Special Issue "STAT3 Signalling in Cancer: Friend or Foe"

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A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (30 November 2013)

Special Issue Editor

Guest Editor
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
Website: http://www.uhcancercenter.org/about-us/directory/faculty-staff/2-directory/84
E-Mail: jturkson@cc.hawaii.edu
Phone: +1-808-356-5784
Fax: +1-808-587-0742
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

Special Issue Information

Dear Colleague,

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
Guest Editor

Submission

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.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 800 CHF (Swiss Francs).

Keywords

  • STAT signaling
  • STAT3
  • malignant transformation
  • tumorigenesis
  • oncogenes
  • tumor suppressor function
  • cell proliferation
  • apoptosis
  • small-molecules inhibitors
  • tyrosine kinases
  • growth factor receptors

Published Papers (12 papers)

by  and
Cancers 2014, 6(3), 1408-1440; doi:10.3390/cancers6031408
Received: 17 April 2014; in revised form: 19 June 2014 / Accepted: 20 June 2014 / Published: 3 July 2014
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by , , ,  and
Cancers 2014, 6(3), 1394-1407; doi:10.3390/cancers6031394
Received: 5 March 2014; in revised form: 13 June 2014 / Accepted: 20 June 2014 / Published: 3 July 2014
Show/Hide Abstract | PDF Full-text (414 KB) | HTML Full-text | XML Full-text
abstract graphic

by ,  and
Cancers 2014, 6(2), 958-968; doi:10.3390/cancers6020958
Received: 24 January 2014; in revised form: 19 March 2014 / Accepted: 28 March 2014 / Published: 23 April 2014
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by , , ,  and
Cancers 2014, 6(2), 926-957; doi:10.3390/cancers6020926
Received: 13 December 2013; in revised form: 11 March 2014 / Accepted: 18 March 2014 / Published: 16 April 2014
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by  and
Cancers 2014, 6(2), 897-925; doi:10.3390/cancers6020897
Received: 3 January 2014; in revised form: 22 March 2014 / Accepted: 28 March 2014 / Published: 16 April 2014
Show/Hide Abstract | Cited by 1 | PDF Full-text (708 KB) | HTML Full-text | XML Full-text
abstract graphic

by ,  and
Cancers 2014, 6(2), 829-859; doi:10.3390/cancers6020829
Received: 8 February 2014; in revised form: 11 March 2014 / Accepted: 17 March 2014 / Published: 9 April 2014
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by ,  and
Cancers 2014, 6(2), 708-722; doi:10.3390/cancers6020708
Received: 5 December 2013; in revised form: 23 February 2014 / Accepted: 7 March 2014 / Published: 26 March 2014
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by , ,  and
Cancers 2014, 6(2), 646-662; doi:10.3390/cancers6020646
Received: 14 November 2013; in revised form: 11 February 2014 / Accepted: 27 February 2014 / Published: 25 March 2014
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by ,  and
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
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by
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
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by , , ,  and
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
Show/Hide Abstract | Cited by 1 | PDF Full-text (398 KB) | HTML Full-text | XML Full-text

by , , , , , , , ,  and
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
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Last update: 1 July 2013

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