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E-Poster Display

1951P - Niraparib and irinotecan combination in ATM-mutated colorectal cancer

Date

17 Sep 2020

Session

E-Poster Display

Topics

Translational Research

Tumour Site

Colon and Rectal Cancer

Presenters

Pietro Paolo Vitiello

Citation

Annals of Oncology (2020) 31 (suppl_4): S1034-S1051. 10.1016/annonc/annonc294

Authors

P.P. Vitiello1, G. Martini1, L. Mele2, E.F. Giunta1, V. De Falco1, D. Ciardiello1, V. Belli1, C. Cardone1, N. Matrone1, L. Poliero1, V. Tirino2, F. Selvaggi3, G. Papaccio2, T. Troiani1, V. Desiderio2, F. Ciardiello1, E. Martinelli1

Author affiliations

  • 1 Oncologia Medica-dipartimento Medicina Di Precisione, Università degli Studi della Campania Luigi Vanvitelli, 80131 - Napoli/IT
  • 2 Dipartimento Di Medicina Sperimentale, Università degli Studi della Campania Luigi Vanvitelli, 80131 - Napoli/IT
  • 3 Chirurgia Generale E Oncologica, Università degli Studi della Campania Luigi Vanvitelli, 80131 - Napoli/IT

Resources

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Abstract 1951P

Background

Despite the advancement in new therapies in colorectal cancer (CRC), chemotherapy still constitutes the mainstay of the treatment. Poly-ADP-Ribose Polymerase inhibitors (PARPi) have the potential to increase the activity of DNA damaging chemotherapeutics such as 5-fluorouracil (5FU), oxaliplatin and irinotecan, even if dose-limiting toxicities have emerged at the currently used doses in previous clinical trials in molecularly unselected CRC patients.

Methods

We tested the combination of the PARPi niraparib (MK-4827) with either 5-fluorouracil, oxaliplatin or irinotecan (SN38) in a panel of 12 molecularly annotated CRC cell lines, encompassing the 4 consensus molecular subtypes (CMSs). Synergism was calculated using the Chou-Talalay method for drug interaction. A correlation between synergism and genetic alterations in genes involved in homologous recombination (HR) repair was performed. We used clonogenic assays, mice xenograft models and patient-derived 3D spheroids to validate the results. The induction of DNA damage was studied by immunofluorescence.

Results

Irinotecan/SN38 is the best candidate for combination with niraparib, showing strong synergism is 6/12 cell lines. Synergism was independent from CMS and microsatellite status. Strong synergistic activity of low-dose combinations of SN38 and niraparib was found in cell lines carrying a pathogenic mutation in ATM by induction of DNA double strand breaks. The strong activity of the low-dose combination was further confirmed in clonogenic assays and in mice xenografts. The presence of an ATM mutation predicted the activity of the combination in a model of patient-derived 3D spheroid.

Conclusions

This work demonstrates that the subset of CRCs carrying heterozygous ATM mutations may benefit from a combination treatment with low doses of niraparib and irinotecan. These data suggest a new potential approach in the treatment of ATM-mutated CRC, up to 10% in large datasets, that deserves to be validated prospectively in clinical trials.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.

Funding

Regione Campania - progetto I-CURE Università della Campania \"Luigi Vanvitelli\".

Disclosure

P.P. Vitiello: Advisory/Consultancy: Biocartis. T. Troiani: Advisory/Consultancy: Amgen; Advisory/Consultancy: Bayer; Advisory/Consultancy: Merck; Advisory/Consultancy: Novartis; Advisory/Consultancy: Roche; Advisory/Consultancy: Sanofi. F. Ciardiello: Advisory/Consultancy, Research grant/Funding (institution): Amgen; Advisory/Consultancy, Research grant/Funding (institution): Bayer; Advisory/Consultancy, Research grant/Funding (institution): Merck; Advisory/Consultancy, Research grant/Funding (institution): Roche; Advisory/Consultancy: Servier; Advisory/Consultancy: Pfizer; Advisory/Consultancy: Symphogen; Research grant/Funding (institution): Ipsen. E. Martinelli: Advisory/Consultancy: Amgen; Advisory/Consultancy: Bayer; Advisory/Consultancy: Merck; Advisory/Consultancy: Roche; Advisory/Consultancy: Servier; Advisory/Consultancy: Sanofi. All other authors have declared no conflicts of interest.

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