Special Issue "STAT3 Signalling in Cancer: Friend or Foe"
A special issue of Cancers (ISSN 2072-6694).
Deadline for manuscript submissions: closed (30 November 2013)
Prof. Dr. James Turkson
Cell and Molecular Biology Department, John A. Burns School of Medicine, University of Hawaii 701 Ilalo Street, Suite 344, Honolulu, HI 96813, USA
Interests: STAT signaling; Stat3; tumorigenesis; small-molecules; peptides; peptidomimetics; inhibitors; computational modeling; natural products; rational drug design; signal transduction; tyrosine kinases; growth factor receptor signaling
Aberrantly-active Signal Transducer and Activator of Transcription (STAT)3 has long been strongly implicated in malignant transformation and the development of human tumors, with the prevailing knowledge that it dysregulates cellular gene expression leading to uncontrolled cell growth and survival, and promotes tumor progression. Further, new mechanisms of STAT3-mediated oncogenesis that extend beyond the traditional transcriptional function have also been reported in recent years. Notwithstanding, evidence is also emerging that leads to the suggestion that STAT3 maintains contradictory functions, and that in certain contexts the protein might regulate cellular events that promote cell death and suppress cell proliferation. These data together indicate the biological functions of STAT3 are far more complex than presently known and that the overall responses to STAT3-inhibiting drugs are likely to be context dependent. In this Issue of Cancers, “STAT3 Signaling in Cancer: Friend or Foe”, experts are invited to contribute original research papers or review articles that will provide further insights on the seemingly divergent functions of STAT3 in cellular processes.
Prof. Dr. James Turkson
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 quarterly journal published by MDPI.
- STAT signaling
- malignant transformation
- tumor suppressor function
- cell proliferation
- small-molecules inhibitors
- tyrosine kinases
- growth factor receptors
Cancers 2014, 6(1), 193-210; doi:10.3390/cancers6010193
Received: 2 December 2013; in revised form: 8 January 2014 / Accepted: 16 January 2014 / Published: 27 January 2014| Download PDF Full-text (764 KB) | Download XML Full-text
Cancers 2014, 6(1), 376-395; doi:10.3390/cancers6010376
Received: 16 December 2013; in revised form: 19 January 2014 / Accepted: 29 January 2014 / Published: 10 February 2014| Download PDF Full-text (398 KB)
Cancers 2014, 6(1), 494-525; doi:10.3390/cancers6010494
Received: 13 November 2013; in revised form: 18 February 2014 / Accepted: 20 February 2014 / Published: 6 March 2014| Download PDF Full-text (629 KB) | Download XML Full-text
Cancers 2014, 6(1), 526-544; doi:10.3390/cancers6010526
Received: 16 December 2013; in revised form: 15 February 2014 / Accepted: 27 February 2014 / Published: 6 March 2014| Download PDF Full-text (403 KB) | Download XML Full-text
Last update: 1 July 2013