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Cancers
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Targeting the JAK–STAT Signaling Axis in Cancer
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Targeting the JAK–STAT Signaling Axis in Cancer

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: closed (15 June 2024) | Viewed by 6000

Special Issue Editor

Prof. Dr. Alister C. Ward

E-Mail Website
Guest Editor
School of Medicine, Institute for Mental and Physical Health, Deakin University, Waurn Ponds, VIC 3216, Australia
Interests: cell–cell signaling; cytokines; JAK–STAT pathway; hematology; immunology; developmental biology; oncology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancers represent one of the leading causes of death worldwide, afflicting every organ system and impacting all stages of the life course. A myriad of genetic, epigenetic and other causes have been identified that complicates the development of strategies for treatment. However, many of these underlying causes utilize common mechanisms to promote cancer formation and progression. These include the Janus kinase–signal transducer and activator of transcription (JAK–STAT) signaling axis, which contributes to a wide range of hematologic malignancies and solid tumors. As such, this pathway represents an attractive target for therapy across a broad range of cancers.

We are pleased to invite you to submit articles including to this Special Issue, including in the form of research papers and reviews.

Consistent with the scope and aims of Cancers, this Special Issue ‘Targeting the JAK–STAT Signaling Axis in Cancer’ aims to provide basic, translational and clinical perspectives on the JAK–STAT pathway across a variety of cancer types, including well-executed studies showing meaningful but negative results. In this Special Issue, original high-quality research articles and reviews are welcome. Research areas may include (but are not limited to) mechanistic and etiological investigations, therapeutic development and testing in both preclinical and clinical settings.

I look forward to receiving your contributions.

Prof. Dr. Alister C. Ward
Guest Editor

Manuscript Submission Information

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. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (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 thoroughly refereed through a single-blind 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 semimonthly 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 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cell–cell signaling
  • cytokines
  • JAK–STAT pathway
  • hematology
  • immunology
  • developmental biology
  • oncology
  • ADAMTS

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Published Papers (2 papers)

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Review

28 pages, 2163 KiB  
Review
Oncogenic STAT Transcription Factors as Targets for Cancer Therapy: Innovative Strategies and Clinical Translation
by Weiyuan Wang, Melanie Cristina Lopez McDonald, Rajashree Hariprasad, Tiara Hamilton and David A. Frank
Cancers 2024, 16(7), 1387; https://doi.org/10.3390/cancers16071387 - 31 Mar 2024
Cited by 6 | Viewed by 3131
Abstract
Despite advances in our understanding of molecular aspects of oncogenesis, cancer remains a leading cause of death. The malignant behavior of a cancer cell is driven by the inappropriate activation of transcription factors. In particular, signal transducers and activators of transcription (STATs), which [...] Read more.
Despite advances in our understanding of molecular aspects of oncogenesis, cancer remains a leading cause of death. The malignant behavior of a cancer cell is driven by the inappropriate activation of transcription factors. In particular, signal transducers and activators of transcription (STATs), which regulate many critical cellular processes such as proliferation, apoptosis, and differentiation, are frequently activated inappropriately in a wide spectrum of human cancers. Multiple signaling pathways converge on the STATs, highlighting their importance in the development and progression of oncogenic diseases. STAT3 and STAT5 are two members of the STAT protein family that are the most frequently activated in cancers and can drive cancer pathogenesis directly. The development of inhibitors targeting STAT3 and STAT5 has been the subject of intense investigations in the last decade, although effective treatment options remain limited. In this review, we investigate the specific roles of STAT3 and STAT5 in normal physiology and cancer biology, discuss the opportunities and challenges in pharmacologically targeting STAT proteins and their upstream activators, and offer insights into novel therapeutic strategies to identify STAT inhibitors as cancer therapeutics. Full article
(This article belongs to the Special Issue Targeting the JAK–STAT Signaling Axis in Cancer)
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13 pages, 1581 KiB  
Review
Myeloproliferative Neoplasms: Diseases Mediated by Chronic Activation of Signal Transducer and Activator of Transcription (STAT) Proteins
by Clifford Liongue and Alister C. Ward
Cancers 2024, 16(2), 313; https://doi.org/10.3390/cancers16020313 - 11 Jan 2024
Cited by 3 | Viewed by 2234
Abstract
Myeloproliferative neoplasms (MPNs) are hematopoietic diseases characterized by the clonal expansion of single or multiple lineages of differentiated myeloid cells that accumulate in the blood and bone marrow. MPNs are grouped into distinct categories based on key clinical presentations and distinctive mutational hallmarks. [...] Read more.
Myeloproliferative neoplasms (MPNs) are hematopoietic diseases characterized by the clonal expansion of single or multiple lineages of differentiated myeloid cells that accumulate in the blood and bone marrow. MPNs are grouped into distinct categories based on key clinical presentations and distinctive mutational hallmarks. These include chronic myeloid leukemia (CML), which is strongly associated with the signature BCR::ABL1 gene translocation, polycythemia vera (PV), essential thrombocythemia (ET), and primary (idiopathic) myelofibrosis (PMF), typically accompanied by molecular alterations in the JAK2, MPL, or CALR genes. There are also rarer forms such as chronic neutrophilic leukemia (CNL), which involves mutations in the CSF3R gene. However, rather than focusing on the differences between these alternate disease categories, this review aims to present a unifying molecular etiology in which these overlapping diseases are best understood as disruptions of normal hematopoietic signaling: specifically, the chronic activation of signaling pathways, particularly involving signal transducer and activator of transcription (STAT) transcription factors, most notably STAT5B, leading to the sustained stimulation of myelopoiesis, which underpins the various disease sequalae. Full article
(This article belongs to the Special Issue Targeting the JAK–STAT Signaling Axis in Cancer)
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