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Cancers
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Oncogenes in Cancer 2.0
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Oncogenes in Cancer 2.0

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

Deadline for manuscript submissions: closed (30 September 2023) | Viewed by 6572

Special Issue Editor

Dr. Ignacio Gil-Bazo

E-Mail Website
Guest Editor
Instituto Valenciano de Oncología (IVO), 46009 Valencia, Spain
Interests: lung cancer; immunotherapy; targeted therapy; treatment resistance; liquid biopsy

Special Issue Information

Dear Colleagues,

This Special Issue is the second edition of a previous one, “Oncogenes in Cancer”.

The first oncogenes were discovered more than three decades ago. Since then, remarkable development has been achieved by the scientific community unraveling the biological impact of these oncogenes in the development and progression of different neoplasms as well as their potential clinical applicability in the design of targeted therapies. All this knowledge has made it possible to conceive of the personalized treatment of cancer.

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

This Special Issue is 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 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

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

Published Papers (4 papers)

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Research

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12 pages, 1177 KiB  
Article
Phase II Trial Evaluating Olaparib Maintenance in Patients with Metastatic Castration-Resistant Prostate Cancer Responsive or Stabilized on Docetaxel Treatment: SOGUG-IMANOL Study
by María José Juan Fita, Urbano Anido Herranz, María José Mendez-Vidal, Regina Gironés-Sarrió, José Muñoz-Langa, Juan Sepúlveda-Sánchez, Begoña Mellado, Carlos Alvarez-Fernandez, Lucía Heras López, José Antonio López-Guerrero, Zaida García-Casado, Ana Calatrava and Miguel Ángel Climent
Cancers 2023, 15(21), 5223; https://doi.org/10.3390/cancers15215223 - 31 Oct 2023
Viewed by 1311
Abstract
The SOGUG-IMANOL trial was a phase 2, uncontrolled, Spanish multicenter study to assess the effect of maintenance treatment with olaparib on radiographic progression-free survival (PFS) in patients with metastatic castration-resistant prostate cancer (mCRPC) who achieved partial or complete response or disease stabilization on [...] Read more.
The SOGUG-IMANOL trial was a phase 2, uncontrolled, Spanish multicenter study to assess the effect of maintenance treatment with olaparib on radiographic progression-free survival (PFS) in patients with metastatic castration-resistant prostate cancer (mCRPC) who achieved partial or complete response or disease stabilization on docetaxel treatment and had a documented germline/somatic mutation in any of the homologous recombination repair (HRR) genes. Patients received olaparib 300 mg orally twice daily. From the screened population (n = 134), 26 (19.4%) somatic mutations were found, and 14 patients were included in the study. The median radiographic PFS was 11.1 (95%CI, 5.7 to 16.5) months. The median PSA-PFS was 3.5 (95%CI, 1.0 to 6.0) months, and the median clinical PFS was 14.7 (95%CI, 1.8 to 27.5 months). Clinical benefit was observed in 12 patients (85.7%, 95%CI 67.4% to 100%), including two patients with partial response and 10 with stable disease. Six patients reported grade 3–5 adverse events: asthenia (n = 3), anemia (n = 2) and neutropenia (n = 1). In this setting, olaparib has been shown to be an efficacious maintenance treatment in terms of radiographic PFS and clinical benefit, becoming a therapeutic option for some patients harboring an HRR gene mutation and in scenarios where further investigation is needed. Full article
(This article belongs to the Special Issue Oncogenes in Cancer 2.0)
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23 pages, 12812 KiB  
Article
c-MYC-Induced AP4 Attenuates DREAM-Mediated Repression by p53
by Markus Kaller, Wenjing Shi and Heiko Hermeking
Cancers 2023, 15(4), 1162; https://doi.org/10.3390/cancers15041162 - 11 Feb 2023
Cited by 1 | Viewed by 2001
Abstract
Background: The deregulated expression of the c-MYC oncogene activates p53, which is presumably mediated by ARF/INK4, as well as replication-stress-induced DNA damage. Here, we aimed to determine whether the c-MYC-inducible AP4 transcription factor plays a role in this context using a genetic approach. [...] Read more.
Background: The deregulated expression of the c-MYC oncogene activates p53, which is presumably mediated by ARF/INK4, as well as replication-stress-induced DNA damage. Here, we aimed to determine whether the c-MYC-inducible AP4 transcription factor plays a role in this context using a genetic approach. Methods: We used a CRISPR/Cas9 approach to generate AP4- and/or p53-deficient derivatives of MCF-7 breast cancer cells harboring an ectopic, inducible c-MYC allele. Cell proliferation, senescence, DNA damage, and comprehensive RNA expression profiles were determined after activation of c-MYC. In addition, we analyzed the expression data from primary breast cancer samples. Results: Loss of AP4 resulted in elevated levels of both spontaneous and c-MYC-induced DNA damage, senescence, and diminished cell proliferation. Deletion of p53 in AP4-deficient cells reverted senescence and proliferation defects without affecting DNA damage levels. RNA-Seq analyses showed that loss of AP4 enhanced repression of DREAM and E2F target genes after p53 activation by c-MYC. Depletion of p21 or the DREAM complex component LIN37 abrogated this effect. These p53-dependent effects were conserved on the level of clinical and gene expression associations found in primary breast cancer tumors. Conclusions: Our results establish AP4 as a pivotal factor at the crossroads of c-MYC, E2F, and p53 target gene regulation. Full article
(This article belongs to the Special Issue Oncogenes in Cancer 2.0)
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Review

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21 pages, 3014 KiB  
Review
Soft Tissue Sarcomas with Chromosomal Alterations in the 12q13-15 Region: Differential Diagnosis and Therapeutic Implications
by Javier Lavernia, Reyes Claramunt, Ignacio Romero, José Antonio López-Guerrero, Antonio Llombart-Bosch and Isidro Machado
Cancers 2024, 16(2), 432; https://doi.org/10.3390/cancers16020432 - 19 Jan 2024
Viewed by 1106
Abstract
The chromosomal region 12q13-15 is rich in oncogenes and contains several genes involved in the pathogenesis of various mesenchymal neoplasms. Notable genes in this region include MDM2, CDK4, STAT6, DDIT3, and GLI1. Amplification of MDM2 and CDK4 genes [...] Read more.
The chromosomal region 12q13-15 is rich in oncogenes and contains several genes involved in the pathogenesis of various mesenchymal neoplasms. Notable genes in this region include MDM2, CDK4, STAT6, DDIT3, and GLI1. Amplification of MDM2 and CDK4 genes can be detected in various mesenchymal and nonmesenchymal neoplasms. Therefore, gene amplification alone is not entirely specific for making a definitive diagnosis and requires the integration of clinical, radiological, morphological, and immunohistochemical findings. Neoplasms with GLI1 alterations may exhibit either GLI1 rearrangements or amplifications of this gene. Despite the diagnostic implications that the overlap of genetic alterations in neoplasms with changes in genes within the 12q13-15 region could create, the discovery of coamplifications of MDM2 with CDK4 and GLI1 offers new therapeutic targets in neoplasms with MDM2/CDK4 amplification. Lastly, it is worth noting that MDM2 or CDK4 amplification is not exclusive to mesenchymal neoplasms; this genetic alteration has also been observed in other epithelial neoplasms or melanomas. This suggests the potential use of MDM2 or CDK4 inhibitors in neoplasms where alterations in these genes do not aid the pathological diagnosis but may help identify potential therapeutic targets. In this review, we delve into the diagnosis and therapeutic implications of tumors with genetic alterations involving the chromosomal region 12q13-15, mainly MDM2, CDK4, and GLI1. Full article
(This article belongs to the Special Issue Oncogenes in Cancer 2.0)
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Other

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17 pages, 4589 KiB  
Systematic Review
A Comprehensive Transcriptional Signature in Pancreatic Ductal Adenocarcinoma Reveals New Insights into the Immune and Desmoplastic Microenvironments
by Irene Pérez-Díez, Zoraida Andreu, Marta R. Hidalgo, Carla Perpiñá-Clérigues, Lucía Fantín, Antonio Fernandez-Serra, María de la Iglesia-Vaya, José A. Lopez-Guerrero and Francisco García-García
Cancers 2023, 15(11), 2887; https://doi.org/10.3390/cancers15112887 - 24 May 2023
Cited by 4 | Viewed by 1744
Abstract
Pancreatic ductal adenocarcinoma (PDAC) prognoses and treatment responses remain devastatingly poor due partly to the highly heterogeneous, aggressive, and immunosuppressive nature of this tumor type. The intricate relationship between the stroma, inflammation, and immunity remains vaguely understood in the PDAC microenvironment. Here, we [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) prognoses and treatment responses remain devastatingly poor due partly to the highly heterogeneous, aggressive, and immunosuppressive nature of this tumor type. The intricate relationship between the stroma, inflammation, and immunity remains vaguely understood in the PDAC microenvironment. Here, we performed a meta-analysis of stroma-, and immune-related gene expression in the PDAC microenvironment to improve disease prognosis and therapeutic development. We selected 21 PDAC studies from the Gene Expression Omnibus and ArrayExpress databases, including 922 samples (320 controls and 602 cases). Differential gene enrichment analysis identified 1153 significant dysregulated genes in PDAC patients that contribute to a desmoplastic stroma and an immunosuppressive environment (the hallmarks of PDAC tumors). The results highlighted two gene signatures related to the immune and stromal environments that cluster PDAC patients into high- and low-risk groups, impacting patients’ stratification and therapeutic decision making. Moreover, HCP5, SLFN13, IRF9, IFIT2, and IFI35 immune genes are related to the prognosis of PDAC patients for the first time. Full article
(This article belongs to the Special Issue Oncogenes in Cancer 2.0)
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