Asymmetrical proliferative pattern loss linked to cyclin D1 overexpression during malignant transformation of the lip epithelium

Garcia, Natália; González‐Moles, Miguel Ángel; Ruiz‐Ávila, Isabel; Bravo, Manuel; Ramos‐García, Pablo; Minicucci, Eliana Maria; Domingues, Maria Aparecida Custódio; Oliveira, Denise Tostes

doi:10.1111/jdv.13671

Cited by 11 publications

(28 citation statements)

References 4 publications

(8 reference statements)

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“…Immunohistochemistry yields information on the differential topography of cyclin D1 expression at both intracellular and epithelial level. The images show: ( a ) High expression of cyclin D1 in parabasal layer of hyperplastic oral epithelium (40×); ( b ) marked nuclear expression in basal and parabasal layers of a dysplastic oral epithelium (40×) alongside an elevated cytoplasmic expression whose significance has not yet been fully elucidated, although it may reflect the amplification of gene CCND 1 with intense overexpression of cyclin D1, which may not only translocate to the nucleus but also accumulate in the cytoplasm (see reference Garcia et al , ); ( c ) high nuclear expression of cyclin D1 in carcinoma in situ (20×); and ( d ) peripheral expression in tumor nests with central negativity in basal and parabasal layers of a well‐differentiated squamous cell carcinoma (40×)…”

Section: Reflections and Future Research Linesmentioning

confidence: 99%

An update on the implications of cyclin D1 in oral carcinogenesis

et al. 2017

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Cyclin D1 promotes cell cycle progression during G1 phase, a key event in G1-S transition. The protein is encoded by gene CCND1, located in chromosomal band 11q13. Cyclin D1 plays key roles in cell biology, including cell proliferation and growth regulation, mitochondrial activity modulation, DNA repair, and cell migration control. CCND1 gene and its protein cyclin D1 are frequently altered by different molecular mechanisms, including amplification, chromosomal translocations, mutations, and activation of the pathways involved in cyclin D1 expression, alterations which appear to be essential in the development of human cancers, including oral carcinoma. This is the first published review of the specific features of cyclin D1 overexpression in oral oncogenesis. Starting with the physiological regulation of cyclin D1, there is an evaluation of its functions, overexpression mechanisms, and the implications of the oncogenic activation of CCND1/cyclin D1 in oral squamous cell carcinoma. The potential diagnostic and prognostic value of cyclin D1 is reviewed. The influence of CCND1/cyclin D1 on tumor size and clinical stage is reported, and an update is provided on the utilization of cyclin D1 as therapeutic target and on the combination of cyclin D1 inhibitors with cytotoxic agents. Future research lines in this field are also proposed.

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Section: Reflections and Future Research Linesmentioning

confidence: 99%

An update on the implications of cyclin D1 in oral carcinogenesis

et al. 2017

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“…-Meta-analysis Three studies were selected for meta-analysis (11,12,23). We compared the mean expression of Ki-67 among the groups of AC, LSCC and control and observed a high heterogeneity among the studies (tau 2 =241.02; I 2 =95.91%).…”

Section: Resultsmentioning

confidence: 99%

“…Since only three articles could be included for statistical analysis, we observed high heterogeneity among results, specially between AC groups, and this may not represent the reality of Ki-67 staining in AC or LSCC. One of the studies that investigated this protein (10) had to be excluded from meta-analysis since we believe the authors analysed the same sample used in their previous study (11), which was included.…”

Section: Discussionmentioning

confidence: 99%

Can immunohistochemical biomarkers distinguish epithelial dysplasia degrees in actinic cheilitis? A systematic review and meta-analysis

Santana

Matuck²,

Tenório³

et al. 2020

Med Oral

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Background: Actinic cheilitis (AC) is a potentially malignant disorder of the lip, characterized by epithelial and connective tissue alterations caused by chronic exposure to ultraviolet radiation. In the past decades, diverse studies have been conducted in lip carcinogenesis and many biomarkers have been identified in lip lesions, yet there is no scientific evidence that determines its usefulness in the clinical setting or in histopathological routine. Therefore, we conducted the first systematic review in this field to summarize the results of published studies on immunohistochemical biomarkers in lip carcinogenesis, to evaluate if there is a marker than can distinguish the different histological grades of AC. Material and Methods: Retrospective studies that investigated immunohistochemical biomarkers in AC defined on standardised histological assessment were gathered from five databases and evaluated. Each study was qualitatively evaluated using the Critical Appraisal Tools from SUMARI. Results: The proliferation marker Ki-67 was the most studied biomarker and we observed, through meta-analysis, that it was differently expressed between AC and lip cancer, but not in AC subgroups. Most articles had a high risk of bias. Conclusions: In summary, the literature lacks quality follow up studies in actinic cheilitis. Multi-centre cohort studies, with patients stratified by treatment type and the use of image analysis software, could be the solution to further address the issues of investigating potentially malignant lesions and help change clinical practice, in terms of individualizing patients' treatment and prognosis prediction.

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“…Cyclin D1 upregulation is related to multiple molecular mechanisms, notably amplification of its gene (CCND1) or the chromosome band (11q13) in which it is located (Ramos-García, Ramos-García, Ruiz-Ávila, et al, 2017). This phenomenon has frequently been documented in breast, lung, colon, and oral cancers (Garcia et al, 2016;Ramos-García, Bravo, González-Ruiz, & González-Moles, 2018; Ramos-García, González-Moles, Santarius, Shipley, Brewer, Stratton, & Cooper, 2010), and melanoma (Alonso et al, 2004;Demirkan, Kesen, Akdag, Larue, & Delmas, 2007;Marzuka-Alcalá, Gabree, & Tsao, 2014). CCND1/cyclin D1 is currently classified as an oncogene that can promote uncontrolled cell proliferation, a hallmark of cancer (Hanahan & Weinberg, 2011).…”

Section: Introductionmentioning

confidence: 99%

An update on the implications of cyclin D1 in melanomas

González‐Ruiz

González‐Moles

González‐Ruiz

et al. 2020

Pigment Cell Melanoma Res

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Cyclin D1 is a protein encoded by the CCND1 gene, located on 11q13 chromosome, which is a key component of the physiological regulation of the cell cycle. CCND1/ cyclin D1 is upregulated in several types of human tumors including melanoma and is currently classified as an oncogene that promotes uncontrolled cell proliferation. Despite the demonstrated importance of CCND1/cyclin D1 as a central oncogene in several types of human tumors, its knowledge in melanoma is still limited. This review examines data published on upregulation of the CCND1 gene and cyclin D1 protein in the melanoma setting, focusing on the pathways and molecular mechanisms involved in the activation of the gene and on the clinical and therapeutic implications.

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Asymmetrical proliferative pattern loss linked to cyclin D1 overexpression during malignant transformation of the lip epithelium

Abstract: Lip carcinogenesis was associated with loss of the asymmetrical proliferative pattern, a preventive mechanism against lip oncogenesis, and with cyclin D1 overexpression.

Cited by 11 publications

References 4 publications

An update on the implications of cyclin D1 in oral carcinogenesis

An update on the implications of cyclin D1 in oral carcinogenesis

Can immunohistochemical biomarkers distinguish epithelial dysplasia degrees in actinic cheilitis? A systematic review and meta-analysis

An update on the implications of cyclin D1 in melanomas

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