Cyclin D1 in parathyroid disease

Mallya, Sanjay M.; Arnold, Andrew

doi:10.2741/mallya

Cited by 47 publications

(25 citation statements)

References 36 publications

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“…CCND1 binds to and activates its kinase partners CDK4 and CDK6, which results in the phosphorylation of the retinoblastoma protein and further affects the transcription of genes that promote progression to the S-phase of the cell cycle (Mallya and Arnold, 2000). Experimental models showed that upregulation of CCND1 expression enhanced the metastatic efficiency of esophageal cancer (Zhou et al, 2009), supporting the notion that CCND1 plays a pivotal role in the development of esophageal cancer.…”

Section: Introductionsupporting

confidence: 57%

Lack of association between Cyclin D1 gene G870A polymorphism and esophageal cancer: evidence from a meta-analysis

Cai

Wang²,

Zhong³

et al. 2013

Genet. Mol. Res.

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ABSTRACT. The association between the Cyclin D1 gene (CCND1) G870A polymorphism and esophageal cancer has been widely evaluated, with conflicting results. As meta-analysis is a reliable approach to resolving discrepancies, we aimed to evaluate this association. Data were available from 9 study populations incorporating 1898 cases and 3046 controls. Overall, the allelic/genotypic association between the G870A polymorphism and esophageal cancer was nonsignificant [for allele: odds ratio (OR) = 1.14, 95% confidence interval (95%CI) = 0.94-1.38, P = 0.184; for genotype homozygous comparison: OR = 1.36, 95%CI = 0.90-2.06, P = 0.140; for dominant model: OR = 1.24, 95%CI = 0.88-1.75, P = 0.222; for recessive model: OR = 1.13, 95%CI = 0.90-1.43, P = 0.292]. Moreover, subgroup analyses according to study designs, geographic areas, types of esophageal cancer, genotyping methods, and ethnicities failed to demonstrate a significant association between this polymorphism and esophageal cancer. In addition, there was significant publication bias as reflected by funnel plots and the 6637 CCND1 G870A and esophageal cancer ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 12 (4): 6636-6645 (2013) Egger test (P = 0.042). Taken together, our results suggest that the CCND1 G870A polymorphism might not be a potential candidate for predicting esophageal cancer risk.

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Section: Introductionsupporting

confidence: 57%

Lack of association between Cyclin D1 gene G870A polymorphism and esophageal cancer: evidence from a meta-analysis

Cai

Wang²,

Zhong³

et al. 2013

Genet. Mol. Res.

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“…Overexpression of this cell cycle regulator is observed in several human cancers such as breast, colon, lymphoma, melanoma and prostate (23). Cyclin D1 overexpression has been implicated through abnormal expression levels in the pathogenesis of 20-40% of sporadic parathyroid tumours (24,25).…”

Section: Introductionmentioning

confidence: 99%

MEN1 intragenic deletions may represent the most prevalent somatic event in sporadic primary hyperparathyroidism

Alvelos

Vinagre

Fonseca

et al. 2013

European Journal of Endocrinology

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Objective: Primary hyperparathyroidism (pHPT) is characterised by an inappropriate over production of parathyroid hormone and it is the most frequent pathological condition of the parathyroid glands. A minority of the cases belong to familial forms, but most of them are sporadic. The genetic alterations underlying the sporadic forms of pHPT remain poorly understood. The main goal of our study is to perform the molecular characterisation of a series of sporadic pHPT cases. Design and methods: We have studied matched blood and tumour from 24 patients with pHPT, who went to a medical appointment in Hospital Pedro Hispano. Informed consent was obtained from all individuals. The MEN1, RET and CDKN1B molecular study was carried out in the germline DNA by PCR/SSCP and direct sequencing. Parathyroid tumours were further analysed by the same methods for MEN1, CDKN1B and CTNNB1 genetic alterations. The multiplex ligation-dependent probe amplification technique enabled the evaluation of MEN1 gene deletions. Protein expression for menin, cyclin D1, parafibromin, p27Kip1 , b-catenin and Ki-67 was conducted by immunohistochemistry. Results: The study of parathyroid tumours detected two somatic MEN1 mutations (c.249_252delGTCT and c.115_163del49bp) and revealed the presence of MEN1 intragenic deletions in 54% (13/24) of the tumours. In RET and CDKN1B genes only previously described, non-pathogenic variants were found. Cyclin D1 protein was overexpressed in 13% (3/24) of tumours. Conclusions: These results suggest that MEN1 alterations, remarkably intragenic deletions, may represent the most prevalent genetic alteration in sporadic parathyroid tumours.

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“…In these particular tumors, the relation between menin expression and cyclin D1 or NF-kB activity is not well documented. Overexpression of cyclin D1 frequently occurs in pancreatic endocrine tumors (Chung et al, 2000;Guo et al, 2003) or in parathyroid adenomas (Mallya et al, 2000), and this overexpression has been postulated to be an early event in neuroendocrine tumorigenesis (Chung, 2004). Parathyroid tumorigenesis is dependent on both cyclin D1 and menin (Rosenberg et al, 1991;Bhuiyan et al, 2000) and parathyroid hyperplasia is induced by an overexpression of cyclin D1 or a loss of menin function in transgenic mice (Imanishi et al, 2001;Bertolino et al, 2003;Libutti et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Relation between menin expression and NF-κB activity in an intestinal cell line

Theillaumas

Blanc

Couderc

et al. 2008

Molecular and Cellular Endocrinology

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This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A c c e p t e d M a n u s c r i p t AbstractIn a previous study, we demonstrated that the Men1 gene is mainly expressed in the proliferative crypt compartment of the small intestine and that a reduction of menin expression in the crypt-like IEC-17 cell line induces an increase in proliferation rate concomitant with an increase in cyclin D1 expression. The aim of the present study was to test the hypothesis that the NF-kB pathway may be involved in cyclin D1 overexpression.Transcriptional activity of the cyclin D1 gene promoter was increased upon reduction of menin expression. Blockade of the NF-kB pathway restored proliferation, cell cycle, cyclin D1 gene transcription and cyclin D1 expression levels to those observed in the presence of menin. These data support a correlation between cyclin D1 expression, NF-kB activity and menin expression in this epithelial cell line and are relevant to the physiological function of menin in regulating proliferation in the intestinal epithelium.

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Cyclin D1 in parathyroid disease

Cited by 47 publications

References 36 publications

Lack of association between Cyclin D1 gene G870A polymorphism and esophageal cancer: evidence from a meta-analysis

Lack of association between Cyclin D1 gene G870A polymorphism and esophageal cancer: evidence from a meta-analysis

MEN1 intragenic deletions may represent the most prevalent somatic event in sporadic primary hyperparathyroidism

Relation between menin expression and NF-κB activity in an intestinal cell line

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