Kinases and Other Molecular Targets in Cancer: Recent Advances, Therapeutic Opportunities, and Clinical Challenges

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 4660

Special Issue Editor

The Olivia Newton-John Cancer Research Institute, Level 5, ONJ Centre, 145 Studley Rd, Heidelberg, VIC 3084, Australia
Interests: SRC family kinases; myeloid cells; hematopoietic cell kinase; tumor immunology; immunotherapy; drug resistance

Special Issue Information

Dear Colleagues,

Aberrant activation of signaling pathways (including those regulated by kinases) can result in oncogenic changes that enable cellular transformation, tumor development, and metastasis. This may occur due to the acquisition of mutations, constitutive expression and/or amplification, epigenetic alterations, and chromosomal translocations. While targeted therapies have revolutionized the treatment landscape of numerous malignancies, these drugs are not curative, and few patients derive long-term clinical benefit. Thus, gaining deeper insights into the immunological and molecular mechanisms that underpin drug resistance remains a prime focus in oncology.

This Special Issue aims to address new therapeutic opportunities, issues, and challenges surrounding kinases and other molecular targets in cancer. These include, but are not limited to:

  • Identification of new diagnostic, prognostic, and predictive biomarkers;
  • The multi-faceted role of kinases and other molecular targets in various malignancies;
  • New and emerging therapies, including the latest advances in drug discovery and development;
  • Molecular, cellular, and pathological factors that underpin drug resistance.

Original research and reviews are welcome.

Dr. Ashleigh Poh
Guest Editor

Manuscript Submission Information

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Keywords

  • kinases
  • kinase inhibitors
  • drug resistance
  • targeted therapies
  • tumor immunology
  • cancer biology
  • oncogenic signaling
  • immunotherapy
  • biomarkers
  • tumor microenvironment

Published Papers (2 papers)

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Review

20 pages, 4181 KiB  
Review
Structure-Guided Prediction of the Functional Impact of DCLK1 Mutations on Tumorigenesis
by Annalisa L. E. Carli, Joshua M. Hardy, Hanadi Hoblos, Matthias Ernst, Isabelle S. Lucet and Michael Buchert
Biomedicines 2023, 11(3), 990; https://doi.org/10.3390/biomedicines11030990 - 22 Mar 2023
Viewed by 1962
Abstract
Doublecortin-like kinase 1 (DCLK1) is a functional serine/threonine (S/T)-kinase and a member of the doublecortin family of proteins which are characterized by their ability to bind to microtubules (MTs). DCLK1 is a proposed cancer driver gene, and its upregulation is associated with poor [...] Read more.
Doublecortin-like kinase 1 (DCLK1) is a functional serine/threonine (S/T)-kinase and a member of the doublecortin family of proteins which are characterized by their ability to bind to microtubules (MTs). DCLK1 is a proposed cancer driver gene, and its upregulation is associated with poor overall survival in several solid cancer types. However, how DCLK1 associates with MTs and how its kinase function contributes to pro-tumorigenic processes is poorly understood. This review builds on structural models to propose not only the specific functions of the domains but also attempts to predict the impact of individual somatic missense mutations on DCLK1 functions. Somatic missense mutations in DCLK1 are most frequently located within the N-terminal MT binding region and likely impact on the ability of DCLK1 to bind to αβ-tubulin and to polymerize and stabilize MTs. Moreover, the MT binding affinity of DCLK1 is negatively regulated by its auto-phosphorylation, and therefore mutations that affect kinase activity are predicted to indirectly alter MT dynamics. The emerging picture portrays DCLK1 as an MT-associated protein whose interactions with tubulin heterodimers and MTs are tightly controlled processes which, when disrupted, may confer pro-tumorigenic properties. Full article
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24 pages, 1659 KiB  
Review
Eph Receptors in Cancer
by Sakshi Arora, Andrew M. Scott and Peter W. Janes
Biomedicines 2023, 11(2), 315; https://doi.org/10.3390/biomedicines11020315 - 23 Jan 2023
Cited by 9 | Viewed by 2210
Abstract
Eph receptor tyrosine kinases play critical functions during development, in the formation of tissue and organ borders, and the vascular and neural systems. Uniquely among tyrosine kinases, their activities are controlled by binding to membrane-bound ligands, called ephrins. Ephs and ephrins generally have [...] Read more.
Eph receptor tyrosine kinases play critical functions during development, in the formation of tissue and organ borders, and the vascular and neural systems. Uniquely among tyrosine kinases, their activities are controlled by binding to membrane-bound ligands, called ephrins. Ephs and ephrins generally have a low expression in adults, functioning mainly in tissue homeostasis and plasticity, but are often overexpressed in cancers, where they are especially associated with undifferentiated or progenitor cells, and with tumour development, vasculature, and invasion. Mutations in Eph receptors also occur in various tumour types and are suspected to promote tumourigenesis. Ephs and ephrins have the capacity to operate as both tumour promoters and tumour suppressors, depending on the circumstances. They have been demonstrated to impact tumour cell proliferation, migration, and invasion in vitro, as well as tumour development, angiogenesis, and metastases in vivo, making them potential therapeutic targets. However, successful development of therapies will require detailed understanding of the opposing roles of Ephs in various cancers. In this review, we discuss the variations in Eph expression and functions in a variety of malignancies. We also describe the multiple strategies that are currently available to target them in tumours, including preclinical and clinical development. Full article
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