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Poster display session: Basic science, Endocrine tumours, Gastrointestinal tumours - colorectal & non-colorectal, Head and neck cancer (excluding thyroid), Melanoma and other skin tumours, Neuroendocrine tumours, Thyroid cancer, Tumour biology & pathology

1425 - Combined inhibition of MEK and PI3KCA pathway induces synergic antitumor activity in HER2 amplified human colorectal cancer models

Date

21 Oct 2018

Session

Poster display session: Basic science, Endocrine tumours, Gastrointestinal tumours - colorectal & non-colorectal, Head and neck cancer (excluding thyroid), Melanoma and other skin tumours, Neuroendocrine tumours, Thyroid cancer, Tumour biology & pathology

Topics

Cancer Biology

Tumour Site

Colon and Rectal Cancer

Presenters

Valentina Belli

Citation

Annals of Oncology (2018) 29 (suppl_8): viii150-viii204. 10.1093/annonc/mdy281

Authors

V. Belli1, N. Matrone1, S. Napolitano1, E. Martinelli1, M.D. Castellone2, L. Trusolino3, E.F. Giunta1, V. De Falco1, N. Zanaletti1, P.P. Vitiello1, D. Ciardiello1, M. Terminiello1, F. Ciardiello4, T. Troiani1

Author affiliations

  • 1 Medicina Di Precisione, Università degli Studi della Campania Luigi Vanvitelli, 80131 - Napoli/IT
  • 2 Università Degli Studi Dellistitute Of Experimental Endocrinology And Oncology, CNR, 80131 - Napoli/IT
  • 3 Irccs, Istituto di Candiolo, 10060 - Candiolo/IT
  • 4 Dipartimento Di Medicina Di Precisione, Università degli Studi della Campania Luigi Vanvitelli, 80131 - Napoli/IT

Resources

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Abstract 1425

Background

Cetuximab and panitumumab, monoclonal antibodies direct against the epidermal growth factor receptor (EGFR) are a therapeutic option for mCRC patients wild type for KRAS and NRAS genes. However, only a subset of mCRC patients receives clinical benefit from these therapies due to the development of resistance mechanisms. HER2 gene amplification or HER2 activating mutations have been implicated as resistance mechanisms to anti-EGFR therapies. However, little is known about the role of HER2 in cancer resistance to anti-EGFR antibodies.

Methods

We transfected colon cancer cells sensitive to anti-EGFR antibodies (LIM1215 and SW48) with HER2 vector in order to obtain stable clones overexpressing HER2 protein. LIM1215-HER2 and SW48-HER2 cells were characterized by their morphological and molecular profile through cell migration and WB assays. Moreover, different drugs sensitivity was evaluated by MTT and colony formation. Furthermore, HER2 amplified cells were engrafted into nude mice and treated with different drugs.

Results

HER2 amplified cells show an overexpression and activation of the HER family receptors coupled by an intracellular downstream activation pathway of AKT, MAPK, and MEK proteins compared to parental cells. HER2 amplified cells were treated with several combinations of drugs directed against HER receptors, such as anti-EGFR antibodies of first, second and third generation (cetuximab, SYM004 and MM151); trastuzumab, pertuzumab and lapatinib directed against HER2 receptor; and duligotuzumab direct against HER3. Subsequently, both cells were treated with drugs directed against MEK and PI3KCA proteins, such as refametinib and pictilisib. Among these therapeutic options, the combination of refametinib and pictilisib have shown the most synergist anti-proliferative activity. The in vivo xenograft CRC models have confirmed the synergistic antitumor activity of this combined treatment. Moreover, PDTX HER amplified CRC models will be used to validate the previous results.

Conclusions

These results suggest that the treatment with refamentinib and pictilisib could be a strategy for patients with HER2 amplification that do not receive clinical benefit from standard anti-EGFR therapies.

Clinical trial identification

Legal entity responsible for the study

Università Degli Studi della Campania Luigi Vanvitelli.

Funding

Has not received any funding.

Editorial Acknowledgement

Disclosure

All authors have declared no conflicts of interest.

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