• Genetic predisposition and mutations in the CDKN2A (p16INK4a) gene are important in the development of a subset of dysplastic (atypical, Clark) melanocytic nevi in patients with familial atypical multiple mole syndrome. (medscape.com)
  • Somatic mutations in CTNNB1 gene encoding ß-catenin have been exclusively detected in adamantinomatous craniopharyngiomas, which predominantly manifest as cystic lesions, while papillary craniopharyngiomas are driven by BRAF V600E mutations in up to 95% of cases and are typically solid masses. (bvsalud.org)
  • Initiation and propagation of tumors reflect underlying genomic alterations such as mutations, polymorphisms, and copy number variations found in genes of multiple cellular pathways. (hindawi.com)
  • Inherited mutations in a small number of genes account for about five to ten percent of women's cancers.These inherited variations, identified in breast, ovarian, and endometrial cancer susceptibility, can be characterized in the general population by their frequency and the magnitude of their impact upon a patient (Table 1 ).Some inherited variants occur rarely in the general population, but confer large risks to the individual. (hindawi.com)
  • Although inherited mutations in a small number of genes account for only about five to ten percent of women's cancers, by far the BRCA1 and BRCA2 gene mutations are the most common examples of this observation (50-70% of familial breast cancers) [ 2 ]. (hindawi.com)
  • It is possible that missense variants of genes for which truncating mutations are clearly pathogenic may also be deleterious, but with reduced penetrance. (bmj.com)
  • Normal meninges harbor oncogenic somatic mutations in meningioma-driver genes. (amedeo.com)
  • Several genetic alterations have been described in SCCHN, including mutations in the p53 tumor suppressor gene and mutations in genes that encode cell cycle proteins such as p16 and cyclin D1. (oncotarget.com)
  • Scope includes mutations and abnormal protein expression. (cancerindex.org)
  • The mutations of BRCA2 gene predispose the cells towards neoplastic development. (biomedcentral.com)
  • Mutations in this gene can result in Wolman disease and cholesteryl ester storage disease. (cancerindex.org)
  • ALL cancers have lots of additional changes, the so-called 'passenger' mutations, that may contribute to the cancer, but are not the main genes. (cancerquest.org)
  • Mutations in this gene as well as in its related proteins including D-type cyclins, p16(INK4a) and Rb were all found to be associated with tumorigenesis of a variety of cancers. (thermofisher.com)
  • We integrated data from multiple analytes (HPV DNA, HPV RNA, and p16), assays (immunohistochemistry, polymerase chain reaction [PCR], quantitative PCR [qPCR], and digital PCR), and molecular changes (somatic mutations and DNA methylation) from 153 patients with OSCC to correlate p16 expression, HPV DNA, and HPV RNA with HPV incidence and patient survival. (univ-nantes.fr)
  • A direct link between DNA DSBs, genomic instability, and cancer is evidenced the fact that many cancer-predisposition syndromes in humans characterized by genomic instability are caused by mutations in DSB-responsive genes ( 16 , 17 ). (amegroups.org)
  • BACKGROUND: : Inherited mutations in the CDKN2A tumor suppressor gene, which encodes the p16(INK4a) protein, and in the cyclin-dependent kinase 4 (CDK4) gene confer susceptibility to cutaneous malignant melanoma. (lu.se)
  • We analyzed families with two or more cases of melanoma for germline mutations in CDKN2A and CDK4 to elucidate the contribution of these gene defects to familial malignant melanoma and to the occurrence of other cancer types. (lu.se)
  • METHODS: : The entire CDKN2A coding region and exon 2 of the CDK4 gene of an affected member of each of 52 families from southern Sweden with at least two cases of melanoma in first- or second-degree relatives were screened for mutations by use of polymerase chain reaction-single-strand conformation polymorphism analysis. (lu.se)
  • Expression of p63 is almost exclusively restricted to epithelial cells, mutations in this gene are infrequent, and its expression is increased in a variety of solid tumors, particularly those of the head and neck area 12,13 . (bvsalud.org)
  • We did simultaneous introduction of two tumor suppressor peptides (p14 ARF and p16 INK4a or p16 INK4a and p21 CIP1 functional peptides) compared with single-peptide introduction using Wr-T-mediated peptide delivery. (aacrjournals.org)
  • Transcription levels of Dnmt1, mbd2, MeCP2, p16 INK4A , hMSH2 and c-myc were detected by using real-time PCR or RT-PCR. (wjgnet.com)
  • Promoter methylation of p16 INK4A , c-myc and hMSH2 genes was assayed by methylation-specific PCR (MSP) and sequencing (mapping). (wjgnet.com)
  • The transcriptional levels of p16 INK4A and MeCP2 genes did not display any difference between gastric cancerous and matched non-cancerous tissues. (wjgnet.com)
  • SnCs exhibit irreversible growth arrest accompanied by increased expression of cyclin-dependent kinase inhibitors (CDKi) such as p16 INK4a , and p21 Cip1 , accumulation of DNA damages, and secretion of diverse bioactive molecules known as the senescence-associated secretory phenotype (SASP). (aging-us.com)
  • The activity of this kinase is restricted to the G1-S phase, which is controlled by the regulatory subunits D-type cyclins and CDK inhibitor p16(INK4a). (thermofisher.com)
  • Furthermore, the cell cycle regulatory genes p16 INK4a and p14 ARF are noted to be altered in lesions of proliferative verrucous leukoplakia. (medscape.com)
  • Nine families carried an identical alteration consisting of the insertion of arginine at position 113 of p16(INK4a), and one carried a missense mutation, in which the valine at position 115 was replaced with a glycine. (lu.se)
  • The 113insArg mutant p16(INK4a) was unable to bind cdk4 and cdk6 in an in vitro binding assay. (lu.se)
  • This gene lies adjacent to the tumor suppressor gene CDKN2A in a region that is frequently mutated, deleted, or disregulated in a wide variety of cancer. (wikipedia.org)
  • A common missense variant of the CDKN2A gene (A148T) predisposes to malignant melanoma in Poland. (bmj.com)
  • CDKN2A appears to be a low penetrance breast cancer susceptibility gene in Poland. (bmj.com)
  • The CDKN2A (OMIM 600160) gene is a tumour suppressor gene that is involved in susceptibility to malignant melanoma 1 and has also been implicated in familial pancreatic cancer. (bmj.com)
  • Correction: Increased mRNA expression of CDKN2A is a transcriptomic marker of clinically aggressive meningiomas. (amedeo.com)
  • 30. Mohseny AB, Tieken C, van der Velden PA, mAChR5 Agonist Storage & Stability Szuhai K, de AC, Hogendoorn PCW, Cleton-Jansen AM: Compact deletions but not methylation underlie CDKN2A/ p16 loss of expression in conventional osteosarcoma. (achrinhibitor.com)
  • 0001). Families with breast cancer also had a propensity for multiple melanomas in females, suggesting that a sex-dependent factor may modify the phenotypic expression of CDKN2A alterations. (lu.se)
  • Two alternatively spliced transcripts of this gene encode proteins that share the N-terminal sequence but completely differ in the C-terminus. (wikipedia.org)
  • [ 12 ] Genetic alterations in dysplastic (atypical, Clark) melanocytic nevi appear complex and include loss of tumor suppressor genes and altered function of oncogenes, housekeeping genes, growth factors, and extracellular matrix proteins. (medscape.com)
  • Mechanistically, both peptides caused a significant reduction at G0/G1 phase, in correlation with an augmented expression of the cell cycle inhibitory proteins p53, p27, p21, necrosis, exacerbated generation of reactive oxygen species and diminished mitochondrial membrane potential, all hallmarks of cellular stress. (nature.com)
  • Structural genes encode proteins that are not involved in gene regulation. (p450inhibitors.com)
  • The availability of tools to interrogate the transcriptome and proteome, such as expression profiling, have identified a substantial library of products that could aid in distinguishing a well-differentiated pancreatic carcinoma from a benign pancreatic lesion.2 Many of these proteins can be detected immunohistochemically and are thus available to the practicing pathologist (Table 2).3 Some of these markers have been validated on biopsy specimens as well. (coek.info)
  • Note that by convention gene names are italicized and the proteins they make are not. (cancerquest.org)
  • Genes that suppress carcinogenesis have been classified as gatekeepers that regulate cellular proliferation and cell death and as caretakers that are primarily encode DNA repair proteins required for the maintenance of genome integrity ( 15 ). (amegroups.org)
  • To explore the effect of DNA methyltransferase, demethylase and methyl-CpG binding protein MeCP2 on the expressions and methylation of hMSH2 and proto-oncogene in human gastric cancer. (wjgnet.com)
  • The inactivation of tumor suppressor genes (TSGs) by aberrant DNA methylation plays an important role in the development of malignancy. (biomedcentral.com)
  • Results: We found that LOH and methylation of the PTEN promoter were significantly associated with loss of PTEN protein expression, while, PTEN mutation was a rare event. (cancerindex.org)
  • Furthermore, out of 46 double hit cases (i.e., having both methylation and LOH), 70% (32/46) cases showed complete loss of PTEN expression (P= 0.0249). (cancerindex.org)
  • Both LOH and PTEN promoter methylation were associated significantly with age and clinical stage, while, methylation and loss of PTEN expression were associated with high grade and Her-2 negativity. (cancerindex.org)
  • Several hallmarks of cellular senescence, such as cell cycle arrest, expression of cyclin-dependent kinase inhibitors, DNA damages, and senescence-associated secretory profile were evaluated. (aging-us.com)
  • however, studies suggest that there may be alterations in the same set of susceptibility genes in dysplastic (atypical, Clark) melanocytic nevi and cutaneous melanoma. (medscape.com)
  • Despite these advances made in identifying inherited breast cancer susceptibility genes, the vast majority of breast cancers are sporadic, that is, no identifiable mutation in one of the known breast cancer susceptibility genes. (hindawi.com)
  • While this may reflect the fact that we have yet to identify the next BRCA gene, it may also reflect the polygenic nature of breast cancer susceptibility. (hindawi.com)
  • There is continuing interest in identifying low penetrance genes that are associated with increased susceptibility to common types of cancer. (bmj.com)
  • Carcinogenesis is a multi-step process wherein abrogation of multiple cancer susceptibility genes leads to cancer development. (amegroups.org)
  • Cyclin-dependent kinase 4 inhibitor B also known as multiple tumor suppressor 2 (MTS-2) or p15INK4b is a protein that is encoded by the CDKN2B gene in humans. (wikipedia.org)
  • This gene encodes a cyclin-dependent kinase inhibitor, also known as p15Ink4b protein, which forms a complex with CDK4 or CDK6, and prevents the activation of the CDK kinases by cyclin D, thus the encoded protein functions as a cell growth regulator that inhibits cell cycle G1 progression. (wikipedia.org)
  • 2 The p16 protein is a cyclin dependent kinase inhibitor that suppresses cell proliferation 3 and is expressed in a wide range of tissues, including the breast, and in breast cancers. (bmj.com)
  • This gene encodes lipase A, the lysosomal acid lipase (also known as cholesterol ester hydrolase). (cancerindex.org)
  • HER2/neu (also called ERB B2 ) is the gene that encodes the human epidermal growth factor receptor type 2. (cancerquest.org)
  • These include dysfunctional telomeres, DNA damage, the expression of certain oncogenes, perturbations to chromatin organization and strong mitogenic signals. (nature.com)
  • Oral carcinogenesis is known as multifactorial process which engaged plentiful genetic events that transform normal activity of tumor suppressor genes and oncogenes. (ujds.in)
  • The normal versions of genes in the first group are called proto-oncogenes. (cancerquest.org)
  • The mutated or otherwise damaged versions of these genes are called oncogenes. (cancerquest.org)
  • We have two copies of each gene and for oncogenes, a single defective copy is enough to cause a cell to divide. (cancerquest.org)
  • Numerous genes have been identified as proto-oncogenes. (cancerquest.org)
  • As stated in the introduction to this section, the defective versions of these genes, known as oncogenes, can cause a cell to divide in an unregulated manner. (cancerquest.org)
  • Genome wide association studies, fluorescence in situ hybridization, comparative genomic hybridization, and candidate gene studies have enumerated genetic contributors to cancers in women. (hindawi.com)
  • Examples of these genes are BRCA1 and BRCA2 in breast and ovarian cancers. (hindawi.com)
  • Candidate genes for cancers at a particular site may be selected because they are known to predispose to malignancies in other organs, or because they are mutated somatically in the cells from the cancer of the interest. (bmj.com)
  • In various human cancers poor outcome for the patients has been associated with increase expression of EphA2 and EphrinA-1 [ 16 , 17 , 19 , 24 , 26 ]. (medsci.org)
  • However, the transcription level of the above genes was not associated with biological behaviours of gastric cancers. (wjgnet.com)
  • 29. Carter SL, Eklund AC, Kohane IS, Harris LN, Szallasi Z: A signature of chromosomal instability inferred from gene expression profiles predicts clinical outcome in numerous human cancers. (achrinhibitor.com)
  • A diagram showing the major cancer genes for some cancers. (cancerquest.org)
  • The proliferative arrest is mediated by transcriptional repression of genes essential for cell division by the retinoblastoma protein family. (biomedcentral.com)
  • The molecular events which direct melanocytic proliferation to the pathogenesis of dysplastic (atypical, Clark) melanocytic nevi formation from melanoma is unknown, but it appears to include a constellation of genetic, epigenetic, and environmental factors (eg, B-RAF mutation status, cell cycle protein expression, histone modifications, and ultraviolet radiation exposure), which may regulate cellular mechanisms that bypass cellular senescence. (medscape.com)
  • [ 6 ] However, a role for the TP53 gene mutation or inactivation has not been found in the pathogenesis of proliferative verrucous leukoplakia. (medscape.com)
  • Figure 4: Senescence controlled by the p53 and p16-pRB pathways. (nature.com)
  • Prior to senescence, mutant RasV12 activation in primary human fibroblasts compromised mitosis, associated with abnormal expression of mitotic genes that enter M-phase. (nih.gov)
  • Importantly, mitotic slippage and oncogene signalling synergistically induced senescence and key senescence regulators p21 and p16. (nih.gov)
  • We found that both deacetylation of H4-K16Ac and expression of HMGA1/2 can contribute to DNA compaction during senescence. (biomedcentral.com)
  • Variable DNA compaction observed during senescence is explained in part by cell-type specific regulation of H4 deacetylation and HMGA1/2 expression. (biomedcentral.com)
  • Chronic exposure to IL-1β induces only partial expression of senescence markers and does not allow us to conclude on its ability to induce senescence in chondrocytes. (aging-us.com)
  • On the other hand, etoposide treatment reliably induces DNA damage-related senescence in human articular chondrocytes evidenced by loss of proliferative capacity, DNA damage accumulation, and expression of some SASP components. (aging-us.com)
  • Considering the role of cellular senescence in age-related diseases including OA, the therapeutic potential of senolytic (drugs that induced SnCs death) and senomorphic (drugs that modulate the SASP) compounds have been contemplated with growing interest [ 15 ]. (aging-us.com)
  • Gene ontology (GO) analysis revealed that inflammatory pathways were most frequently implicated in RTK. (aging-us.com)
  • What pathways are this gene/protein implicaed in? (cancerindex.org)
  • These findings were verified in vivo, where activation of the SHH pathway significantly promoted GLI1 and IL-6 expressions in nude mice, inducing inflammation and tumor growth. (bvsalud.org)
  • This first category also includes genes that contribute to tumor growth by inhibiting cell death. (cancerquest.org)
  • Increased expression of immunoreactive tumor growth factor-alpha has been noted in lesions of both proliferative verrucous leukoplakia and oral squamous cell cancer, but not in healthy oral mucosa. (medscape.com)
  • The various markers that enable assessment of the progression of preneoplastic lesions to spindle cell carcinoma include the p16 protein, which halts the cell cycle and induces apoptosis by pRb-mediated phosphorylation of cyclin-dependent kinase 4 (CDK4). (bvsalud.org)
  • For EphA2 expression, 21 tumors (10%) showed negative, 108 (50%) weak positive, 69 (32%) moderate positive and 19 (9%) strong positive, whereas for EphrinA-1 expression, 33 tumors (15%) showed negative, 91 (42%) weak positive, 67 (31%) moderate positive and 26 (12%) strong positive. (medsci.org)
  • Previous studies have reported that 10-15% of patients with RTKs had primary central nervous system (CNS) disease, which is currently designated as atypical teratoid-rhabdoid tumors [ 2 ]. (aging-us.com)
  • Conclusion: p63, p16, MIB, Cal A, Cys A are markedly expressed and p16 is strongly suppressed in oral cavity tumors, which suggests that the latter protein may play a role in negative regulation of cell cycle progression. (bvsalud.org)
  • An example of this class of genes is a mutation in the CHEK2 gene in breast cancer. (hindawi.com)
  • In addition, they all had a common deletion of the last base G of codon 249 (AGG to AG_) of the p53 gene, which resulted in generation of its nonsense gene product. (biomedcentral.com)
  • Consideration of tumor heterogeneity is therefore important in the critical analysis of gene associations in cancer. (hindawi.com)
  • Modern approaches to treating cancer take advantage of critical biochemical differences between cancer cells and normal cells - from radiation therapy to chemotherapy to experimental gene therapy. (janechin.net)
  • The up-regulation of proto-oncogene may be the consequence of epigenetic control of gene expression by demethylase, and mbd2 is involved in the regulation of hMSH2 expression in human gastric cancer. (wjgnet.com)
  • To investigate the in vitro effects of suicide gene therapy system of herpes simplex virus thymidine kinase gene (HSV-TK) in combination with the treatment of nucleotide analog-ganciclovir (GCV) on human pancreatic cancer, and to provide a novel clinical therapeutic method for human pancreatic cancer. (wjgnet.com)
  • Our data demonstrate that HSV-TK/GCV suicide gene therapy system is effective for treating experimental human pancreatic cancer, which is largely resistant to the common therapies, so the suicide gene therapy system may be a potential treatment approach for pancreatic cancer. (wjgnet.com)
  • Loss of expression of the homeobox transcription factor NKX3.1 in the prostate is frequently associated with human prostate cancer. (pharmaceuticalintelligence.com)
  • The Selenium and Vitamin E Cancer Prevention Trial (SELECT) was initiated in 2001 to conduct a large, randomized controlled clinical trial on the efficacy of the antioxidants selenium and vitamin E in the prevention of prostate cancer [15]. (pharmaceuticalintelligence.com)
  • Gera R, Mokbel L, Jiang WG, Mokbel K mRNA Expression of Cancer Genomics Proteomics. (cancerindex.org)
  • Our objective was to determine if CDK2AP1 mRNA expression levels were consistent with tumour-suppressive functions in breast cancer. (cancerindex.org)
  • Normalised CDK2AP1 expression was 38-fold higher in adjacent non-cancerous breast tissue than in breast cancer. (cancerindex.org)
  • CDK2AP1 expression in disease-free patients at 10 years was more than threefold that of patients who died of breast cancer. (cancerindex.org)
  • To our knowledge, this is the first study in the literature to examine the mRNA expression of CDK2AP1 in human breast cancer over a long-term follow-up period. (cancerindex.org)
  • While studying the activity of BRCA2 gene promoter in breast cancer cells, we discovered that this promoter has bi-directional activity and the product of the reverse activity (a ZAR1-like protein, we named ZAR2) silences the forward promoter at the G0/G1 phase of the cell. (biomedcentral.com)
  • The notion could be that unique cellular mechanisms are triggered in the breast cancer cells to stimulate BRCA2 gene expression as a temporary measure to regulate the growth of the breast cancer cells. (biomedcentral.com)
  • One potential mechanism of BRCA2 involvement in breast cancer progression may be through deregulation of the BRCA2 gene expression. (biomedcentral.com)
  • Int J Cancer 1975, 15:239. (achrinhibitor.com)
  • Genes Chromosomes Cancer 2010, 49:1095103. (achrinhibitor.com)
  • Background: Breast cancer is a heterogeneous disease that can be subdivided on the basis of histopathological features, genetic alterations, and gene-expression profiles. (cancerindex.org)
  • PTEN gene is considered an established tumor suppressor gene in different types of cancer including breast cancer. (cancerindex.org)
  • The larger the gene name, the more frequently that gene is defective in that cancer type. (cancerquest.org)
  • Of the 30,000 or so genes that are currently thought to exist in the human genome , there is a small subset that seems to be particularly important in the prevention, development, and progression of cancer. (cancerquest.org)
  • These genes have been found to be either malfunctioning or non-functioning in many different kinds of cancer. (cancerquest.org)
  • GLI1 interaction with p300 modulates SDF1 expression in cancer-associated fibroblasts to promote pancreatic cancer cells migration. (mayo.edu)
  • Clinical studies indicate that expression and activity of DNA-PKcs is correlated with cancer progression and response to treatment. (amegroups.org)
  • Park H, Imoto S , Miyano S. Comprehensive information-based differential gene regulatory networks analysis (CIdrgn): Application to gastric cancer and chemotherapy-responsive gene network identification. (google.com)
  • L'étude menée en Iraq a utilisé la méthode d'hybridation in situ pour déterminer la fréquence du papillomavirus humain et pour son génotypage dans les échantillons de tissus prélevés auprès de 129 patientes ayant reçu un diagnostic de cancer du sein malin, de 24 patientes porteuses d'une tumeur du sein bénigne et de 20 femmes témoins en bonne santé. (who.int)
  • Studies suggest that expression of cystatin A is inversely associated with malignant progression of cancer 9 . (bvsalud.org)
  • By using immunohistochemistry we investigated the expression of EphA2 and EphrinA-1 in 217 early squamous cell cervical carcinomas and examine their prognostic relevance. (medsci.org)
  • We analyzed the clinical data and performed immunohistochemistry for Epidermal growth factor receptor (EGFR) and Aurora kinase A (Aurora-A) expression in 180 SCCHN patients. (oncotarget.com)
  • While, for PTEN protein expression, we used immunohistochemistry. (cancerindex.org)
  • This gene thus plays a role in both cell-cycle and epigenetic regulation. (cancerindex.org)
  • While BRCA2 expression is involved in cell cycle checkpoints and DNA repair, the mechanisms of cell cycle-dependent regulation of BRCA2 gene expression remains elusive. (biomedcentral.com)
  • In Gene Regulation: Procedures and Protocols, Procedures in Molecular Biology. (achrinhibitor.com)
  • We further identified a binding site between GLI1 and the promoter region of IL-6, demonstrating that GLI1 can enhance the expression of IL-6. (bvsalud.org)
  • Standard techniques like cell synchronization by serum starvation, flow cytometry, N-terminal or C-terminal FLAG epitope-tagged protein expression, immunofluorescence confocal microscopy, dual luciferase assay for promoter evaluation, and chromatin immunoprecipitation assay were employed during this study. (biomedcentral.com)
  • Human BRCA2 gene promoter is active in both the forward and the reverse orientations. (biomedcentral.com)
  • In the G0/G1 growth phase ZAR2 is predominantly located inside the nucleus of the breast cells, binds to the BRCA2 promoter and inhibits the expression of BRCA2. (biomedcentral.com)
  • BRCA2 gene promoter has bi-directional activity, expressing BRCA2 and a novel C4-type zinc finger containing transcription factor ZAR2. (biomedcentral.com)
  • Subcellular location of ZAR2 and its expression from the reverse promoter of the BRCA2 gene are stringently regulated in a cell cycle dependent manner. (biomedcentral.com)
  • ZAR2 binds to BRCA2/ZAR2 bi-directional promoter in vivo and is responsible, at least in part, for the silencing of BRCA2 gene expression in the G0/G1 phase in human breast cells. (biomedcentral.com)
  • Patients characterized by elevated EGFR and elevated Aurora-A protein expression in tumor tissue represent a risk group with poor disease-free and overall survival (EGFR low Aurora-A low versus EGFR high Aurora-A high , p=0.024). (oncotarget.com)
  • Comparing pan-Aurora kinase and Aurora-A targeting hints towards a strong and clinically relevant biological effect mediated via Aurora kinase B. Taken together, our findings characterize a new poor risk group in SCCHN patients defined by elevated EGFR and Aurora-A protein expression. (oncotarget.com)
  • Liu Y, Zhang YZ, Imoto S . Microbial Gene Ontology informed deep neural network for microbe functionality discovery in human diseases. (google.com)
  • They were characterized by immunofluorescence, classical cytogenetics, p53 gene mutational analysis, fluorescence in-situ hybridization, and histopathological and immunohistochemical examinations of their xenografts, to demonstrate their potency of secondary transformation. (biomedcentral.com)
  • [ 15 ] A helpful review of the molecular aspects of dysplastic (atypical, Clark) melanocytic nevi is available by Hussein and Wood. (medscape.com)
  • In our previous study, we proposed a concept of focal carcinomas in pleomorphic adenoma which is an advanced stage of accumulated atypical cells with P53 over-expressions as an initial stage or a latent form of apparent carcinomas secondarily arising in pleomorphic adenoma [ 3 ]. (biomedcentral.com)
  • We discovered that GLI1 regulates the expression of IL-6, thereby triggering inflammatory responses in ACP and influencing the tumor's progression. (bvsalud.org)
  • Despite the differences in their normal roles, these genes all contribute to unregulated cell division if they are present in a mutant (oncogenic) form. (cancerquest.org)
  • The protein encoded by this gene is a cyclin-dependent kinase 2 (CDK2) -associated protein which is thought to negatively regulate CDK2 activity by sequestering monomeric CDK2, and targeting CDK2 for proteolysis. (cancerindex.org)
  • There were no significant associations between CDK2AP1 expression and estrogen receptor status, tumour grade and tumour type. (cancerindex.org)
  • This is in contrast with tumor suppressor genes which must BOTH be defective to lead to abnormal cell division. (cancerquest.org)
  • These events are dependent on the proper levels of transcription and translation of certain genes. (cancerquest.org)
  • Functional loss of p16 may lead to uncontrolled cell proliferation 3,4 . (bvsalud.org)
  • Analyzing the Gene Expression Omnibus (GEO) database chip GSE68015, we found that GLI1 is overexpressed in ACP, correlating positively with the spite of ACP and inflammation markers. (bvsalud.org)
  • Search the gene expression profiles from curated DataSets in the Gene Expression Omnibus (GEO) repository. (cancerindex.org)
  • The expression of this gene was found to be dramatically induced by TGF beta, which suggested its role in the TGF beta induced growth inhibition. (wikipedia.org)
  • 95% within the first 72 h, whereas the growth inhibition was ∼40% by p14 or p16 single-peptide introduction. (aacrjournals.org)