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CCND1 (B-cell leukemia/lymphoma 1)

Written1998-05Jean-Loup Huret
Genetics, Dept Medical Information, University of Poitiers, CHU Poitiers Hospital, F-86021 Poitiers, France
Updated2015-04Shreya Sarkar, Chinmay Kumar Panda
Department of Oncogene Regulation, Chittaranjan National Cancer Institute, Kolkata, West Bengal, India; ckpanda.cnci@gmail.com

Abstract Review on CCND1, with data on DNA, on the protein encoded, and where the gene is implicated.

Keywords CCND1; Cell cycle

(Note : for Links provided by Atlas : click)

Identity

Alias_namesBCL1
D11S287E
PRAD1
cyclin D1 (PRAD1: parathyroid adenomatosis 1)
Alias_symbol (synonym)U21B31
Other aliasBCL1 (B-cell leukemia/lymphoma 1)
PRAD1 (parathyroid adenomatosis 1)
HGNC (Hugo) CCND1
LocusID (NCBI) 595
Atlas_Id 36
Location 11q13.3  [Link to chromosome band 11q13]
Location_base_pair Starts at 69641105 and ends at 69654474 bp from pter ( according to hg19-Feb_2009)  [Mapping CCND1.png]
 
  The figure shows the chromosomal location of CCND1 (Red line). Image courtesy genecards.org
 
  BCL1 (11q13) - Courtesy Mariano Rocchi, Resources for Molecular Cytogenetics.
Fusion genes
(updated 2016)
CCND1 (11q13.3) / ATP5J2-PTCD1 (7q22.1)CCND1 (11q13.3) / CCND1 (11q13.3)CCND1 (11q13.3) / CDK2 (12q13.2)
CCND1 (11q13.3) / CDK4 (12q14.1)CCND1 (11q13.3) / DPP6 (7q36.2)CCND1 (11q13.3) / FSTL3 (19p13.3)
CCND1 (11q13.3) / GMFB (14q22.2)CCND1 (11q13.3) / IGH (14q32.33)CCND1 (11q13.3) / IGHG1 (14q32.33)
CCND1 (11q13.3) / IGLL1 (22q11.23)CCND1 (11q13.3) / NFAT5 (16q22.1)CCND1 (11q13.3) / TACSTD2 (1p32.1)
CHAF1A (19p13.3) / CCND1 (11q13.3)FSTL3 (19p13.3) / CCND1 (11q13.3)GNB1 (1p36.33) / CCND1 (11q13.3)
IGH (14q32.33) / CCND1 (11q13.3)IGHG1 (14q32.33) / CCND1 (11q13.3)IGK (14q32.33) / CCND1 (11q13.3)
IGL (22q11.22) / CCND1 (11q13.3)IGLV3-10 () / CCND1 (11q13.3)Ig () / CCND1 (11q13.3)
PHYHIPL (10q21.1) / CCND1 (11q13.3)RPS16 (19q13.2) / CCND1 (11q13.3)TMA7 (3p21.31) / CCND1 (11q13.3)
UBE3C (7q36.3) / CCND1 (11q13.3)

DNA/RNA

 
  Diagram shows the different transcripts of CCND1 (BROWN, BLUE AND MAROON BOXES). Beginning of boxes represents transcription start sites. Filled areas represent translated regions. The brown box representing transcript CCND- 001 forms the full length, active protein. Image adapted from Ensembl.org
Description Located in the long (q) arm of chromosome 11 in the 13th band, the length of the CCND 1 gene is about 13.38 Kb (precisely 13,388 bases), contains 5 exons and is arranged in a telomere to centromere orientation.
Transcription According to Ensembl, the full length, functional transcript of CCND1 (Transcript ID ENST00000227507) is 4307 bp in length, encoding 5 coding exons. From the total of 6 transcripts generated, only two are protein coding.
Pseudogene None reported.

Protein

 
  Schematic diagram of full length CCND1, showing different domains. Adapted from PDB P24385.
Data origin/ Colour codes: Data in Green originates from UniProtKB.; Data in blue originates from PDB. Secstruc- Secondary structure projected from representative PDB entries onto the UniProt sequence. a. Red box- Helix. b. Grey tube- Coil. Data in red indicates combined ranges of Homology Models from SBKB and the Protein Model Portal. Figure shows RNA expression data (presence/absence) for RNA genes is according to H-InvDB, NONCODE, miRBase, and RNAdb. The expression images based on data from BioGPS, Illumina Human BodyMap, and SAGE, with SAGE tags from CGAP.
BioGPS
76 normal tissues were used and compartments hybridized against HG-U133A, with Affymetrix MAS5 algorithm used in array processing.
Illumina body map
Transcripts were mapped to genes from 16 normal human tissues by sequencing. Cufflinks program was used to calculate Fragments per Kilobase of exon per Million fragments mapped (FPKM) and rescaled by multiplying FPKM by 100 and calculating the root.
CGAP: SAGE Normal
For Serial Analysis of Gene Expression (SAGE) of 19 normal human tissues, Hs frequencies and Hs libraries in CGAP datasets are mined for information regarding the number of SAGE tags per tissue. Unigene clustering was applied to Tags, followed by a particular gene by mining Hs best gene, Hs best tag and Hs GeneData. The number of appearances of the corresponding tag divided by the total number of tags in libraries derived from that tissue was used in calculating the level of expression of a particular gene, which were then rescaled by making the genomic mean of all tissues equal.
Intermediate between log and linear scales are normalized intensities drawn on root scale, with values not comparable between datasets (i.e. Microarray, RNAseq and SAGE).
Figure courtesy: genecards.org.
Description The full length CCND1 protein has a length of 295 amino acids, having a molecular weight of 33729 Da. CCND1 is a member of the cyclin family, Cyclin D subfamily and contains 1 cyclin N-terminal domain.
 
  The RNA expression data of CCND1 based on data from BioGPS, Illumina Human BodyMap, and SAGE, with SAGE tags from CGAP,
The RNA expression data of CCND1 based on data from BioGPS, Illumina Human BodyMap, and SAGE, with SAGE tags from CGAP,
Figure shows RNA expression data (presence/absence) for RNA genes is according to H-InvDB, NONCODE, miRBase, and RNAdb. The expression images based on data from BioGPS, Illumina Human BodyMap, and SAGE, with SAGE tags from CGAP.
BioGPS
76 normal tissues were used and compartments hybridized against HG-U133A, with Affeymetrix MAS5 algorithm used in array processing.
Illumina body map
Transcripts were mapped to genes from 16 normal human tissues by sequencing. Cufflinks program was used to calculate Fragments per Kilobase of exon per Million fragments mapped (FPKM) and rescaled by multiplying FPKM by 100 and calculating the root.
CGAP: SAGE Normal
For Serial Analysis of Gene Expression (SAGE) of 19 normal human tissues, Hs frequencies and Hs libraries in CGAP datasets are mined for information regarding the number of SAGE tags per tissue. Unigene clustering was applied to Tags, followed by a particular gene by mining Hs best gene, Hs best tag and Hs GeneData. The number of appearances of the corresponding tag divided by the total number of tags in libraries derived from that tissue was used in calculating the level of expression of a particular gene, which were then rescaled by making the genomic mean of all tissues equal.
Intermediate between log and linear scales are normalized intensities drawn on root scale, with values not comparable between datasets (i.e. Microarray, RNAseq and SAGE).
Figure courtesy: genecards.org.
 
  Presentation of protein expression images for 35 tissues, fluids and cells. Data sources:
1- MOPED - Eugene Kolker, Bioinformatics & High-throughput Analysis Lab, Seattle Children's Research Institute
. 2- PaxDb - Christian von Mering, Bioinformatics Group, Institute of Molecular Life Sciences, University of Zurich.
3- MAXQB - Matthias Mann, Department of Proteomics and Signal Transduction, Max-Planck Institute of Biochemistry, Germany.
The data was normalized as follows:
For each sample, ppm protein values were calculated, if not provided so by data sources. For each sample from MAXQB, iBAQ expression values were divided by sum of values of each sample, and multiplied by 1,000,000. For all samples, data was gene centrically aggregated by summing expression values of all isoforms for each gene. For better visualization of graphs, expression values are drawn on a root scale, which is an intermediate between log and linear scales as used for our mRNA expression graphs (PMID 12519968).
Localisation Nuclear, cytoplasmic and membrane.
NOTE: Accumulation of CCND1- CDK4 complexes occur in the nuclear membrane, which are then transported to the nucleus through interactions with KIP-CIP family member proteins (By similarity, a LaBaer et. al.,1997).
 
  EXPRESSION IN TISSUES:
TOP: Cyclin D1 overexpression in keratoacanthomas (KAs) and squamous cell carcinomas (SCCs). CCND1 (brown), counterstain hemalaun (blue). (a) Normal skin and (b) actinic keratosis, a precursor lesion of SCCs. (c-f) Representative KAs (c) Higher magnification of a different tumor (d); medium expression (e); and low expression (f) of cyclin D1. Bar=50 micro-m. Image courtesy Burnworth et. al., 2006.
MIDDLE: The figure shows the localization of CCND1 in Ramos cells. Image courtesy Abcam ®
BOTTOM: EXPRESSION DURING CELL CYCLE:
Image shows the levels expression of CCND1 during different phases of the cell cycle (left panel) and the function associated in each phase (right). Image courtesy kinexux.ca (left) and Yang et. al., 2006 (right).
Function CCND1 binds and activates the G1 cyclin dependent kinases, Cdk4 and Cdk6. The complex then phosphorylates and inhibits members of the retinoblastoma (RB) family of protein including RB1, thereby regulating the G1/S transition in the cell cycle (Kato et al., 1993).
CCND1 has a kinase-independent function of sequestering CDK inhibitors such as p27 Kip1 and p21Cip1and promoting efficient activation of Cyclin E/CDK2-containing complexes (Polyak et al., 1994; Sherr and Roberts, 1999).
CCND1 phosphorylates Smad3 and inhibits its transcriptional activity and antiproliferative function (Matsuura et. al., 2004).
 
Homology The CCND1 gene is conserved in chimpanzee, Rhesus monkey, dog, cow, mouse, rat, chicken, zebrafish, and frog (According to Homologene, NCBI).
 
  Top: String model depicting probable binding partners on CCND1. Image adapted from string-db.org; Bottom: The figure shows the different proteins with which CCND1 interact and the different functions that result from such interactions. Picture courtesy: Pestell, 2013.
 
  Gene tree of CCND1 Human has been encircled in red. Adapted from ensembl.org.

Mutations

 
  Figure shows the predicted miRNA binding sites in the 3' UTR of CCND1. Image courtesy TargetScan 6.2.
  ../Genes/Images/CCND1Fig11.png   ../Genes/Images/CCND1Fig12.png   ../Genes/Images/CCND1Fig13.png  
Epigenetics CCND1 and miRNAs:

miR365
in Gastric cancer cell line BGC-823
Binds to 3' UTR of CCND1 in gastric cancer. miR-365 markedly decreased the expression (mRNA and protein) of CCND1. Conversely, miR365 knockdown repressed cell growth, which can be overcome by CCND1 over-expression. Similar inverse co-relation was obtained between miR-365 and CCND1 expression in patient samples. (Long-Guo et. al., 2013).
in Vascular smooth muscle cell (VSMC)
miR-365 suppresses CCND1 significantly in mRNA and protein levels in primary rat VSMC. CCND1 is a direct target of miR-365 in vascular smooth muscle cells, as shown by significant inhibition of the luciferase activity of wild type CCND1 3' UTR, but not the mutant cyclinD1 3' UTR with the mutant biding site of miR-365 (Zhang et. al., 2014). CCND1 is a potential target of mir-365 through direct binding. (Kim et. al., 2014).
in Colon cancer
miRNA directly binds to the 3'UTR of CCND1, proved by luciferase reporter assay. Transfection of miR365 significantly decreased CCND1 expression in HT29 and LoVo cells. Pearson's co-relation between miR-365 levels and CCND1 expression by qRT-PCR and western blot showed that they were inversely correlated (Nie et. al., 2012).

miR-338-3p in Hepatocyte cell line LO2
miR-338-3p binds at two regions in the 3' UTR of CCND1( mainly at the site spanning nucleotides 2397-2403). Overexpression of miR-338-3p downregulates endogenous CyclinD1 protein, while inhibition upregulates CyclinD1 protein, without any change in CCND1 mRNA levels. miR-338-3p post-transcriptionally regulates CCND1 (Fu et. al., 2012).

miR-19a in Human umbilical vein endothelial cells (HUVECs)
miR-19a binding site (nucleotides 1,778-1,785 in human CCND1) identified by sequence alignment, which is highly conserved among different species. Binding of miR-19a to 3' UTR of CCND1 verified by luciferase assay. CCND1 protein expression markedly reduced upon over-expression of miR-19a, although no change in RNA expression. miR-19a post-transcriptionally regulates CCND1 expression (Qin et. al., 2010).

miR-490-3p in A549 Lung cancer cell line
miR-490-3p binds to 3' UTR of CCND1. Over-expression decreased the expression of CCND1, both at the RNA and protein levels (Gu et. al., 2014).

miR-302 in Endometrial cell line Ishikawa
Directly targets CCND1 and significantly inhibited protein expression (Yan et. al., 2014).

miR-449-a in Gastric cancer cell line SGC7901
miR-449a inhibited SGC7901 cells proliferation and enhanced cisplatin chemosensitivity by downregulating expression of CCND1, respectively, via directly targeting the 3'-untranslated regions of CCND1 mRNA (Hu et. al., 2014).

miR-16 in Bladder cancer cell line TCHu-1
Binding of miR16 to 3' UTR of CCND1 and its reduced expression was validated by luciferase assay, while the reverse result was obtained by mutation of the conserved miR-16 binding motif. Overexpression of miR-16 in TCHu-1 cells led to reduced CCND1 protein expression, whereas its inhibition led to an increased expression of CCND1 (Jiang et. al., 2013).

miR-9 in Gastric cancer
Databases indicated potential binding site of miR-9 with high complementarity at CCND1 39-UTR (bases 2974-2995), which was validated by luciferase reporter assay. Significant inverse correlation between miR-9 expression and CCND1 transcript levels in gastric cancer tissues and cell lines. Overexpression of miR9 in gastric cancer cell lines SGC-7901 and AGS resulted in reduced RNA and protein expression of CCND1, whereas knockdown of miR-9 produced the opposite result, proving that miR-9 considerably inhibited the expression of CCND1 through post-transcriptional repression. Results validated by in-vitro experiments (Zheng et. al., 2013).

miR-195 in Glioma
Analysis using publicly available algorithms (TargetScan, Pictar, miRANDA) indicates that CCND1 is a predicted target of miR-195, which was validated by overexpression of miR- 195, which reduced, but inhibition of miR-195 increased, the luciferase activity of CCND1-39UTR in a consistent and dose-dependent manner. Upregulation of miR-195 decreased, but inhibition of miR-195 increased, the expression levels of CCND1 in LN18 and T98G glioma cells. The findings were also validated in a model system in mice (Hui et. al., 2013).

miR-155 in Human extravillous trophoblast derived HTR-8/SVneo cells
Bioinformatics analysis showed that, at the 3' untranslated region (UTR) of CCND1, six bases are complementary to the seed region of miR-155. Luciferase assays and CCND1 3'UTR transfection assays validated that CCND1 3'UTR was the target of miR-155 in HTR-8/SVneo cells. Overexpression of miR-155 in HTR-8/SVneo cells reduced the level of CCND1 protein (Dai et. al., 2012).

miR-143 in Mesenchymal stem cells from the bone marrow of male Fischer 344 rats
Ectopic expression of miR-143 also increased CCND1 in the native MSC as compared with scramble transfected cells .On the contrary, pre-treatment of AAMSC with miR-143 specific antagomir significantly abolished CCND1 expression (Lai et. al., 2012).

miR-21
in Mouse liver regeneration
Cyclin D expression and G1 phase transition of hepatocytes after 2/3 PH depend on induced miR-21 expression. Knockdown of miR-21 impaired progression of hepatocytes into S phase of the cell cycle, mainly through a decrease in levels of cyclinD1 protein, but not Ccnd1 mRNA, whereas increased miR-21 expression facilitated CCND1 translation in the early phase of liver regeneration (Ng et. al., 2012).
in Renal cancer
miR-21 controlled the expression of CCND1 through NF?B-dependent transcription and mediated renal cancer cell proliferation by CCND1 (Bera et. al., 2013).

miR-520-b in Hepatoma cell lines
miR520-b directly targets the 3 'UTR of CCND1; proved by dual luciferase reporter system. Down-regulation of protein levels of CCND1 occurred on over-expression of miR520-b in HepG2 and H7402 cells, while the over-expression occurred on inhibition in miR520-b. Tumors in mice over-expressing miR520-b also showed lower CCND1 expression (Zhang et. al., 2012).

miR-193b in Melanoma
TargetScan showed that miR193b binds to the 3'UTR of CCND1, which was proved by luciferase reporter assay. miR-193b over-expression led to nearly 50% reduction in CCND1 mRNA and protein levels in Malme-3M cells than in control (Chen et. al., 2010).

miR-17/20 in Breast cancer
Levels of the miR-17-5p/miR-20a miRNA cluster were inversely correlated to CCND1 abundance in human breast tumors and cell lines. miR 17/20 negatively regulates the expression of CCND1 by binding to a conserved 3'UTR region (nucleotides 2,109-2,117) of the gene (Yu et. al., 2008).

miR-20 and miR106-a in Spermatogonial stem cells (SCC)
They promote renewal at the post-transcriptional level via targeting CCND1. Knockdown of CCND1 results in renewal of SCCs (He et. al., 2013).

miR-503 in Endometrioid endometrial cancer (EEC)
Binds to 5' UTR of CCND1 and its expression is inversely co-related with CCND1 in EEC tissues and cell lines (Xu et. al., 2013).

miR-449b in SW116 colon cancer stem cell
Transfecting pre-miR-449b and inhibiting miR-449b altered protein expression levels of CCND1 (Fang, 2013).

miR-15a and miR16-1 in Osteosarcoma
They bind to 3'-UTR of CCND1 and suppress transcription of CCND1 (Cai et. al., 2012).

miR-138 in Nasopharyngeal carcinoma
CCND1 is a novel direct target of miR138. mRNA levels of CCND1 were inversely correlated with miR-138 expression (Liu et. al., 2012).

miR-34a in A549 cell line
Ectopic expression of miR-34a reduces both mRNA and protein levels of CCND1 by targeting the 3'-untranslated mRNA region of CCND1 (Sun et. al., 2008).

miR-29a in Breast cancer cell lines
Over-expression of miR29a down-regulation of CCND1 expression in MDA-MB-453 cells, whereas in MCF-10A cells with Mir-29a knockdown, CCND1 was up-regulated (Wu et. al., 2013).

miR-7 in Colorectal cancer cell lines
Over-expression of miR-7 significantly decreased CCND1 expression (Xu et. al., 2014).

miR-545 in Lung cancer
miR-545 caused cell cycle arrest at the G0/G1 phase and induced cell apoptosis in lung cancer cells by targeting CCND1. The effects of CCND1 down-regulated by miR-545 were similar to those caused by siRNAs of CCND1 and over-expression of CCND1 could abolish the miR-545-induced inhibition of cell proliferation (Du et. al., 2014).

miR-125b in Melanoma
Cells over-expressing miR-125b exhibited reduced expression of CCND1 (Nyholm et. al., 2014).

miR-147 in Colon and lung cancer cells.
Transfection of miR147 led to down-regulation of CCND1 (Lee et. al., 2014).

Implicated in

Note
  
Entity t(11;14)(q13;q32)/B-cell malignancies CCND1/ IgH
Disease The t(11;14) is mainly found in mantle cell lymphoma; also in: B-prolymphocytic leukaemia, plasma cell leukaemia, splenic lymphoma with villous lymphocytes; rarely in: chronic lymphocytic leukaemia, multiple myeloma
Prognosis according to the disease.
Cytogenetics Complex karyotypes.
Hybrid/Mutated Gene 5' CCND1 translocated on chromosome 14 near JH (junctions genes of IgH) and C in 3'.
 
Fluorescence in situ hybridization (FISH) for identification of t(11;14)(q13;q32) chromosomal translocation in metaphase nuclei. Orange probe represents CCND1 (chromosome 11q13), green represents IGH (chromosome 14q32). Fusion signals representing translocations are encircled in white. Image courtesy Ghielmini et. al., 2009.
Abnormal Protein no fusion protein, but promoter exchange; the immunoglobulin gene enhancer stimulates the expression of CCND1.
Oncogenesis Overexpression of CCND1 accelerates the cell transit through the G1 phase (Williams et. al., 1993, Williams et. al., 1994, Rimokh et. al., 1994, Wlodarska et. al., 1994, de Boer et. al., 1997, Stilgenbauer et. al., 1998, Donnellan et. al., 1998, Li et. al., 1999, Wlodarska et. al., 2004, Sander et. al., 2008).
  
  
Entity t(11;19)(q13;p13) CCND1/ FSTL3
Note Found in a case of chronic lymphocytic leukaemia (Hayette et al., 1998).
  
  
Entity Acute Lymphoblastic Leukemia (ALL)
Note Routinely used ALL drugs: Routinely used drugs failed to bind to CCND1 in in vitro docking studies (Jayaraman et. al., 2014).
  
  
Entity Adrenocortical tumors (AC)
Note CCND1 was over-expression in 31.0% (13/42) in AC tumors compared to 17.5 % (4/23) in normal adrenal samples. Similarly, mRNA of CCND1 was significantly over-expressed in AC compared to normal samples (Mitsui et. al., 2014).
  
  
Entity B cell neoplasia
Note Strong CCND1 mRNA over-expression was detected in mantle cell lymphomas (23 of 23), hairy cell leukemias (5 of 19), and multiple myelomas (7 of 23) with particularly high levels in 2 of the latter cases. Intermediate CCND1 transcripts were detected in multiple myeloma (5 / 23), hairy cell leukemia (7 / 19) Low of no CCND1 was detected in B -cell chronic lymphocytic leukemias (10 / 10), follicular lymphomas (9 / 9), mucosa associated lymphoid tissue lymphomas (5 / 5) and reactive lymphoid tissues (Specht et. al., 2002).
  
  
Entity Biliary Intraepithelial Neoplasia (BilIN) / Pancreatic Intraepithelial Neoplasia (PanIN)
Note Immunohistochemical expression of CCND1 was absent or focal in nonneoplastic epithelium of the bile ducts and the pancreatic ducts, and were occasionally observed in BilIN-1 and PanIN-1 and more frequently in BilIN-2/3 and PanIN-2/3. No significant difference was obtained between expression of BilIN and PanIN in semi-quantitative analysis (Sato et. al., 2014).
  
  
Entity Bladder cancer
Note Increased CCND1 levels were not correlated with OS with a pooled HR estimate, but were significantly correlated with progression-free survival (Ren et. al., 2014)
Over-expression of Pin X1 in T24 cells leads to greater than 2 fold increase in mRNA expression of CCND1 than in control cell, with similar results obtained by Western blotting. A significant correlation between the immune-histochemical expression of PinX1 and CCND1 was also observed in the UCB tissues (Liu et. al., 2013).
Ursane triterpenoid isopropyl 3?-hydroxyurs-12-en-28-oat (UA17) (Natural compound) : Protein level of CCND1 was down-regulated in a dose-dependent manner when treated with UA17or Cisplatin in NTUB1 cells. Enhanced decrease of level of CCND1 when treated with a combination of Cisplatin (20 ?M) + UA17 (20 ?M) (Lin et. al., 2014)
Metformin : Treatment with metformin leads to reduction in expression of CCND1 in a dose-dependent manner. Metformin treatment also markedly reduced the expression of CCND1 in Human Bladder Tumor Xenografts in Nude Mice compared to control (Zhang et. al., 2013).
  
  
Entity Breast cancer
Note CCND1 induction of Dicer coordinates microRNA biogenesis by its transcriptional targeting (Yu et. al., 2013).
CCND1 overexpression is associated with longer DSS, but not recurrence-free survival, in patients with breast cancer (Chung et. al., 2014).
There was a statistically significant reverse relationship of CCND1 with tumor grade and both ER and PR hormone receptors (Mohammadizadeh et. al., 2013).
CCND1 was one of the most frequently altered genes in breast cancer (Wheler et. al., 2014).
Activation of Notch-1 signaling up-regulated expression of CCND1 through NF-kB (Li et. al., 2014).
Acylglycerol kinase (AGK) over-expression led to concurrent increase in levels of CCND1 (Wang et. al., 2014).
over-expression led to blockade of CCND1 expression via BCAS2 and ?-catenin (Sengupta et. al., 2014).
Enhanced expression of Vav1 led to the elevation of CCND1 and the progression of cell cycle (Du et. al., 2014).
CCND1 was frequently more positive in ER alpha positive and Bmi1 positive breast tumors than ER alpha negative and Bmi1 negative groups (Wang et. al., 2014).
Progesterone induced the assembly of a transcriptional complex among AP-1, Stat3, PR, and ErbB-2 at the CCND1 promoter, which functions as an enhanceosome to drive breast cancer growth (Flaqué et. al., 2013).
Prolactin-induced protein (PIP) silenced cells showed marked decrease in CCND1 expression (Naderi et. al., 2014).
Calcitriol (Natural compound): In calcitriol-treated cells, the presence of antiestrogen ICI-182 down-regulated CCND1 gene expression (Martinez et. al., 2014).
Euginol (Natural compound): Treatment of euginol decreased CCND1 level 3 fold in MDA-MB-231 cells and 20 fold in MCF7 cells compared to control (Sharif et. al., 2013).
Fangchinoline (Fan) (Natural compound): Fan decreased the expression of CCND1 both in the RNA and protein level (Wang et. al., 2014).
Gallotannin (Natural compound): Nanostring and qPCR data showed that CCND1 was exclusively downregulated on treatment with gallotannin in triple negative breast cancer (Zhao et. al., 2014).
8bromo7methoxychrysin (BrMC) (Natural compound): BrMC caused a dosedependent reduction of CCND1 in HER2/neu over-expressing breast cancer cells (Cao et. al., 2014).
Panepoxydone (Natural compound): CCND1 was down-regulated by dose-dependent treatment of Panepoxydone (Arora et. al., 2014).
Thymus caramanicus extract (TCE) (Natural compound): TCE led to reduction in expression of CCND1, either alone or in combination with Vincristine (Mahani et. al., 2014).
Tea polyphenols (Natural compound): Tea polyphenols did not significantly alter the expression of CCND1 in breast cancer cell lines (Chen et. al., 2014).
Fenofibrate : Fenofibrate decreased the expression of CCND1 in a time and dose dependent manner in Triple negative breast cancer cells (Li et. al., 2014).
Obatoclax analog SC-2001 : SC-2001 down-regulated CCND1 in TNBC cell lines in a dose- dependent manner (Liu et. al., 2014).
  
  
Entity Chronic Myeloid Leukemia (CML)
Note Resveratrol (Res) (Natural compound): Res reduced expression of CCND1 in K562 cells (Siu et. al., 2014).
Quercetin (Natural compound): CML KBM7 Cells demonstrated reduction in expression on CCND1 on treatment with quercetin ((Li et. al., 2014).
  
  
Entity Chronic Myeloid Leukemia (CML)
Note Resveratrol (Res) (Natural compound): Res reduced expression of CCND1 in K562 cells (Siu et. al., 2014).
Quercetin (Natural compound): CML KBM7 Cells demonstrated reduction in expression on CCND1 on treatment with quercetin ((Li et. al., 2014).
  
  
Entity Colorectal cancer
Note There was significant association between post-menopausal hormone therapy (HRT) and CCND1 negative-tumors, as well as significantly increased risk in CCND1 positive tumours (Brändstedt et. al., 2014).
High height and weight was associated with risk of CCND1 positive CRC in women. Increased hip circumference, high BMI, high WHR and high waist circumference was associated with CCND1 positive tumours in men (Brändstedt et. al., 2013).
CCND1 over-expression was significantly associated with both poor OS, DFS, relatively older patients (?60 years), T3,4 tumor invasion, N positive and distant metastasis (Li et. al., 2104).
Galectin-3 knockdown decreased the mRNA expression level of CCND1, whereas epirubicin significantly up-regulated their expression. Combined treatment effectively reduced the mRNA expression of CCND1 (Lee et. al., 2013).
HMGCR expression was significantly associated with expression of CCND1 (Bengtsson et. al., 2014).
CoCl2 : Treatment of COCl2 leads to dose-dependent decrease in expression of CCND1 and cell cycle arrest (Lopez-Sanchez et. al., 2014).
SW620-S and TGF-b1 : Fibroblasts induced by Colorectal cancer cells, treated with SW620-S and TGF-b-1 separately showed high expression of CCND1 (Rao et. al., 2014).
  
  
Entity Diffuse large B-cell lymphoma
Note A case of diffuse large B-cell lymphoma was described, which developed within a rectal tubular adenoma with low-graded dysplasia. The mass showed positive staining of CCND1 (Genovese et. al., 2014).
  
  
Entity Esophageal cancer
Note CCND1 G870A polymorphism had no significant association with esophageal squamous cell carcinoma (ESCC) or esophageal adenocarcinoma (EADC) in Caucasian or the Asian populations. However, the comparison of A vs. G in CCND1 G870A showed significant differential susceptibility to esophageal cancer, suggesting that the CCND1 G870A polymorphism has no association with esophageal cancer risk in ethnicity and histology, respectively (He et. al., 2013).
No significantly statistical differences between the two groups were observed in distribution of genotypes or alleles at CCND1 807 (Jang et. al., 2013).
  
  
Entity Fibrosarcoma
Note KIOM-C (Natural compound) : Treatment of HT1080 human fibrosarcoma cells led to down-regulated expression of CCND1 compared to control (Kim et. al., 2014).
  
  
Entity Gastric cancer
Note Down regulation of CCND1 by ShCCND1 in NCI-N87 cells showed significant inhibition of cell proliferation, cell motility, clonogenicity, G1 arrest and apoptosis. Results were validated by in vivo studies in mice, suggesting the possibility of developing new gastric cancer therapies using lentivirus-mediated shRNA (Seo et. al., 2014).
Odd-skipped related 1 (OSR1) suppressed the expression of CCND1 (Otani et. al., 2014).
Knockdown of P115 led to reduction in expression of CCND1, whereas its over-expression led to up-regulation of CCND1 (Li et. al., 2013).
Caudatin 3-O-?-D-cymaropyranosyl-(1 ? 4)-?-D-oleandropyranosyl-(1 ? 4)-?-D-cymaropyranosyl-(1 ? 4)- ? -D-cymaropyranoside (CGII) (Drug): CGII induced down-regulation of expression of CCND1 in a dose-dependent manner in Gastric Cancer SGC-7901 Cells (Wang et. al., 2013)
Tetramethypyrazine (TMP) (Natural compound): Expression of CCND1 gradually decreased with increasing concentrations of TMP in Gastric cancer 7901 cells (Ji et. al., 2014).
Resveratrol (Res) (Natural compound) : Res reduced expression of CCND1 (Yang et. al., 2013).
  
  
Entity Gastric cancer
Note Down regulation of CCND1 by ShCCND1 in NCI-N87 cells showed significant inhibition of cell proliferation, cell motility, clonogenicity, G1 arrest and apoptosis. Results were validated by in vivo studies in mice, suggesting the possibility of developing new gastric cancer therapies using lentivirus-mediated shRNA (Seo et. al., 2014).
Odd-skipped related 1 (OSR1) suppressed the expression of CCND1 (Otani et. al., 2014).
Knockdown of P115 led to reduction in expression of CCND1, whereas its over-expression led to up-regulation of CCND1 (Li et. al., 2013).
Caudatin 3-O-?-D-cymaropyranosyl-(1 ? 4)-?-D-oleandropyranosyl-(1 ? 4)-?-D-cymaropyranosyl-(1 ? 4)- ? -D-cymaropyranoside (CGII) (Drug): CGII induced down-regulation of expression of CCND1 in a dose-dependent manner in Gastric Cancer SGC-7901 Cells (Wang et. al., 2013)
Tetramethypyrazine (TMP) (Natural compound): Expression of CCND1 gradually decreased with increasing concentrations of TMP in Gastric cancer 7901 cells (Ji et. al., 2014).
Resveratrol (Res) (Natural compound) : Res reduced expression of CCND1 (Yang et. al., 2013).
  
  
Entity Glioma
Note Expression of Alpha enolase (ENO-1) inhibited the expression of CCND1 (Song et. al., 2014).
  
  
Entity Hairy Cell Leukemia (HCL)
Note CCND1 displayed nuclear staining at variable intensities but with high specificity and accuracy in HCL biopsies, thus representing it as a valuable tool in the differential diagnosis of HCL and its mimics (Tóth-Lipták et. al., 2014).
  
  
Entity Head and neck squamous cell carcinoma
Note Amplification, over-expression and translocation of CCND1 has been reported (Akervall et. al., 1997, Akervall et. al., 2002, Utikal et. al., 2005, Sabbir et. al., 2006). However, expression of CCND1 did not change in post-therapy tumors compared to pre-therapy (Sarkar et. al., 2014).
  
  
Entity Head and neck squamous cell carcinoma
Note Amplification, over-expression and translocation of CCND1 has been reported (Akervall et. al., 1997, Akervall et. al., 2002, Utikal et. al., 2005, Sabbir et. al., 2006). However, expression of CCND1 did not change in post-therapy tumors compared to pre-therapy (Sarkar et. al., 2014).
  
  
Entity Hepatocellular Carcinoma (HCC)
Note Ectopic expression of miR-184 led to down-regulation of the SOX7 protein, resulting in up-regulation of CCND1, cell proliferation and tumorigenesis (Wu et. al., 2014). SOX7-overexpression inhibited cell growth by down-regulating CCND1, which could be over-ridden by ectopic expression of CCND1 and induction of SOX7. Over-expression of SOX7 suppressed tumor formation with down-regulation of CCND1 in vivo (Wang et. al., 2014).
Knockdown of TRIM24 led to decreased CCND1 expression (Liu et. al., 2014).
KIF14 knockdown suppresses tumor cell growth through decrease in levels of cyclins including CCND1 (Xu et. al., 2014).
Knockdown of expression of SHC SH2-domain binding protein 1 (SHCBP1) led to reduction in expression of CCND1 (Tao et. al., 2013).
7. 3, 3'DiOmethyl ellagic acid4'O?dxylopyranoside (JNE2). JNE2 induced down-regulation of expression of CCND1 in HepG2 cells (Zhang et. al., 2014).
Silybin (SIL) (Natural compound): Treatment of HepG2 cells with SIL led to down-regulation of expression of CCND1 (Zhang et. al., 2013).
SL1122-37: SL1122-37 induced down-regulation of expression of CCND1 in PLC/ PRF/5 HCC cells (Qin et. al., 2013).
IBN-65 (1-benzyl-2-phenyl-3-(4-isopropyl)-benzyl-imidazolium chloride) : IBN-65 decreased levels of CCND1 in Huh7 cells in Mouse model of HCC (Gopalan et. al., 2014).
Sorafenib and YC-1 : Treatment with the sorafenib and YC-1 combination led to a significant reduction in CCND1 (Kong et. al., 2014).
  
  
Entity Hepatoma
Note Over-expression of HAFHIT inhibited the expression of CCND1 in the cells. In HepG2 cells which were transfected with a fulllength CCND1 promoterluciferase reporter, cotransfection with increasing quantities of FHIT plasmid DNA caused a concentrationdependent inhibition of the transcriptional activity of the CCND1 promoter (Ge et. al., 2014).
  
  
Entity Lung Cancer
Note 1. PAX6 down-regulation led to reduction in protein levels of CCND1 (Zhao et. al., 2014).
Over-expression of Ubiquitin- conjugating enzyme E2C (UBE2C) increased expression of CCND1 in L-78 and SC-1680 cells, as well as in tumor transplants in nude mice (Tang et. al., 2014).
Met- F-AEA in combination with URB597 induced down-regulation of CCND1 and subsequent G0/ G1 cell cycle arrest (Ravi et. al., 2014).
Up-regulation of decorin led to significant decrease in expression of CCND1 (Liang et. al., 2013).
The expression of CCND1 was significantly decreased upon knockdown of Claudin-2 in lung adenocarcinoma (Ikari et. al., 2014).
Knockdown of JAM-A decreased protein levels of CCND1 (Zhang et. al., 2013).
Tea polyphenols (Natural compound): Epigallocatechin gallate, epicatechin gallate and theaflavin reduced the expression of CCND1 in benzo(a)pyrene-induced lung carcinogenesis in mice (Manna et al., 2009).
Polydatin: PD suppressed expression of CCND1 in A549 and NCIH1975 lung cancer cell lines (Zhang et. al., 2014).
  
  
Entity Mantle Cell Lymphoma (MCL)
Note 1. Decrease in expression of CCND1 by RNSi induced partial inhibition and reduced expression of AKT and/or S6, which may in turn lead to decrease in NOXA mRNA levels (Dengler et. al., 2014).
85% were weakly positive and 15%, moderately positive with labelled streptavidin biotin, whereas 75% were weakly positive and 25% moderately positive for CCND1 with EnVision. All 20 mantle cell lymphoma cases were strongly CCN D1 positive with catalyzed signal amplification. No evidence of CCND1 immunostaining was obtained in any of the small lymphocytic lymphoma and follicular centre cell lymphoma instances with any of the three methods used (Barranco et. al., 2003).
CCND1 showed exclusive nuclear staining and directly compared with the expression observed by immunoblot analysis with the same antibody, as well as with mRNA expression and with the occurrence of genomic rearrangements within the B CL-1 locus. 12/13 MCL showed over-expression by immunohistochemistry or immunoblot, with similar results for additional 13 MCLs, indicating its importance for routine diagnostic purposes (Boer et. al., 2014).
CCND1 mRNA could be detected in 23 of 24 mantle-cell lymphomas by reverse transcription polymerase chain reaction (RT-PCR) whereas only 9 of 24 demonstrated a t(11;14) by PCR (Aguilera et. al., 1998).
In 16 of 21 cases of MCL with overt disease, the ratio of CCND1 mRNA to ?2-microglobulin mRNA was increased, but all 21 cases showed increased ratios of CCND1 mRNA to CD19 mRNA (Howe et. al., 2004)
  
  
Entity Melanoma
Note Piperine (Natural compound) : Piperine induced reduction in expression of CCND1 in a dose- dependent manner in SK MEL 28 and B16 F0 melanoma cells (Fofaria et. al., 2014).
  
  
Entity Multiple myeloma
Note CCND1 expression was observed in 57% cases. CCND1 positive group had significantly lower hemoglobin level than CCND1 negative group, though both groups showed no statistical significance in regard to age, gender, Durie and Salmon stage, lytic bone lesions, light chain phenotype, creatinine, calcium, lactate dehydrogenase, leukocyte and platelet count and bone marrow histology (Padhi et. al., 2013).
  
  
Entity Nasopharyngeal cancer
Note No significant association was found between CCND1 G870A polymorphism and nasopharyngeal carcinoma risk in total population meta-analysis. In the subgroup meta-analysis by ethnicity, a negative association was shown in Caucasian subgroup, and no significant association in any genetic models among Asians was observed (Li et. al., 2013).
Indole-3-carbinol (I3C) : I3C induced G1 arrest by decreasing CCND1 expression (Chen et. al., 2013).
  
  
Entity Neuroblastoma
Note CCND1 showed strong nuclear reactivity in a case study on Primary localized congenital sacrococcygeal neuroblastomas (SCNs) (Khandeparkar et. al., 2013).
Over-expression of n-myc downstream regulated gene 2 (NDRG2) induced down-regulation of expression of CCND1 (Zhang et. al., 2014).
A negative co-relation existed between WWOX and CCND1 expression (Nowakowska et. al., 2014)
  
  
Entity Odontogenic tumors
Note Using immune-labelling of CCND1, no statistical difference was observed between primary and recurrent KOT (keratocystic odontogenic tumors), sporadic and NBCCS-KOT (nevoid basal cell carcinoma syndrome), and unicystic and solid AB (ameloblastomas) (Gurgel et. al., 2014).
  
  
Entity Oral cancer
Note Expression of CCND1 in group 3 (leukoplakias exhibiting dysplasias) was significantly higher than in group 1 (normal buccal mucosa without any habits) and 2 (clinically normal mucosa from tobacco habits), expression in group 2 was significantly higher than in group and were statistically significant. CCND1 was mostly expressed in the lower third of epithelium. Highest expression was obtained in mild dysplasias, with expression consistently correlating with basilar hyperplasia among atypical morphological features (Ramakrishna et. al., 2013).
Clinico-pathological correlation showed that CCND1 over-expression was related to increase in tumor size, tumor differentiation and higher clinical stages and lymph node metastasis and adversely affected overall survival (Zhao et. al., 2014).
HPV-negative patients, heavy alcohol consumption was significantly associated with somatic copy-number alterations (SCNAs) in CCND1 (Urashima et. al., 2013).
The proportions of positive staining in well, moderately and poorly differentiated laryngeal SCC were 50, 66.7, 100%, respectively, for CCND1, and were statistically significant, with the expression being positively correlated with Ang-2 expression. Tumor grading and CCND1 were independent factors affecting laryngeal SCC patient survival by the Cox regression model of risk factors proportion analysis, which may possess clinical significance in evaluating the prognosis and guiding the clinical treatment of SCC (Liu et. al., 2013).
Knockdown of Nemo-like kinases (NLK) led to significant reduction in the levels of CCND1 (Dong et. al., 2013).
2,4-bis (p-hydroxyphenyl)-2-butenal : HPB 242 significantly decreased CCND1 expression in HN22 and HSC4 Oral squamous cell carcinoma cell lines (Chae et. al., 2014).
  
  
Entity Osteosarcoma
Note Selective inhibition of Ether à go-go 1 (Eag1) led to significant decrease in expression of CCND1 (Wu et. al. 2014).
  
  
Entity Ovarian serious carcinoma
Note Compared with NOT (Normal Ovarian Tissue), CCND1 expression in the OSA (ovarian serous cystadenomas) and OSC (Ovarian serous carcinoma) groups was significantly elevated. Expression of CCND1 was positively associated with lymphatic metastasis and the expression gradually increased in the NOT, OSA, OSBT and OSC groups and was associated with tumor metastasis (Song et. al., 2014).
  
  
Entity Pancreatic cancer
Note Silencing of Frizzled (Fz)2 by siRNA or shRNA induced significant reduction of expression on CCND1 (Tomizawa et. al., 2014).
Down-regulation of miR-196a led to decrease in expression of CCND1 via Nuclear Factor Kappa-B-Inhibitor Alpha (Huang et. al., 2014).
Diallyl trisulfide (DATS) (Natural compound) : DATS reduced levels of CCND1 and DATS-induced apoptosis was correlated with down-regulation of CCND1 protein levels in Capan-2 cells (Ma et. al., 2014).
alpha-Mangostin (Natural compound) : alpha--Mangostin led to decrease in expression of CCND1 (Xu et. al., 2014).
Pristimerin (PM) : PM treatment produced decreased expression of CCND1 in MiaPaCa-2 and Panc-1 cells (Deeb et. al., 2014).
  
  
Entity Plasmacytoma
Note A solitary plasmacytoma following complete remission from an intravascular large B-cell lymphoma, stained strongly for CCND1 while the initial tumor was negative for CCND1, proving different clonal origins of the tumors (Lee et. al., 2014).
  
  
Entity Prostate cancer
Note CNCD1 staining was positive (expression in .5% of tumor cells) in 64 cases (75.4%) and negative (expression in ?5% of tumor cells) in 21 cases (including 15 cases with no immunostaining) with normal prostate tissues being negative for CCND1. Patients with high grade Gleason score and perineural invasion showed significant association with CCND1 expression, but not with PSA levels or other parameters. Thus, high CCND1 expression could be a potential marker for tumor aggressiveness (Pereira et. al., 2014).
Univariate analyses showed that lymph node positivity, surgical margin positivity, non-localized tumor, age at prostatectomy and CCND1 in malignant epithelium were significantly associated with time to BF (Biochemical failure) (Rizzardi et. al., 2014).
Reevesioside A (Natural compound) : Reevesioside A inhibited expression of CCND1 in Hormone-Refractory Prostate Cancers (Leu et. al., 2014).
Scoparone (Natural compound) : Scoparone suppressed the transcription of STAT3 target CCND1 in DU-145 cells (Kim et. al., 2013).
Triptolide (Natural compound) : Triptolide induced significant decrease of expression of CCND1 through EZH2 (Tamgue et. al., 2014).
Pifithrin (PFT) : Combination therapy with suboptimal doses of PFT-m and HT decreased expression of CCND1 (Sekihara et. al., 2013).
  
  
Entity Renal cancer
Note Microvessicles : CCND1 protein expression in tumor tissues was markedly up-regulated by MVs released from human Wharton's jelly mesenchymal stem cells (hWJ-MSCs) (Du et. al., 2014).
  
  
Entity Sarcoma
Note Tea polyphenol epigallocatechin gallate (EGCG) did not alter expression of CCND1 in Sarcoma180 cells in vivo (Manna et. al., 2006)
  
  
Entity T-cell Acute Lymphoblastic Leukemia
Note Resveratrol (Res) (Natural compound): Expression of CCND1 was attenuated in Res treated T-ALL CEM-C1-15 cells (Ge et. al., 2013).
  
  
Entity T-cell Acute Lymphoblastic Leukemia
Note Resveratrol (Res) (Natural compound): Expression of CCND1 was attenuated in Res treated T-ALL CEM-C1-15 cells (Ge et. al., 2013).
  
  
Entity Uterine cervical cancer
Note Bcl-1/Cyclin D1 alterations are associated with the development of uterine cervical carcinoma (Singh et. al., 2005).
  
  
Entity Various cancers
Note Ursolic acid (UA) (Natural compound) : UA in combination with other drugs led to down-regulation of expression of CCND1 (Doudican et. al., 2014).
Salinomycin-: Salinomycin induced lowering of expression of CCND1 in Breast and prostate cancer cells (Lu et. al., 2014).
  
  
Entity Non-cancerous tissues
Note Primary human cardiomyocytes: Thrombin time-dependently up-regulated CCND1 expression, with a significant response within 36-48 h (Chien et. al., 2014).
Human diploid fibroblast (HDFs): CCND1 gene was significantly up-regulated in irradiated (1 Gy) HDFs as compared to untreated control, while bothHDFs treated with Gelam honey and irradiated HDFs pre-treated with Gelam honey showed down- regulation of cyclin D1 gene as compared to irradiated HDFs. HDFs treated with Gelam honey during radiation and post-irradiation however showed significant up-regulation of cyclin D1 gene as compared to untreated control (Ahmed et. al., 2014).
Human coronary artery smooth muscle cells (HCASMCs): FABP4 induced increase in expression of the downstream genes CCND1 (Girona et. al., 2013).
Vascular smooth muscle cells: STS (sodium tanshinone IIA silate) decreased the expression of cell cycle-associated protein, CCND1 (Wu et. al., 2014)
. Vascular smooth muscle cells: PDGF-induced CCND1 mRNA and protein expression was inhibited by TGFb. PDGF-induced CCND1 expression requiring KLF5 was inhibited by TGFb via a Smad dependent mechanism, leading to G1 cell cycle arrest of VSMs (Garrido et. al., 2013).
Nuroectodermal stem cells: PGE2 (Prostaglandin E2) treatment significantly up-regulated CCND1 (Wong et. al., 2014).
Neurons: DYRK1A (dual specificity tyrosine-phosphorylation-regulated kinase 1A) reduced cellular CCND1 levels by phosphorylation on Thr286, which is known to induce proteasomal degradation (Soppa et. al., 2014).
Renal intestinal fibroblasts: Exposure of NRK-49F to resulted in reduced expression proliferation markers CCND1 in a dose and time dependent manner (Ponnusamy et. al., 2014).
Idiopathic pulmonary fibrosis (IPF): Cell cycle regulatory protein CCND1 was significantly enhanced in AEC (alveolar epithelial cell) within the remodelled fibrotic areas of IPF lungs but expression was negligible in myofibroblasts (Akram et. al., 2014).
Human Rheumatoid Arthritis Synovial Cells: The protein and mRNA levels of CCND1 decreased gradually with the increasing of thapsigargin concentration and treatment times (Wang et. al., 2014).
  
  
Entity Other mammals
Note Mouse:
Adult mice cardiomyocytes:
Silencing the CCND1 expression is necessary for the maintenance of the cell cycle exit, and suggests a mechanism that involves inhibition of M-phase entry (Tane et. al., 2004).
Mouse hair follicle (HF):
Real-time PCR analysis revealed an inverse relationship between CCND1 expression pattern and that of Sfrp2 throughout the HF cycle (Kim et. al., 2014).
Mouse mammary gland:
CCND1 was more frequently up-regulated in mammary tumors from transgenic mice (expressing myristoylated-Akt1 (myr-Akt1) under the control of the MMTV-LTR promoter) compared to tumors from wild-type mice. Increased expression of CCND1 was incompletely dependent on Akt1 expression. Low expression of CCND1 and increased expression of Twist and Slug was observed in mammary tumors that had metastasized to secondary sites (Wu et. al., 2014).
Atherosclerosis in mice:
The expression levels of CCND1 in smooth muscle cells were restrained by CD59 and C-PC (C-phycocyanin) (Li et. al., 2013).
Mouse pancreatic cancer:
Embelin-treated mice showed significant inhibition in tumor growth, which was associated with reduced expression of CCND1 (Huang et. al., 2014).
Human umbilical cord mesenchymal stem cells (hUCMSCs) in nude mice:
In mice treated with hUCMSCs-LV-IL-21, Expression of cyclin-D1 was simultaneously low compared to control group, hUCMSCs group and hUCMSCs-LV-Vec group (Zhang et. al., 2014).
Partial hepatectomy
Following seventy percent partial hepatectomy (PH) in wild type (WT) mice IL-6 serum levels increased, resulting in increased CCND1 (Tachibana et. al., 2014).

Cow:
Dairy Cow Mammary Epithelial Cells:
Treatment with leucine induced LeuRS, increasing CCND1 mRNA and protein expression (Wang et. al., 2014).

Rat:
Rat epithelial cells:
CCND1 accumulation due to differential effects of of PKC? and PKC? was likely contribute to the opposing tumor suppressive and tumor promoting activities in the intestinal epithelium (Pyfz et. al., 2014). Hyperbilirubinemic Gunn Rat:
Decreased expression in CCND1 in the cerebellum of the hyperbilirubinemic Gunn rats led to significant increased cell cycle arrest in the late G0/G1 phase (Robert et. al., 2013).
Neonatal hypoxia-ischemia in rat:
IGF-1R activation together with EGFR co-signaling decreased the percentage of cells in G1 and enhanced cell progression into S and G2 by increases in expression of CCND1 (Alagappan et. al., 2014).
Rat balloon injury model:
CCND1 mRNA was significantly decreased by sodium ferulate in cells under serum stimulation (Zhang et. al., 2014).
Rat liver fibrosis:
Sophocarpine inhibited the proliferation of HSCs by a decrease in the expression of CCND1 (Qian et. al., 2014).
Rat Airway Smooth Muscle Cells:
Nicotine significantly increased expression of CCND1 (He et. al., 2014).

Chicken:
Chicken fetal myoblasts (CFMs):
Increased CCND1 expression during acceleration of cell cycle at G1/ S phase in CMF was due to CARP (cardiac ankyrin repeat protein) over-expression (Ma. et. al., 2014).

  

Breakpoints

 

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Pathol Oncol Res 2015 Jan;21(1):203-11
PMID 24903677
 
Interleukin-6 is required for cell cycle arrest and activation of DNA repair enzymes after partial hepatectomy in mice
Tachibana S, Zhang X, Ito K, Ota Y, Cameron AM, Williams GM, Sun Z
Cell Biosci 2014 Feb 3;4(1):6
PMID 24484634
 
Triptolide inhibits histone methyltransferase EZH2 and modulates the expression of its target genes in prostate cancer cells
Tamgue O, Chai CS, Hao L, Zambe JC, Huang WW, Zhang B, Lei M, Wei YM
Asian Pac J Cancer Prev 2013;14(10):5663-9
PMID 24289559
 
Repression of cyclin D1 expression is necessary for the maintenance of cell cycle exit in adult mammalian cardiomyocytes
Tane S, Kubota M, Okayama H, Ikenishi A, Yoshitome S, Iwamoto N, Satoh Y, Kusakabe A, Ogawa S, Kanai A, Molkentin JD, Nakamura K, Ohbayashi T, Takeuchi T
J Biol Chem 2014 Jun 27;289(26):18033-44
PMID 24821722
 
Effects of ubiquitin-conjugating enzyme 2C on invasion, proliferation and cell cycling of lung cancer cells
Tang XK, Wang KJ, Tang YK, Chen L
Asian Pac J Cancer Prev 2014;15(7):3005-9
PMID 24815438
 
Targeting SHCBP1 inhibits cell proliferation in human hepatocellular carcinoma cells
Tao HC, Wang HX, Dai M, Gu CY, Wang Q, Han ZG, Cai B
Asian Pac J Cancer Prev 2013;14(10):5645-50
PMID 24289556
 
Gelam honey attenuated radiation-induced cell death in human diploid fibroblasts by promoting cell cycle progression and inhibiting apoptosis
Tengku Ahmad TA, Jaafar F, Jubri Z, Abdul Rahim K, Rajab NF, Makpol S
BMC Complement Altern Med 2014 Mar 24;14:108
PMID 24655584
 
Frizzled-2: A potential novel target for molecular pancreatic cancer therapy
Tomizawa M, Shinozaki F, Sugiyama T, Yamamoto S, Sueishi M, Yoshida T
Oncol Lett 2014 Jan;7(1):74-78
PMID 24348824
 
Distinct effects of alcohol consumption and smoking on genetic alterations in head and neck carcinoma
Urashima M, Hama T, Suda T, Suzuki Y, Ikegami M, Sakanashi C, Akutsu T, Amagaya S, Horiuchi K, Imai Y, Mezawa H, Noya M, Nakashima A, Mafune A, Kato T, Kojima H
PLoS One 2013 Nov 20;8(11):e80828
PMID 24278325
 
Numerical abnormalities of the Cyclin D1 gene locus on chromosome 11q13 in non-melanoma skin cancer
Utikal J, Udart M, Leiter U, Kaskel P, Peter RU, Krähn G
Cancer Lett 2005 Mar 10;219(2):197-204
PMID 15723720
 
The suppressive role of SOX7 in hepatocarcinogenesis
Wang C, Guo Y, Wang J, Min Z
PLoS One 2014 May 9;9(5):e97433
PMID 24816720
 
Fangchinoline inhibits cell proliferation via Akt/GSK-3beta/ cyclin D1 signaling and induces apoptosis in MDA-MB-231 breast cancer cells
Wang CD, Yuan CF, Bu YQ, Wu XM, Wan JY, Zhang L, Hu N, Liu XJ, Zu Y, Liu GL, Song FZ
Asian Pac J Cancer Prev 2014;15(2):769-73
PMID 24568493
 
Effects of thapsigargin on the proliferation and survival of human rheumatoid arthritis synovial cells
Wang H, Jia XZ, Sui CJ, Zhao YP, Mei YF, Zheng YN, Zhang ZY
ScientificWorldJournal 2014 Feb 9;2014:605416
PMID 24688409
 
Estrogen receptor -coupled Bmi1 regulation pathway in breast cancer and its clinical implications
Wang H, Liu H, Li X, Zhao J, Zhang H, Mao J, Zou Y, Zhang H, Zhang S, Hou W, Hou L, McNutt MA, Zhang B
BMC Cancer 2014 Feb 24;14:122
PMID 24559156
 
Leucyl-tRNA synthetase regulates lactation and cell proliferation via mTOR signaling in dairy cow mammary epithelial cells
Wang L, Lin Y, Bian Y, Liu L, Shao L, Lin L, Qu B, Zhao F, Gao X, Li Q
Int J Mol Sci 2014 Apr 9;15(4):5952-69
PMID 24722568
 
Acylglycerol kinase promotes cell proliferation and tumorigenicity in breast cancer via suppression of the FOXO1 transcription factor
Wang X, Lin C, Zhao X, Liu A, Zhu J, Li X, Song L
Mol Cancer 2014 May 8;13:106
PMID 24886245
 
A C 21 -Steroidal Glycoside Isolated from the Roots of Cynanchum auriculatum Induces Cell Cycle Arrest and Apoptosis in Human Gastric Cancer SGC-7901 Cells
Wang YQ, Zhang SJ, Lu H, Yang B, Ye LF, Zhang RS
Evid Based Complement Alternat Med 2013;2013:180839
PMID 24454488
 
Unique molecular signatures as a hallmark of patients with metastatic breast cancer: implications for current treatment paradigms
Wheler JJ, Parker BA, Lee JJ, Atkins JT, Janku F, Tsimberidou AM, Zinner R, Subbiah V, Fu S, Schwab R, Moulder S, Valero V, Schwaederle M, Yelensky R, Miller VA, Stephens MP, Meric-Bernstam F, Kurzrock R
Oncotarget 2014 May 15;5(9):2349-54
PMID 24811890
 
Cyclin D1 overexpression in non-Hodgkin's lymphoma with chromosome 11 bcl-1 rearrangement
Williams ME, Swerdlow SH
Ann Oncol 1994;5 Suppl 1:71-3
PMID 8172823
 
Variant t(2;11)(p11;q13) associated with the IgK-CCND1 rearrangement is a recurrent translocation in leukemic small-cell B-non-Hodgkin lymphoma
Wlodarska I, Meeus P, Stul M, Thienpont L, Wouters E, Marcelis L, Demuynck H, Rummens JL, Madoe V, Hagemeijer A
Leukemia 2004 Oct;18(10):1705-10
PMID 15306823
 
Prostaglandin E2 alters Wnt-dependent migration and proliferation in neuroectodermal stem cells: implications for autism spectrum disorders
Wong CT, Ahmad E, Li H, Crawford DA
Cell Commun Signal 2014 Mar 23;12:19
PMID 24656144
 
Mir-184 post-transcriptionally regulates SOX7 expression and promotes cell proliferation in human hepatocellular carcinoma
Wu GG, Li WH, He WG, Jiang N, Zhang GX, Chen W, Yang HF, Liu QL, Huang YN, Zhang L, Zhang T, Zeng XC
PLoS One 2014 Feb 18;9(2):e88796
PMID 24558429
 
Silencing of Ether à go-go 1 by shRNA inhibits osteosarcoma growth and cell cycle progression
Wu J, Zhong D, Fu X, Liu Q, Kang L, Ding Z
Int J Mol Sci 2014 Apr 1;15(4):5570-81
PMID 24694542
 
Sodium tanshinone IIA silate inhibits high glucose-induced vascular smooth muscle cell proliferation and migration through activation of AMP-activated protein kinase
Wu WY, Yan H, Wang XB, Gui YZ, Gao F, Tang XL, Qin YL, Su M, Chen T, Wang YP
PLoS One 2014 Apr 16;9(4):e94957
PMID 24739942
 
Activation of Akt1 accelerates carcinogen-induced tumorigenesis in mammary gland of virgin and post-lactating transgenic mice
Wu Y, Kim J, Elshimali Y, Sarkissyan M, Vadgama JV
BMC Cancer 2014 Apr 17;14:266
PMID 24742286
 
The inhibitory role of Mir-29 in growth of breast cancer cells
Wu Z, Huang X, Huang X, Zou Q, Guo Y
J Exp Clin Cancer Res 2013 Dec 1;32:98
PMID 24289849
 
Silencing of KIF14 interferes with cell cycle progression and cytokinesis by blocking the p27(Kip1) ubiquitination pathway in hepatocellular carcinoma
Xu H, Choe C, Shin SH, Park SW, Kim HS, Jung SH, Yim SH, Kim TM, Chung YJ
Exp Mol Med 2014 May 23;46:e97
PMID 24854087
 
miR-7 inhibits colorectal cancer cell proliferation and induces apoptosis by targeting XRCC2
Xu K, Chen Z, Qin C, Song X
Onco Targets Ther 2014 Feb 20;7:325-32
PMID 24570594
 
-Mangostin suppresses the viability and epithelial-mesenchymal transition of pancreatic cancer cells by downregulating the PI3K/Akt pathway
Xu Q, Ma J, Lei J, Duan W, Sheng L, Chen X, Hu A, Wang Z, Wu Z, Wu E, Ma Q, Li X
Biomed Res Int 2014;2014:546353
PMID 24812621
 
MicroRNA-503 suppresses proliferation and cell-cycle progression of endometrioid endometrial cancer by negatively regulating cyclin D1
Xu YY, Wu HJ, Ma HD, Xu LP, Huo Y, Yin LR
FEBS J 2013 Aug;280(16):3768-79
PMID 23731275
 
MicroRNA miR-302 inhibits the tumorigenicity of endometrial cancer cells by suppression of Cyclin D1 and CDK1
Yan GJ, Yu F, Wang B, Zhou HJ, Ge QY, Su J, Hu YL, Sun HX, Ding LJ
Cancer Lett 2014 Apr 1;345(1):39-47
PMID 24333727
 
Variations in cyclin D1 levels through the cell cycle determine the proliferative fate of a cell
Yang K, Hitomi M, Stacey DW
Cell Div 2006 Dec 18;1:32
PMID 17176475
 
Resveratrol inhibits the growth of gastric cancer by inducing G1 phase arrest and senescence in a Sirt1-dependent manner
Yang Q, Wang B, Zang W, Wang X, Liu Z, Li W, Jia J
PLoS One 2013 Nov 21;8(11):e70627
PMID 24278101
 
A cyclin D1/microRNA 17/20 regulatory feedback loop in control of breast cancer cell proliferation
Yu Z, Wang C, Wang M, Li Z, Casimiro MC, Liu M, Wu K, Whittle J, Ju X, Hyslop T, McCue P, Pestell RG
J Cell Biol 2008 Aug 11;182(3):509-17
PMID 18695042
 
Cyclin D1 induction of Dicer governs microRNA processing and expression in breast cancer
Yu Z, Wang L, Wang C, Ju X, Wang M, Chen K, Loro E, Li Z, Zhang Y, Wu K, Casimiro MC, Gormley M, Ertel A, Fortina P, Chen Y, Tozeren A, Liu Z, Pestell RG
Nat Commun 2013;4:2812
PMID 24287487
 
Antitumor effect and mechanism of an ellagic acid derivative on the HepG2 human hepatocellular carcinoma cell line
Zhang H, Guo ZJ, Xu WM, You XJ, Han L, Han YX, Dai LJ
Oncol Lett 2014 Feb;7(2):525-530
PMID 24396481
 
Sodium ferulate inhibits neointimal hyperplasia in rat balloon injury model
Zhang J, Chen J, Yang J, Xu C, Ding J, Yang J, Guo Q, Hu Q, Jiang H
PLoS One 2014 Jan 29;9(1):e87561
PMID 24489938
 
Overexpression of JAM-A in non-small cell lung cancer correlates with tumor progression
Zhang M, Luo W, Huang B, Liu Z, Sun L, Zhang Q, Qiu X, Xu K, Wang E
PLoS One 2013 Nov 12;8(11):e79173
PMID 24265754
 
MicroRNA-365 inhibits vascular smooth muscle cell proliferation through targeting cyclin D1
Zhang P, Zheng C, Ye H, Teng Y, Zheng B, Yang X, Zhang J
Int J Med Sci 2014 May 21;11(8):765-70
PMID 24936138
 
Silybin-mediated inhibition of Notch signaling exerts antitumor activity in human hepatocellular carcinoma cells
Zhang S, Yang Y, Liang Z, Duan W, Yang J, Yan J, Wang N, Feng W, Ding M, Nie Y, Jin Z
PLoS One 2013 Dec 27;8(12):e83699
PMID 24386256
 
The antidiabetic drug metformin inhibits the proliferation of bladder cancer cells in vitro and in vivo
Zhang T, Guo P, Zhang Y, Xiong H, Yu X, Xu S, Wang X, He D, Jin X
Int J Mol Sci 2013 Dec 18;14(12):24603-18
PMID 24351837
 
MicroRNA-520b inhibits growth of hepatoma cells by targeting MEKK2 and cyclin D1
Zhang W, Kong G, Zhang J, Wang T, Ye L, Zhang X
PLoS One 2012;7(2):e31450
PMID 22319632
 
Gene therapy of ovarian cancer using IL-21-secreting human umbilical cord mesenchymal stem cells in nude mice
Zhang Y, Wang J, Ren M, Li M, Chen D, Chen J, Shi F, Wang X, Dou J
J Ovarian Res 2014 Jan 20;7:8
PMID 24444073
 
Polydatin inhibits growth of lung cancer cells by inducing apoptosis and causing cell cycle arrest
Zhang Y, Zhuang Z, Meng Q, Jiao Y, Xu J, Fan S
Oncol Lett 2014 Jan;7(1):295-301
PMID 24348867
 
Overexpression of NDRG2 can inhibit neuroblastoma cell proliferation through negative regulation by CYR61
Zhang ZG, Li G, Feng DY, Zhang J, Zhang J, Qin HZ, Ma LT, Gao GD, Wu L
Asian Pac J Cancer Prev 2014;15(1):239-44
PMID 24528032
 
Gallotannin imposes S phase arrest in breast cancer cells and suppresses the growth of triple-negative tumors in vivo
Zhao T, Sun Q, del Rincon SV, Lovato A, Marques M, Witcher M
PLoS One 2014 Mar 21;9(3):e92853
PMID 24658335
 
Downregulation of PAX6 by shRNA inhibits proliferation and cell cycle progression of human non-small cell lung cancer cell lines
Zhao X, Yue W, Zhang L, Ma L, Jia W, Qian Z, Zhang C, Wang Y
PLoS One 2014 Jan 15;9(1):e85738
PMID 24454925
 
Cyclin D1 overexpression is associated with poor clinicopathological outcome and survival in oral squamous cell carcinoma in Asian populations: insights from a meta-analysis
Zhao Y, Yu D, Li H, Nie P, Zhu Y, Liu S, Zhu M, Fang B
PLoS One 2014 Mar 27;9(3):e93210
PMID 24675814
 
microRNA-9 suppresses the proliferation, invasion and metastasis of gastric cancer cells through targeting cyclin D1 and Ets1
Zheng L, Qi T, Yang D, Qi M, Li D, Xiang X, Huang K, Tong Q
PLoS One 2013;8(1):e55719
PMID 23383271
 
Bcl-1/cyclin D1 in malignant lymphoma
de Boer CJ, van Krieken JH, Schuuring E, Kluin PM
Ann Oncol 1997;8 Suppl 2:109-17
PMID 9209653
 

Citation

This paper should be referenced as such :
Sarkar S, Panda CK
CCND1 (B-cell leukemia/lymphoma 1);
Atlas Genet Cytogenet Oncol Haematol. in press
On line version : http://AtlasGeneticsOncology.org/Genes/BCL1ID36.html
History of this paper:
Huret, JL. BCL1 (B-cell leukemia/lymphoma 1). Atlas Genet Cytogenet Oncol Haematol. 1998;2(4):111-112.
http://documents.irevues.inist.fr/bitstream/handle/2042/37448/05-1998-BCL1.pdf


Other Leukemias implicated (Data extracted from papers in the Atlas) [ 20 ]
  3q27 rearrangements (BCL6) in non Hodgkin lymphoma::t(3;Var)(q27;Var) in non Hodgkin lymphoma
Atypical Chronic Myeloid Leukemia (aCML)
Classification of B-cell chronic lymphoproliferative disorders (CLD)
Classification of B-cell non-Hodgkin lymphomas (NHL)
B-cell prolymphocytic leukemia (B-PLL)
Chronic lymphocytic leukaemia (CLL)
Hairy Cell Leukemia (HCL) and Hairy Cell Leukemia Variant (HCL-V)
Mantle cell lymphoma (incomplete)
Multiple myeloma in 2004
Multiple Myeloma in 2017
Plasma cell leukemia (PCL)
Small lymphocytic lymphoma
Splenic lymphoma with villous lymphocytes (SLVL)
t(3;7)(q26;q21) CDK6/MECOM
t(5;7)(q35;q21) TLX3/CDK6
t(9;13)(p12;q21) PAX5/DACH1
t(11;14)(q13;q32) IGH/CCND1
t(11;14)(q13;q32) IGH/CCND1 in multiple myeloma
t(11;19)(q13;p13) FSTL3/CCND1
t(2;12)(p12;p13) IGK/CCND2::t(12;14)(p13;q32) IGH/CCND2::t(12;22)(p13;q11) IGL/CCND2


Other Solid tumors implicated (Data extracted from papers in the Atlas) [ 20 ]
  Thyroid: Anaplastic (undifferentiated) carcinoma
Bladder: Urothelial carcinomas
Breast tumors : an overview
Neuro-Endocrine/Endocrine System: Carcinoid tumors
Breast: Ductal carcinoma
Nervous system: Ependymomas
Nervous System: Glioma: an overview
Head and Neck: Squamous cell carcinoma: an overview
Head and Neck: Epidermoid carcinoma
Liver: Hepatocellular carcinoma
Head and Neck: Laryngeal tumors: an overview
Head and Neck: Laryngeal squamous cell carcinoma
Lung: Non-small cell carcinoma
Male breast cancer
Nervous system: Peripheral neuroblastic tumours (Neuroblastoma, Ganglioneuroblastoma, Ganglioneuroma)
Head and Neck: Oral squamous cell carcinoma
Bone: Osteosarcoma
Ovarian tumours : an overview
Squamous cell cancer
Eye: Posterior uveal melanoma


Other Cancer prone implicated (Data extracted from papers in the Atlas) [ 1 ]
  Von Hippel-Lindau


External links

Nomenclature
HGNC (Hugo)CCND1   1582
LRG (Locus Reference Genomic)LRG_990
Cards
AtlasBCL1ID36
Entrez_Gene (NCBI)CCND1  595  cyclin D1
AliasesBCL1; D11S287E; PRAD1; U21B31
GeneCards (Weizmann)CCND1
Ensembl hg19 (Hinxton)ENSG00000110092 [Gene_View]
Ensembl hg38 (Hinxton)ENSG00000110092 [Gene_View]  chr11:69641105-69654474 [Contig_View]  CCND1 [Vega]
ICGC DataPortalENSG00000110092
TCGA cBioPortalCCND1
AceView (NCBI)CCND1
Genatlas (Paris)CCND1
WikiGenes595
SOURCE (Princeton)CCND1
Genetics Home Reference (NIH)CCND1
Genomic and cartography
GoldenPath hg38 (UCSC)CCND1  -     chr11:69641105-69654474 +  11q13.3   [Description]    (hg38-Dec_2013)
GoldenPath hg19 (UCSC)CCND1  -     11q13.3   [Description]    (hg19-Feb_2009)
EnsemblCCND1 - 11q13.3 [CytoView hg19]  CCND1 - 11q13.3 [CytoView hg38]
Mapping of homologs : NCBICCND1 [Mapview hg19]  CCND1 [Mapview hg38]
OMIM168461   193300   254500   
Gene and transcription
Genbank (Entrez)AB075505 AK299044 AK313136 AM393193 AM393430
RefSeq transcript (Entrez)NM_053056
RefSeq genomic (Entrez)
Consensus coding sequences : CCDS (NCBI)CCND1
Cluster EST : UnigeneHs.523852 [ NCBI ]
CGAP (NCI)Hs.523852
Alternative Splicing GalleryENSG00000110092
Gene ExpressionCCND1 [ NCBI-GEO ]   CCND1 [ EBI - ARRAY_EXPRESS ]   CCND1 [ SEEK ]   CCND1 [ MEM ]
Gene Expression Viewer (FireBrowse)CCND1 [ Firebrowse - Broad ]
SOURCE (Princeton)Expression in : [Datasets]   [Normal Tissue Atlas]  [carcinoma Classsification]  [NCI60]
GenevisibleExpression in : [tissues]  [cell-lines]  [cancer]  [perturbations]  
BioGPS (Tissue expression)595
GTEX Portal (Tissue expression)CCND1
Protein : pattern, domain, 3D structure
UniProt/SwissProtP24385   [function]  [subcellular_location]  [family_and_domains]  [pathology_and_biotech]  [ptm_processing]  [expression]  [interaction]
NextProtP24385  [Sequence]  [Exons]  [Medical]  [Publications]
With graphics : InterProP24385
Splice isoforms : SwissVarP24385
PhosPhoSitePlusP24385
Domaine pattern : Prosite (Expaxy)CYCLINS (PS00292)   
Domains : Interpro (EBI)Cyclin-like    Cyclin_C-dom    Cyclin_D    Cyclin_N   
Domain families : Pfam (Sanger)Cyclin_C (PF02984)    Cyclin_N (PF00134)   
Domain families : Pfam (NCBI)pfam02984    pfam00134   
Domain families : Smart (EMBL)CYCLIN (SM00385)  Cyclin_C (SM01332)  
Conserved Domain (NCBI)CCND1
DMDM Disease mutations595
Blocks (Seattle)CCND1
PDB (SRS)2W96    2W99    2W9F    2W9Z   
PDB (PDBSum)2W96    2W99    2W9F    2W9Z   
PDB (IMB)2W96    2W99    2W9F    2W9Z   
PDB (RSDB)2W96    2W99    2W9F    2W9Z   
Structural Biology KnowledgeBase2W96    2W99    2W9F    2W9Z   
SCOP (Structural Classification of Proteins)2W96    2W99    2W9F    2W9Z   
CATH (Classification of proteins structures)2W96    2W99    2W9F    2W9Z   
SuperfamilyP24385
Human Protein AtlasENSG00000110092
Peptide AtlasP24385
HPRD01346
IPIIPI00028098   IPI01009315   IPI00815934   IPI01013571   IPI01013164   IPI01011321   
Protein Interaction databases
DIP (DOE-UCLA)P24385
IntAct (EBI)P24385
FunCoupENSG00000110092
BioGRIDCCND1
STRING (EMBL)CCND1
ZODIACCCND1
Ontologies - Pathways
QuickGOP24385
Ontology : AmiGOG1/S transition of mitotic cell cycle  G1/S transition of mitotic cell cycle  negative regulation of transcription from RNA polymerase II promoter  cyclin-dependent protein kinase holoenzyme complex  re-entry into mitotic cell cycle  positive regulation of protein phosphorylation  transcription corepressor activity  protein kinase activity  protein binding  intracellular  nucleus  nucleoplasm  nucleoplasm  cytosol  bicellular tight junction  transcription, DNA-templated  protein phosphorylation  cellular response to DNA damage stimulus  lactation  transcription factor binding  response to iron ion  response to X-ray  response to organonitrogen compound  positive regulation of G2/M transition of mitotic cell cycle  membrane  cyclin-dependent protein serine/threonine kinase regulator activity  transcriptional repressor complex  enzyme binding  protein kinase binding  negative regulation of Wnt signaling pathway  negative regulation of epithelial cell differentiation  endoplasmic reticulum unfolded protein response  mitotic G1 DNA damage checkpoint  response to magnesium ion  response to estradiol  protein complex binding  response to vitamin E  Leydig cell differentiation  mammary gland epithelial cell proliferation  positive regulation of mammary gland epithelial cell proliferation  response to drug  histone deacetylase binding  response to estrogen  response to leptin  fat cell differentiation  response to ethanol  positive regulation of cyclin-dependent protein serine/threonine kinase activity  positive regulation of cell cycle  cell division  response to corticosterone  response to calcium ion  canonical Wnt signaling pathway  mammary gland alveolus development  proline-rich region binding  response to UV-A  negative regulation of cell cycle arrest  liver regeneration  
Ontology : EGO-EBIG1/S transition of mitotic cell cycle  G1/S transition of mitotic cell cycle  negative regulation of transcription from RNA polymerase II promoter  cyclin-dependent protein kinase holoenzyme complex  re-entry into mitotic cell cycle  positive regulation of protein phosphorylation  transcription corepressor activity  protein kinase activity  protein binding  intracellular  nucleus  nucleoplasm  nucleoplasm  cytosol  bicellular tight junction  transcription, DNA-templated  protein phosphorylation  cellular response to DNA damage stimulus  lactation  transcription factor binding  response to iron ion  response to X-ray  response to organonitrogen compound  positive regulation of G2/M transition of mitotic cell cycle  membrane  cyclin-dependent protein serine/threonine kinase regulator activity  transcriptional repressor complex  enzyme binding  protein kinase binding  negative regulation of Wnt signaling pathway  negative regulation of epithelial cell differentiation  endoplasmic reticulum unfolded protein response  mitotic G1 DNA damage checkpoint  response to magnesium ion  response to estradiol  protein complex binding  response to vitamin E  Leydig cell differentiation  mammary gland epithelial cell proliferation  positive regulation of mammary gland epithelial cell proliferation  response to drug  histone deacetylase binding  response to estrogen  response to leptin  fat cell differentiation  response to ethanol  positive regulation of cyclin-dependent protein serine/threonine kinase activity  positive regulation of cell cycle  cell division  response to corticosterone  response to calcium ion  canonical Wnt signaling pathway  mammary gland alveolus development  proline-rich region binding  response to UV-A  negative regulation of cell cycle arrest  liver regeneration  
Pathways : BIOCARTA [Genes]   
Pathways : KEGG   
REACTOMEP24385 [protein]
REACTOME PathwaysR-HSA-8849470 [pathway]   
NDEx NetworkCCND1
Atlas of Cancer Signalling NetworkCCND1
Wikipedia pathwaysCCND1
Orthology - Evolution
OrthoDB595
GeneTree (enSembl)ENSG00000110092
Phylogenetic Trees/Animal Genes : TreeFamCCND1
HOVERGENP24385
HOGENOMP24385
Homologs : HomoloGeneCCND1
Homology/Alignments : Family Browser (UCSC)CCND1
Gene fusions - Rearrangements
Fusion : MitelmanCCND1/TACSTD2 [11q13.3/1p32.1]  
Fusion : MitelmanFSTL3/CCND1 [19p13.3/11q13.3]  [t(11;19)(q13;p13)]  
Fusion : MitelmanIGH/CCND1 [14q32.33/11q13.3]  [ins(14;11)(q32;q13q13)]  [t(11;14)(q13;q32)]  
[t(11;19;14)(q13;q13;q32)]  [t(14;16)(q32;q23)]  [t(14;20)(q32;q12)]  
[t(1;11;14)(q32;q13;q32)]  [t(3;14;11)(q21;q32;q13)]  [t(4;14)(p16;q32)]  [t(6;14)(p21;q32)]  
Fusion : MitelmanIGK/CCND1 [2p11.2/11q13.3]  [t(2;11)(p11;q13)]  
Fusion : MitelmanIGL/CCND1 [22q11.22/11q13.3]  [t(11;22)(q13;q11)]  
Fusion : TICdbCCND1 [11q13.3]  -  FSTL3 [19p13.3]
Fusion : TICdbIg [CCND1]  -  11q13.3 []
Polymorphisms : SNP and Copy number variants
NCBI Variation ViewerCCND1 [hg38]
dbSNP Single Nucleotide Polymorphism (NCBI)CCND1
dbVarCCND1
ClinVarCCND1
1000_GenomesCCND1 
Exome Variant ServerCCND1
ExAC (Exome Aggregation Consortium)CCND1 (select the gene name)
Genetic variants : HAPMAP595
Genomic Variants (DGV)CCND1 [DGVbeta]
DECIPHERCCND1 [patients]   [syndromes]   [variants]   [genes]  
CONAN: Copy Number AnalysisCCND1 
Mutations
ICGC Data PortalCCND1 
TCGA Data PortalCCND1 
Broad Tumor PortalCCND1
OASIS PortalCCND1 [ Somatic mutations - Copy number]
Cancer Gene: CensusCCND1 
Somatic Mutations in Cancer : COSMICCCND1  [overview]  [genome browser]  [tissue]  [distribution]  
Mutations and Diseases : HGMDCCND1
intOGen PortalCCND1
LOVD (Leiden Open Variation Database)Whole genome datasets
LOVD (Leiden Open Variation Database)LOVD - Leiden Open Variation Database
LOVD (Leiden Open Variation Database)LOVD 3.0 shared installation
BioMutasearch CCND1
DgiDB (Drug Gene Interaction Database)CCND1
DoCM (Curated mutations)CCND1 (select the gene name)
CIViC (Clinical Interpretations of Variants in Cancer)CCND1 (select a term)
intoGenCCND1
NCG5 (London)CCND1
Cancer3DCCND1(select the gene name)
Impact of mutations[PolyPhen2] [SIFT Human Coding SNP] [Buck Institute : MutDB] [Mutation Assessor] [Mutanalyser]
Diseases
OMIM168461    193300    254500   
Orphanet8776    10899    10693   
MedgenCCND1
Genetic Testing Registry CCND1
NextProtP24385 [Medical]
TSGene595
GENETestsCCND1
Target ValidationCCND1
Huge Navigator CCND1 [HugePedia]
snp3D : Map Gene to Disease595
BioCentury BCIQCCND1
ClinGenCCND1
Clinical trials, drugs, therapy
Chemical/Protein Interactions : CTD595
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