Open AccessThis article is
- freely available
EGFR-Targeting as a Biological Therapy: Understanding Nimotuzumab’s Clinical Effects
Center of Molecular Immunology, P.O. Box 16040, Havana 11600, Cuba
* Author to whom correspondence should be addressed.
Received: 4 February 2011; in revised form: 19 March 2011 / Accepted: 24 March 2011 / Published: 18 April 2011
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.
Keywords: EGFR; Nimotuzumab; cancer treatment; targeted therapy; biological therapy
Citations to this Article
Cite This Article
MDPI and ACS Style
Perez, R.; Moreno, E.; Garrido, G.; Crombet, T. EGFR-Targeting as a Biological Therapy: Understanding Nimotuzumab’s Clinical Effects. Cancers 2011, 3, 2014-2031.
Perez R, Moreno E, Garrido G, Crombet T. EGFR-Targeting as a Biological Therapy: Understanding Nimotuzumab’s Clinical Effects. Cancers. 2011; 3(2):2014-2031.
Perez, Rolando; Moreno, Ernesto; Garrido, Greta; Crombet, Tania. 2011. "EGFR-Targeting as a Biological Therapy: Understanding Nimotuzumab’s Clinical Effects." Cancers 3, no. 2: 2014-2031.