- Ian Cree, University Hospitals Coventry and Warwickshire
- John A Hartley, University College London
- Manami Inoue, University of Tokyo
- Ferdinando Mannello, University Carlo Bo of Urbino
- Christophe Nicot, Kansas University Medical Center
- Stephen P Povoski, The Ohio State University
- Charles Rosser, University of Hawaii Cancer Center
- Dirk Vordermark, Martin Luther University Halle-Wittenberg
- Dafne Solera, BioMed Central
Tumor-induced downregulation of Connexin 43, a component of Gap Junctions and regulator of vessel quiescence, frees endothelium to respond to angiogenic cues and may be an imprortant mechanism of tumor vascularization.
BMC Cancer 2015, 15:645
BMC Cancer is an open access, peer-reviewed journal that considers articles on all aspects of cancer research, including the pathophysiology, prevention, diagnosis and treatment of cancers. The journal welcomes submissions concerning molecular and cellular biology, genetics, epidemiology, and clinical trials.
BMC Cancer is part of the BMC series which publishes subject-specific journals focused on the needs of individual research communities across all areas of biology and medicine. We offer an efficient, fair and friendly peer review service, and are committed to publishing all sound science, provided that there is some advance in knowledge presented by the work.
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Christudas Morais, David W Johnson, David A Vesey, and Glenda C Gobe1BMC Cancer 2013, 13:14 (10 January 2013)
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