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Martin Fenner

Researcher at Hannover Medical School

Publications -  119
Citations -  3705

Martin Fenner is an academic researcher from Hannover Medical School. The author has contributed to research in topics: Scholarly communication & Computer science. The author has an hindex of 29, co-authored 105 publications receiving 3423 citations. Previous affiliations of Martin Fenner include Charité & PLOS.

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European Consensus Conference on Diagnosis and Treatment of Germ Cell Cancer: A Report of the Second Meeting of the European Germ Cell Cancer Consensus group (EGCCCG): Part I

Susanne Krege, +82 more
- 01 Mar 2008 - 
TL;DR: F refinements in the treatment of early- and advanced-stage testicular cancer have emerged from clinical trials, and expert clinical skills will continue to be one of the major determinants for the prognosis of patients with germ cell cancer.
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X inactivation in the mouse embryo deficient for Dnmt1: distinct effect of hypomethylation on imprinted and random X inactivation.

TL;DR: It is suggested that maintenance of imprinted X in activation in the extraembryonic lineage can tolerate extensive demethylation while normal levels of methylation are required for stable maintenance of X inactivation in the embryonic lineage.
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Maintaining success, reducing treatment burden, focusing on survivorship: highlights from the third European consensus conference on diagnosis and treatment of germ-cell cancer

TL;DR: The main recommendations and controversies of this meeting are presented, with a particular focus on acute and late toxic effects as well as on survivorship issues.
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ORCID: a system to uniquely identify researchers

TL;DR: Use cases for embedding ORCID identifiers in manuscript submission workflows, prior work searches, manuscript citations, and repository deposition are described and recommendations for storing and displaying ORC ID identifiers in publication metadata are made.
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PPARγ Ligands and ATRA Inhibit the Invasion of Human Breast Cancer Cells in vitro

TL;DR: Treatment of the highly aggressive human breast cancer cell line MDA-MB-231 with the synthetic PPARγ ligands pioglitazone (PGZ), rosiglitazonesone (RGZ), GW7845 or its natural ligand 15-deoxy-Δ 12, 14-prostaglandin J2(15d-PGJ2), at concentrations at which no obvious cytotoxicity was observed in vitro, led to a significant inhibition of