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Personalized Treatment Strategy in Early Breast Cancer
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Personalized Treatment Strategy in Early Breast Cancer

A special issue of Journal of Personalized Medicine (ISSN 2075-4426). This special issue belongs to the section "Mechanisms of Diseases".

Deadline for manuscript submissions: closed (31 July 2022) | Viewed by 6487

Special Issue Editor

Dr. Giovanni Tazzioli

E-Mail Website
Guest Editor
Oncologic Breast Surgery Unit, Department of Medical and Surgical Sciences for Mother, Child and Adult, University of Modena and Reggio Emilia, Azienda Ospedaliero-Universitaria Policlinico, 41125 Modena, Italy
Interests: breast cancer surgery; nutrigenetics; biomarkers; genomic risk profile

Special Issue Information

Dear Colleagues,

Treatment for early breast cancer usually involves a combination of surgery, radiation therapy, chemotherapy, hormone therapy, and/or HER2-targeted therapy based on the breast cancer subtype. Neoadjuvant therapy (chemotherapy, HER2-targeted therapy, or endocrine therapy) is a well-known treatment strategy mainly in cases of locally advanced tumor, as well as triple-negative or HER2 positive breast cancer. The timing of chemotherapy around surgery does not affect survival outcome, but it is well known that patients who achieve a complete pathological response have better long-term outcomes. Moreover, neoadjuvant chemotherapy is an optimal setting for studying both breast cancer biology and the upcoming drug resistance due to the pressure of therapies. Finally, based on tumor response to preoperative therapy, adjuvant treatment can be tailored for every patient. In fact, the optimal therapeutic algorithms, including the type of drugs to administer, the duration of the treatment, and the ideal local treatment, are still unclear. This Special Issue will highlight the current state of the art in neoadjuvant treatment of breast cancer and will focus on the possibility of tailoring the best treatment strategy for every patient based on tumor biology and/or patients’ characteristics.

Dr. Giovanni Tazzioli
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. Journal of Personalized Medicine 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

  • breast cancer 
  • neoadjuvant chemotherapy 
  • HER2 positive breast cancer 
  • radiotherapy 
  • breast cancer surgery 
  • primary endocrine therapy

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Published Papers (2 papers)

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Research

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13 pages, 983 KiB  
Article
A Novel Surrogate Nomogram Capable of Predicting OncotypeDX Recurrence Score©
by Matthew G. Davey, Amirhossein Jalali, Éanna J. Ryan, Ray P. McLaughlin, Karl J. Sweeney, Michael K. Barry, Carmel M. Malone, Maccon M. Keane, Aoife J. Lowery, Nicola Miller and Michael J. Kerin
J. Pers. Med. 2022, 12(7), 1117; https://doi.org/10.3390/jpm12071117 - 8 Jul 2022
Cited by 2 | Viewed by 2307
Abstract
Background: OncotypeDX Recurrence Score© (RS) is a commercially available 21-gene expression assay which estimates prognosis and guides chemoendocrine prescription in early-stage estrogen-receptor positive, human epidermal growth factor receptor-2-negative (ER+/HER2−) breast cancer. Limitations of RS testing include the cost and turnaround time of several [...] Read more.
Background: OncotypeDX Recurrence Score© (RS) is a commercially available 21-gene expression assay which estimates prognosis and guides chemoendocrine prescription in early-stage estrogen-receptor positive, human epidermal growth factor receptor-2-negative (ER+/HER2−) breast cancer. Limitations of RS testing include the cost and turnaround time of several weeks. Aim: Our aim is to develop a user-friendly surrogate nomogram capable of predicting RS. Methods: Multivariable linear regression analyses were performed to determine predictors of RS and RS > 25. Receiver operating characteristic analysis produced an area under the curve (AUC) for each model, with training and test sets were composed of 70.3% (n = 315) and 29.7% (n = 133). A dynamic, user-friendly nomogram was built to predict RS using R (version 4.0.3). Results: 448 consecutive patients who underwent RS testing were included (median age: 58 years). Using multivariable regression analyses, postmenopausal status (β-Coefficient: 0.25, 95% confidence intervals (CIs): 0.03–0.48, p = 0.028), grade 3 disease (β-Coefficient: 0.28, 95% CIs: 0.03–0.52, p = 0.026), and estrogen receptor (ER) score (β-Coefficient: −0.14, 95% CIs: −0.22–−0.06, p = 0.001) all independently predicted RS, with AUC of 0.719. Using multivariable regression analyses, grade 3 disease (odds ratio (OR): 5.67, 95% CIs: 1.32–40.00, p = 0.037), decreased ER score (OR: 1.33, 95% CIs: 1.02–1.66, p = 0.050) and decreased progesterone receptor score (OR: 1.16, 95% CIs: 1.06–1.25, p = 0.002) all independently predicted RS > 25, with AUC of 0.740 for the static and dynamic online nomogram model. Conclusions: This study designed and validated an online user-friendly nomogram from routinely available clinicopathological parameters capable of predicting outcomes of the 21-gene RS expression assay. Full article
(This article belongs to the Special Issue Personalized Treatment Strategy in Early Breast Cancer)
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Review

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12 pages, 586 KiB  
Review
Kinesin Family Member C1 (KIFC1/HSET): A Potential Actionable Biomarker of Early Stage Breast Tumorigenesis and Progression of High-Risk Lesions
by Nikita Wright, Zhihong Gong, Rick Kittles, Rama Natarajan, Tijana Jovanovic-Talisman, Padmashree Rida, Mark LaBarge and Victoria Seewaldt
J. Pers. Med. 2021, 11(12), 1361; https://doi.org/10.3390/jpm11121361 - 14 Dec 2021
Cited by 7 | Viewed by 3628
Abstract
The enigma of why some premalignant or pre-invasive breast lesions transform and progress while others do not remains poorly understood. Currently, no radiologic or molecular biomarkers exist in the clinic that can successfully risk-stratify high-risk lesions for malignant transformation or tumor progression as [...] Read more.
The enigma of why some premalignant or pre-invasive breast lesions transform and progress while others do not remains poorly understood. Currently, no radiologic or molecular biomarkers exist in the clinic that can successfully risk-stratify high-risk lesions for malignant transformation or tumor progression as well as serve as a minimally cytotoxic actionable target for at-risk subpopulations. Breast carcinogenesis involves a series of key molecular deregulatory events that prompt normal cells to bypass tumor-suppressive senescence barriers. Kinesin family member C1 (KIFC1/HSET), which confers survival of cancer cells burdened with extra centrosomes, has been observed in premalignant and pre-invasive lesions, and its expression has been shown to correlate with increasing neoplastic progression. Additionally, KIFC1 has been associated with aggressive breast tumor molecular subtypes, such as basal-like and triple-negative breast cancers. However, the role of KIFC1 in malignant transformation and its potential as a predictive biomarker of neoplastic progression remain elusive. Herein, we review compelling evidence suggesting the involvement of KIFC1 in enabling pre-neoplastic cells to bypass senescence barriers necessary to become immortalized and malignant. We also discuss evidence inferring that KIFC1 levels may be higher in premalignant lesions with a greater inclination to transform and acquire aggressive tumor intrinsic subtypes. Collectively, this evidence provides a strong impetus for further investigation into KIFC1 as a potential risk-stratifying biomarker and minimally cytotoxic actionable target for high-risk patient subpopulations. Full article
(This article belongs to the Special Issue Personalized Treatment Strategy in Early Breast Cancer)
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