Background Genomic deletion at tumor suppressor loci is a common genetic aberration in human cancers. The study aimed to explore candidate tumor suppressor genes at chromosome 4q25-q28.2 and to delineate novel prognostic biomarkers associated with colorectal cancer (CRC). Methods Deletion mapping of chromosome 4q25-q28.2 was conducted in 114 sporadic CRC by loss of heterozygosity study with 11 microsatellite markers. A novel candidate tumor suppressor gene, namely NDST4, was identified at 4q26. Gene expression of NDST4 was investigated in 52 pairs of primary CRC tissues by quantitative reverse transcription-polymerase chain reaction. Allelic loss of NDST4 gene was further determined in 174 colorectal carcinomas by loss of heterozygosity analysis, and then was assessed for clinical relevance. Results One minimal deletion region was delineated between D4S2297 and D4S2303 loci at 4q26, where NDST4 was the only gene that had markedly been downregulated in CRC tumors. By laser capture microdissection,
Autori: Lefter LP, Sunamura M, Furukawa T, Yastsuoka T, Abe H, Inoue H, Abe T, Egawa S, Miura K, Morita R, Horii A, Matsuno S.. Editorial: Asian J Surg. 2004 Apr;27(2):85-92., 2004.. Rezumat:. BACKGROUND: In a previous work, we demonstrated that loss of heterozygosity of 18q is a frequent event significantly associated with poor prognosis in pancreatic cancer. We hypothesized that restoration of heterozygosity of chromosome 18 in pancreatic cancer cells would reduce their tumorigenicity. This study was intended to provide functional evidence for the existence of new tumour suppressor gene(s) located on chromosome 18. METHOD: Restoration of heterozygosity was achieved by introducing a normal copy of chromosome 18 into pancreatic ductal carcinoma using a microcell-mediated chromosome transfer technique. The tumorigenicity and metastatic ability of both the parental cells and resulting hybrids were assessed in vitro and in vivo. RESULTS: In vitro growth of hybrid clones was significantly delayed ...
Recently, abnormal tumor suppressor gene (TSG) methylation has become a hotspot in the research on colorectal cancer (CRC). This study aimed to explore the influence of CHD5 methylation of CRC TSG on its clinical and pathological characteristics.
The long arm of chromosome 16 is a frequent target for loss of heterozygosity (LOH) in sporadic breast cancer [1]. Detailed mapping of LOH revealed at least two frequently deleted genomic regions on chromosome 16q22.1 and 16q24.3 that could harbour classical tumour suppressor genes (TSGs) [2, 3]. Mutation analysis identified the homophilic epithelial cell adhesion gene CDH1 encoding E-cadherin, located at 16q22.1, as a TSG, but only in the histological subset of lobular breast cancer and not in the more frequent ductal breast cancer [4]. Thus, the TSGs in ductal breast cancer remain elusive. To identify these TSGs, many genes have already been screened and excluded as candidates [5-8]. Although some studies have suggested other genes as potential candidates (e.g. the transcriptional co-repressor CBFA2T3 (MTG16) [9], the zinc finger transcription factor CTCF [10] or the oxidoreductase WWOX [11]), these genes fail to fit the classic two-hit model for a TSG because no inactivating mutations could ...
Tumour suppressor gene function, focusing on several hematopoietic transcription factors recurrently mutated in acute lymphoblastic and myeloid leukemias (ALL and AML).. Cancer results from an accumulation of genetic mutations that disable the normal regulation of cell growth and survival. In the last decade, large scale cancer genome sequencing of all the major cancer types has identified ~150 genes that promote oncogenesis when mutated. To develop more effective cancer therapies, now the key challenge is to understand how these cancer driver genes, comprising a similar number of oncogenes and tumour suppressor genes, contribute to tumourigenesis and treatment response.. Our laboratory is interested in understanding tumour suppressor gene function, focusing on several hematopoietic transcription factors recurrently mutated in acute lymphoblastic and myeloid leukemias (ALL and AML). Our general approach uses shRNA-mediated inhibition of these transcription factors to drive leukemogenesis in ...
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inproceedings{1148146, abstract = {Identification of tumor suppressor genes (TSGs) silenced by CpG methylation uncovers the molecular mechanism of tumorigenesis and potential tumor biomarkers. GULP1, a molecule not previously related to cancer, is a cytoplasmic adaptor protein with a phosphotyrosine binding domain that plays a role in one of two partially redundant pathways that lead to the engulfment and clearance of apoptotic cells, according to several genetic studies performed in Caenorhabditis elegans. Performing a pharmacologic unmasking technique we observed that this molecule is downregulated in ovarian tumor tissues when compared to normal ovary. Ovarian cancer is the leading cause of death among gynaecological cancers worldwide, this due to the fact that women are diagnosed with advanced stage disease and because of the lack of truly sensitive/specific screening techniques and unavailability of individualized therapy. We performed an expression microarray on 15 ovarian tumor samples, ...
SNPwatch gives you the latest news about research linking various traits and conditions to individual genetic variations. These studies are exciting becaus
Many of the genes in which we found high FSM rates have known potential links to carcinogenesis. For example, ACTRII is a member of the TGF-β receptor family that is involved in the induction of differentiation, growth suppression, and apoptosis. Mutant ACTRII inhibits activin-mediated induction of differentiation (12) . DKFZ564K112 is a human homologue of the Drosophila tumor suppressor gene multi-sex-comb (mxc), a member of the homeobox gene transcription repressor family Polycomb group. Mxc is ubiquitously expressed, and its loss of function provokes uncontrolled malignant cell growth (13) . ICE/caspase-1, a human homologue of Caenorhabditis elegans CED3, is a mediator of Fas-mediated apoptosis. Down-regulation of ICE/caspase-1 is observed in various human cancers (14) , and overexpression of ICE/caspase-1 inhibits the growth of renal cell carcinoma cell lines in vivo (15) . KIAA0896 (hHYD) is a human homologue of the Drosophila tumor suppressor gene hyperplastic discs. hHYD is expressed at ...
Deleted in malignant brain tumours 1 (DMBT1), a candidate tumour suppressor gene located on chromosome 10q25.3-q26.1, has recently been identified and found to be deleted in several different types of human tumours. In melanomas, the chromosomal regi
Qiu, G.-H.,Lim, C.Y.,Tao, Q.,Tan, L.K.S.,Loh, K.S.,Srivastava, G.,Tsai, S.-T.,Tsao, S.W. (2004). The candidate tumor suppressor gene BLU, located at the commonly deleted region 3p21.3, is an E2F-regulated, stress-responsive gene and inactivated by both epigenetic and genetic mechanisms in nasopharyngeal carcinoma. Oncogene 23 (27) : 4793-4806. [email protected] Repository. https://doi.org/10.1038/sj.onc.1207632 ...
Cut62 is a putative tumor suppressor gene. than in regular Compact disc34-positive cells recommending that Cut62 loss may be involved with leukemogenesis but had not been associated with particular karyotypic TWS119 abnormalities or Nucleophosmin (NPM1) Fms-like Tyrosine Kinase-3 (FLT3) or rat sarcoma viral oncogene (RAS) mutational position. Low Cut62 levels had been connected with shorter comprehensive remission length of time and considerably shorter event-free and general survival rates especially among sufferers with intermediate-risk cytogenetics. For the reason that AML subgroup age group and Cut62 amounts were the most powerful self-employed prognostic factors for survival. TRIM62 protein levels further processed the risk associated with NPM1 and FLT3 mutational status. TRIM62 loss was associated with modified expression TWS119 of proteins involved in leukemia stem cell homeostasis (β-catenin and Notch) cell motility and adhesion (integrin-β3 ras-related C3 botulinum toxin substrate ...
In this study we examined the LOH of 11 dinucleotide repeat loci on chromosome 10 in 208 meningiomas of all grades. We investigated the incidence and complexity of LOH relative to tumor progression. For all alleles examined, the incidence of LOH was much higher in all grades than that reported previously, with incidence and complexity of LOH increasing with tumor grade. Mapping of the regions of LOH of all of the tumors defined four regions of chromosomal deletion. These deletions coincide with those found in other cancers, supporting the hypothesis that candidate tumor suppressor genes in these regions contribute to meningeal tumorigenesis and progression.. To expand on previous studies, we examined LOH of alleles used in previous meningioma reports (11, 12, 13, 14, 15) , as well as additional loci mapping near known and candidate tumor suppressor genes on 10q. The present data are in good agreement with our reported data (11) that LOH occurs at markers D10S89 and D10S169 and with the 10q LOH ...
By activating a cancer suppressor gene, a small molecule called nutlin-3a can block cancer cell division, according to researchers at the National Cancer Institute (NCI), part of the National Institutes of Health. This activation of the p53 gene leads to cellular senescence, a process by which cells lose their ability to grow and divide. An opportunity for new genetic mutations occurs each time a cell divides, so limiting the number of cell divisions in a cancer cell inhibits tumor progression. This study is published in the May 1, 2008, issue of Cancer Research.
Traditionally, it has been held that a central characteristic of stem cells is their ability to divide asymmetrically. Recent advances in inducible genetic labeling provided ample evidence that symmetric stem cell divisions play an important role in adult mammalian homeostasis. It is well understood that the two types of cell divisions differ in terms of the stem cells flexibility to expand when needed. On the contrary, the implications of symmetric and asymmetric divisions for mutation accumulation are still poorly understood. In this paper we study a stochastic model of a renewing tissue, and address the optimization problem of tissue architecture in the context of mutant production. Specifically, we study the process of tumor suppressor gene inactivation which usually takes place as a sequence of two consecutive "hits", and which is one of the most common patterns in carcinogenesis. We compare and contrast symmetric and asymmetric (and mixed) stem cell divisions, and focus on the rate at ...
Slit, Netrin, Ephrin, and Semaphorins roles in development have expanded greatly in the past decade from their original characterization as axon guidance molecules (AGMs) to include roles as regulato
Cancer cells escape normal growth control mechanisms as a consequence of activating (i.e., gain-of-function) mutations and/or increased expression of one or more cellular protooncogenes and/or inactivating (i.e., loss-of function) mutations and/or decreased expression of one or more tumor suppressor genes. Most oncogene and tumor suppressor gene products are components of signal transduction pathways that control cell cycle entry or exit, promote differentiation, sense DNA damage and initiate repair mechanisms, and/or regulate cell death programs. Several oncogenes and tumor suppressor genes belong to the same signaling pathway. Perhaps the best-characterized pathway includes D-type cyclin/cdk complexes, which can be oncogenes, and two tumor suppressor genes, the p16 cyclin/cdk inhibitor and the retinoblastoma gene product (reviewed in ref. 1). Nearly all tumors have mutations in multiple oncogenes and tumor suppressor genes, indicating that cells employ multiple parallel mechanisms to regulate ...
Oncogenes and tumor suppressor genes (TSGs) both play a role in oncogenesis via opposite mechanisms. Proto-oncogenes promote normal cell growth. Occasionally, a mutation increases their activity or a duplication, translocation, or other genetic event increases their expression. Under such conditions, these genes, now called oncogenes, cause abnormal unchecked cell growth. Examples of proto-oncogenes include growth factors, tyrosine kinases, regulatory GTPases, and transcription factors. TSGs inhibit cell growth in normal cells. However, decreases in TSG activity, often caused by mutation or promoter hypermethylation, prevents their ability to stop abnormal cell growth. Examples of TSGs include genes that regulate apoptosis, cell adhesion, or DNA damage signaling. Genes may have oncogenic properties, tumor suppressor properties, or both. These properties depend not only on the tumor type, but also on the known or observed differences in gene expression or epigenetic marks. Genetic differences in ...
You have 2 copies of most genes - one from each parent. When someone has inherited an abnormal copy of a gene, their cells already start out with one mutation. If the other copy of the gene stops working (because of an acquired mutation, for example), the gene can stop functioning altogether. When the gene that stops working is a cancer susceptibility gene, cancer can develop. Some cancer susceptibility genes function as tumor suppressor genes. Tumor suppressor genes are normal genes that slow down cell division, repair DNA mistakes, or tell cells when to die (a process known as apoptosis or programmed cell death). When tumor suppressor genes dont work properly, cells can grow out of control, which can lead to cancer. Many family cancer syndromes are caused by inherited defects of tumor suppressor genes ...
Extensive studies are now being conducted on adoptively transferred tumor-reactive T cells in an attempt to identify characteristics of those cells that are associated with tumor regression. The results of several studies suggest that HLA class I-restricted T cells that recognize nonmutated shared Ags such as the melanocyte differentiation Ags MART-1 and gp100 play a role in tumor regression in some patients (23, 26). It is more difficult to assess the role of T cells that are reactive with mutated Ags in tumor regression, because individual mutations are generally restricted to only one or a relatively small percentage of tumors. Nevertheless, TIL that are associated with tumor regression have been found to contain T cells that recognize mutated Ags (27), suggesting that they may in some cases play a role in this process.. This study presents the analysis of a TIL 1913 that was associated with a nearly complete regression of multiple metastatic lesions following adoptive immunotherapy. The ...
FGF2 is expressed in all stages of human prostate cancer. To determine whether FGF2 plays a critical role in prostate cancer progression, we have compared prostate cancer progression in TRAMP mice with hemi- or homozygous inactivation of FGF2 with that of WT littermate controls. Our results show that inactivation of either one or both alleles of FGF2 leads to significantly increased survival by inhibiting progression to the poorly differentiated phenotype and metastatic disease. It is noteworthy that inactivation of even one FGF2 allele has a strong influence on tumor progression. Analysis of mouse models of cancer has revealed that profound phenotypic consequence can result from haploinsufficiency of tumor suppressor gene function. For example, we have demonstrated previously that loss of even one PTEN allele is associated with increased rates of tumor progression in TRAMP mice (21) . Similarly, Goss et al. (30) have recently demonstrated that mice carrying only one allele of the Bloom syndrome ...
In most myeloid leukemias induced in mice by γ-radiation, one copy of chromosome 2 has suffered a deletion. To search for a potential tumor suppressor gene in that region, we have delineated the deletions in a panel of these tumors. A commonly deleted region of 2 megabase pairs (Mbp) includes the gene encoding the PU.1 transcription factor, a powerful inducer of granulocytic/monocytic differentiation. Significantly, in 87% of these tumors the remaining PU.1 allele exhibited point mutations in the PU.1 DNA binding domain. Surprisingly, 86% of these mutations altered a single CpG, implicating deamination of deoxycytidine, a common mutational mechanism, as the origin of this lesion. The "hot spot" resides in the codon for a contact residue essential for DNA binding by PU.1. In keeping with a tumor suppressor role for PU.1, enforced expression of wild-type PU.1 in the promyelocytic leukemia cells inhibited their clonogenic growth, induced monocytic differentiation, and elicited apoptosis. The ...
Powerful new tools are now available to discover and understand tumor suppressor genes (TSGs) and the biochemical mechanisms by which they control cancer
Lowe, S. (November 2002) Roles of oncogenes and tumor suppressor genes in apoptosis. European Journal of Cancer, 38. S15-S15. ISSN 0959-8049 ...
Human cancer develops as a result of accumulation of mutations in oncogenes and tumor suppressor genes. Zinc finger protein 668 (ZNF668) has recently been identified and validated as one of the highly mutated genes in breast cancer, but its function is entirely unknown. Here, we report two major functions of ZNF668 in cancer development. (1) ZNF668 functions as a tumor suppressor by regulating p53 protein stability and function. We demonstrate that ZNF668 is a nucleolar protein that physically interacts with both MDM2 and p53. By binding to MDM2, ZNF668 regulates MDM2 autoubiquitination and prevents MDM2-mediated p53 ubiquitination and degradation; ZNF668 deficiency impairs DNA damage-induced p53 stabilization. Notably, ZNF668 effectively suppresses breast cancer cell proliferation and transformation in vitro and tumorigenicity in vivo. Consistently, ZNF668 knockdown readily transforms normal mammary epithelial cells. Together, our studies identify ZNF668 as a novel breast tumor suppressor gene that
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Tumor suppressor genes are protective genes. Normally, they limit cell growth by monitoring how quickly cells divide into new cells, repairing mismatched DNA, and controlling when a cell dies. When a tumor suppressor gene is mutated, cells grow uncontrollably and may eventually form a mass called a tumor. BRCA1, BRCA2, and p53 are examples of tumor suppressor genes. Germline mutations in BRCA1 or BRCA2 genes increase a womans risk of developing hereditary breast or ovarian cancers. The most commonly mutated gene in people who have cancer is p53. In fact, more than 50% of all cancers involve a missing or damaged p53 gene. Most p53 gene mutations are acquired mutations. Germline p53 mutations are rare ...
WES of patient-matched tumor pairs from 23 individuals with HNSCC demonstrates the intertumor genetic heterogeneity of this cancer. To our knowledge, this is the first study of HNSCC to examine intertumor genetic heterogeneity in synchronous nodal metastases and metachronous recurrence across multiple patients; it provides a model to determine patterns of mutation and clonal evolution that may be targetable for the treatment of recurrent/metastatic disease.. Primary tumors in our study averaged 67.6 nonsynonymous SSNVs per tumor, including mutations in tumor suppressor genes, oncogenes, and genes that have previously been found to be significantly mutated in HNSCC, such as AJUBA, CASP8, FAT1, FBXW7, NFE2L2, and TP53 (Supplemental Table 10 and Supplemental Table 4). Interestingly, primary tumors were not found to harbor mutations in several tumor suppressor genes and oncogenes previously implicated in HNSCC, including CCND1, PIK3CA, NOTCH1, PTEN, CDKN2A, HRAS, and EGFR. However, copy number ...
Mutation is nothing but change in the building block of genome that is DNA. The mutations in the Oncogene and Tumor suppressor gene may lead to the formation of tumor or cancer.
Colorectal Cancer (CRC) is a genetic disease in which progression is driven by the accumulation of mutations or epigenetic alterations in oncogenes and tumor su...
In the present study, we investigated serum DNA methylation for p16, p15, and RASSF1A, three tumor suppressor genes frequently hypermethylated in HCC. Blood samples were collected from 50 HCC cases 0 to 9 years before diagnosis. The frequencies of detection of gene methylation in the available samples collected closest to diagnosis are consistent with previous studies of serum DNA from HCC patients using blood collected at the time of diagnosis: p16, 44.% versus 48% (22); p15, 22% versus 25% (12); and RASSF1A, 70% versus 43% (19). The detection frequencies for p16 and RASSF1A are also similar to our previous findings in HCC tissue DNAs (14). Hypermethylation was detected 1 to 8 years before clinical diagnosis for p16, 1 to 5 years for p15, and 1 to 9 years for RASSF1A. These findings show that p16, p15, and RASSF1A hypermethylation are early events in the development of HCC.. A specific missense mutation in the p53 tumor suppressor gene at codon 249 has been reported in ,50% of HCC tumors and in ...
SnoN is a negative regulator of TGF-β signaling and also an activator of the tumor suppressor p53 in response to cellular stress. Its role in human cancer is complex and controversial with both pro-oncogenic and anti-oncogenic activities reported. To clarify its role in human cancer and provide clinical relevance to its signaling activities, we examined SnoN expression in normal and cancerous human esophageal, ovarian, pancreatic and breast tissues. In normal tissues, SnoN is expressed in both the epithelium and the surrounding stroma at a moderate level and is predominantly cytoplasmic. SnoN levels in all tumor epithelia examined are lower than or similar to that in the matched normal samples, consistent with its anti-tumorigenic activity in epithelial cells. In contrast, SnoN expression in the stroma is highly upregulated in the infiltrating inflammatory cells in high-grade esophageal and ovarian tumor samples, suggesting that SnoN may potentially promote malignant progression through ...
Transcriptional Regulation in Hematopoiesis and Leukemogenesis. Dr. McNerneys research focuses on the genomics of therapy-related and de novo acute myeloid leukemias (AML). A high-risk subset of patients is unresponsive to treatment and their survival is less than a year. Understanding the underlying genetic changes in these neoplasms is essential to identifying new therapeutic strategies for patients. Using next-generation sequencing and other genomic approaches, Dr. McNerney determined the genetic changes that occur in high-risk myeloid leukemias. She demonstrated that these leukemias have a distinct mutational profile. Half of high-risk myeloid neoplasms exhibit haploinsufficiency of the CUX1 transcription factor, a tumor suppressor gene on chromosome 7 (McNerney et al. 2013, Blood 121:869 link= http://www.ncbi.nlm.nih.gov/pubmed/23212519). In addition, mutations that activate the RAS signaling pathway occur at significantly higher frequency than other AMLs (McNerney et al. 2014, British ...
CRC, a type of malignant tumor, is the second leading cause of cancer-associated mortality in Asia (43). It is also the third most commonly diagnosed type of cancer in men and the second in women worldwide (44). Despite advances in treatment modalities, the prognosis for patients with CRC has not significantly improved (45). miR-27a-3p (has-miR-27a-3p) has been identified as an onco-miRNA in several solid tumors, including breast (46), ovarian (47), pancreatic (48) and gastric (16) cancer. miR-27a has also been reported to be a key oncogenic component in CRC and miR-27a is overexpressed in CRC (49). miR-27a-3p may accelerate tumorigenesis by targeting several tumor suppressors, including BTG2 (15), F-box and WD repeat domain containing 7 (19), Yes associated protein 1 (50) and Wnt family member 3A (51). Regarding BTG1, it has been reported that the tumor suppressor enhances Hoxb9-mediated transcription and inhibits HeLa cell proliferation (52). Overexpression of BTG1 has been detected in ...
1. Arnold CN, Goel A, Blum HE, Boland CR. Molecular pathogenesis of colorectal cancer: implications for molecular diagnosis. Cancer. 2005;104:2035-47 2. Palii SS, Robertson KD. Epigenetic control of tumor suppression. Crit Rev Eukaryot Gene Expr. 2007;17:295-316 3. Baylin SB, Ohm JE. Epigenetic gene silencing in cancer - a mechanism for early oncogenic pathway addiction?. Nat Rev Cancer. 2006;6:107-16 4. Duffy MJ, Napieralski R, Martens JW, Span PN, Spyratos F, Sweep FC. et al. Methylated genes as new cancer biomarkers. Eur J Cancer. 2009;45:335-46 5. Rodriguez-Paredes M, Esteller M. Cancer epigenetics reaches mainstream oncology. Nat Med. 2011;17:330-9 6. Jin H, Wang X, Ying J, Wong AH, Li H, Lee KY. et al. Epigenetic identification of ADAMTS18 as a novel 16q23.1 tumor suppressor frequently silenced in esophageal, nasopharyngeal and multiple other carcinomas. Oncogene. 2007;26:7490-8 7. Lo KW, Teo PM, Hui AB, To KF, Tsang YS, Chan SY. et al. High resolution allelotype of microdissected primary ...
A natural tumor suppressor that could potentially be turned on in cert...Located on chromosome 18 and called PH domain Leucine-rich repeat Prot... A drug that turns on PHLPP so that it suppresses cell growth caused ...Scientists have known that Akt is critical in regulating cell growth a...Since the Akt molecule is locked in the on position when it has phos...,Natural,tumor,suppressor,in,body,discovered,by,UCSD,medical,researchers,biological,biology news articles,biology news today,latest biology news,current biology news,biology newsletters
Mestre-Escorihuela C, Rubio-Moscardo F, Richter JA, Siebert R, Climent J, Fresquet V, Beltran E, Agirre X, Marugan I, Marín M, Rosenwald A, Sugimoto KJ, Wheat LM, Karran EL, García JF, Sanchez L, Prosper F, Staudt LM, Pinkel D, Dyer MJ, Martinez-Climent JA (2007). Homozygous deletions localize novel tumor suppressor genes in B-cell lymphomas. Blood 109, 271-280 ...
Tumor suppressor proteins control the proliferation and survival of normal cells; consequently, their inactivation by gene mutations can initiate or drive cancer progression. Most tumor suppressors have been identified by genetic screening, and in many cases their function and regulation are poorly …
Background Ephrin receptor B2 (EPHB2) has recently been proposed as a novel tumor suppressor gene in colorectal cancer (CRC). Inactivation of the gene has been shown to correlate with progression of colorectal tumorigenesis ...
Abstract: IKKβ (encoded by IKBKB) is a protein kinase that regulates the activity of numerous proteins important in several signaling pathways, such as the nuclear factor kappa B (NF-κB) pathway. IKKβ exerts a pro-tumorigenic role in several animal models of lung, hepatic, intestinal and oral cancer. In addition, genomic and proteomic studies of human tumors also indicate that IKBKB gene is amplified or overexpressed in multiple tumor types. Here, the relevance of IKKβ in skin cancer was determined by performing carcinogenesis studies in animal models overexpressing IKKβ in the basal skin layer. IKKβ overexpression resulted in a striking resistance to skin cancer development and an increased expression of several tumor suppressor proteins, such as p53, p16 and p19. Mechanistically, this skin tumor-protective role of IKKβ is independent of p53 but dependent on the activity of the p16INK4A/p19ARF locus. Interestingly, in the absence of p16 and p19, IKKβ increased expression favors the ...
LATS1 tumor suppressor is a serine/threonine kinase of the AGC kinase family and a core component of the Hippo pathway in mammals. LATS1 regulates various biological processes such as cell cycle progression, genetic stability, cell motility and adhesion, apoptosis, stem cell renewal and differentiation (Visser and Yang, 2010; Mo et al., 2014). LATS1 performs these functions by phosphorylating various substrates such as transcriptional co-activators YAP and TAZ (Zhao et al., 2007; Hao et al., 2008). LATS1 is also required for tissue homeostasis in both flies and mice (Visser et al., 2010). In addition to its roles in a broad spectrum of normal biological processes, loss of LATS1 has been shown to be important for the development of cancer and resistance to chemotherapeutic drugs (Visser et al., 2010). Therefore, understanding the molecular mechanisms underlying loss-of-LATS1-induced tumorigenesis and drug resistance will shed light on the design of new cancer treatment strategies in the future ...
The hLIMD1 gene is located at chromosome 3p21 and was identified as a putative tumor suppressor gene using an elimination test assay. Chromosome 3p21 loci are frequently deleted in a number of cancers, including breast. The 3p21.3 locus harbors a number of tumor suppressor candidates, including LIMD …
Because uncertainties remain about the nature of the cell population that gives rise to cancer, we have investigated different assumptions. According to one scenario, we assume that cancer is initiated in adult stem cells. There is a single stem cell per compartment, such as the crypt of the colon. Division of the stem cell is assumed to be asymmetric, and these dynamics are described by a stochastic model. When a TSP gene becomes inactivated in the stem cell, clonal expansion occurs, which is described with deterministic equations. Alternatively, we can assume that a healthy compartment contains a population of (stem or differentiated) cells that is kept at a constant size. Depending on the number of cells, this scenario is described either with a stochastic or a deterministic model (see Supporting Methods, which is published as supporting information on the PNAS web site). Again, inactivation of a TSP gene results in clonal expansion. It turns out that the results presented here remain the ...
Cancer is caused by an accumulation of genetic alterations that confer a survival advantage to the neoplastic cell. J. L. Jameson(p73) Oncogenes are
Cancer is caused by an accumulation of genetic alterations that confer a survival advantage to the neoplastic cell. J. L. Jameson(p73) Oncogenes are
A gene that halts cell division to prevent the formation of a cancerous tumour. If mutated they can act like a broken brake, allowing cell division to occur at an uncontrollable rate. ...
Principal Investigator:UEDA Masato, Project Period (FY):1998 - 1999, Research Category:Grant-in-Aid for Scientific Research (C), Section:一般, Research Field:Dermatology
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The Phospho-p35 Antibody is involved in cell cycle regulation, and acts as a tumor suppressor in many tumor types. Order the TP53 antibody from Abgent today!
View Notes - Lecture 29 Oncogenes and Tumor Suppressors from PHARM HB at UCSD. Recognize that most cancers originate in tissues and cell types that undergo continuous regeneration Explain the