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Oral Cancer and Disease in Humans and Animals
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Oral Cancer and Disease in Humans and Animals

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 November 2024) | Viewed by 5506

Special Issue Editors

Dr. Maria Leonor Delgado

E-Mail Website
Guest Editor
1. Department of Veterinary Medicine, University Institute of Health Sciences (IUCS-CESPU), 4585-116 Gandra, Portugal
2. UNIPRO—Oral Pathology and Rehabilitation Research Unit, University Institute of Health Sciences (IUCS-CESPU), Gandra, Portugal
3. Pathology Department, INNO Serviços Especializados em Veterinária, Braga, Portugal
Interests: oral cancer; veterinary pathology; comparative pathology; molecular pathology; immunohistochemistry
Special Issues, Collections and Topics in MDPI journals
Dr. Luís Monteiro

E-Mail Website
Guest Editor
1. Department of Veterinary Medicine, University Institute of Health Sciences (IUCS-CESPU), 4585-116 Gandra, Portugal
2. UNIPRO—Oral Pathology and Rehabilitation Research Unit, University Institute of Health Sciences (IUCS-CESPU), Gandra, Portugal
3. Pathology Department, INNO Serviços Especializados em Veterinária, Braga, Portugal
Interests: oral medicine; oral cancer; carcinogenesis; premalignant lesions; biomarkers; laser
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The increase in the mean life expectancy of humans as well as companion animals probably contributes to a higher incidence of neoplasms, with oncological disease today representing a major cause of death; however, there are important gaps in the knowledge of and subsequent interventions in these neoplasms, including many factors, such as the late diagnosis of neoplastic lesions and a lack of treatment options, that contribute to the poor survival of these patients. From this point of view, the molecular study of tumors and the search for molecules with prognostic value (cancer biomarkers, molecular diagnostics, immunotherapy, etc.) can open doors for a specialized characterization of tumors of each human or companion animal patient and better prognoses. This Special Issue is interested in the molecular pathology of oral carcinogenesis (including head and neck neoplasms) in human and veterinary patients that might contribute to an increase in the knowledge on oral oncology.

Dr. Maria Leonor Delgado
Dr. Luís Monteiro
Guest Editors

Manuscript Submission Information

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Keywords

  • cancer biomarkers
  • mitosis
  • cell cycle
  • animal models
  • comparative pathology
  • cancer stem cell
  • cancer epidemiology
  • cancer risk factors
  • cancer biomarker
  • tissue microarray
  • immunohistochemistry
  • microarray
  • microRNA
  • molecular diagnostics
  • proteomics
  • tumor microenvironment
  • treatment response
  • targeted therapy
  • immunotherapy
  • translation cancer research
  • zoonosis
  • gross pathology

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Published Papers (5 papers)

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Research

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11 pages, 1507 KiB  
Article
Drugs That Induce Gingival Overgrowth Drive the Pro-Inflammatory Polarization of Macrophages In Vitro
by Annalisa Palmieri, Agnese Pellati, Dorina Lauritano, Alberta Lucchese, Francesco Carinci, Luca Scapoli and Marcella Martinelli
Int. J. Mol. Sci. 2024, 25(21), 11441; https://doi.org/10.3390/ijms252111441 - 24 Oct 2024
Viewed by 545
Abstract
Several attempts have been made to elucidate the pathogenesis of drug-induced gingival overgrowth (DIGO), which is triggered by the chronic use of certain drugs that fall into three main categories: anticonvulsants, immunosuppressants, and calcium channel blockers. Previous research suggests that cytokines and impaired [...] Read more.
Several attempts have been made to elucidate the pathogenesis of drug-induced gingival overgrowth (DIGO), which is triggered by the chronic use of certain drugs that fall into three main categories: anticonvulsants, immunosuppressants, and calcium channel blockers. Previous research suggests that cytokines and impaired cellular functions play a role in DIGO. Of particular interest are macrophages, immune cells that can switch between M1 (pro-inflammatory) and M2 (anti-inflammatory) phenotypes in response to exogenous signals and stimuli. An imbalance between M1 and M2 macrophage populations may underlie DIGO. M1 may contribute to the initial tissue damage in DIGO, while M2 may then attempt to repair the damage with anti-inflammatory mechanisms. To test the hypothesis that drugs associated with DIGO could influence macrophage polarization, human monocytes (precursors of macrophages) were induced to differentiate into M0-naïve macrophages and then exposed to drugs: diphenylhydantoin, gabapentin, mycophenolate, and amlodipine. Quantitative real-time PCR amplification was used to measure the expression of specific genes associated with macrophage polarization. All of the drugs tested induced M0 macrophages to overexpress genes typical of the M1 phenotype, such as CCL5, CXCL10, and IDO1. This investigation provides the first evidence of a link between drugs that cause DIGO and M1 pro-inflammatory macrophage polarization. The knowledge gained from this research could be valuable for future DIGO treatment strategies. Full article
(This article belongs to the Special Issue Oral Cancer and Disease in Humans and Animals)
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19 pages, 2188 KiB  
Article
Splicing Machinery Is Impaired in Oral Squamous Cell Carcinomas and Linked to Key Pathophysiological Features
by Alba Sanjuan-Sanjuan, Emilia Alors-Perez, Marina Sanchez-Frías, José A. Monserrat-Barbudo, Mabel Falguera Uceda, Susana Heredero-Jung and Raúl M. Luque
Int. J. Mol. Sci. 2024, 25(13), 6929; https://doi.org/10.3390/ijms25136929 - 25 Jun 2024
Cited by 1 | Viewed by 787
Abstract
Alternative splicing dysregulation is an emerging cancer hallmark, potentially serving as a source of novel diagnostic, prognostic, or therapeutic tools. Inhibitors of the activity of the splicing machinery can exert antitumoral effects in cancer cells. We aimed to characterize the splicing machinery (SM) [...] Read more.
Alternative splicing dysregulation is an emerging cancer hallmark, potentially serving as a source of novel diagnostic, prognostic, or therapeutic tools. Inhibitors of the activity of the splicing machinery can exert antitumoral effects in cancer cells. We aimed to characterize the splicing machinery (SM) components in oral squamous cell carcinoma (OSCC) and to evaluate the direct impact of the inhibition of SM-activity on OSCC-cells. The expression of 59 SM-components was assessed using a prospective case-control study of tumor and healthy samples from 37 OSCC patients, and the relationship with clinical and histopathological features was assessed. The direct effect of pladienolide-B (SM-inhibitor) on the proliferation rate of primary OSCC cell cultures was evaluated. A significant dysregulation in several SM components was found in OSCC vs. adjacent-healthy tissues [i.e., 12 out of 59 (20%)], and their expression was associated with clinical and histopathological features of less aggressiveness and overall survival. Pladienolide-B treatment significantly decreased OSCC-cell proliferation. Our data reveal a significantly altered expression of several SM-components and link it to pathophysiological features, reinforcing a potential clinical and pathophysiological relevance of the SM dysregulation in OSCC. The inhibition of SM-activity might be a therapeutic avenue in OSCC, offering a clinically relevant opportunity to be explored. Full article
(This article belongs to the Special Issue Oral Cancer and Disease in Humans and Animals)
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Review

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34 pages, 664 KiB  
Review
Unraveling the Keratin Expression in Oral Leukoplakia: A Scoping Review
by Guru Murthy O, Jeremy Lau, Ramesh Balasubramaniam, Agnieszka M. Frydrych and Omar Kujan
Int. J. Mol. Sci. 2024, 25(11), 5597; https://doi.org/10.3390/ijms25115597 - 21 May 2024
Viewed by 1090
Abstract
Intermediate filaments are one of three polymeric structures that form the cytoskeleton of epithelial cells. In the epithelium, these filaments are made up of a variety of keratin proteins. Intermediate filaments complete a wide range of functions in keratinocytes, including maintaining cell structure, [...] Read more.
Intermediate filaments are one of three polymeric structures that form the cytoskeleton of epithelial cells. In the epithelium, these filaments are made up of a variety of keratin proteins. Intermediate filaments complete a wide range of functions in keratinocytes, including maintaining cell structure, cell growth, cell proliferation, cell migration, and more. Given that these functions are intimately associated with the carcinogenic process, and that hyperkeratinization is a quintessential feature of oral leukoplakias, the utility of keratins in oral leukoplakia is yet to be fully explored. This scoping review aims to outline the current knowledge founded on original studies on human tissues regarding the expression and utility of keratins as diagnostic, prognostic, and predictive biomarkers in oral leukoplakias. After using a search strategy developed for several scientific databases, namely, PubMed, Scopus, Web of Science, and OVID, 42 papers met the inclusion and exclusion criteria. One more article was added when it was identified through manually searching the list of references. The included papers were published between 1989 and 2024. Keratins 1–20 were investigated in the 43 included studies, and their expression was assessed in oral leukoplakia and dysplasia cases. Only five studies investigated the prognostic role of keratins in relation to malignant transformation. No studies evaluated keratins as a diagnostic adjunct or predictive tool. Evidence supports the idea that dysplasia disrupts the terminal differentiation pathway of primary keratins. Gain of keratin 17 expression and loss of keratin 13 were significantly observed in differentiated epithelial dysplasia. Also, the keratin 19 extension into suprabasal cells has been associated with the evolving features of dysplasia. The loss of keratin1/keratin 10 has been significantly associated with high-grade dysplasia. The prognostic value of cytokeratins has shown conflicting results, and further studies are required to ascertain their role in predicting the malignant transformation of oral leukoplakia. Full article
(This article belongs to the Special Issue Oral Cancer and Disease in Humans and Animals)
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21 pages, 1574 KiB  
Review
A Review of the Repair of DNA Double Strand Breaks in the Development of Oral Cancer
by Stephen S. Prime, Piotr Darski, Keith D. Hunter, Nicola Cirillo and E. Kenneth Parkinson
Int. J. Mol. Sci. 2024, 25(7), 4092; https://doi.org/10.3390/ijms25074092 - 7 Apr 2024
Viewed by 1614
Abstract
We explore the possibility that defects in genes associated with the response and repair of DNA double strand breaks predispose oral potentially malignant disorders (OPMD) to undergo malignant transformation to oral squamous cell carcinoma (OSCC). Defects in the homologous recombination/Fanconi anemia (HR/FA), but [...] Read more.
We explore the possibility that defects in genes associated with the response and repair of DNA double strand breaks predispose oral potentially malignant disorders (OPMD) to undergo malignant transformation to oral squamous cell carcinoma (OSCC). Defects in the homologous recombination/Fanconi anemia (HR/FA), but not in the non-homologous end joining, causes the DNA repair pathway to appear to be consistent with features of familial conditions that are predisposed to OSCC (FA, Bloom’s syndrome, Ataxia Telangiectasia); this is true for OSCC that occurs in young patients, sometimes with little/no exposure to classical risk factors. Even in Dyskeratosis Congenita, a disorder of the telomerase complex that is also predisposed to OSCC, attempts at maintaining telomere length involve a pathway with shared HR genes. Defects in the HR/FA pathway therefore appear to be pivotal in conditions that are predisposed to OSCC. There is also some evidence that abnormalities in the HR/FA pathway are associated with malignant transformation of sporadic cases OPMD and OSCC. We provide data showing overexpression of HR/FA genes in a cell-cycle-dependent manner in a series of OPMD-derived immortal keratinocyte cell lines compared to their mortal counterparts. The observations in this study argue strongly for an important role of the HA/FA DNA repair pathway in the development of OSCC. Full article
(This article belongs to the Special Issue Oral Cancer and Disease in Humans and Animals)
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Other

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16 pages, 3567 KiB  
Case Report
Exceptional Evolution of a Squamous Odontogenic Tumor in the Jaw: Molecular Approach
by Miguel Alonso-Juarranz, Oscar De La Sen, Pablo Pérez, Maria Aranzazu González-Corchón, Santiago Cabezas-Camarero, Melchor Saiz-Pardo, Jesus Viñas-Lopez, Lucia Recio-Poveda, Luisa María Botella and Farzin Falahat
Int. J. Mol. Sci. 2024, 25(17), 9547; https://doi.org/10.3390/ijms25179547 - 2 Sep 2024
Viewed by 814
Abstract
A squamous odontogenic tumor (SOT) is an epithelial locally benign neoplasia derived from the periodontium of the jaws. It is considered a lesion of low incidence. Predominantly, it affects the mandible, although both jaw bones may be involved. Here, we discuss the malignant [...] Read more.
A squamous odontogenic tumor (SOT) is an epithelial locally benign neoplasia derived from the periodontium of the jaws. It is considered a lesion of low incidence. Predominantly, it affects the mandible, although both jaw bones may be involved. Here, we discuss the malignant clinical evolution of an SOT lesion in an 80-year-old female patient. The patient exhibited an expansive triangular lesion at the inferior right quadrant. Surgery was performed and an SOT was diagnosed (2019). Two years after, the lesion grew, and the analysis of the biopsy revealed SOT malignization with pleomorphic atypical squamous cells, characteristics of a squamous cell carcinoma (2021). Massive DNA sequencing of formalin-fixed–paraffin-embedded specimens of the initial and relapsed tumors indicated pathogenic mutations in RET and POLE genes in both tumors, loss of ALK, and gain of CDKN1B and MAP2K in the relapse. In addition, the clinical, radiographic, and microscopic features of this neoplasm are discussed and compared with those already published. The case presented contributes to the better understanding of this SOT tumor entity and to indicates its malignant evolution, together with its biological behavior and its histologic, clinical, and radiographic features. Also, it aims to stress the importance of deeper genetic analyses in rare diseases to uncover mutations that help to select a personalized treatment. Full article
(This article belongs to the Special Issue Oral Cancer and Disease in Humans and Animals)
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