Prognostics of Cyclin-D1 expression with chemoradiation response in patients of locally advanced oral squamous cell carcinoma

Khan, Huma; Gupta, Seema; Husain, Nuzhat; Misra, Sanjeev; Singh, Navneet; Negi, Mahendra Pal Singh

doi:10.4103/0973-1482.136549

Cited by 9 publications

(8 citation statements)

References 11 publications

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“…A key focus for researchers has been the role of cyclin D1 in loco-regional lymph node metastasis. Many authors found a significant correlation between cyclin D1 overexpression or gene amplification and N stage (Mineta et al, 2000;Carlos de Vicente et al, 2002;Myo et al, 2005;Wang et al, 2006b;Das et al, 2011;Mahdey et al, 2011;Huang et al, 2012;Gupta et al, 2014;van Kempen et al, 2015), and this association has been corroborated by two meta-analyses (Zhao et al, 2014;Noorlag et al, 2015). Extracapsular spread, one of the worst prognostic features in oral cancer, has been positively correlated with CCND1 copy-number aberrations in primary tumors (P = 0.011; Michikawa et al, 2011).…”

Section: Tumor Size and Clinical Stagementioning

confidence: 90%

“…Higher levels of cyclin D1 expression have been found in OSCCs of larger size (Carlos de Vicente et al , ; Das et al , ; Gupta et al , ; Guimarães et al , ). In their meta‐analysis, Zhao et al (Zhao et al , ) reported a significant correlation between cyclin D1 overexpression and higher T stage.…”

Section: Diagnostic and Prognostic Implications Of Cyclin D1 In Oral mentioning

confidence: 99%

“…However, the oncogenic role of cyclin D1 is not limited to advanced tumor stages. Many authors found this protein to be overexpressed in potentially malignant disorders (Castle et al, 1999;Sartor et al, 1999;Rousseau et al, 2001;Huang et al, 2006b;Tsui et al, 2009;Ramakrishna et al, 2013;Mishra et al, 2015), with a tendency for higher cyclin D1 expression with each stage of oral carcinogenesis from oral dysplasia to locally advanced OSCC (Carlos de Vicente et al, 2002;Das et al, 2011;Gupta et al, 2014;Guimarães et al, 2015). Indeed, cyclin D1 overexpression was positively correlated with more advanced clinical stages of OSCC (Huang et al, 2012;Gupta et al, 2014), as corroborated by the meta-analysis of Zhao et al (Zhao et al, 2014), consistent with the correlation of this overexpression with larger tumor size and lymph node invasion.…”

Section: Tumor Size and Clinical Stagementioning

confidence: 99%

“…The effect of cyclin D1 overexpression or CCND1 gene amplification on the response to radiotherapy and/or chemotherapy has also been widely studied (Henriksson et al, 2006;Zhang et al, 2006;Zhou et al, 2009;Feng et al, 2011;Zhong et al, 2013;Gupta et al, 2014). Most studies analyzed the response to cisplatin, but there were contradictory results.…”

Section: Influence Of Cyclin D1/ccnd1 Overexpression On the Response mentioning

confidence: 99%

“…The same research group demonstrated that gene silencing by transfection of various cyclin D1 short hairpin RNAs (shRNAs), inhibiting cyclin D1 expression, enhances the sensitivity of tumors to cisplatin, increasing apoptosis and reducing NF-jb-mediated oncogenic activity (Zhou et al, 2009). In a more recent study by Gupta et al (2014) of patients with locally advanced OSCC treated with cisplatin, paclitaxel, and radiotherapy, those with higher cyclin D1 expression had a worse prognosis and response to treatment. A clinical trial in patients with locally advanced HNSCC (stage III/IV), mainly OSCC (89.7% of cases), found that patients with tumors that overexpressed cyclin D1 had a poor response to cisplatin chemotherapy…”

Section: Influence Of Cyclin D1/ccnd1 Overexpression On the Response mentioning

confidence: 99%

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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: Tumor Size and Clinical Stagementioning

confidence: 90%

Section: Diagnostic and Prognostic Implications Of Cyclin D1 In Oral mentioning

confidence: 99%

Section: Tumor Size and Clinical Stagementioning

confidence: 99%

Section: Influence Of Cyclin D1/ccnd1 Overexpression On the Response mentioning

confidence: 99%

Section: Influence Of Cyclin D1/ccnd1 Overexpression On the Response mentioning

confidence: 99%

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An update on the implications of cyclin D1 in oral carcinogenesis

et al. 2017

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Age and risk of recurrence in oral tongue squamous cell carcinoma: Systematic review

et al. 2020

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The incidence of oral tongue squamous cell carcinoma has been increasing in young patients (≤45 years) without a clear etiologic driver. It is unknown if younger patients have an increased risk of recurrence compared to older patients. A literature search was conducted through January 2020 using PubMed/MEDLINE, Embase, Cochrane, Scopus, Science Direct, and clinicaltrials.gov. This review was registered with PROSPERO (ID: CRD42020167498) and the PRISMA statement was followed. Studies were eligible for inclusion if they assessed risk of recurrence by age using a timeto-event analysis, used an age cutoff of ≤45 years or less for the younger cohort, and limited the analysis to the oral tongue subsite. Data were extracted independently by two reviewers using a form with a prespecified list of variables. There were 13 articles that met criteria for the qualitative synthesis (n = 1763 patients). The reported 5-year rates of disease-free survival ranged from 30% to 72% for the younger cohorts and 42% to 81% for the older cohorts. Three studies reported a statistically significant increased risk of recurrence in younger patients, three studies reported a nonsignificant increased risk in younger patients, and seven studies reported a similar risk in younger patients based on the time-to-event analyses. There may be an increased risk of recurrence for younger patients with oral tongue cancer. A definitive conclusion is precluded by limitations among individual studies, and additional research is warranted to examine this question.

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