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Cancers
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Bone Metastasis in Breast Cancer
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Bone Metastasis in Breast Cancer

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

Deadline for manuscript submissions: closed (1 August 2023) | Viewed by 15955

Special Issue Editor

Prof. Dr. Penelope Dawn Ottewell

E-Mail Website
Guest Editor
Department of Oncology and Metabolism, University of Sheffield, Sheffield S10 2RX, UK
Interests: breast and prostate cancer bone metastasis; clinically relevant models; role of cytokine and immune cell regulation

Special Issue Information

Dear Colleagues, 

We are putting together a Special Issue focussed on breast cancer bone metastasis for publication in Cancers. For this issue, we would like to provide a mixture of data from clinical and pre-clinical studies in order to showcase recent developments in our understanding of this condition that will ultimately lead to improved patient benefit. We are interested in high quality original research or clinical reviews covering the following topics:

  • Predictive biomarkers for bone metastasis.
  • Mechanisms that promote breast cancer spread to bone.
  • Immune cell regulation of breast cancer bone metastasis.
  • Mechanisms of tumour cell dormancy in bone.
  • Mechanisms of drug resistance in bone metastases.
  • Novel therapeutic strategies/agents for treatment/prevention of bone metastasis.

We believe that bringing together clinical and preclinical research focussed on breast cancer bone metastasis in this Special Issue will help bridge the knowledge gaps that are currently impeding the development of effective targeted treatments for this condition. Ultimately, we hope that by showcasing your new research we will help drive the development of better treatment options for patients with breast cancer bone metastasis.

Dr. Penelope Dawn Ottewell
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 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. 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

  • breast cancer bone metastasis
  • biomarkers
  • immune regulation
  • dormancy
  • drug resistance
  • novel therapies
  • treatment strategies

Published Papers (5 papers)

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Research

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23 pages, 5115 KiB  
Article
The CDK4/6 Inhibitor Palbociclib Inhibits Estrogen-Positive and Triple Negative Breast Cancer Bone Metastasis In Vivo
by Lubaid Saleh, Penelope D. Ottewell, Janet E. Brown, Steve L. Wood, Nichola J. Brown, Caroline Wilson, Catherine Park, Simak Ali and Ingunn Holen
Cancers 2023, 15(8), 2211; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers15082211 - 08 Apr 2023
Viewed by 2222
Abstract
CDK 4/6 inhibitors have demonstrated significant improved survival for patients with estrogen receptor (ER) positive breast cancer (BC). However, the ability of these promising agents to inhibit bone metastasis from either ER+ve or triple negative BC (TNBC) remains to be established. We therefore [...] Read more.
CDK 4/6 inhibitors have demonstrated significant improved survival for patients with estrogen receptor (ER) positive breast cancer (BC). However, the ability of these promising agents to inhibit bone metastasis from either ER+ve or triple negative BC (TNBC) remains to be established. We therefore investigated the effects of the CDK 4/6 inhibitor, palbociclib, using in vivo models of breast cancer bone metastasis. In an ER+ve T47D model of spontaneous breast cancer metastasis from the mammary fat pad to bone, primary tumour growth and the number of hind limb skeletal tumours were significantly lower in palbociclib treated animals compared to vehicle controls. In the TNBC MDA-MB-231 model of metastatic outgrowth in bone (intracardiac route), continuous palbociclib treatment significantly inhibited tumour growth in bone compared to vehicle. When a 7-day break was introduced after 28 days (mimicking the clinical schedule), tumour growth resumed and was not inhibited by a second cycle of palbociclib, either alone or when combined with the bone-targeted agent, zoledronic acid (Zol), or a CDK7 inhibitor. Downstream phosphoprotein analysis of the MAPK pathway identified a number of phosphoproteins, such as p38, that may contribute to drug-insensitive tumour growth. These data encourage further investigation of targeting alternative pathways in CDK 4/6-insensitive tumour growth. Full article
(This article belongs to the Special Issue Bone Metastasis in Breast Cancer)
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20 pages, 4033 KiB  
Article
Novel Methods of Targeting IL-1 Signalling for the Treatment of Breast Cancer Bone Metastasis
by Jiabao Zhou, Jennifer M. Down, Christopher N. George, Jessica Murphy, Diane V. Lefley, Claudia Tulotta, Marwa A. Alsharif, Michael Leach and Penelope D. Ottewell
Cancers 2022, 14(19), 4816; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14194816 - 01 Oct 2022
Cited by 5 | Viewed by 2202
Abstract
Breast cancer bone metastasis is currently incurable. Evidence suggests that inhibiting IL-1 signalling with the IL1R antagonist, Anakinra, or the IL1β antibody, Canakinumab, prevents metastasis and almost eliminates breast cancer growth in the bone. However, these drugs increase primary tumour growth. We, therefore, [...] Read more.
Breast cancer bone metastasis is currently incurable. Evidence suggests that inhibiting IL-1 signalling with the IL1R antagonist, Anakinra, or the IL1β antibody, Canakinumab, prevents metastasis and almost eliminates breast cancer growth in the bone. However, these drugs increase primary tumour growth. We, therefore, investigated whether targeting other members of the IL-1 pathway (Caspase-1, IL1β or IRAK1) could reduce bone metastases without increasing tumour growth outside of the bone. Inhibition of IL-1 via MLX01 (IL1β secretion inhibitor), VRT043198/VX765 (Caspase-1 inhibitor), Pacritinib (IRAK1 inhibitor) or Anakinra (IL1R antagonist) on tumour cell viability, migration and invasion were assessed in mouse mammary E0771 and Py8119 cells in vitro and on primary tumour growth, spontaneous metastasis and metastatic outgrowth in vivo. In vitro, Inhibition of IL-1 signalling by MLX01, VRT043198 and Anakinra reduced migration of E0771 and Py8119 cells and reversed tumour-derived IL1β induced-increased invasion and migration towards bone cells. In vivo, VX765 and Anakinra significantly reduced spontaneous metastasis and metastatic outgrowth in the bone, whereas MLX01 reduced primary tumour growth and bone metastasis. Pacritinib had no effect on metastasis in vitro or in vivo. Targeting IL-1 signalling with small molecule inhibitors may provide a new therapeutic strategy for breast cancer bone metastasis. Full article
(This article belongs to the Special Issue Bone Metastasis in Breast Cancer)
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33 pages, 10093 KiB  
Article
Decoding Single Cell Morphology in Osteotropic Breast Cancer Cells for Dissecting Their Migratory, Molecular and Biophysical Heterogeneity
by Lila Bemmerlein, Ilker A. Deniz, Jana Karbanová, Angela Jacobi, Stephan Drukewitz, Theresa Link, Andy Göbel, Lisa Sevenich, Anna V. Taubenberger, Pauline Wimberger, Jan Dominik Kuhlmann and Denis Corbeil
Cancers 2022, 14(3), 603; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14030603 - 25 Jan 2022
Cited by 6 | Viewed by 3926
Abstract
Breast cancer is a heterogeneous disease and the mechanistic framework for differential osteotropism among intrinsic breast cancer subtypes is unknown. Hypothesizing that cell morphology could be an integrated readout for the functional state of a cancer cell, we established a catalogue of the [...] Read more.
Breast cancer is a heterogeneous disease and the mechanistic framework for differential osteotropism among intrinsic breast cancer subtypes is unknown. Hypothesizing that cell morphology could be an integrated readout for the functional state of a cancer cell, we established a catalogue of the migratory, molecular and biophysical traits of MDA-MB-231 breast cancer cells, compared it with two enhanced bone-seeking derivative cell lines and integrated these findings with single cell morphology profiles. Such knowledge could be essential for predicting metastatic capacities in breast cancer. High-resolution microscopy revealed a heterogeneous and specific spectrum of single cell morphologies in bone-seeking cells, which correlated with differential migration and stiffness. While parental MDA-MB-231 cells showed long and dynamic membrane protrusions and were enriched in motile cells with continuous and mesenchymal cell migration, bone-seeking cells appeared with discontinuous mesenchymal or amoeboid-like migration. Although non-responsive to CXCL12, bone-seeking cells responded to epidermal growth factor with a morphotype shift and differential expression of genes controlling cell shape and directional migration. Hence, single cell morphology encodes the molecular, migratory and biophysical architecture of breast cancer cells and is specifically altered among osteotropic phenotypes. Quantitative morpho-profiling could aid in dissecting breast cancer heterogeneity and in refining clinically relevant intrinsic breast cancer subtypes. Full article
(This article belongs to the Special Issue Bone Metastasis in Breast Cancer)
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14 pages, 4471 KiB  
Article
Quantitative Analysis of SPECT-CT Data in Metastatic Breast Cancer Patients—The Clinical Significance
by Mirela Gherghe, Mario-Demian Mutuleanu, Adina Elena Stanciu, Ionela Irimescu, Alexandra Lazar, Xenia Bacinschi and Rodica Maricela Anghel
Cancers 2022, 14(2), 273; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14020273 - 06 Jan 2022
Cited by 13 | Viewed by 3482
Abstract
Purpose: To assess the potential added value of the SPECT-CT quantitative analysis in metastatic breast cancer lesions detection and differentiation from degenerative lesions. Methods: This prospective monocentric study was conducted on 70 female patients who underwent SPECT-CT bone scans using 99mTc–HDP that [...] Read more.
Purpose: To assess the potential added value of the SPECT-CT quantitative analysis in metastatic breast cancer lesions detection and differentiation from degenerative lesions. Methods: This prospective monocentric study was conducted on 70 female patients who underwent SPECT-CT bone scans using 99mTc–HDP that identified the presence of metastatic bone lesions and degenerative lesions in each patient. Once the lesions were identified, a quantitative analysis of radiotracer uptake was conducted. The highest one to five SUVmax values for both metastatic and degenerative bone lesions were identified in each patient and the data were then statistically analyzed. Results: The SUVmax value was significantly higher in metastatic bone lesions than in degenerative lesions (p < 0.001). The diagnostic accuracy of SPECT-CT quantitative data analysis revealed a sensitivity of 91.5% and a specificity of 93.3% at a cut-off value of the SUVmax of 16.6 g/mL. Conclusion: Quantitative analysis performed using SPECT-CT data can improve the diagnostic accuracy in differentiating between metastatic bone lesions and degenerative lesions, thus leading to appropriate treatment and better follow-up in metastatic breast cancer patients. Full article
(This article belongs to the Special Issue Bone Metastasis in Breast Cancer)
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Review

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12 pages, 1513 KiB  
Review
Re-Evaluating the Role of PTHrP in Breast Cancer
by Jeremy F. Kane and Rachelle W. Johnson
Cancers 2023, 15(10), 2670; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers15102670 - 09 May 2023
Viewed by 2811
Abstract
Parathyroid-hormone-related protein (PTHrP) is a protein with a long history of association with bone metastatic cancers. The paracrine signaling of PTHrP through the parathyroid hormone receptor (PTHR1) facilitates tumor-induced bone destruction, and PTHrP is known as the primary driver of humoral hypercalcemia of [...] Read more.
Parathyroid-hormone-related protein (PTHrP) is a protein with a long history of association with bone metastatic cancers. The paracrine signaling of PTHrP through the parathyroid hormone receptor (PTHR1) facilitates tumor-induced bone destruction, and PTHrP is known as the primary driver of humoral hypercalcemia of malignancy. In addition to paracrine signaling, PTHrP is capable of intracrine signaling independent of PTHR1 binding, which is essential for cytokine-like functions in normal physiological conditions in a variety of tissue types. Pre-clinical and clinical studies evaluating the role of PTHrP in breast cancer have yielded contradictory conclusions, in some cases indicating the protein is tumor suppressive, and in other studies, pro-growth. This review discusses the possible molecular basis for the disharmonious prognostic indications of these studies and highlights the implications of the paracrine, intracrine, and nuclear functions of the protein. This review also examines the current understanding of the functional domains of PTHrP and re-evaluates their role in the unique context of the breast cancer environment. This review will expand on the current understanding of PTHrP by attempting to reconcile the functional domains of the protein with its intracrine signaling in cancer. Full article
(This article belongs to the Special Issue Bone Metastasis in Breast Cancer)
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