This result is in agreement with experimental data [5]. Our model also accounts for the variability of the expression of connexin 43 (the major junctional protein in astrocytes) through different tumours. We suggest that

the various migrating behaviours observed among cells in a tumour correspond to different expressions of connexin 43 and we propose a model for the “go or grow” hypothesis, based on a differential connexin 43 expression. [1] Aubert M et al, 2008, A model for glioma cell migration on collagen and astrocytes, AZD1390 cell line J. R. Soc. Interface, 5, 75. [2] Deroulers C et al, Modeling tumor cell migration: From microscopic to macroscopic models, 2009, Phys Rev E Stat Nonlin Soft Matter Phys. 79, 031917. [3] Oliveira R et al, 2005, Contribution of gap junctional communication between tumor cells and astroglia to the invasion of the brain parenchyma by human glioblastomas BMC Cell Biol., 6, 7. Poster No. 123 Nerve Growth Factor-Expressing Stromal Cells in the Microenvironment

of Hepatic Colorectal Carcinoma Metastasis: Clinical Occurrence and Functional Implicationsin Preclinical Models Felisa Basaldua 1 PI3K inhibitor , Aritz Lopategi1, Beatriz Arteta1, Andrés Valdivieso2, Jorge Ortiz de Urbina2, Fernando Vidal-Vanaclocha2 1 Department of Cell Biology and Histology, Basque Country University School of Medicine, Leioa, Bizkaia, Spain, 2 Hepatobiliar Tumor Surgery Sevice, Cruces Hospital, Cruces-Baracaldo, Bizkaia, Spain Nerve growth factor (NGF) is increased during hepatic regeneration and carcinogenesis, but its role during hepatic metastasis is unknown. A tissue-array collection of metastases from 24 patients who had undergone hepatic excision of colorectal adenocarcinoma metastases was used to investigate NGF and neurotrophin receptor expression by cancer and stromal cells. NGF immunostaining of cancer cells only occurred in 2 out of 24 patients with hepatic metastases, while around 80%

of patients had metastases with NGF-expressing stromal cells. Conversely, high affinity TrkA neurotrophin receptor immunoreactivity was mainly concentrated in cancer cells, with low expression occurring in tumor stroma. However, NGF immunostaining Gefitinib chemical structure of tumor stroma and cancer cell immunostaining with anti-ki67 antibodies did not correlate, suggesting that NGF was not associated to metastatic cell proliferation. Anti-alpha-smooth muscle actin antibodies revealed that majority of metastasis-associated NGF-expressing cells had a myofibroblast phenotype. Interestingly, NGF immunoreactivity was unequivocally localized to desmin-expressing hepatic stellate cells (HSC) —prototypic myofibroblast precursors—, and perimetastatic hepatocytes, located at the invasion front of metastases. NGF-expressing hepatocytes had phenotypic features suggesting epithelial-to-mesenchymal transition.