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Cancers
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Oncogenes in Cancer
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Oncogenes in Cancer

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

Deadline for manuscript submissions: closed (31 October 2021) | Viewed by 30644

Special Issue Editor

Dr. Ignacio Gil-Bazo

E-Mail Website
Guest Editor
Universidad de Navarra, Pamplona, Spain
Interests: lung cancer; immunotherapy; targeted therapy; treatment resistance; liquid biopsy

Special Issue Information

Dear Colleagues,

The first oncogenes were discovered more than three decades ago. Since then, a remarkable development has been achieved by the scientific community in order to unravel the biological impact of those oncogenes in the development and progression of different neoplasms and their potential clinical applicability in designing targeted therapies. All this knowledge has made it possible to think of a personalized treatment of cancer.

In this Special Issue entitled “Oncogenes in Cancer”, we approach the role of actionable genomic somatic alterations able to driver different solid tumors, their biological context, and the different therapeutic strategies evaluated.

This Special Issue has being conceived as a comprehensive review of the most frequently present oncogenes in major solid malignancies, updating the most relevant advances leading to the development and eventual approval of new targeted therapeutic compounds.

Dr. Ignacio Gil-Bazo
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 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

  • driver oncogenes
  • personalized medicine
  • targeted therapies
  • somatic mutations

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Published Papers (7 papers)

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Editorial

Jump to: Research, Review

3 pages, 193 KiB  
Editorial
Oncogenes in Cancer: Using the Problem as Part of the Solution
by Ignacio Gil-Bazo
Cancers 2020, 12(11), 3373; https://doi.org/10.3390/cancers12113373 - 14 Nov 2020
Cited by 1 | Viewed by 1554
Abstract
Human cancer is considered to have a multifactorial origin [...] Full article
(This article belongs to the Special Issue Oncogenes in Cancer)

Research

Jump to: Editorial, Review

22 pages, 2967 KiB  
Article
Id1 and PD-1 Combined Blockade Impairs Tumor Growth and Survival of KRAS-mutant Lung Cancer by Stimulating PD-L1 Expression and Tumor Infiltrating CD8+ T Cells
by Iosune Baraibar, Marta Roman, María Rodríguez-Remírez, Inés López, Anna Vilalta, Elisabeth Guruceaga, Margarita Ecay, María Collantes, Teresa Lozano, Diego Alignani, Ander Puyalto, Ana Oliver, Sergio Ortiz-Espinosa, Haritz Moreno, María Torregrosa, Christian Rolfo, Christian Caglevic, David García-Ros, María Villalba-Esparza, Carlos De Andrea, Silvestre Vicent, Rubén Pío, Juan José Lasarte, Alfonso Calvo, Daniel Ajona and Ignacio Gil-Bazoadd Show full author list remove Hide full author list
Cancers 2020, 12(11), 3169; https://doi.org/10.3390/cancers12113169 - 28 Oct 2020
Cited by 12 | Viewed by 4939
Abstract
The use of PD-1/PD-L1 checkpoint inhibitors in advanced NSCLC is associated with longer survival. However, many patients do not benefit from PD-1/PD-L1 blockade, largely because of immunosuppression. New immunotherapy-based combinations are under investigation in an attempt to improve outcomes. Id1 (inhibitor of differentiation [...] Read more.
The use of PD-1/PD-L1 checkpoint inhibitors in advanced NSCLC is associated with longer survival. However, many patients do not benefit from PD-1/PD-L1 blockade, largely because of immunosuppression. New immunotherapy-based combinations are under investigation in an attempt to improve outcomes. Id1 (inhibitor of differentiation 1) is involved in immunosuppression. In this study, we explored the potential synergistic effect of the combination of Id1 inhibition and pharmacological PD-L1 blockade in three different syngeneic murine KRAS-mutant lung adenocarcinoma models. TCGA analysis demonstrated a negative and statistically significant correlation between PD-L1 and Id1 expression levels. This observation was confirmed in vitro in human and murine KRAS-driven lung cancer cell lines. In vivo experiments in KRAS-mutant syngeneic and metastatic murine lung adenocarcinoma models showed that the combined blockade targeting Id1 and PD-1 was more effective than each treatment alone in terms of tumor growth impairment and overall survival improvement. Mechanistically, multiplex quantification of CD3+/CD4+/CD8+ T cells and flow cytometry analysis showed that combined therapy favors tumor infiltration by CD8+ T cells, whilst in vivo CD8+ T cell depletion led to tumor growth restoration. Co-culture assays using CD8+ cells and tumor cells showed that T cells present a higher antitumor effect when tumor cells lack Id1 expression. These findings highlight that Id1 blockade may contribute to a significant immune enhancement of antitumor efficacy of PD-1 inhibitors by increasing PD-L1 expression and harnessing tumor infiltration of CD8+ T lymphocytes. Full article
(This article belongs to the Special Issue Oncogenes in Cancer)
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Review

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18 pages, 1200 KiB  
Review
Synthetic Vulnerabilities in the KRAS Pathway
by Marta Roman, Elizabeth Hwang and E. Alejandro Sweet-Cordero
Cancers 2022, 14(12), 2837; https://doi.org/10.3390/cancers14122837 - 8 Jun 2022
Cited by 3 | Viewed by 6108
Abstract
Mutations in Kristen Rat Sarcoma viral oncogene (KRAS) are among the most frequent gain-of-function genetic alterations in human cancer. Most KRAS-driven cancers depend on its sustained expression and signaling. Despite spectacular recent success in the development of inhibitors targeting specific KRAS [...] Read more.
Mutations in Kristen Rat Sarcoma viral oncogene (KRAS) are among the most frequent gain-of-function genetic alterations in human cancer. Most KRAS-driven cancers depend on its sustained expression and signaling. Despite spectacular recent success in the development of inhibitors targeting specific KRAS alleles, the discovery and utilization of effective directed therapies for KRAS-mutant cancers remains a major unmet need. One potential approach is the identification of KRAS-specific synthetic lethal vulnerabilities. For example, while KRAS-driven oncogenesis requires the activation of a number of signaling pathways, it also triggers stress response pathways in cancer cells that could potentially be targeted for therapeutic benefit. This review will discuss how the latest advances in functional genomics and the development of more refined models have demonstrated the existence of molecular pathways that can be exploited to uncover synthetic lethal interactions with a promising future as potential clinical treatments in KRAS-mutant cancers. Full article
(This article belongs to the Special Issue Oncogenes in Cancer)
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14 pages, 531 KiB  
Review
The BRCA Gene in Epithelial Ovarian Cancer
by Luisa Sánchez-Lorenzo, Diego Salas-Benito, Julia Villamayor, Ana Patiño-García and Antonio González-Martín
Cancers 2022, 14(5), 1235; https://doi.org/10.3390/cancers14051235 - 27 Feb 2022
Cited by 12 | Viewed by 3843
Abstract
Epithelial ovarian cancer (EOC) is still the most lethal gynecological cancer. Germline alterations in breast cancer 1 (gBRCA1) and breast cancer 2 (gBRCA2) genes have been identified in up to 18% of women diagnosed with EOC, and somatic mutations are found in an [...] Read more.
Epithelial ovarian cancer (EOC) is still the most lethal gynecological cancer. Germline alterations in breast cancer 1 (gBRCA1) and breast cancer 2 (gBRCA2) genes have been identified in up to 18% of women diagnosed with EOC, and somatic mutations are found in an additional 7%. Testing of BRCA at the primary diagnosis of patients with EOC is recommended due to the implications in the genomic counseling of the patients and their families, as well as for the therapeutic implications. Indeed, the introduction of poly-(ADP ribose) polymerase inhibitors (PARPis) has changed the natural history of patients harboring a mutation in BRCA, and has resulted in a new era in the treatment of patients with ovarian cancer harboring a BRCA mutation. Full article
(This article belongs to the Special Issue Oncogenes in Cancer)
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16 pages, 321 KiB  
Review
Plasma-Based Genotyping in Advanced Solid Tumors: A Comprehensive Review
by Maisam Makarem, Miguel García-Pardo and Natasha B. Leighl
Cancers 2021, 13(21), 5299; https://doi.org/10.3390/cancers13215299 - 22 Oct 2021
Cited by 3 | Viewed by 2217
Abstract
Molecular genotyping for advanced solid malignancies has transformed the clinical management of patients with metastatic disease. Treatment decisions in a growing number of tumors require knowledge of molecularly driven alterations in order to select optimal targeted therapy. Although genomic testing of tumor tissue [...] Read more.
Molecular genotyping for advanced solid malignancies has transformed the clinical management of patients with metastatic disease. Treatment decisions in a growing number of tumors require knowledge of molecularly driven alterations in order to select optimal targeted therapy. Although genomic testing of tumor tissue is the gold standard for identifying targetable genomic alterations, biopsy samples are often limited or difficult to access. This has paved the way for the development of plasma-based approaches for genomic profiling. Recent advances in the detection of plasma-circulating tumor DNA (ctDNA) have enabled the integration of plasma-based molecular profiling into clinical practice as an alternative or complementary tool for genomic testing in the setting of advanced cancer, to facilitate the identification of driver mutations to guide initial treatment and diagnose resistance. Several guidelines now recommend the use of plasma where tumor tissue is limited to identify a targetable genomic alteration. Current plasma-based assays can evaluate multiple genes in comprehensive panels, and their application in advanced disease will be increasingly incorporated into standard practice. This review focuses on current and future applications of plasma ctDNA-based assays in advanced solid malignancies, while highlighting some limitations in implementing this technology into clinical practice. Full article
(This article belongs to the Special Issue Oncogenes in Cancer)
77 pages, 2619 KiB  
Review
Targeting Notch to Maximize Chemotherapeutic Benefits: Rationale, Advanced Strategies, and Future Perspectives
by Nadezda Zhdanovskaya, Mariarosaria Firrincieli, Sara Lazzari, Eleonora Pace, Pietro Scribani Rossi, Maria Pia Felli, Claudio Talora, Isabella Screpanti and Rocco Palermo
Cancers 2021, 13(20), 5106; https://doi.org/10.3390/cancers13205106 - 12 Oct 2021
Cited by 16 | Viewed by 4613
Abstract
Notch signaling guides cell fate decisions by affecting proliferation, apoptosis, stem cell self-renewal, and differentiation depending on cell and tissue context. Given its multifaceted function during tissue development, both overactivation and loss of Notch signaling have been linked to tumorigenesis in ways that [...] Read more.
Notch signaling guides cell fate decisions by affecting proliferation, apoptosis, stem cell self-renewal, and differentiation depending on cell and tissue context. Given its multifaceted function during tissue development, both overactivation and loss of Notch signaling have been linked to tumorigenesis in ways that are either oncogenic or oncosuppressive, but always context-dependent. Notch signaling is critical for several mechanisms of chemoresistance including cancer stem cell maintenance, epithelial-mesenchymal transition, tumor-stroma interaction, and malignant neovascularization that makes its targeting an appealing strategy against tumor growth and recurrence. During the last decades, numerous Notch-interfering agents have been developed, and the abundant preclinical evidence has been transformed in orphan drug approval for few rare diseases. However, the majority of Notch-dependent malignancies remain untargeted, even if the application of Notch inhibitors alone or in combination with common chemotherapeutic drugs is being evaluated in clinical trials. The modest clinical success of current Notch-targeting strategies is mostly due to their limited efficacy and severe on-target toxicity in Notch-controlled healthy tissues. Here, we review the available preclinical and clinical evidence on combinatorial treatment between different Notch signaling inhibitors and existent chemotherapeutic drugs, providing a comprehensive picture of molecular mechanisms explaining the potential or lacking success of these combinations. Full article
(This article belongs to the Special Issue Oncogenes in Cancer)
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9 pages, 793 KiB  
Review
Neuregulin 1 Gene (NRG1). A Potentially New Targetable Alteration for the Treatment of Lung Cancer
by Daniel Rosas, Luis E. Raez, Alessandro Russo and Christian Rolfo
Cancers 2021, 13(20), 5038; https://doi.org/10.3390/cancers13205038 - 9 Oct 2021
Cited by 20 | Viewed by 5978
Abstract
Oncogenic gene fusions are hybrid genes that result from structural DNA rearrangements, leading to unregulated cell proliferation by different mechanisms in a wide variety of cancer. This has led to the development of directed therapies to antagonize a variety of mechanisms that lead [...] Read more.
Oncogenic gene fusions are hybrid genes that result from structural DNA rearrangements, leading to unregulated cell proliferation by different mechanisms in a wide variety of cancer. This has led to the development of directed therapies to antagonize a variety of mechanisms that lead to cell growth or proliferation. Multiple oncogene fusions are currently targeted in lung cancer treatment, such as those involving ALK, RET, NTRK and ROS1 among many others. Neuregulin (NRG) gene fusion has been described in the development of normal tissue as well as in a variety of diseases, such as schizophrenia, Hirschsprung’s disease, atrial fibrillation and, most recently, the development of various types of solid tumors, such as renal, gastric, pancreatic, breast, colorectal and, more recently, lung cancer. The mechanism for this is that the NRG1 chimeric ligand leads to aberrant activation of ERBB2 signaling via PI3K-AKT and MAPK cellular cascades, leading to cell division and proliferation. Details regarding the incidence of these gene rearrangements are lacking. Limited case reports and case series have evaluated their clinicopathologic features and prognostic significance in the lung cancer population. Taking this into account, NRG1 could become a targetable alteration in selected patients. This review highlights how the knowledge of new molecular mechanisms of NRG1 fusion may help in gaining new insights into the molecular status of lung cancer patients and unveil a novel targetable molecular marker. Full article
(This article belongs to the Special Issue Oncogenes in Cancer)
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