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Review
. 2019 Nov;18(11):1909-1915.
doi: 10.1158/1535-7163.MCT-19-0214.

Targeting the EGFR and Immune Pathways in Squamous Cell Carcinoma of the Head and Neck (SCCHN): Forging a New Alliance

Nabil F Saba  1 , Zhuo Gerogia Chen  2 , Missak Haigentz  3 , Paolo Bossi  4 , Alessandra Rinaldo  5 , Juan P Rodrigo  6 , Antti A Mäkitie  7 , Robert P Takes  8 , Primoz Strojan  9 , Jan B Vermorken  10 , Alfio Ferlito  11
Affiliations
Review

Targeting the EGFR and Immune Pathways in Squamous Cell Carcinoma of the Head and Neck (SCCHN): Forging a New Alliance

Nabil F Saba et al. Mol Cancer Ther. 2019 Nov.

Abstract

Despite the recent approval of immune-modulatory agents, EGFR inhibition continues to be a cornerstone in the management of squamous cell carcinoma of the head and neck (SCCHN) namely in combination with radiotherapy in the treatment of locoregionally advanced disease as well as in platinum-sensitive recurrent or metastatic disease in the first-line setting. Importantly, recent evidence has emerged supporting also an immune-modulatory effect of EGFR inhibition, and interest has now focused on utilizing these effects in the current treatment approaches for SCCHN. In this report, we review the rationale and evidence supporting the forging of this new alliance in optimizing the treatment of SCCHN.

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Conflict of interest statement

Conflict of Interest (COI):

NFS reports receiving compensation for advisory role from BMS, Merck, Lilly, GSK, Roche, J.B.V.: Has had in the last 3 years or has consulting/ advisory relationships with: Amgen, AstraZeneca, Boehringer Ingelheim, Innate Pharma, Merck Serono, Merck Sharp & Dome Corp, PCI Biotech, Synthon Biopharmaceuticals, Debiopharm and Wnt Research and has received lecture fees from Merck-Serono, Sanofi and BMS. PB reports Advisory role for BMS, MSD, Astra Zeneca, Sanofi, Roche, Angelini

MH, reports: Advisory role to Astra Zeneka and Takeda Oncology,

ER, AR, PB, PS, JPR, and GZC report no COI

Figures

Figure 1
Figure 1
Resistant mechanisms of EGFR targeted therapy. The following molecular activities will result in bypassing EGFR blockade: (A) Activation mutations or amplification of EGFR downstream signaling effectors; (B) Overexpression of MET proto-oncogene and expression of EGFR variant III; (C) Hetero-dimerization between EGFR family members; and (D) Activation of TGF-beta IL-6 axis
See this image and copyright information in PMC

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