- cell neoplastic transformation
- small room in which a monk or nun lives (同)cubicle
- a device that delivers an electric current as the result of a chemical reaction (同)electric cell
- a room where a prisoner is kept (同)jail cell, prison cell
- (biology) the basic structural and functional unit of all organisms; they may exist as independent units of life (as in monads) or may form colonies or tissues as in higher plants and animals
- any small compartment; "the cells of a honeycomb"
- a small unit serving as part of or as the nucleus of a larger political movement (同)cadre
- (mathematics) a function that changes the position or direction of the axes of a coordinate system
- the act of changing in form or shape or appearance; "a photograph is a translation of a scene onto a two-dimensional surface" (同)translation
- (genetics) modification of a cell or bacterium by the uptake and incorporation of exogenous DNA
- a qualitative change (同)transmutation, shift
- a rule describing the conversion of one syntactic structure into another related syntactic structure
- of or related to or having the properties of a neoplasm; "neoplastic cells"
- a cell that is part of tumor
- (刑務所の)『独房』;(修道院の)小さい独居室 / (ミツバチの)みつ房,巣穴 / 小さい部屋 / 『細胞』 / 電池 / 花粉室 / (共産党などの)細胞
- 変形,変質;変身 / (物理学で)変換;(電流の)変圧 / (言吾学で)変形
全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.
- Neoplastic-like transformation effect of single-walled and multi-walled carbon nanotubes compared to asbestos on human lung small airway epithelial cells.
- Wang L, Stueckle TA, Mishra A, Derk R, Meighan T, Castranova V, Rojanasakul Y.Author information HELD/PPRB, National Institute for Occupational Safety and Health , Morgantown, WV 26505 , USA.AbstractAbstract Accumulating evidence indicates that carbon nanotubes (CNTs) are biopersistent and can cause lung damage. With similar fibrous morphology and mode of exposure to asbestos, a known human carcinogen, growing concern has arisen for elevated risk of CNT-induced lung carcinogenesis; however, relatively little is known about the long-term carcinogenic effect of CNT. Neoplastic transformation is a key early event leading to carcinogenesis. We studied the ability of single- and multi-walled CNTs to induce neoplastic transformation of human lung epithelial cells compared to asbestos. Long-term (6-month) exposure of the cells to occupationally relevant concentrations of CNT in culture caused a neoplastic-like transformation phenotype as demonstrated by increased cell proliferation, anchorage-independent growth, invasion and angiogenesis. Whole-genome expression signature and protein expression analyses showed that single- and multi-walled CNTs shared similar signaling signatures which were distinct from asbestos. These results provide novel toxicogenomic information and suggest distinct particle-associated mechanisms of neoplasia promotion induced by CNTs and asbestos.
- Nanotoxicology.Nanotoxicology.2014 Aug;8:485-507. doi: 10.3109/17435390.2013.801089. Epub 2013 May 28.
- Abstract Accumulating evidence indicates that carbon nanotubes (CNTs) are biopersistent and can cause lung damage. With similar fibrous morphology and mode of exposure to asbestos, a known human carcinogen, growing concern has arisen for elevated risk of CNT-induced lung carcinogenesis; however, rel
- PMID 23634900
- Cytochrome P450 2A13 mediates the neoplastic transformation of human bronchial epithelial cells at a low concentration of aflatoxin B1.
- Zhang Z, Lu H, Huan F, Meghan C, Yang X, Wang Y, Wang X, Wang X, Wang SL.Author information Key Lab of Modern Toxicology of Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing, People's Republic of China; State Key Lab of Reproductive Medicine, Institute of Toxicology, Nanjing Medical University, Nanjing, People's Republic of China.AbstractCytochrome P450 2A13 (CYP2A13), mainly expressed in human respiratory tract, is highly efficient in the metabolic activation of aflatoxin (AF) B1 (AFB1) and is assumed to play a role in human lung tumorigenesis in airborne AFB1 exposure. To validate the assumption, we exposed human bronchial epithelial (BEAS-2B) cells stably expressing CYP2A13 (B-2A13), CYP1A2 (B-1A2) and CYP2A6 (B-2A6) to 0.1-10 nM AFB1 for 30-50 passages. B-2A13 cells showed increased sensitivity to 0.1 nM AFB1-induced neoplastic transformation and the formation of tumors in nude mice were observed at passage 30 (P30) while it occurred at P50 B-1A2 cells. B-2A6, similar to vector control, showed no neoplastic transformation in this condition. Additionally, AFB1-DNA adducts and 8-OHdG significantly increased in transformed P40 B-2A13, in parallel with the upregulation of p-ATR, p-BRCA1, Mre11, Rad50 and Rad51. However, the apoptosis of P40 cells was near normal, while the expression of Bax, C-Caspase 3 and C-PARP increased passage-dependently. Inhibition of ATR (ATR siRNA or NU6027) reversely increased the apoptosis of P40 B-2A13 cells in parallel with the upregulation of Bax, C-Caspase 3 and C-PARP, suggesting that ATR plays an important role in maintaining cell survival via antiapoptosis. Additionally, activation of ATR was necessary to neoplastic transformation since blockage of ATR in P40 cells inhibited DNA damage repair response and anchorage-independent growth. Our data demonstrated that CYP2A13 played a critical role in AFB1-induced neoplastic transformation. ATR-mediated the dysfunction of apoptosis and DNA damage repair might be involved. These results help establish a linkage between airborne AFB1 and human respiratory carcinoma.
- International journal of cancer. Journal international du cancer.Int J Cancer.2014 Apr 1;134(7):1539-48. doi: 10.1002/ijc.28489. Epub 2013 Oct 11.
- Cytochrome P450 2A13 (CYP2A13), mainly expressed in human respiratory tract, is highly efficient in the metabolic activation of aflatoxin (AF) B1 (AFB1) and is assumed to play a role in human lung tumorigenesis in airborne AFB1 exposure. To validate the assumption, we exposed human bronchial epithel
- PMID 24114584
- Identification of H ferritin-dependent and independent genes in K562 differentiating cells by targeted gene silencing and expression profiling.
- Misaggi R1, Di Sanzo M1, Cosentino C1, Bond HM1, Scumaci D1, Romeo F1, Stellato C2, Giurato G2, Weisz A2, Quaresima B1, Barni T1, Amato F1, Viglietto G1, Morrone G1, Cuda G1, Faniello MC3, Costanzo F1.Author information 1Department of Experimental and Clinical Medicine, Magna Græcia University of Catanzaro, Salvatore Venuta Campus, Viale Europa, 88100 Catanzaro, Italy.2Laboratory of Molecular Medicine and Genomics, Department of Medicine and Surgery, University of Salerno, via Allende, 84081 Baronissi, Salerno, Italy.3Department of Experimental and Clinical Medicine, Magna Græcia University of Catanzaro, Salvatore Venuta Campus, Viale Europa, 88100 Catanzaro, Italy. Electronic address: firstname.lastname@example.org.AbstractFerritin is best known as the key molecule in intracellular iron storage, and is involved in several metabolic processes such as cell proliferation, differentiation and neoplastic transformation. We have recently demonstrated that the shRNA silencing of the ferritin heavy subunit (FHC) in a melanoma cell line is accompanied by a consistent modification of gene expression pattern leading to a reduced potential in terms of proliferation, invasiveness, and adhesion ability of the silenced cells. In this study we sought to define the repertoire of genes whose expression might be affected by FHC during the hemin-induced differentiation of the erythromyeloid cell line K562. To this aim, gene expression profiling was performed in four different sets of cells: i) wild type K562; ii) sh-RNA FHC-silenced K562; iii) hemin-treated wild-type K562; and iv) hemin-treated FHC-silenced K562. Statistical analysis of the gene expression data, performed by two-factor ANOVA, identified three distinct classes of transcripts: a) Class 1, including 657 mRNAs whose expression is modified exclusively during hemin-induced differentiation of K562 cells, independently from the FHC relative amounts; b) Class 2, containing a set of 70 mRNAs which are consistently modified by hemin and FHC-silencing; and c) Class 3, including 128 transcripts modified by FHC-silencing but not by hemin. Our data indicate that FHC may function as a modulator of gene expression during erythroid differentiation and add new findings to the knowledge of the complex gene network modulated during erythroid differentiation.
- Gene.Gene.2014 Feb 10;535(2):327-35. doi: 10.1016/j.gene.2013.10.067. Epub 2013 Nov 14.
- Ferritin is best known as the key molecule in intracellular iron storage, and is involved in several metabolic processes such as cell proliferation, differentiation and neoplastic transformation. We have recently demonstrated that the shRNA silencing of the ferritin heavy subunit (FHC) in a melanoma
- PMID 24239552
- Senescence-inducing stress promotes proteolysis of phosphoglycerate mutase via ubiquitin ligase Mdm2.
- Mikawa Takumi,Maruyama Takeshi,Okamoto Koji,Nakagama Hitoshi,Lleonart Matilde E,Tsusaka Takeshi,Hori Kousuke,Murakami Itsuo,Izumi Taisuke,Takaori-Kondo Akifumi,Yokode Masayuki,Peters Gordon,Beach David,Kondoh Hiroshi
- The Journal of cell
- … Mutations in PGAM and Mdm2 that abrogate ubiquitination of PGAM restored the proliferative potential of primary cells under stress conditions and promoted neoplastic transformation. …
- NAID 120005385888
- Protooncogene TCL1b functions as an Akt kinase co-activator that exhibits oncogenic potency in vivo
- Hashimoto M,Suizu F,Tokuyama W,Noguchi H,Hirata N,Matsuda-Lennikov M,Edamura T,Masuzawa M,Gotoh N,Tanaka S,Noguchi M
- Oncogenesis 2(9), e70, 2013-09-16
- … Protooncogene T-cell leukemia 1 (TCL1), which is implicated in human T-cell prolymphocytic leukemia (T-PLL), interacts with Akt and enhances its kinase activity, functioning as an Akt kinase co-activator. … TCL1b exhibited oncogenicity in in vitro colony-transformation assay. … The current study disclosed TCL1b bears oncogenicity and hence serves as a novel therapeutic target for human neoplastic diseases. …
- NAID 120005385329
- MDM2 regulates a novel form of incomplete neoplastic transformation of Theileria parva infected lymphocytes
- Hayashida Kyoko,Kajino Kiichi,Hattori Masakazu,Wallace Maura,Morrison Ivan,Greene Mark I.,Sugimoto Chihiro
- Experimental and Molecular Pathology 94(1), 228-238, 2013-02
- … Our efforts are concerned with identifying features of incomplete malignant transformation caused by non viral pathogens. … parva-infected lymphocytes display a transformed phenotype and proliferate in culture media like the other tumor cells, however those cells will return to normal after antiprotozoal treatment reflecting the incomplete nature of transformation. … To identify signaling pathways involved in this form of transformation of T. …
- NAID 120005228347
- neoplastic cell transformation
- neoplastic cell transformation
- cellular transformation