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Abstract 69P

Background

Quantitative ctDNA is emerging as a sensitive and specific non-invasive marker of active cancer. However, it has not been studied in patients (pts) undergoing hepatic artery infusion (HAI) therapy for liver metastases from colorectal cancer (CRC) or intrahepatic cholangiocarcinoma (IHCC). We sought to test ctDNA as a noninvasive biomarker to correlate with outcomes to HAI therapy.

Methods

Pts with liver-only metastatic CRC or IHCC underwent standard of care surgical placement of HAI pump. Treatment was initiated with Day 1 floxuridine (FUDR) via HAI pump. On Day 15, FUDR was replaced with heparin saline (HS), and pts were given systemic therapy (SYS). Thereafter, cycles were repeated every 4 weeks with Day 1 (FUDR HAI and SYS) and Day 15 (HS HAI and SYS). We measured ctDNA on Day 1, Day 15, and every 4 weeks thereafter, and evaluated radiographic response using RECIST v1.1.

Results

We tracked ctDNA in 14 pts who underwent HAI: 10 with CRC and 4 with IHCC. Median age was 60 years (range 45-76), 11 pts were male, and 4 were receiving HAI therapy at time of analysis. 3 pts received adjuvant HAI and baseline ctDNA was 0; all 3 pts remained ctDNA-negative with no radiographic evidence of recurrence after completion of HAI (median 8.3 mo). Of the remaining 11 pts, 1 pt did not have reduction in ctDNA to baseline; this pt had initial ctDNA rise, one of the lowest hepatic responses (20%), and early extrahepatic progression (2.7mo). 7 pts had ctDNA Day 1 and Day 15, representing first dose of FUDR HAI (no SYS). 2 of these pts had initial rise in ctDNA; these pts had the lowest hepatic responses (10%, 20%). Of pts with hepatic response (n=7), all had a decrease in ctDNA of 97% or greater from baseline. Decrease in ctDNA to very low values <1 mTM/mL was associated with lower risk of extrahepatic progression (p=0.015). In all pts with extrahepatic PD (n=6), ctDNA increases by at least 2-fold preceded CT progression by approximately 1 mo.

Conclusions

We demonstrate that ctDNA corresponds to radiographic response to HAI. This proof-of-concept study supports development of prospective longitudinal tracking of ctDNA in pts undergoing HAI to correlate to response, early identification of treatment resistance, and survival.

Legal entity responsible for the study

The authors.

Funding

Has not received any funding.

Disclosure

All authors have declared no conflicts of interest.

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