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Inflammatory Breast Cancer: Biology, Mechanisms, Diagnostics, and Therapeutics
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Inflammatory Breast Cancer: Biology, Mechanisms, Diagnostics, and Therapeutics

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (10 February 2023) | Viewed by 9421

Special Issue Editor

Dr. Hugo Arias-Pulido

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Guest Editor
Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, 621 Rubin Building - HB7936, 1 Medical Center Dr., Lebanon, NH 03756, USA
Interests: inflammatory breast cancer; triple-negative breast cancer in young women; patient-derived xenograft models; canine mammary tumors; canine clinical trials; prognostic and predictive biomarkers

Special Issue Information

Dear Colleagues,

Inflammatory breast cancer (IBC) is a rare but aggressive form of breast cancer. The annual IBC incidence in the US is between 1.6 and 3.1 per 100,000 women. In humans, IBC was first described in 1814 by Charles Bell as a painful breast tumor with a poor prognosis, presenting purple discoloration of the overlying skin. IBC does not commonly form a lump as occurs with other forms of breast cancer. IBC causes symptoms of breast inflammation such as swelling and redness, which is caused by cancer cells blocking lymph vessels in the skin causing the breast to look “inflamed”. Pathogenesis and behavior of IBC are closely related to components of the tumor microenvironment (TME), including tumor surrounding inflammatory and immune cells, blood vessels, extracellular matrix, etc.

Although we have achieved enormous progress in refining diagnostic criteria and establishing multimodality treatment strategies, outcomes remain unsatisfactory. The purpose of this Special Issue is to highlight recent findings regarding mechanisms, diagnostics, and therapies for inflammatory breast cancer. We welcome the submission of both original research articles and reviews.

Dr. Hugo Arias-Pulido
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. Cells 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 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

  • inflammatory breast cancer
  • IBC
  • cellular mechanism
  • molecular mechanism
  • diagnosis
  • biomarkers
  • tumor microenvironment
  • targeted therapy
  • chemotherapy
  • radiation treatments
  • biologic targeted therapy
  • hormonal therapy
  • neoadjuvant chemotherapy
  • prognosis
  • immunotherapy
  • immune checkpoint inhibitor
  • tumor microenvironment
  • tumor immunology

Published Papers (3 papers)

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12 pages, 3312 KiB  
Communication
Copy Number Variation in Inflammatory Breast Cancer
by Aditi Hazra, Andrea O’Hara, Kornelia Polyak, Faina Nakhlis, Beth T. Harrison, Antonio Giordano, Beth Overmoyer and Filipa Lynce
Cells 2023, 12(7), 1086; https://doi.org/10.3390/cells12071086 - 04 Apr 2023
Cited by 1 | Viewed by 1998
Abstract
Identification of a unique genomic biomarker in de novo inflammatory breast cancer (IBC) may provide an insight into the biology of this aggressive disease. The goal of our study was to elucidate biomarkers associated with IBC. We examined breast biopsies collected from Dana–Farber [...] Read more.
Identification of a unique genomic biomarker in de novo inflammatory breast cancer (IBC) may provide an insight into the biology of this aggressive disease. The goal of our study was to elucidate biomarkers associated with IBC. We examined breast biopsies collected from Dana–Farber Cancer Institute patients with IBC prior to initiating preoperative systemic treatment (30 samples were examined, of which 14 were eligible). Patients without available biopsies (n = 1), with insufficient tumor epithelial cells (n = 10), or insufficient DNA yield (n = 5) were excluded from the analysis. Molecular subtype and tumor grade were abstracted from a medical records’ review. Ten IBC tumors were estrogen-receptor-positive (ER+) and human epidermal growth factor receptor 2 (HER2)-negative (n = 10 out of 14). Sufficient RNA and DNA were simultaneously extracted from 14 biopsy specimens using the Qiagen AllPrep Kit. RNA was amplified using the Sensation kit and profiled using the Affymetrix Human Transcriptome Array 2.0. DNA was profiled for genome-wide copy number variation (CNV) using the Affymetrix OncoScan Array and analyzed using the Nexus Chromosome Analysis Suite. Among the 14 eligible samples, we first confirmed biological concordance and quality control metrics using replicates and gene expression data. Second, we examined CNVs and gene expression change by IBC subtype. We identified significant CNVs in IBC patients after adjusting for multiple comparisons. Next, to assess whether the CNVs were unique to IBC, we compared the IBC CNV data to fresh-frozen non-IBC CNV data from The Cancer Genome Atlas (n = 388). On chromosome 7p11.2, we identified significant CN gain located at position 58,019,983-58,025,423 in 8 ER+ IBC samples compared to 338 non-IBC ER+ samples (region length: 5440 bp gain and 69,039 bp, False Discovery Rate (FDR) p-value = 3.12 × 10−10) and at position 57,950,944–58,025,423 in 3 TN-IBC samples compared to 50 non-IBC TN samples (74,479 base pair, gain, FDR p-value = 4.27 × 10−5; near the EGFR gene). We also observed significant CN loss on chromosome 21, located at position 9,648,315–9,764,385 (p-value = 4.27 × 10−5). Secondarily, differential gene expression in IBC patients with 7p11.2 CN gain compared to SUM149 were explored after FDR correction for multiple testing (p-value = 0.0016), but the results should be interpreted with caution due to the small sample size. Finally, the data presented are hypothesis-generating. Validation of CNVs that contribute to the unique presentation and biological features associated with IBC in larger datasets may lead to the optimization of treatment strategies. Full article
(This article belongs to the Special Issue Inflammatory Breast Cancer: Biology, Mechanisms, Diagnostics, and Therapeutics)
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20 pages, 20183 KiB  
Article
MARCKS as a Potential Therapeutic Target in Inflammatory Breast Cancer
by Maroua Manai, Ines ELBini-Dhouib, Pascal Finetti, Haifa Bichiou, Carolina Reduzzi, Dorra Aissaoui, Naziha Ben-Hamida, Emilie Agavnian, Najet Srairi-Abid, Marc Lopez, Fatma Amri, Lamia Guizani-Tabbane, Khaled Rahal, Karima Mrad, Mohamed Manai, Daniel Birnbaum, Emilie Mamessier, Massimo Cristofanilli, Hamouda Boussen, Maher Kharrat, Raoudha Doghri and François Bertucciadd Show full author list remove Hide full author list
Cells 2022, 11(18), 2926; https://doi.org/10.3390/cells11182926 - 19 Sep 2022
Cited by 3 | Viewed by 2851
Abstract
Inflammatory breast cancer (IBC) is the most pro-metastatic form of breast cancer (BC). We previously demonstrated that protein overexpression of Myristoylated Alanine-Rich C Kinase Substrate (MARCKS) protein was associated with shorter survival in IBC patients. MARCKS has been associated with the PI3K/AKT pathway. [...] Read more.
Inflammatory breast cancer (IBC) is the most pro-metastatic form of breast cancer (BC). We previously demonstrated that protein overexpression of Myristoylated Alanine-Rich C Kinase Substrate (MARCKS) protein was associated with shorter survival in IBC patients. MARCKS has been associated with the PI3K/AKT pathway. MARCKS inhibitors are in development. Our objective was to investigate MARCKS, expressed preferentially in IBC that non-IBC (nIBC), as a novel potential therapeutic target for IBC. The biologic activity of MPS, a MARCKS peptide inhibitor, on cell proliferation, migration, invasion, and mammosphere formation was evaluated in IBC (SUM149 and SUM190) and nIBC (MDA-MB-231 and MCF7) cell lines, as well as its effects on protein expression in the PTEN/AKT and MAPK pathways. The prognostic relevance of MARCKS and phosphatase and tensin homolog (PTEN) protein expression as a surrogate marker of metastasis-free survival (MFS) was evaluated by immunohistochemistry (IHC) in a retrospective series of archival tumor samples derived from 180 IBC patients and 355 nIBC patients. In vitro MPS impaired cell proliferation, migration and invasion, and mammosphere formation in IBC cells. MARCKS inhibition upregulated PTEN and downregulated pAKT and pMAPK expression in IBC cells, but not in nIBC cells. By IHC, MARCKS expression and PTEN expression were negatively correlated in IBC samples and were associated with shorter MFS and longer MFS, respectively, in multivariate analysis. The combination of MARCKS-/PTEN+ protein status was associated with longer MFS in IBC patient only (p = 8.7 × 10−3), and mirrored the molecular profile (MARCKS-downregulated/PTEN-upregulated) of MPS-treated IBC cell lines. In conclusion, our results uncover a functional role of MARCKS implicated in IBC aggressiveness. Associated with the good-prognosis value of the MARCKS-/PTEN+ protein status that mirrors the molecular profile of MPS-treated IBC cell lines, our results suggest that MARCKS could be a potential therapeutic target in patients with MARCKS-positive IBC. Future preclinical studies using a larger panel of IBC cell lines, animal models and analysis of a larger series of clinical samples are warranted in order to validate our results. Full article
(This article belongs to the Special Issue Inflammatory Breast Cancer: Biology, Mechanisms, Diagnostics, and Therapeutics)
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11 pages, 3379 KiB  
Commentary
Proactive Immunotherapeutic Approaches against Inflammatory Breast Cancer May Improve Patient Outcomes
by Daniel Alonso-Miguel, Steven Fiering and Hugo Arias-Pulido
Cells 2022, 11(18), 2850; https://doi.org/10.3390/cells11182850 - 13 Sep 2022
Cited by 1 | Viewed by 3369
Abstract
Inflammatory breast cancer (IBC) is highly metastatic at the onset of the disease with no IBC-specific treatments, resulting in dismal patient survival. IBC treatment is a clear unmet clinical need. This commentary highlights findings from a recent seminal approach in which pembrolizumab, a [...] Read more.
Inflammatory breast cancer (IBC) is highly metastatic at the onset of the disease with no IBC-specific treatments, resulting in dismal patient survival. IBC treatment is a clear unmet clinical need. This commentary highlights findings from a recent seminal approach in which pembrolizumab, a checkpoint inhibitor against programmed cell death protein 1 (PD-1), was provided to a triple-negative IBC patient as a neoadjuvant immune therapy combined with anthracycline–taxane-based chemotherapy. We highlight the findings of the case report and offer a perspective on taking a proactive approach to deploy approved immune checkpoint inhibitors. On the basis of our recently published research study, we propose in situ vaccination with direct injection of immunostimulatory agents into the tumor as an option to improve outcomes safely, effectively, and economically for IBC patients. Full article
(This article belongs to the Special Issue Inflammatory Breast Cancer: Biology, Mechanisms, Diagnostics, and Therapeutics)
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