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Cancers
Special Issues
Hormone-Associated Cancers
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Hormone-Associated Cancers

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: closed (31 October 2021) | Viewed by 20633

Special Issue Editors

Prof. Dr. Robert Clarke

E-Mail Website
Guest Editor
The Hormel Institute, University of Minnesota, Minneapolis, MN 55455, USA
Interests: breast cancer; systems biology; molecular endocrinology; endocrine resistance
Dr. Surojeet Sengupta

E-Mail Website
Guest Editor
Department of Oncology, Georgetown-Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington D.C., USA

Special Issue Information

Dear Colleagues,

Hormone-associated cancers are among the most prevalent cancers in both women and men. For example, there will be almost 270,000 new cases of breast cancer diagnosed in the USA in 2019, and over 41,500 women will die from breast cancer—an average of one about every 13 minutes. In women, breast cancer is the most prevalent cancer, and it is second only to lung cancer as the most common cause of cancer mortality. For ovarian cancer, there will be over 22,500 new cases and almost 14,000 deaths; the numbers for endometrial cancer are 13,000 and over 4000, respectively. A total of 175,000 new cases of prostate cancer will be diagnosed, and almost 42,000 men will die from this disease in the USA in 2019. For testicular cancer, 10,000 new cases and over 400 deaths are anticipated in the USA during 2019. Steroid hormone receptors and their ligands are often actionable and effective molecular targets for these cancers. For example, endocrine therapies significantly reduce overall mortality and improve progression-free survival in breast and prostate cancers. Indeed, endocrine-based interventions for these cancers were among the first personalized medicine approaches applied and have been the standard of care for several decades. Despite the many advances, therapy-refractory and advanced diseases remain difficult to manage, and metastatic disease is almost invariably lethal. The inability to cure these cancers reflects an incomplete understanding of the endocrine biology, endocrine immunobiology, and drug resistance mechanisms intrinsic and extrinsic to these tumors. The Special Issue entitled “Hormone-Associated Cancers” will explore advances in basic, translational, and clinical research across a spectrum of cancers that exhibit endocrine regulation.

Prof. Dr. Robert Clarke
Dr. Surojeet Sengupta
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 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. Cancers 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 2900 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

  • hormones
  • growth factors
  • cancer immunology
  • drug sensitivity and resistance
  • molecular signaling
  • invasion
  • metastasis
  • clinical outcomes

Published Papers (5 papers)

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Research

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13 pages, 26713 KiB  
Article
Identification of BXDC2 as a Key Downstream Effector of the Androgen Receptor in Modulating Cisplatin Sensitivity in Bladder Cancer
by Guiyang Jiang, Yuki Teramoto, Takuro Goto, Taichi Mizushima, Satoshi Inoue, Hiroki Ide, Yujiro Nagata, Eiji Kashiwagi, Alexander S. Baras, George J. Netto, Zhiming Yang and Hiroshi Miyamoto
Cancers 2021, 13(5), 975; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13050975 - 26 Feb 2021
Cited by 11 | Viewed by 1721
Abstract
Underlying mechanisms for resistance to cisplatin-based chemotherapy in bladder cancer patients are largely unknown, although androgen receptor (AR) activity, as well as extracellular signal-regulated kinase (ERK) signaling, has been indicated to correlate with chemosensitivity. We also previously showed ERK activation by androgen treatment [...] Read more.
Underlying mechanisms for resistance to cisplatin-based chemotherapy in bladder cancer patients are largely unknown, although androgen receptor (AR) activity, as well as extracellular signal-regulated kinase (ERK) signaling, has been indicated to correlate with chemosensitivity. We also previously showed ERK activation by androgen treatment in AR-positive bladder cancer cells. Because our DNA microarray analysis in control vs. AR-knockdown bladder cancer lines identified BXDC2 as a potential downstream target of AR, we herein assessed its functional role in cisplatin sensitivity, using bladder cancer lines and surgical specimens. BXDC2 protein expression was considerably downregulated in AR-positive or cisplatin-resistant cells. BXDC2-knockdown sublines were significantly more resistant to cisplatin, compared with respective controls. Without cisplatin treatment, BXDC2-knockdown resulted in significant increases/decreases in cell proliferation/apoptosis, respectively. An ERK activator was also found to reduce BXDC2 expression. Immunohistochemistry showed downregulation of BXDC2 expression in tumor (vs. non-neoplastic urothelium), higher grade/stage tumor (vs. lower grade/stage), and AR-positive tumor (vs. AR-negative). Patients with BXDC2-positive/AR-negative muscle-invasive bladder cancer had a significantly lower risk of disease-specific mortality, compared to those with a BXDC2-negative/AR-positive tumor. Additionally, in those undergoing cisplatin-based chemotherapy, BXDC2 positivity alone (p = 0.083) or together with AR negativity (p = 0.047) was associated with favorable response. We identified BXDC2 as a key molecule in enhancing cisplatin sensitivity. AR-ERK activation may thus be associated with chemoresistance via downregulating BXDC2 expression in bladder cancer. Full article
(This article belongs to the Special Issue Hormone-Associated Cancers)
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23 pages, 3515 KiB  
Article
A Comprehensive Molecular and Clinical Analysis of the piRNA Pathway Genes in Ovarian Cancer
by Eunice Lee, Noor A. Lokman, Martin K. Oehler, Carmela Ricciardelli and Frank Grutzner
Cancers 2021, 13(1), 4; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13010004 - 22 Dec 2020
Cited by 3 | Viewed by 3124
Abstract
Ovarian cancer (OC) is one of the most lethal gynecological malignancies, yet molecular mechanisms underlying its origin and progression remain poorly understood. With increasing reports of piRNA pathway deregulation in various cancers, we aimed to better understand its role in OC through a [...] Read more.
Ovarian cancer (OC) is one of the most lethal gynecological malignancies, yet molecular mechanisms underlying its origin and progression remain poorly understood. With increasing reports of piRNA pathway deregulation in various cancers, we aimed to better understand its role in OC through a comprehensive analysis of key genes: PIWIL1-4, DDX4, HENMT1, MAEL, PLD6, TDRD1,9 and mutants of PIWIL1 (P1∆17) and PIWIL2 (PL2L60). High-throughput qRT-PCR (n = 45) and CSIOVDB (n = 3431) showed differential gene expression when comparing benign ovarian tumors, low grade OC and high grade serous OC (HGSOC). Significant correlation of disparate piRNA pathway gene expression levels with better progression free, post-progression free and overall survival suggests a complex role of this pathway in OC. We discovered PIWIL3 expression in chemosensitive but not chemoresistant primary HGSOC cells, providing a potential target against chemoresistant disease. As a first, we revealed that follicle stimulating hormone increased PIWIL2 expression in OV-90 cells. PIWIL1, P1∆17, PIWIL2, PL2L60 and MAEL overexpression in vitro and in vivo decreased motility and invasion of OVCAR-3 and OV-90 cells. Interestingly, P1∆17 and PL2L60, induced increased motility and invasion compared to PIWIL1 and PIWIL2. Our results in HGSOC highlight the intricate role piRNA pathway genes play in the development of malignant neoplasms. Full article
(This article belongs to the Special Issue Hormone-Associated Cancers)
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9 pages, 902 KiB  
Article
Fertility Sparing Treatment of Endometrial Cancer with and without Initial Infiltration of Myometrium: A Single Center Experience
by Paolo Casadio, Mariangela La Rosa, Andrea Alletto, Giulia Magnarelli, Alessandro Arena, Enrico Fontana, Matilde Fabbri, Kevin Giovannico, Agnese Virgilio, Diego Raimondo, Francesca Guasina, Roberto Paradisi and Renato Seracchioli
Cancers 2020, 12(12), 3571; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers12123571 - 29 Nov 2020
Cited by 39 | Viewed by 2644
Abstract
Endometrial cancer (EC) is the fourth largest female cancer in Europe and North America. In 5% of cases, the diagnosis is made in women who wish to become pregnant. In our retrospective study, we reported our experience about fertility sparing treatment of G1 [...] Read more.
Endometrial cancer (EC) is the fourth largest female cancer in Europe and North America. In 5% of cases, the diagnosis is made in women who wish to become pregnant. In our retrospective study, we reported our experience about fertility sparing treatment of G1 endometrioid endometrial cancer (G1 EEC) or atypical endometrial hyperplasia/endometrial intraepithelial neoplasm (AEH/EIN) in young women desiring pregnancy treated in our Center. Conservative treatment was based on operative hysteroscopy and hormone therapy with megestrol acetate (160 mg/die for 9 months). For the first time we included women with G1 EEC with minimal myometrial infiltration. The minimum follow-up period was two years and consisted of serial outpatient hysteroscopies with endometrial biopsies. Among the 36 women with G1 EEC we observed one case of disease persistence and four recurrences and four recurrences among the 46 women diagnosed with AEH/EIN. To date, 35 live births were obtained in both groups. Our results advance the hypothesis that conservative treatment can represent a safe and feasible alternative to propose to young women with desire for pregnancy. Further randomized and multicentric studies are needed to arrive at unambiguous and standardized guidelines on the surgical and medical treatment of young women with EEC or AEH/EIN. Full article
(This article belongs to the Special Issue Hormone-Associated Cancers)
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18 pages, 7700 KiB  
Article
Hormonal Receptor Status Determines Prognostic Significance of FGFR2 in Invasive Breast Carcinoma
by Marcin Braun, Dominika Piasecka, Bartlomiej Tomasik, Kamil Mieczkowski, Konrad Stawiski, Aleksandra Zielinska, Janusz Kopczynski, Dariusz Nejc, Radzislaw Kordek, Rafal Sadej and Hanna M. Romanska
Cancers 2020, 12(9), 2713; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers12092713 - 22 Sep 2020
Cited by 8 | Viewed by 4209
Abstract
Interaction between fibroblast growth factor receptor 2 (FGFR2) and estrogen/progesterone receptors (ER/PR) affects resistance to anti-ER therapies, however the prognostic value of FGFR2 in breast cancer (BCa) remains largely unexplored. We have recently showed in vitro that FGFR2-mediated signaling alters PR activity and [...] Read more.
Interaction between fibroblast growth factor receptor 2 (FGFR2) and estrogen/progesterone receptors (ER/PR) affects resistance to anti-ER therapies, however the prognostic value of FGFR2 in breast cancer (BCa) remains largely unexplored. We have recently showed in vitro that FGFR2-mediated signaling alters PR activity and response to anti-ER treatment. Herein, prognostic significance of FGFR2 in BCa was evaluated in relation to both ER/PR protein status and a molecular signature designed to reflect PR transcriptional activity. FGFR2 was examined in 353 BCa cases using immunohistochemistry and Nanostring-based RNA quantification. FGFR2 expression was higher in ER+PR+ and ER+PR- compared to ER−PR− cases (p < 0.001). Low FGFR2 was associated with higher grade (p < 0.001), higher Ki67 proliferation index (p < 0.001), and worse overall and disease-free survival (HR = 2.34 (95% CI: 1.26–4.34), p = 0.007 and HR = 2.22 (95% CI: 1.25–3.93), p = 0.006, respectively). The poor prognostic value of low FGFR2 was apparent in ER+PR+, but not in ER+PR− patients, and it did not depend on the expression level of PR-dependent genes. Despite the functional link between FGFR2 and ER/PR revealed by preclinical studies, the data showed a link between FGFR2 expression and poor prognosis in BCa patients. Full article
(This article belongs to the Special Issue Hormone-Associated Cancers)
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Review

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20 pages, 1641 KiB  
Review
Nexus between PI3K/AKT and Estrogen Receptor Signaling in Breast Cancer
by Aditi S. Khatpe, Adedeji K. Adebayo, Christopher A. Herodotou, Brijesh Kumar and Harikrishna Nakshatri
Cancers 2021, 13(3), 369; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13030369 - 20 Jan 2021
Cited by 34 | Viewed by 8067
Abstract
Signaling from estrogen receptor alpha (ERα) and its ligand estradiol (E2) is critical for growth of ≈70% of breast cancers. Therefore, several drugs that inhibit ERα functions have been in clinical use for decades and new classes of anti-estrogens are continuously being developed. [...] Read more.
Signaling from estrogen receptor alpha (ERα) and its ligand estradiol (E2) is critical for growth of ≈70% of breast cancers. Therefore, several drugs that inhibit ERα functions have been in clinical use for decades and new classes of anti-estrogens are continuously being developed. Although a significant number of ERα+ breast cancers respond to anti-estrogen therapy, ≈30% of these breast cancers recur, sometimes even after 20 years of initial diagnosis. Mechanism of resistance to anti-estrogens is one of the intensely studied disciplines in breast cancer. Several mechanisms have been proposed including mutations in ESR1, crosstalk between growth factor and ERα signaling, and interplay between cell cycle machinery and ERα signaling. ESR1 mutations as well as crosstalk with other signaling networks lead to ligand independent activation of ERα thus rendering anti-estrogens ineffective, particularly when treatment involved anti-estrogens that do not degrade ERα. As a result of these studies, several therapies that combine anti-estrogens that degrade ERα with PI3K/AKT/mTOR inhibitors targeting growth factor signaling or CDK4/6 inhibitors targeting cell cycle machinery are used clinically to treat recurrent ERα+ breast cancers. In this review, we discuss the nexus between ERα-PI3K/AKT/mTOR pathways and how understanding of this nexus has helped to develop combination therapies. Full article
(This article belongs to the Special Issue Hormone-Associated Cancers)
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