CDKN2 (MTS1) tumor suppressor gene mutations in human tumor cell lines.

Abstract:

:Tumor suppressor gene CDKN2 (also called MTS1, CDK4I and p16INK4) is located in 9p21 and deleted homozygously in a high percentage of tumor cell lines. We have examined the sequence of CDKN2 in 154 tumor cell lines that are not homozygously deleted for CDKN2. Overall, 18% (27/154) of the cell lines carried mutations in CDKN2. These mutations were found in cell lines derived from melanoma, bladder, lung and prostate cancers, as well as sarcomas of various origin. The spectrum of the CDKN2 mutations found in melanoma cell lines indicated a major role for ultraviolet light in generating the mutations, suggesting the mutations occurred in vivo. The frequency of loss of heterozygosity in 9p21 in this set of lines is only slightly higher than the background rate of aneuploidy, suggesting that a second 9p21 tumor suppressor gene, if it exists, must lie near CDKN2.

journal_name

Oncogene

journal_title

Oncogene

authors

Liu Q,Neuhausen S,McClure M,Frye C,Weaver-Feldhaus J,Gruis NA,Eddington K,Allalunis-Turner MJ,Skolnick MH,Fujimura FK

subject

Has Abstract,Author List Incomplete

pub_date

1995-03-16 00:00:00

pages

1061-7

issue

6

eissn

0950-9232

issn

1476-5594

journal_volume

10

pub_type

杂志文章

相关文献

ONCOGENE文献大全
  • Role of the integrin-linked kinase (ILK)/Rictor complex in TGFβ-1-induced epithelial-mesenchymal transition (EMT).

    abstract::Epithelial-to-mesenchymal transition (EMT) causes fibrosis, cancer progression and metastasis. Integrin-linked kinase (ILK) is a focal adhesion adaptor and a serine/threonine protein kinase that regulates cell proliferation, survival and EMT. Elucidating the molecular mechanisms necessary for development and progressi...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/onc.2012.30

    authors: Serrano I,McDonald PC,Lock FE,Dedhar S

    更新日期:2013-01-03 00:00:00

  • Critical roles of AMP-activated protein kinase in constitutive tolerance of cancer cells to nutrient deprivation and tumor formation.

    abstract::As tumors grow and invade beyond their homeostatic limits, the tumor cells are subjected to insufficient nutrient and oxygen supplies because of excessive demand for nutrition and oxygen, and insufficient vascularization. We therefore hypothesized that tolerance to nutrient deprivation as well as angiogenesis may be c...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/sj.onc.1205737

    authors: Kato K,Ogura T,Kishimoto A,Minegishi Y,Nakajima N,Miyazaki M,Esumi H

    更新日期:2002-09-05 00:00:00

  • Inactivation of promoter 1B of APC causes partial gene silencing: evidence for a significant role of the promoter in regulation and causative of familial adenomatous polyposis.

    abstract::Familial adenomatous polyposis (FAP) is caused by germline mutations in the adenomatous polyposis coli (APC) gene. Two promoters, 1A and 1B, have been recognized in APC, and 1B is thought to have a minor role in the regulation of the gene. We have identified a novel deletion encompassing half of this promoter in the l...

    journal_title:Oncogene

    pub_type: 临床试验,杂志文章,多中心研究

    doi:10.1038/onc.2011.201

    authors: Rohlin A,Engwall Y,Fritzell K,Göransson K,Bergsten A,Einbeigi Z,Nilbert M,Karlsson P,Björk J,Nordling M

    更新日期:2011-12-15 00:00:00

  • Silencing the cochaperone CDC37 destabilizes kinase clients and sensitizes cancer cells to HSP90 inhibitors.

    abstract::The cochaperone CDC37 promotes the association of HSP90 with the protein kinase subset of client proteins to maintain their stability and signalling functions. HSP90 inhibitors induce depletion of clients, which include several oncogenic kinases. We hypothesized that the targeting of CDC37 using siRNAs would compromis...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/onc.2008.380

    authors: Smith JR,Clarke PA,de Billy E,Workman P

    更新日期:2009-01-15 00:00:00

  • Anthracyclines induce the accumulation of mutant p53 through E2F1-dependent and -independent mechanisms.

    abstract::Mutant p53 frequently accumulates in cancer cells and promotes tumor cell invasion, as part of its gain of function. Its accumulation is partially due to enhanced stability, but little is known about how the mRNA levels of mutant p53 can be regulated. Likewise, the impact of cancer therapy on the levels of mutant p53 ...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/onc.2011.72

    authors: Bug M,Dobbelstein M

    更新日期:2011-08-18 00:00:00

  • Adrenomedullin promotes formation of xenografted endometrial tumors by stimulation of autocrine growth and angiogenesis.

    abstract::The angiogenic peptide adrenomedullin (ADM) has been implicated as a mediator of the increased risk of endometrial hyperplasia and cancer resulting from the use of tamoxifen for the treatment and prevention of breast cancer. ADM has been shown to be induced by tamoxifen in the endometrium and to be a growth factor for...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/sj.onc.1205374

    authors: Oehler MK,Hague S,Rees MC,Bicknell R

    更新日期:2002-04-25 00:00:00

  • Prevalence and specificity of LKB1 genetic alterations in lung cancers.

    abstract::Germline LKB1 mutations cause Peutz-Jeghers syndrome, a hereditary disorder that predisposes to gastrointestinal hamartomatous polyposis and several types of malignant tumors. Somatic LKB1 alterations are rare in sporadic cancers, however, a few reports showed the presence of somatic alterations in a considerable frac...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/sj.onc.1210418

    authors: Matsumoto S,Iwakawa R,Takahashi K,Kohno T,Nakanishi Y,Matsuno Y,Suzuki K,Nakamoto M,Shimizu E,Minna JD,Yokota J

    更新日期:2007-08-30 00:00:00

  • Tumor formation in mice with somatic inactivation of the retinoblastoma gene in interphotoreceptor retinol binding protein-expressing cells.

    abstract::The retinoblastoma suppressor gene product Rb has been assigned a critical role in cell cycle regulation, the induction of differentiation, and inhibition of oncogenic transformation. Inheritance of a mutant RB allele in humans is responsible for bilateral retinoblastoma, a malignant tumor of the retina. Trilateral re...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/sj.onc.1205575

    authors: Vooijs M,te Riele H,van der Valk M,Berns A

    更新日期:2002-07-11 00:00:00

  • Selective activation of Akt1 by mammalian target of rapamycin complex 2 regulates cancer cell migration, invasion, and metastasis.

    abstract::Mammalian target of rapamycin complex (mTORC) regulates a variety of cellular responses including proliferation, growth, differentiation and cell migration. In this study, we show that mammalian target of rapamycin complex 2 (mTORC2) regulates invasive cancer cell migration through selective activation of Akt1. Insuli...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/onc.2011.22

    authors: Kim EK,Yun SJ,Ha JM,Kim YW,Jin IH,Yun J,Shin HK,Song SH,Kim JH,Lee JS,Kim CD,Bae SS

    更新日期:2011-06-30 00:00:00

  • The 'WS motif' common to v-mpl and members of the cytokine receptor superfamily is dispensable for myeloproliferative leukemia virus pathogenicity.

    abstract::Several motifs are conserved in the extracellular domain of the cloned chains of the recently described cytokine receptor superfamily. One of them, usually close to the transmembrane region, is the 'WS motif'. Its function remains unknown, but it has been recently shown that the integrity of this motif is essential fo...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:

    authors: Bénit L,Charon M,Cocault L,Wendling F,Gisselbrecht S

    更新日期:1993-03-01 00:00:00

  • Intracellular signaling of the Ufo/Axl receptor tyrosine kinase is mediated mainly by a multi-substrate docking-site.

    abstract::Ufo/Axl belongs to a new family of receptor tyrosine kinases with an extracellular structure similar to that of neural cell adhesion molecules. In order to elucidate intracellular signaling, the cytoplasmic moiety of Ufo/Axl was used to screen an expression library according to the CORT (cloning of receptor targets) m...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/sj.onc.1201123

    authors: Braunger J,Schleithoff L,Schulz AS,Kessler H,Lammers R,Ullrich A,Bartram CR,Janssen JW

    更新日期:1997-06-05 00:00:00

  • Mammary epithelial-specific expression of the integrin-linked kinase (ILK) results in the induction of mammary gland hyperplasias and tumors in transgenic mice.

    abstract::The integrin linked kinase (ILK) is a cytoplasmic effector of integrin receptors, involved in the regulation of integrin binding properties as well as the activation of cell survival and proliferative pathways, including those involving MAP kinase, PKB/Akt and GSK-3beta. Overexpression of ILK in cultured intestinal an...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/sj.onc.1204910

    authors: White DE,Cardiff RD,Dedhar S,Muller WJ

    更新日期:2001-10-25 00:00:00

  • Role of MMP-2 in the regulation of IL-6/Stat3 survival signaling via interaction with α5β1 integrin in glioma.

    abstract::Matrix metalloproteinase-2 (MMP-2) has pivotal role in the degradation of extracellular matrix, and thereby enhances the invasive, proliferative and metastatic potential in cancer. Knockdown of MMP-2 using MMP-2 small interfering RNA (pM) in human glioma xenograft cell lines 4910 and 5310 decreased cell proliferation ...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/onc.2012.52

    authors: Kesanakurti D,Chetty C,Dinh DH,Gujrati M,Rao JS

    更新日期:2013-01-17 00:00:00

  • CDX2 has tumorigenic potential in the human colon cancer cell lines LOVO and SW48.

    abstract::CDX2 is a Drosophila caudal-related homeobox transcription factor that is important for the establishment and maintenance of intestinal epithelial cells. CDX2 is a marker of colon cancer, with strong staining in up to 90% of colonic adenocarcinomas. CDX2 heterozygous-null mice develop colonic neoplasms, which have sug...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/sj.onc.1209247

    authors: Dang LH,Chen F,Ying C,Chun SY,Knock SA,Appelman HD,Dang DT

    更新日期:2006-04-06 00:00:00

  • A novel translational approach for human malignant pleural mesothelioma: heparanase-assisted dual virotherapy.

    abstract::Malignant pleural mesothelioma (MPM) is a highly aggressive tumor that is related to asbestos exposure. MPM is characterized by rapid and diffuse local growth in the thoracic cavity, and it has a poor prognosis because it is often refractory to conventional therapy. Although MPM is an extraordinarily challenging disea...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/onc.2009.415

    authors: Watanabe Y,Kojima T,Kagawa S,Uno F,Hashimoto Y,Kyo S,Mizuguchi H,Tanaka N,Kawamura H,Ichimaru D,Urata Y,Fujiwara T

    更新日期:2010-02-25 00:00:00

  • Ets-related protein E1A-F can activate three different matrix metalloproteinase gene promoters.

    abstract::An Ets-related E1A-F has been characterized as an enhancer-binding protein for the adenovirus E1A gene. Here we show, in transient expression assays, that E1A-F can activate three different subclasses of the matrix metalloproteinase gene promoters. Expressions of the chloramphenicol acetyltransferase (CAT) reporter ge...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:

    authors: Higashino F,Yoshida K,Noumi T,Seiki M,Fujinaga K

    更新日期:1995-04-06 00:00:00

  • DBC1 promotes castration-resistant prostate cancer by positively regulating DNA binding and stability of AR-V7.

    abstract::Constitutively active AR-V7, one of the major androgen receptor (AR) splice variants lacking the ligand-binding domain, plays a key role in the development of castration-resistant prostate cancer (CRPC) and anti-androgen resistance. However, our understanding of the regulatory mechanisms of AR-V7-driven transcription ...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/s41388-017-0047-5

    authors: Moon SJ,Jeong BC,Kim HJ,Lim JE,Kwon GY,Kim JH

    更新日期:2018-03-01 00:00:00

  • Heterogeneity of lung cancer cells with respect to the amplification and rearrangement of myc family oncogenes.

    abstract::Seventy lung tumors from 53 patients were analysed for alterations of myc family oncogenes, c-myc, N-myc and L-myc, to evaluate when activation of these genes occurs during tumor development. The 53 cases were 17 small cell carcinomas (SCCs), 18 adenocarcinomas, 12 squamous cell carcinomas (SqCs), 4 large cell carcino...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:

    authors: Yokota J,Wada M,Yoshida T,Noguchi M,Terasaki T,Shimosato Y,Sugimura T,Terada M

    更新日期:1988-06-01 00:00:00

  • A peptide that inhibits function of Myristoylated Alanine-Rich C Kinase Substrate (MARCKS) reduces lung cancer metastasis.

    abstract::Myristoylated Alanine-Rich C Kinase Substrate (MARCKS), a substrate of protein kinase C, is a key regulatory molecule controlling mucus granule secretion by airway epithelial cells as well as directed migration of leukocytes, stem cells and fibroblasts. Phosphorylation of MARKCS may be involved in these responses. How...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/onc.2013.336

    authors: Chen CH,Thai P,Yoneda K,Adler KB,Yang PC,Wu R

    更新日期:2014-07-10 00:00:00

  • Transformation of Balb 3T3 cells by the BNLF-1 gene of Epstein-Barr virus.

    abstract::The BNLF-1 protein is the only non-nuclear Epstein-Barr virus (EBV) encoded protein that has been detected in B-lymphocytes immortalized by EBV. We demonstrate that the BNLF-1 gene induces anchorage-independent growth and tumorigenic transformation of the murine cell-line, Balb/3T3. This demonstration extends the earl...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:

    authors: Baichwal VR,Sugden B

    更新日期:1988-05-01 00:00:00

  • Cooperative activity between HER oncogenes and the tumor suppressor IRF-1 results in apoptosis.

    abstract::The tumor suppressor transcription factor IRF-1 inhibits cell growth. In this report we show that IRF-1 also induces apoptosis of highly transformed and tumorigenic cell lines. This activity of IRF-1 is demonstrated with cell lines expressing HER oncogenes and an activatable IRF-1 fusion protein. Growth of cell lines ...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/sj.onc.1202704

    authors: Kirchhoff S,Hauser H

    更新日期:1999-06-24 00:00:00

  • Amplification of 11q13 DNA sequences in human breast cancer: D11S97 identifies a region tightly linked to BCL1 which can be amplified separately.

    abstract::In the course of our study on the amplification of 11q13 sequences in human breast cancer, we have investigated the amplification status of the anonymous DNA fragment D11S97 in a series of 125 mammary tumors. Our results indicate that, as with bladder carcinomas, D11S97 can be amplified separately from BCL1. In additi...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:

    authors: Szepetowski P,Courseaux A,Carle GF,Theillet C,Gaudray P

    更新日期:1992-04-01 00:00:00

  • An N-terminal region of adenovirus E1a essential for cell transformation and induction of an epithelial cell growth factor.

    abstract::A new region of the adenovirus E1a protein essential for immortalization and transformation of primary rat kidney cells has been identified. This region is located between amino acid residues 18 to 20 in an N-terminal domain that is not conserved among the various adenovirus serotypes. The transformation defective mut...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:

    authors: Subramanian T,Kuppuswamy M,Nasr RJ,Chinnadurai G

    更新日期:1988-02-01 00:00:00

  • Cucurbitacin Q: a selective STAT3 activation inhibitor with potent antitumor activity.

    abstract::Constitutive activation of the JAK/STAT3 pathway is a major contributor to oncogenesis. In the present study, structure-activity relationship (SAR) studies with five cucurbitacin (Cuc) analogs, A, B, E, I, and Q, led to the discovery of Cuc Q, which inhibits the activation of STAT3 but not JAK2; Cuc A which inhibits J...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/sj.onc.1208470

    authors: Sun J,Blaskovich MA,Jove R,Livingston SK,Coppola D,Sebti SM

    更新日期:2005-05-05 00:00:00

  • Regulation of cell cycle checkpoint kinase WEE1 by miR-195 in malignant melanoma.

    abstract::WEE1 kinase has been described as a major gate keeper at the G2 cell cycle checkpoint and to be involved in tumour progression in different malignant tumours. Here we analysed the expression levels of WEE1 in a series of melanoma patient samples and melanoma cell lines using immunoblotting, quantitative real-time PCR ...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/onc.2012.324

    authors: Bhattacharya A,Schmitz U,Wolkenhauer O,Schönherr M,Raatz Y,Kunz M

    更新日期:2013-06-27 00:00:00

  • The new truncated somatostatin receptor variant sst5TMD4 is associated to poor prognosis in breast cancer and increases malignancy in MCF-7 cells.

    abstract::Somatostatin receptors (sst1-5) are present in different types of tumors, where they inhibit key cellular processes such as proliferation and invasion. Although ssts are densely expressed in breast cancer, especially sst2, their role and therapeutic potential remain uncertain. Recently, we identified a new truncated s...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/onc.2011.389

    authors: Durán-Prado M,Gahete MD,Hergueta-Redondo M,Martínez-Fuentes AJ,Córdoba-Chacón J,Palacios J,Gracia-Navarro F,Moreno-Bueno G,Malagón MM,Luque RM,Castaño JP

    更新日期:2012-04-19 00:00:00

  • Targeting WNT1-inducible signaling pathway protein 2 alters human breast cancer cell susceptibility to specific lysis through regulation of KLF-4 and miR-7 expression.

    abstract::The molecular basis for the resistance of tumor cells to cell-mediated cytotoxicity remains poorly understood and thus poses a major challenge for cancer immunotherapy. The present study was designed to determine whether the WNT1-inducible signaling pathway protein 2 (WISP2, also referred to as CCN5), a key regulator ...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/onc.2014.151

    authors: Akalay I,Tan TZ,Kumar P,Janji B,Mami-Chouaib F,Charpy C,Vielh P,Larsen AK,Thiery JP,Sabbah M,Chouaib S

    更新日期:2015-04-23 00:00:00

  • Alternative splicing in cancer: implications for biology and therapy.

    abstract::Alternative splicing has critical roles in normal development and can promote growth and survival in cancer. Aberrant splicing, the production of noncanonical and cancer-specific mRNA transcripts, can lead to loss-of-function in tumor suppressors or activation of oncogenes and cancer pathways. Emerging data suggest th...

    journal_title:Oncogene

    pub_type: 杂志文章,评审

    doi:10.1038/onc.2013.570

    authors: Chen J,Weiss WA

    更新日期:2015-01-02 00:00:00

  • Gene amplification-associated overexpression of the RNA editing enzyme ADAR1 enhances human lung tumorigenesis.

    abstract::The introduction of new therapies against particular genetic mutations in non-small-cell lung cancer is a promising avenue for improving patient survival, but the target population is small. There is a need to discover new potential actionable genetic lesions, to which end, non-conventional cancer pathways, such as RN...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/onc.2015.469

    authors: Anadón C,Guil S,Simó-Riudalbas L,Moutinho C,Setien F,Martínez-Cardús A,Moran S,Villanueva A,Calaf M,Vidal A,Lazo PA,Zondervan I,Savola S,Kohno T,Yokota J,Ribas de Pouplana L,Esteller M

    更新日期:2016-08-18 00:00:00

  • Gastrin-mediated activation of cyclin D1 transcription involves beta-catenin and CREB pathways in gastric cancer cells.

    abstract::Gastrin and its precursors promote proliferation in different gastrointestinal cells. Since mature, amidated gastrin (G-17) can induce cyclin D1, we determined whether G-17-mediated induction of cyclin D1 transcription involved Wnt signaling and CRE-binding protein (CREB) pathways. Our studies indicate that G-17 induc...

    journal_title:Oncogene

    pub_type: 杂志文章

    doi:10.1038/sj.onc.1207454

    authors: Pradeep A,Sharma C,Sathyanarayana P,Albanese C,Fleming JV,Wang TC,Wolfe MM,Baker KM,Pestell RG,Rana B

    更新日期:2004-04-29 00:00:00