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Molecular Mechanism of Cancer Research and Therapies

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 31 May 2024 | Viewed by 4851

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Special Issue Editor

Prof. Dr. Hsiu-Hsi Chen

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Guest Editor

Institute of Epidemiology and Preventive Medicine, National Taiwan University, Room 533, No. 17 Xu-Zhou Rd, Taipei 100, Taiwan
Interests: inflammation; epidemiology; nutrition; colorectal cancer

Special Issue Information

Dear Colleagues,

With the advance in both genome-wide association studies (GWAS) and phenome-wide association studies (PHWAS), the era of evidence-based medicine has gradually shifted to that of personalized medicine or individually-tailored health care over the past two decades. Therefore, precision cancer preventive and therapeutic care cannot be overemphasized from the panorama of three levels of prevention (primary, secondary, and tertiary). To this end, it is imperative to elucidate the molecule-based mechanism of cancer research by providing a systematic framework constructed by a multistate disease process from carcinogenesis (occurrence), proliferation (progression), and prognosis (recurrence and survival) onto which a constellation of molecular profiles that are synthesized from both GWAS and PHWAS are mapped. The corresponding state-of-the art effective and cost-effective interventions and therapies can be guided by such a continuous spectrum of molecule-based multistate process to implement three level of prevention.

In this special issue, we first aim to provide an overview of the multistate disease process on which a string of state-speciifc molecule feastures are superimposed to elucidate the mechanism of cancer research trageting at different stages, embracing occurrence, progression, and progression of cancer. Following the synthesis science of combining a series of studies on molecular profiles associated with each stage of cancer development from literatures, the special issue further plan to propose precision preventive and therapeutic care paradigm in comparison with the conventional evidence-based one. Evaluation of this precision care model is also demonstrated by first using artificial intelligence with the machine learning methods and then the digital twin approach. The contexts of cancer include, to a greater extent, five major sites of cancers (including breast, colon &rectum, cervix, lung, and liver) and, to a lesser extent, other sites such as oral cavity. Data on molecular mechanisms or pathophysiology are essential, and papers that only contain clinical trials/data are not acceptable.

Potential topics include, but not limited to:

Molecular Profiles Associated with Multi-step Process of Cancer
Risk Prediciton Model for Multistate Cancer with Molecular Biomarkers
Synthetic Science for Occurrence, Progression, and Prognosis of Cancer Consolidated by the Molecule-guided Mechanisms
Precsion Preventive and Therapeutic Care Model for Cancer
Evaluating Precsion Cancer Care Model particularly preferred by but not limited to Artificial Intelligence (AI)

Prof. Dr. Hsiu-Hsi Chen
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

molecular mechanism
multistate model
cancer
precsion cancer care
preventive and therapeutic care

Published Papers (3 papers)

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Research

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8 pages, 1108 KiB

Open AccessArticle

BRAF Mutations in Patients with Myeloid Neoplasms: A Cancer Center Multigene Next-Generation Sequencing Analysis Experience

by Fei Fei, Caitlin Caporale, Lisa Chang, Barbara K. Fortini, Haris Ali, Diana Bell, Anthony Stein, Guido Marcucci, Milhan Telatar and Michelle Afkhami

Int. J. Mol. Sci. 2024, 25(10), 5183; https://doi.org/10.3390/ijms25105183 - 9 May 2024

Viewed by 363

Abstract

BRAF mutations are rare in myeloid neoplasms and are reported to be associated with poor treatment outcomes. The purpose of our study is to characterize BRAF mutations in myeloid neoplasms using a next-generation sequencing (NGS) panel based on the experiences of a single cancer center. We conducted a retrospective review of patients with myeloid neoplasms who underwent the HopeSeq studies between January 2018 and September 2023. A total of 14 patients with myeloid neoplasms carrying BRAF mutations were included in our cohort. The clinical, pathological, and molecular features of these patients were investigated. Our study indicates that BRAF mutations are rare in myeloid neoplasms, constituting only 0.53% (14/2632) of all myeloid neoplasm cases, with the most common BRAF mutation being BRAF V600E (4/14; 28.6%). Interestingly, we observed that six out of seven patients with acute myeloid leukemia (AML) exhibited AML with monocytic differentiation, and all the patients with AML exhibited an extremely poor prognosis compared to those without BRAF mutations. TET2 (5/14; 35.7%), ASXL1 (4/14; 28.6%), and JAK2 (4/14; 28.6%) were the three most frequently co-mutated genes in these patients. Moreover, we noted concurrent KMT2A gene rearrangement with BRAF mutations in three patients with AML (3/7; 42.9%). Our study suggests that although BRAF mutations are rare in myeloid neoplasms, they play a crucial role in the pathogenesis of specific AML subtypes. Furthermore, RAS pathway alterations, including BRAF mutations, are associated with KMT2A gene rearrangement in AML. However, these findings warrant further validation in larger studies. Full article

(This article belongs to the Special Issue Molecular Mechanism of Cancer Research and Therapies)

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15 pages, 10141 KiB

Open AccessArticle

Does Diffusely Infiltrating Lobular Carcinoma of the Breast Arise from Epithelial–Mesenchymal Hybrid Cells?

by László Tabár, Renáta Bozó, Peter B. Dean, Katalin Ormándi, Olga Puchkova, Orsolya Oláh-Németh, István Balázs Németh, Zoltán Veréb, Ming-Fang Yen, Li-Sheng Chen, Hsiu-Hsi Chen and András Vörös

Int. J. Mol. Sci. 2023, 24(13), 10752; https://doi.org/10.3390/ijms241310752 - 28 Jun 2023

Cited by 5 | Viewed by 1541

Abstract

Classic diffusely infiltrating lobular carcinoma has imaging features divergent from the breast cancers originating from the terminal ductal lobular units and from the major lactiferous ducts. Although the term “invasive lobular carcinoma” implies a site of origin within the breast lobular epithelium, we were unable to find evidence supporting this assumption. Exceptional excess of fibrous connective tissue and the unique cell architecture combined with the aberrant features at breast imaging suggest that this breast malignancy has not originated from cells lining the breast ducts and lobules. The only remaining relevant component of the fibroglandular tissue is the mesenchyme. The cells freshly isolated and cultured from diffusely infiltrating lobular carcinoma cases contained epithelial–mesenchymal hybrid cells with both epithelial and mesenchymal properties. The radiologic and histopathologic features of the tumours and expression of the mesenchymal stem cell positive markers CD73, CD90, and CD105 all suggest development in the direction of mesenchymal transition. These hybrid cells have tumour-initiating potential and have been shown to have poor prognosis and resistance to therapy targeted for malignancies of breast epithelial origin. Our work emphasizes the need for new approaches to the diagnosis and therapy of this highly fatal breast cancer subtype. Full article

(This article belongs to the Special Issue Molecular Mechanism of Cancer Research and Therapies)

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Review

Jump to: Research

16 pages, 591 KiB

Open AccessReview

The Mechanism of DNA Methylation and miRNA in Breast Cancer

by Lingyuan Ma, Chenyu Li, Hanlin Yin, Jiashu Huang, Shenghao Yu, Jin Zhao, Yongxu Tang, Min Yu, Jie Lin, Lei Ding and Qinghua Cui

Int. J. Mol. Sci. 2023, 24(11), 9360; https://doi.org/10.3390/ijms24119360 - 27 May 2023

Cited by 6 | Viewed by 2467

Abstract

Breast cancer is the most prevalent cancer in the world. Currently, the main treatments for breast cancer are radiotherapy, chemotherapy, targeted therapy and surgery. The treatment measures for breast cancer depend on the molecular subtype. Thus, the exploration of the underlying molecular mechanisms and therapeutic targets for breast cancer remains a hotspot in research. In breast cancer, a high level of expression of DNMTs is highly correlated with poor prognosis, that is, the abnormal methylation of tumor suppressor genes usually promotes tumorigenesis and progression. MiRNAs, as non-coding RNAs, have been identified to play key roles in breast cancer. The aberrant methylation of miRNAs could lead to drug resistance during the aforementioned treatment. Therefore, the regulation of miRNA methylation might serve as a therapeutic target in breast cancer. In this paper, we reviewed studies on the regulatory mechanisms of miRNA and DNA methylation in breast cancer from the last decade, focusing on the promoter region of tumor suppressor miRNAs methylated by DNMTs and the highly expressed oncogenic miRNAs inhibited by DNMTs or activating TETs. Full article

(This article belongs to the Special Issue Molecular Mechanism of Cancer Research and Therapies)

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