Dr. Vincent GOFFIN is the Head of the “PRL/GH Pathophysiology: Translational Approaches” laboratory, which is part of INSERM Unit 1151/Institut Necker Enfants Malades (INEM) located on the Necker Campus at Paris (France).

This laboratory aims to identify, understand, predict and target cellular and molecular mechanisms responsible for the initiation, progression and/or resistance to treatment of benign and malignant tumors affecting the breast and the prostate.

This lab is specialized in translational studies that over the years have included the use and analyses of in vitro and in vivo pre-clinical models (cell lines, primary cultures, genetically-modified mouse model, tumor xenografts) and of human material (clinical samples, retrospective/prospective cohorts).

Thanks to this collaboration, Humana Biosciences has access to a validated transgenic mouse model mimicking human Benign Prostatic Hyperplasia. The complementary expertise of Humana Biosciences (unique functional urological tests) and Dr Goffin’s laboratory (histological/molecular characterization of prostates from this preclinical model1-5) offers the opportunity of fruitful partnerships. 

Bibliography :

1— Bernichtein, S. et al. Vitamin D3 prevents calcium-induced progression of early-stage prostate tumors by counteracting TRPC6 and calcium sensing receptor upregulation. Cancer Res 77, 355-365, doi:10.1158/0008-5472.CAN-16-0687 (2017).
2— Sackmann Sala, L. et al. A rare castration-resistant progenitor cell population is highly enriched in Pten-null prostate tumors. J Pathol 243, 54-64, doi:10.1002/path.4924 (2017).
3—Bernichtein, S. et al. Anti-inflammatory properties of Lipidosterolic extract of Serenoa repens (Permixon(R)) in a mouse model of prostate hyperplasia. Prostate 75, 706-722 (2015).
4—Sackmann-Sala, L. et al. Prolactin-Induced Prostate Tumorigenesis Links Sustained Stat5 Signaling with the Amplification of Basal/Stem Cells and Emergence of Putative Luminal Progenitors. Am. J. Pathol 184, 3105-3119 (2014). 
5—Rouet, V. et al. Local prolactin is a target to prevent expansion of basal/stem cells in prostate tumors. Proc Natl. Acad. Sci. U. S. A 107, 15199-15204 (2010).