KRAS mutation testing for predicting response to anti-EGFR therapy for colorectal carcinoma: proposal for an European quality assurance program

Erratum to: Virchows Arch

DOI 10.1007/s00428-008-0665-y

In Fig. 2 of this article the DNA sequencing data were incorrect, and parts of Fig. 3 were illegible.

Fig. 2

Role of KRAS mutations in oncogenic activation of intracellular signaling. The human KRAS gene, located on chromosome 12, encodes a small G-protein that functions downstream of EGFR-induced cell signaling. This G-protein belongs to the family of RAS proteins involved in signal transduction pathways that regulate cell development and function. RAS proteins normally cycle between active (RAS-GTP) and inactive (RAS-GDP) conformations. Somatic missense mutations in codon 12 of the KRAS gene, leading to single amino acid substitutions such as p.Gly12Val, are the most common alterations found in colorectal tumors. These KRAS mutations result in RAS proteins that are constitutively in the active RAS-GTP conformation. Unlike wild-type RAS proteins which are deactivated after a short time, the mutated RAS proteins cause continuous activation of RAS signaling pathways in the absence of upstream stimulation of EGFR/HER receptors. This oncogenic activation of RAS signaling pathways leads to abnormal cell growth, proliferation and differentiation

Fig. 3

Proposed framework for a European quality assurance (QA) program for KRAS mutation testing in colorectal cancer. The European QA program, under the direction of a QA council, will be organized by the European Society of Pathology in close collaboration with existing regional and/or national QA programs. The QA program, together with a designated coordinator, will be responsible for establishing QA guidelines and testing criteria, implementing the QA program and performing laboratory accreditation. Participating laboratories can attain accreditation at the regional or centralized level

Corrected versions of these figures are given here.