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Bioengineering
Special Issues
Engineering-Inspired Cancer Research
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Engineering-Inspired Cancer Research

A special issue of Bioengineering (ISSN 2306-5354).

Deadline for manuscript submissions: closed (31 March 2023) | Viewed by 5411

Special Issue Editors

Dr. Jonathan W. Song

E-Mail Website
Guest Editor
Department of Mechanical and Aerospace Engineering, The Ohio State University, Columbus, OH 43210, USA
Interests: microfluidics; angiogenesis and microcirculation; extracellular matrix; mechanobiology; cancer migration and metastasis
Dr. Kristen L. Mills

E-Mail Website
Guest Editor
Rensselaer Polytechnic Institute, Troy, NY 12180, USA
Interests: cell and tissue biomechanics; experimental mechanics of materials

Special Issue Information

Dear Colleagues,

Cancer microenvironments are physically and biologically complex. The integration of cancer biology with bioengineering has helped address the challenges posed by these complexities with engineered models of organs and tissues. These models have the unique ability to control physical, chemical, and biological complexity across multiple length scales, making them tools rich with possibilities for studying and identifying key drivers of cancer initiation and progression, as well as therapeutic efficacy. This Special Issue will showcase research papers, short communications, and review articles on a range of engineered solutions for investigating cancer mechanisms based in different tissue microenvironments of the body. Topics of interest include: 1) the interaction and crosstalk of cancer cells with cells and tissues of the host microenvironment; 2) physiological properties of the tumor vasculature and extracellular matrix that promote cancer progression and preclude treatment response; 3) sensors and techniques for biomarker discovery; and 4) cancer treatments and interventions that affect cancer cell dynamics, plasticity, and metabolic pathways. 

Dr. Jonathan W. Song
Dr. Kristen L. Mills
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. Bioengineering 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 2700 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

  • physics of cancer
  • cancer cell migration and invasion
  • microfluidics and microfabrication
  • tissue engineering
  • extracellular matrix
  • fibroblasts
  • immune cells

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Further information on MDPI's Special Issue polices can be found here.

Published Papers (2 papers)

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Research

16 pages, 1209 KiB  
Article
Comprehensive Profiling of Cancer-Associated Cells in the Blood of Breast Cancer Patients Undergoing Neoadjuvant Chemotherapy to Predict Pathological Complete Response
by Adity A. Pore, Chathurika S. Dhanasekara, Hunaiz Bin Navaid, Siva A. Vanapalli and Rakhshanda Layeequr Rahman
Bioengineering 2023, 10(4), 485; https://doi.org/10.3390/bioengineering10040485 - 18 Apr 2023
Cited by 3 | Viewed by 2070
Abstract
Neoadjuvant chemotherapy (NAC) can affect pathological complete response (pCR) in breast cancers; the resection that follows identifies patients with residual disease who are then offered second-line therapies. Circulating tumor cells (CTCs) and cancer-associated macrophage-like cells (CAMLs) in the blood can be used as [...] Read more.
Neoadjuvant chemotherapy (NAC) can affect pathological complete response (pCR) in breast cancers; the resection that follows identifies patients with residual disease who are then offered second-line therapies. Circulating tumor cells (CTCs) and cancer-associated macrophage-like cells (CAMLs) in the blood can be used as potential biomarkers for predicting pCR before resection. CTCs are of epithelial origin that undergo epithelial-to-mesenchymal transition to become more motile and invasive, thereby leading to invasive mesenchymal cells that seed in distant organs, causing metastasis. Additionally, CAMLs in the blood of cancer patients are reported to either engulf or aid the transport of cancer cells to distant organs. To study these rare cancer-associated cells, we conducted a preliminary study where we collected blood from patients treated with NAC after obtaining their written and informed consent. Blood was collected before, during, and after NAC, and Labyrinth microfluidic technology was used to isolate CTCs and CAMLs. Demographic, tumor marker, and treatment response data were collected. Non-parametric tests were used to compare pCR and non-pCR groups. Univariate and multivariate models were used where CTCs and CAMLs were analyzed for predicting pCR. Sixty-three samples from 21 patients were analyzed. The median(IQR) pre-NAC total and mesenchymal CTC count/5 mL was lower in the pCR vs. non-pCR group [1(3.5) vs. 5(5.75); p = 0.096], [0 vs. 2.5(7.5); p = 0.084], respectively. The median(IQR) post-NAC CAML count/5 mL was higher in the pCR vs. non-pCR group [15(6) vs. 6(4.5); p = 0.004]. The pCR group was more likely to have >10 CAMLs post-NAC vs. non-pCR group [7(100%) vs. 3(21.4%); p = 0.001]. In a multivariate logistic regression model predicting pCR, CAML count was positively associated with the log-odds of pCR [OR = 1.49(1.01, 2.18); p = 0.041], while CTCs showed a negative trend [Odds Ratio (OR) = 0.44(0.18, 1.06); p = 0.068]. In conclusion, increased CAMLs in circulation after treatment combined with lowered CTCs was associated with pCR. Full article
(This article belongs to the Special Issue Engineering-Inspired Cancer Research)
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22 pages, 6436 KiB  
Article
Oscillatory ERK Signaling and Morphology Determine Heterogeneity of Breast Cancer Cell Chemotaxis via MEK-ERK and p38-MAPK Signaling Pathways
by Kenneth K. Y. Ho, Siddhartha Srivastava, Patrick C. Kinnunen, Krishna Garikipati, Gary D. Luker and Kathryn E. Luker
Bioengineering 2023, 10(2), 269; https://doi.org/10.3390/bioengineering10020269 - 18 Feb 2023
Cited by 2 | Viewed by 2632
Abstract
Chemotaxis, regulated by oscillatory signals, drives critical processes in cancer metastasis. Crucial chemoattractant molecules in breast cancer, CXCL12 and EGF, drive the activation of ERK and Akt. Regulated by feedback and crosstalk mechanisms, oscillatory signals in ERK and Akt control resultant changes in [...] Read more.
Chemotaxis, regulated by oscillatory signals, drives critical processes in cancer metastasis. Crucial chemoattractant molecules in breast cancer, CXCL12 and EGF, drive the activation of ERK and Akt. Regulated by feedback and crosstalk mechanisms, oscillatory signals in ERK and Akt control resultant changes in cell morphology and chemotaxis. While commonly studied at the population scale, metastasis arises from small numbers of cells that successfully disseminate, underscoring the need to analyze processes that cancer cells use to connect oscillatory signaling to chemotaxis at single-cell resolution. Furthermore, little is known about how to successfully target fast-migrating cells to block metastasis. We investigated to what extent oscillatory networks in single cells associate with heterogeneous chemotactic responses and how targeted inhibitors block signaling processes in chemotaxis. We integrated live, single-cell imaging with time-dependent data processing to discover oscillatory signal processes defining heterogeneous chemotactic responses. We identified that short ERK and Akt waves, regulated by MEK-ERK and p38-MAPK signaling pathways, determine the heterogeneous random migration of cancer cells. By comparison, long ERK waves and the morphological changes regulated by MEK-ERK signaling, determine heterogeneous directed motion. This study indicates that treatments against chemotaxis in consider must interrupt oscillatory signaling. Full article
(This article belongs to the Special Issue Engineering-Inspired Cancer Research)
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