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Special Issue "Molecular and Cellular Mechanisms of Cancers: Breast Cancer"
A special issue of Cells (ISSN 2073-4409).
Deadline for manuscript submissions: closed (31 January 2020).
Breast cancer is a molecularly diverse disease which involves complex processes that result in initiation, progression, and metastasis. Traditionally, breast cancers are categorized into three major subgroups. These include the luminal subtype with hormone receptor positivity (HR+), the oncogene HER2 subtype (HER2+), and the triple-negative, basal subtype that lacks hormone receptors and HER2. Lately, additional subtypes within these broad categories have emerged. Together with the discovery of additional driver genes and their mutant variants, they underscore complex molecular mechanisms and pathways of breast carcinogenesis. There is an increasing realization that many oncogenes that control carcinogenesis exert profound effects on malignant transformation and distant metastases. Moreover, mutations in driver oncogenes, such as gene amplification and mutations and concomitant dysregulation of apoptotic pathways, often contribute to the emergence of resistant phenotypes that consequently affect the efficacy of current therapies and patient survival. Therefore, the targeting of such drivers and their downstream, oncogenic signaling nodes have been rationally pursued for many cancers, including breast cancers. For example, endocrine therapies or HER2 targeting have provided clinical benefits for treating luminal or HER2-positive subtypes of breast cancers, respectively. Additional, molecular mechanism-based targeted therapeutics have recently emerged. These include inhibitors of DNA repair PARP protein in a subset of a BRCA-mutant basal breast cancer subtype, or CDK4/6 inhibitors for HR+ HER2- advanced breast cancers. Although a novel class of immune check-point inhibitors have been approved for clinical use in many cancers, a number of clinical trials are currently underway to assess the potential therapeutic use of current immune check-point inhibitors as monotherapies or in combination with other targeted therapies in breast cancers. The primary focus of this topic will be cell signaling in cancer growth and survival, and current and novel strategies to target oncogenic drivers and their downstream signaling nodes. In addition, the reviews and research articles will explore the mechanisms of carcinogenesis and the ways in which tumor cells modulate these processes to optimize their survival and examine current clinical modalities aimed at exploiting these oncogenic targets to selectively inhibit tumor cells.
Prof. Arun K. Rishi
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 papers will be 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 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 2000 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.
- growth and survival
- receptor signaling
- signal transduction nodes: MAPKs, NF-kB
- tumor metabolism
- immune check-point signaling
- epithelial-to-mesenchymal transition