Molecular Targets in Cancer Cell Biology

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

Deadline for manuscript submissions: 30 June 2024 | Viewed by 1464

Special Issue Editors


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Guest Editor
1. School of Health and Medical Sciences, University of Southern Queensland, Toowoomba, Australia
2. Centre for Health Research, University of Southern Queensland, Toowoomba, Australia
Interests: metastatic tumour microenvironment; solid cancers; neuroblastomas; engineered 3D bioscaffolds

E-Mail Website
Guest Editor
School of Health and Medical Sciences, University of Southern Queensland, Toowoomba 4350, Australia
Interests: cancer diagnostics; cancer quality of survivorship; cognition; cerebrovascular function; cardiometabolic disease

Special Issue Information

Dear Colleagues,

We are pleased to invite you to contribute to this Special Issue, titled “Molecular Targets in Cancer Cell Biology”, of biomedicines. A better understanding of the pivotal molecular events underlying the oncogenesis, tumour progression, and therapy resistance of cancer are quintessential in developing new therapeutic and diagnostic approaches and identifying novel targets. These targets may also improve our understanding of the comorbidities and adverse effects that can develop as cancer patients move into survivorship and how these can be mitigated. This Special Issue will focus on recent advances in understanding the molecular mechanisms involved in the development, progression, metastasis and therapy response, and resistance of cancer. Topics of interest for this Special Issue include the role of molecular and genomic alterations, epigenetic changes, and signalling pathways in the response and resistance to current and emerging therapies and the progression to metastasis in cancer, as well as their impact on the development of comorbidities or adverse effects that develop pre- and post-active treatment. For this Special Issue, authors are invited to submit original research articles and/or reviews. Research areas may include, but are not limited to, the following: molecular mechanisms, tumour invasion and metastasis, cancer stem cell biology, combination therapies and approaches aimed at overcoming resistance, tumour microenvironment, molecular pathways, molecular networks, and pathway networks.

Dr. Louisa C. E. Windus
Dr. Edward Bliss
Guest Editors

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 short 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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

  • oncogenesis and cancer progression
  • tumour invasion and metastasis
  • cancer stem cell biology
  • cancer immunology
  • inflammation and cancer
  • DNA damage and genomic instability
  • mechanisms of therapy resistance
  • oxidative stress
  • prognosis
  • cancer-induced systemic pathophysiology

Published Papers (1 paper)

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Research

11 pages, 2871 KiB  
Article
A Mouse Model for the Rapid and Binomial Assessment of Putative WNT/β-Catenin Signalling Inhibitors
by Janson Tse, Ryan O’Keefe, Angela Rigopolous, Annalisa L. E. Carli, Jo Waaler, Stefan Krauss, Matthias Ernst and Michael Buchert
Biomedicines 2023, 11(10), 2719; https://doi.org/10.3390/biomedicines11102719 - 07 Oct 2023
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Abstract
Specific signalling thresholds of the WNT/β-catenin pathway affect embryogenesis and tissue homeostasis in the adult, with mutations in this pathway frequently occurring in cancer. Excessive WNT/β-catenin activity inhibits murine anterior development associated with embryonic lethality and accounts for the driver event in 80% [...] Read more.
Specific signalling thresholds of the WNT/β-catenin pathway affect embryogenesis and tissue homeostasis in the adult, with mutations in this pathway frequently occurring in cancer. Excessive WNT/β-catenin activity inhibits murine anterior development associated with embryonic lethality and accounts for the driver event in 80% of human colorectal cancers. Uncontrolled WNT/β-catenin signalling arises primarily from impairment mutation in the tumour suppressor gene APC that otherwise prevents prolonged stabilisation of β-catenin. Surprisingly, no inhibitor compounds for WNT/β-catenin signalling have reached clinical use in part owing to the lack of specific in vivo assays that discriminate between on-target activities and dose-limiting toxicities. Here, we present a simple in vivo assay with a binary outcome whereby the administration of candidate compounds to pregnant and phenotypically normal Apcflox/flox mice can rescue in utero death of Apcmin/flox mutant conceptus without subsequent post-mortem assessment of WNT/β-catenin signalling. Indeed, the phenotypic plasticity of born Apcmin/flox conceptus enables future refinement of our assay to potentially enable dosage finding and cross-compound comparisons. Thus, we show for the first time the suitability of endogenous WNT/β-catenin signalling during embryonic development to provide an unambiguous and sensitive mammalian in vivo model to assess the efficacy and bioavailability of potential WNT/β-catenin antagonists. Full article
(This article belongs to the Special Issue Molecular Targets in Cancer Cell Biology)
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