Cómo leer los relatos bíblicos. Iniciación al análisis narrativo

La Biblia es uno de los más fabulosos tesoros de historia(s) de la humanidad, pues desde la noche de los tiempos los creyentes relatan. Pero no lo hacen de cualquier manera. Largamente elaborados en su etapa oral, pacientemente redactados, los relatos bíblicos obedecen a unas sutiles reglas de composición. Tras las historias aparentemente ingenuas se esconde la fina estrategia de un narrador. El libro de Daniel Marguerat e Yvan Bourquin -el primer manual de iniciación al análisis narrativo publicado en español- conduce al lector por los entresijos del relato bíblico para observar su construcción. Este descubrimiento de la arquitectura oculta de los textos lleva a plantearse de manera nueva su significación. Con gran claridad pedagógica, los autores han dispuesto un recorrido que permite descubrir los instrumentos del análisis narrativo, estudiar su aplicación y evaluar su eficacia. Toda la magia de la lectura queda con ello iluminada.

Lack of EGFR-activating mutations in European patients with triple-negative breast cancer could emphasise geographic and ethnic variations in breast cancer mutation profiles.

INTRODUCTION: Triple-negative breast cancers (TNBCs) are characterised by lack of expression of hormone receptors and epidermal growth factor receptor 2 (HER-2). As they frequently express epidermal growth factor receptors (EGFRs), anti-EGFR therapies are currently assessed for this breast cancer subtype as an alternative to treatments that target HER-2 or hormone receptors. Recently, EGFR-activating mutations have been reported in TNBC specimens in an East Asian population. Because variations in the frequency of EGFR-activating mutations in East Asians and other patients with lung cancer have been described, we evaluated the EGFR mutational profile in tumour samples from European patients with TNBC. METHODS: We selected from a DNA tumour bank 229 DNA samples isolated from frozen, histologically proven and macrodissected invasive TNBC specimens from European patients. PCR and high-resolution melting (HRM) analyses were used to detect mutations in exons 19 and 21 of EGFR. The results were then confirmed by bidirectional sequencing of all samples. RESULTS: HRM analysis allowed the detection of three EGFR exon 21 mutations, but no exon 19 mutations. There was 100% concordance between the HRM and sequencing results. The three patients with EGFR exon 21 abnormal HRM profiles harboured the rare R836R SNP, but no EGFR-activating mutation was identified. CONCLUSIONS: This study highlights variations in the prevalence of EGFR mutations in TNBC. These variations have crucial implications for the design of clinical trials involving anti-EGFR treatments in TNBC and for identifying the potential target population.