Hormones and Tumors
A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".
Deadline for manuscript submissions: 31 March 2025 | Viewed by 202
Special Issue Editors
Interests: breast cancer; chemoresistance; molecular biology; prostate cancer; tumor microenvironment
Interests: endocrine-related tumor; enzyme; hormone action; pathology; receptor
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
It is well known that hormones contribute immensely not only to normal tissue/cell functions but also to the development of various disorders. Tumors arising from endocrine organs and neuroendocrine neoplasms produce active hormones and cause various clinical symptoms. Endocrine-related cancers such as breast and prostate cancers are common malignant neoplasms worldwide, and hormones are locally produced and act in cancer tissues. In recent years, new techniques have been developed to visualize hormonal dynamics, and new light is being shed on the diagnosis of endocrine-related tumors. Moreover, a detailed investigation of hormonal actions will lead to the development of a new therapeutic strategy for endocrine-related tumors. This Special Issue will be reviewed by experts in this field and encompass new research articles and timely reviews regarding hormones and tumors.
Prof. Dr. Kiyoshi Takagi
Prof. Dr. Takashi Suzuki
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 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. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.
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Keywords
- diagnosis
- hormone
- prognosis
- progression
- therapy
- tumor
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Planned Papers
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Title: Discoidin Domain Receptor 2 contributes to breast cancer progression and chemoresistance by interacting with collagen type I
Authors: Ai Sato; Kiyoshi Takagi; Momoka Yoshida; Mio Yamaguchi-Tanaka; Mikoto Sagehashi; Yasuhiro Miki; Minoru Miyashita; Takashi Suzuki
Affiliation: Department of Pathology and Histotechnology, Tohoku University Graduate School of Medicine, Sendai, Japan
Abstract: Background: Chemoresistance is an important issue to be solved in breast cancer. It is well known that the content and morphology of collagens in tumor tissues are drastically altered following chemotherapy, and discoidin domain receptor 2 (DDR2) is a unique type of receptor tyrosine kinases activated by collagens, playing important roles in human malignancies. However, the contribution to the chemoresistance of DDR2 in terms of the association with collagens remains largely unclear in breast cancer. Methods: We immunolocalized DDR2 and collagen type I in 224 breast cancer tissues and subsequently conducted in vitro studies to confirm the role of DDR2 in breast cancer chemoresistance using chemo-sensitive and chemo-resistant cell lines. Results: DDR2 immunoreactivity was positively correlated with aggressive behaviors of breast cancer and was significantly associated with increased risk of recurrence, especially in those who received chemotherapy. Moreover, in vitro experiments demonstrated that DDR2 promoted the proliferative activity of breast cancer cells, and cell viability was significantly maintained by DDR2 overexpression cells compared to control cells in the presence of Epirubicin. Conclusion: These data suggested that DDR2 could be a poor prognostic factor associated with cell proliferation and chemotherapy resistance in human breast cancer.
