Special Issue "Targeting Solid Tumors"

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: 31 December 2019

Special Issue Editors

Guest Editor
Prof. Elisabetta Ferretti

Dipartimento di Medicina Sperimentale, Università di Roma "La Sapienza", Viale Regina Elena, 291, 00161 Rome, Italy
Website | E-Mail
Interests: solid tumors; metabolic diseases; microRNAs; LncRNA; Hedgehog/Gli signaling; stem cells; circulating biomarkers (microRNAs and cfDNA); cellular models; animal models; oncosuppressor; oncogenes
Guest Editor
Dr. Marco Tafani

Department of Experimental Medicine, Sapienza University of Rome, Viale Regina Elena 324, 00161, Rome, Italy
Website | E-Mail
Interests: hypoxia; inflammation; sirtuins (SIRTs)

Special Issue Information

Dear colleagues,

Despite the fact that scientific achievements in the studies and therapies for cancer have reached levels that were unthinkable a few years ago, we are very far from an effective cure for solid tumors. The reason for this may be ascribed to many different aspects of such tumors, which are unraveling as we speak.

In particular, tumor microenvironment, metabolic and epigenetic changes, and immune evasion and adaptation are some of the aspects that render solid tumor eradication a real challenge.

In that respect, the current Special Issue invites contributions aimed at exploring the different characteristics of solid tumors, focused on, but not limited to, the microenvironment, such as hypoxia, alteration of tumor vasculature; extracellular matrix; pH; epigenetic changes, such as methylation, acetylation, and so on; metabolic changes, such as glucose uptake, glutamine metabolism, and so on; modification of microRNA signature; and interaction with the immune system. At the same time, contributions should provide the state-of-the-art of the therapies associated to or proposed for each solid tumor aspect discussed.

Prof. Elisabetta Ferretti
Dr. Marco Tafani
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 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. Cancers 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 1800 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

  • solid tumors
  • targeted therapies
  • tumor microenvironment (TME)
  • immune evasion
  • epigenetic changes
  • microRNA signature
  • metabolic features
  • precision therapy
  • drug resistance

Published Papers (2 papers)

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Research

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Open AccessArticle Overactive IGF1/Insulin Receptors and NRASQ61R Mutation Drive Mechanisms of Resistance to Pazopanib and Define Rational Combination Strategies to Treat Synovial Sarcoma
Cancers 2019, 11(3), 408; https://doi.org/10.3390/cancers11030408
Received: 5 February 2019 / Revised: 8 March 2019 / Accepted: 18 March 2019 / Published: 22 March 2019
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Abstract
Pazopanib is approved for treatment of advanced soft tissue sarcomas, but primary and secondary drug resistance limits its clinical utility. We investigated the molecular mechanisms mediating pazopanib resistance in human synovial sarcoma (SS) models. We found reduced cell sensitivity to pazopanib associated with [...] Read more.
Pazopanib is approved for treatment of advanced soft tissue sarcomas, but primary and secondary drug resistance limits its clinical utility. We investigated the molecular mechanisms mediating pazopanib resistance in human synovial sarcoma (SS) models. We found reduced cell sensitivity to pazopanib associated with inefficient inhibition of the two critical signaling nodes, AKT and ERKs, despite strong inhibition of the main drug target, PDGFRα. In the CME-1 cell line, overactivation of IGF1 and Insulin receptors (IGF1R/InsR) sustained AKT activation and pazopanib resistance, which was overcome by a combination treatment with the double IGF1R/InsR inhibitor BMS754807. In the highly pazopanib resistant MoJo cell line, NRASQ61R mutation sustained constitutive ERK activation. Transfection of the NRAS mutant in the pazopanib sensitive SYO-1 cell line increased the drug IC50. MoJo cells treatment with pazopanib in combination with the MEK inhibitor trametinib restored ERK inhibition, synergistically inhibited cell growth, and induced apoptosis. The combination significantly enhanced the antitumor efficacy against MoJo orthotopic xenograft abrogating growth in 38% of mice. These findings identified two different mechanisms of intrinsic pazopanib resistance in SS cells, supporting molecular/immunohistochemical profiling of tumor specimens as a valuable approach to selecting patients who may benefit from rational drug combinations. Full article
(This article belongs to the Special Issue Targeting Solid Tumors)
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Review

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Open AccessReview Tumor Energy Metabolism and Potential of 3-Bromopyruvate as an Inhibitor of Aerobic Glycolysis: Implications in Tumor Treatment
Cancers 2019, 11(3), 317; https://doi.org/10.3390/cancers11030317
Received: 16 February 2019 / Revised: 28 February 2019 / Accepted: 1 March 2019 / Published: 6 March 2019
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Abstract
Tumor formation and growth depend on various biological metabolism processes that are distinctly different with normal tissues. Abnormal energy metabolism is one of the typical characteristics of tumors. It has been proven that most tumor cells highly rely on aerobic glycolysis to obtain [...] Read more.
Tumor formation and growth depend on various biological metabolism processes that are distinctly different with normal tissues. Abnormal energy metabolism is one of the typical characteristics of tumors. It has been proven that most tumor cells highly rely on aerobic glycolysis to obtain energy rather than mitochondrial oxidative phosphorylation (OXPHOS) even in the presence of oxygen, a phenomenon called “Warburg effect”. Thus, inhibition of aerobic glycolysis becomes an attractive strategy to specifically kill tumor cells, while normal cells remain unaffected. In recent years, a small molecule alkylating agent, 3-bromopyruvate (3-BrPA), being an effective glycolytic inhibitor, has shown great potential as a promising antitumor drug. Not only it targets glycolysis process, but also inhibits mitochondrial OXPHOS in tumor cells. Excellent antitumor effects of 3-BrPA were observed in cultured cells and tumor-bearing animal models. In this review, we described the energy metabolic pathways of tumor cells, mechanism of action and cellular targets of 3-BrPA, antitumor effects, and the underlying mechanism of 3-BrPA alone or in combination with other antitumor drugs (e.g., cisplatin, doxorubicin, daunorubicin, 5-fluorouracil, etc.) in vitro and in vivo. In addition, few human case studies of 3-BrPA were also involved. Finally, the novel chemotherapeutic strategies of 3-BrPA, including wafer, liposomal nanoparticle, aerosol, and conjugate formulations, were also discussed for future clinical application. Full article
(This article belongs to the Special Issue Targeting Solid Tumors)
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