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Cancer Prevention with Molecular Target Therapies 2.0
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Cancer Prevention with Molecular Target Therapies 2.0

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: closed (31 March 2022) | Viewed by 28588

Special Issue Editor

Dr. Laura Paleari

E-Mail Website
Guest Editor
Research, Innovation and HTA Unit, (A.Li.Sa.) Liguria Health Authority, 16121 Genoa, Italy
Interests: cancer prevention; molecular biology; drug repurposing; health technology assessment; pharmacoeconomics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Personalized medicine is playing an important role in cancer prevention. To date, it is clear that many cancers are molecularly distinct subtypes, and different therapeutic approaches would be required for each. Indeed, the identification of cancer susceptibility genes permits identifying patients “at risk” of developing neoplasia and supports modifying individual risk behaviors or the choice of preventive therapy. Additionally, the efficacy of various targeted therapies in different cancer subtypes suggests that treatment choices in a near future will be more and more centered on molecular signatures. Data from preclinical, clinical, and observational studies have revealed the ability to prevent cancer development for compounds with different indications than cancer. The concept of drug repurposing permits combinations that can target several critical pathways of a specific disease, decreasing the risk of resistance observed when using single agent targeted therapy.

This open-access Special Issue will bring together original research and review articles on molecular oncology with attention to early detection and prevention of cancer. It highlights new findings, methods, and technical advances in molecular cancer research. The main feature of this Special Issue is to provide an open-source sharing of significant works in the field of molecular oncology that can increase our understanding of cancer development, which may lead to the discovery of new molecular diagnostic technologies and targeted therapeutics.

Topics include but are not limited to:
1—Molecular methods to personalize cancer screening and detection;
2—Molecular target therapies to prevent cancer development and metastases;
3—Identification and new aspects of cellular signaling molecules and pathways for target discovery, drug design, and personalized and gender medicine;
4—Drug repurposing for cancer prevention;
5—Molecular modeling studies.

Dr. Laura Paleari
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

  • Cancer prevention
  • Target therapy
  • Personalized screening
  • Drug repurposing
  • Target discovery

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Published Papers (6 papers)

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Editorial

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2 pages, 165 KiB  
Editorial
Cancer Prevention with Molecular Targeted Therapies
by Laura Paleari
Int. J. Mol. Sci. 2022, 23(15), 8429; https://doi.org/10.3390/ijms23158429 - 29 Jul 2022
Cited by 2 | Viewed by 1456
Abstract
Today, the oncologist is like a detective of the human body who, instead of a magnifying glass, uses the new tools of molecular pathology to search not only for genes or molecular targets, to be targeted with innovative anticancer therapies, but also molecular [...] Read more.
Today, the oncologist is like a detective of the human body who, instead of a magnifying glass, uses the new tools of molecular pathology to search not only for genes or molecular targets, to be targeted with innovative anticancer therapies, but also molecular alterations that allow the identification of population groups at risk of developing tumors for preventive purposes [...] Full article
(This article belongs to the Special Issue Cancer Prevention with Molecular Target Therapies 2.0)

Research

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14 pages, 2268 KiB  
Article
A Presurgical Study of Curcumin Combined with Anthocyanin Supplements in Patients with Colorectal Adenomatous Polyps
by Irene Maria Briata, Laura Paleari, Mariangela Rutigliani, Marilena Petrera, Silvia Caviglia, Paola Romagnoli, Mauro Dalla Libera, Massimo Oppezzi, Matteo Puntoni, Giacomo Siri, Matteo Lazzeroni, Lynne Howells, Raj Singh, Karen Brown and Andrea DeCensi
Int. J. Mol. Sci. 2021, 22(20), 11024; https://doi.org/10.3390/ijms222011024 - 13 Oct 2021
Cited by 19 | Viewed by 2848
Abstract
Adenomatous polyps are precancerous lesions associated with a higher risk of colorectal cancer (CRC). Curcumin and anthocyanins have shown promising CRC-preventive activity in preclinical and epidemiological studies. The objective of this window-of-opportunity, proof-of principle trial was to evaluate the effect of curcumin combined [...] Read more.
Adenomatous polyps are precancerous lesions associated with a higher risk of colorectal cancer (CRC). Curcumin and anthocyanins have shown promising CRC-preventive activity in preclinical and epidemiological studies. The objective of this window-of-opportunity, proof-of principle trial was to evaluate the effect of curcumin combined with anthocyanin supplements on tissue biomarkers of colorectal adenomatous polyps. Eligible patients received either anthocyanin and curcumin supplementation or related matching placebo for 4–6 weeks before polyp removal. Adenomatous polyps and adjacent tissue biopsies were collected at baseline and after supplementation for immunohistochemical assessment of β-catenin, NF-kappa B (NF-κB), Ki-67, P53, and dysplasia. No differences were observed in baseline biomarker expression between normal and dysplastic tissues. The combination of anthocyanins and curcumin resulted in a significant borderline reduction of NF-κB immunohistochemistry (IHC) expression in adenoma tissue (geometric mean ratio (GMR): 0.72; 95% confidence interval (CI): 0.51–1.00; p-value: 0.05) and a trend to a reduction of Ki-67 (GMR: 0.73; 95% CI: 0.50–1.08; p-value: 0.11). No significant modulation of biomarkers in normal adjacent mucosa was observed. We concluded that the combined supplementation of anthocyanins and curcumin seems to lead to a potentially favorable modulation of tissue biomarkers of inflammation and proliferation in colon adenomas. Full article
(This article belongs to the Special Issue Cancer Prevention with Molecular Target Therapies 2.0)
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23 pages, 14247 KiB  
Article
Disulfiram Sensitizes a Therapeutic-Resistant Glioblastoma to the TGF-β Receptor Inhibitor
by Chan-Chuan Liu, Cheng-Lin Wu, Meng-Xuan Lin, Chun-I Sze and Po-Wu Gean
Int. J. Mol. Sci. 2021, 22(19), 10496; https://doi.org/10.3390/ijms221910496 - 28 Sep 2021
Cited by 13 | Viewed by 2989
Abstract
Despite neurosurgery following radiation and chemotherapy, residual glioblastoma (GBM) cells develop therapeutic resistance (TR) leading to recurrence. The GBM heterogeneity confers TR. Therefore, an effective strategy must target cancer stem cells (CSCs) and other malignant cancer cells. TGF-β and mesenchymal transition are the [...] Read more.
Despite neurosurgery following radiation and chemotherapy, residual glioblastoma (GBM) cells develop therapeutic resistance (TR) leading to recurrence. The GBM heterogeneity confers TR. Therefore, an effective strategy must target cancer stem cells (CSCs) and other malignant cancer cells. TGF-β and mesenchymal transition are the indicators for poor prognoses. The activity of aldehyde dehydrogenases (ALDHs) is a functional CSC marker. However, the interplay between TGF-β and ALDHs remains unclear. We developed radiation-resistant and radiation-temozolomide-resistant GBM models to investigate the underlying mechanisms conferring TR. Galunisertib is a drug targeting TGF-β receptors. Disulfiram (DSF) is an anti-alcoholism drug which functions by inhibiting ALDHs. The anti-tumor effects of combining DSF and Galunisertib were evaluated by in vitro cell grow, wound healing, Transwell assays, and in vivo orthotopic GBM model. Mesenchymal-like phenotype was facilitated by TGF-β in TR GBM. Additionally, TR activated ALDHs. DSF inhibited TR-induced cell migration and tumor sphere formation. However, DSF did not affect the tumor growth in vivo. Spectacularly, DSF sensitized TR GBM to Galunisertib both in vitro and in vivo. ALDH activity positively correlated with TGF-β-induced mesenchymal properties in TR GBM. CSCs and mesenchymal-like GBM cells targeted together by combining DSF and Galunisertib may be a good therapeutic strategy for recurrent GBM patients. Full article
(This article belongs to the Special Issue Cancer Prevention with Molecular Target Therapies 2.0)
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18 pages, 8610 KiB  
Article
Costunolide Induces Apoptosis via the Reactive Oxygen Species and Protein Kinase B Pathway in Oral Cancer Cells
by Hai Huang, Jun-Koo Yi, Su-Geun Lim, Sijun Park, Haibo Zhang, Eungyung Kim, Soyoung Jang, Mee-Hyun Lee, Kangdong Liu, Ki-Rim Kim, Eun-Kyong Kim, Youngkyun Lee, Sung-Hyun Kim, Zae-Young Ryoo and Myoung Ok Kim
Int. J. Mol. Sci. 2021, 22(14), 7509; https://doi.org/10.3390/ijms22147509 - 13 Jul 2021
Cited by 12 | Viewed by 2610
Abstract
Oral cancer (OC) has been attracted research attention in recent years as result of its high morbidity and mortality. Costunolide (CTD) possesses potential anticancer and bioactive abilities that have been confirmed in several types of cancers. However, its effects on oral cancer remain [...] Read more.
Oral cancer (OC) has been attracted research attention in recent years as result of its high morbidity and mortality. Costunolide (CTD) possesses potential anticancer and bioactive abilities that have been confirmed in several types of cancers. However, its effects on oral cancer remain unclear. This study investigated the potential anticancer ability and underlying mechanisms of CTD in OC in vivo and in vitro. Cell viability and anchorage-independent colony formation assays were performed to examine the antigrowth effects of CTD on OC cells; assessments for migration and invasion of OC cells were conducted by transwell; Cell cycle and apoptosis were investigated by flow cytometry and verified by immunoblotting. The results revealed that CTD suppressed the proliferation, migration and invasion of oral cancer cells effectively and induced cell cycle arrest and apoptosis; regarding the mechanism, CTD bound to AKT directly by binding assay and repressed AKT activities through kinase assay, which thereby downregulating the downstream of AKT. Furthermore, CTD remarkably promotes the generation of reactive oxygen species by flow cytometry assay, leading to cell apoptosis. Notably, CTD strongly suppresses cell-derived xenograft OC tumor growth in an in vivo mouse model. In conclusion, our results suggested that costunolide might prevent progression of OC and promise to be a novel AKT inhibitor. Full article
(This article belongs to the Special Issue Cancer Prevention with Molecular Target Therapies 2.0)
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Review

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19 pages, 2220 KiB  
Review
Role of HSP90 in Cancer
by Bereket Birbo, Elechi E. Madu, Chikezie O. Madu, Aayush Jain and Yi Lu
Int. J. Mol. Sci. 2021, 22(19), 10317; https://doi.org/10.3390/ijms221910317 - 25 Sep 2021
Cited by 126 | Viewed by 10254
Abstract
HSP90 is a vital chaperone protein conserved across all organisms. As a chaperone protein, it correctly folds client proteins. Structurally, this protein is a dimer with monomer subunits that consist of three main conserved domains known as the N-terminal domain, middle domain, and [...] Read more.
HSP90 is a vital chaperone protein conserved across all organisms. As a chaperone protein, it correctly folds client proteins. Structurally, this protein is a dimer with monomer subunits that consist of three main conserved domains known as the N-terminal domain, middle domain, and the C-terminal domain. Multiple isoforms of HSP90 exist, and these isoforms share high homology. These isoforms are present both within the cell and outside the cell. Isoforms HSP90α and HSP90β are present in the cytoplasm; TRAP1 is present in the mitochondria; and GRP94 is present in the endoplasmic reticulum and is likely secreted due to post-translational modifications (PTM). HSP90 is also secreted into an extracellular environment via an exosome pathway that differs from the classic secretion pathway. Various co-chaperones are necessary for HSP90 to function. Elevated levels of HSP90 have been observed in patients with cancer. Despite this observation, the possible role of HSP90 in cancer was overlooked because the chaperone was also present in extreme amounts in normal cells and was vital to normal cell function, as observed when the drastic adverse effects resulting from gene knockout inhibited the production of this protein. Differences between normal HSP90 and HSP90 of the tumor phenotype have been better understood and have aided in making the chaperone protein a target for cancer drugs. One difference is in the conformation: HSP90 of the tumor phenotype is more susceptible to inhibitors. Since overexpression of HSP90 is a factor in tumorigenesis, HSP90 inhibitors have been studied to combat the adverse effects of HSP90 overexpression. Monotherapies using HSP90 inhibitors have shown some success; however, combination therapies have shown better results and are thus being studied for a more effective cancer treatment. Full article
(This article belongs to the Special Issue Cancer Prevention with Molecular Target Therapies 2.0)
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23 pages, 9626 KiB  
Review
Retinoids as Chemo-Preventive and Molecular-Targeted Anti-Cancer Therapies
by Victoria O. Hunsu, Caroline O. B. Facey, Jeremy Z. Fields and Bruce M. Boman
Int. J. Mol. Sci. 2021, 22(14), 7731; https://doi.org/10.3390/ijms22147731 - 20 Jul 2021
Cited by 47 | Viewed by 7322
Abstract
Retinoic acid (RA) agents possess anti-tumor activity through their ability to induce cellular differentiation. However, retinoids have not yet been translated into effective systemic treatments for most solid tumors. RA signaling is mediated by the following two nuclear retinoic receptor subtypes: the retinoic [...] Read more.
Retinoic acid (RA) agents possess anti-tumor activity through their ability to induce cellular differentiation. However, retinoids have not yet been translated into effective systemic treatments for most solid tumors. RA signaling is mediated by the following two nuclear retinoic receptor subtypes: the retinoic acid receptor (RAR) and the retinoic X receptor (RXR), and their isoforms. The identification of mutations in retinoid receptors and other RA signaling pathway genes in human cancers offers opportunities for target discovery, drug design, and personalized medicine for distinct molecular retinoid subtypes. For example, chromosomal translocation involving RARA occurs in acute promyelocytic leukemia (APL), and all-trans retinoic acid (ATRA) is a highly effective and even curative therapeutic for APL patients. Thus, retinoid-based target discovery presents an important line of attack toward designing new, more effective strategies for treating other cancer types. Here, we review retinoid signaling, provide an update on retinoid agents and the current clinical research on retinoids in cancer, and discuss how the retinoid pathway genotype affects the ability of retinoid agents to inhibit the growth of colorectal cancer (CRC) cells. We also deliberate on why retinoid agents have not shown clinical efficacy against solid tumors and discuss alternative strategies that could overcome the lack of efficacy. Full article
(This article belongs to the Special Issue Cancer Prevention with Molecular Target Therapies 2.0)
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