Abstract
Current clinical trials of epidermal growth factor receptor (EGFR)-targeted therapies are mostly guided by a classical approach coming from the cytotoxic paradigm. The predominant view is that the efficacy of EGFR antagonists correlates with skin rash toxicity and induction of objective clinical response. Clinical benefit from EGFR-targeted therapies is well documented; however, chronic use in advanced cancer patients has been limited due to cumulative and chemotherapy-enhanced toxicity. Here we analyze different pieces of data from mechanistic and clinical studies with the anti-EGFR monoclonal antibody Nimotuzumab, which provides several clues to understand how this antibody may induce a biological control of tumor growth while keeping a low toxicity profile. Based on these results and the current state of the art on EGFR-targeted therapies, we discuss the need to evaluate new therapeutic approaches using anti-EGFR agents, which would have the potential of transforming advanced cancer into a long-term controlled chronic disease.
Highlights
Epidermal growth factor receptor (EGFR)-targeted therapies have been extensively evaluated in the clinic [1,2], and several EGFR-targeting products have been registered worldwide for the treatment of different tumor localizations [2]
In this paper, taking the antibody Nimotuzumab as a case study, we would like to share our views regarding clinical implementations of EGFR-targeted therapies that aim to a long-term control of the advanced cancer disease
The relevance of chronic treatment with Nimotuzumab on disease control is currently being assessed in controlled clinical trials (e.g., NCT00561990 and NCT00753246, [51]) comparing a maintenance phase with the antibody versus the best supportive care
Summary
Epidermal growth factor receptor (EGFR)-targeted therapies have been extensively evaluated in the clinic [1,2], and several EGFR-targeting products have been registered worldwide for the treatment of different tumor localizations [2]. No K-Ras mutations have been found in colorectal cancer patients responding to Cetuximab or Panitumumab treatment in different studies [4,5,6,7,8]. The limited effects on survival of EGFR antagonists might be a consequence, at least partially, of administering EGFR-targeting therapies in a non-optimal way. We are lacking in differentiation strategies for individual EGFR antagonists, which could eventually improve their clinical benefit in different patient niches. In this paper, taking the antibody Nimotuzumab as a case study, we would like to share our views regarding clinical implementations of EGFR-targeted therapies that aim to a long-term control of the advanced cancer disease
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