Special Issue "RASSF Signalling in Cancer"
A special issue of Cancers (ISSN 2072-6694).
Deadline for manuscript submissions: closed (15 December 2015)
The Ras Association Domain Family (RASSF) consists of ten members, which encode either a C-Terminal Ras association (RA) domain or a N-terminal RA. Most of the RASSF are tumor suppressor genes that are frequently epigenetically inactivated in human cancers. Functional studies have shown that RASSF signaling is involved in several pathways including Ras and Hippo. Deregulation of the RASSF members alters cell cycle control, growth and apoptosis of cancer cells. Thus aberrant RASSF signaling plays a key role in the pathogenesis of human cancers. In this special issue of cancers we invite you to submit an original manuscript analyzing the function or epigenetic alteration of the RASSF members in cancers.
Prof. Dr. Reinhard Dammann
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed Open Access monthly journal published by MDPI.
- ras Association Domain Family
- N-Terminal RASSF
- C-Terminal RASSF
- epigenetic regulation
- DNA methylation
- tumor suppressor gene
- hippo pathway
- ras signaling
- cell cycle regulation
- growth inhibition
- DNA repair
- genetic alterations