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Titolo:
Stepwise genetic changes associated with progression of nontumorigenic HPV-18 immortalized human prostate cancer-derived cell line to a malignant phenotype
Autore:
Hukku, B; Mally, M; Cher, ML; Peehl, DM; Kung, HF; Rhim, JS;
Indirizzi:
Childrens Hosp Michigan, Dept Pediat, Cell Culture Lab, Detroit, MI 48201 USA Childrens Hosp Michigan Detroit MI USA 48201 e Lab, Detroit, MI 48201 USA Wayne State Univ, Sch Med, Detroit, MI USA Wayne State Univ Detroit MI USA yne State Univ, Sch Med, Detroit, MI USA Wayne State Univ, Karamanos Canc Inst, Dept Urol & Pathol, Detroit, MI USAWayne State Univ Detroit MI USA nst, Dept Urol & Pathol, Detroit, MI USA Stanford Univ, Dept Urol, Sch Med, Stanford, CA 94305 USA Stanford Univ Stanford CA USA 94305 Urol, Sch Med, Stanford, CA 94305 USA NCI, Lab Biochem Physiol, Frederick, MD 21701 USA NCI Frederick MD USA 21701 , Lab Biochem Physiol, Frederick, MD 21701 USA
Titolo Testata:
CANCER GENETICS AND CYTOGENETICS
fascicolo: 2, volume: 120, anno: 2000,
pagine: 117 - 126
SICI:
0165-4608(20000715)120:2<117:SGCAWP>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
PAPILLOMAVIRUS TYPE-18 DNA; ALLELIC LOSS; DELETION; ABNORMALITIES; CARCINOMA; FREQUENCY; LOCI;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
23
Recensione:
Indirizzi per estratti:
Indirizzo: Hukku, B Childrens Hosp Michigan, Dept Cell Culture, 3901 Beaubien Blvd, Detroit, MI 48201 USA Childrens Hosp Michigan 3901 Beaubien Blvd Detroit MI USA 48201 A
Citazione:
B. Hukku et al., "Stepwise genetic changes associated with progression of nontumorigenic HPV-18 immortalized human prostate cancer-derived cell line to a malignant phenotype", CANC GENET, 120(2), 2000, pp. 117-126

Abstract

Cytogenetics, fluorescence in situ hybridization (FISH), and comparative genomic hybridization (CGH) were used to identify genes that are involved inthe development and progression of prostate cancer. For that purpose, we chose a cell line established in vitro from a prostatic adenocarcinoma whichwas nontumorigenic in nude mice and followed its progression to a tumorigenic cell line. Stepwise changes were observed in the cell line as it becametumorigenic. The composite karyotype at the nontumorigenic stage (CA-HPV-10) was 68 similar to 77,XXY, -(1, 9, 13, 14, 19, 22),+(4, 5, 11, 18, 20, 21),+ (del(1) (q23q31)=M1 (two copies), + der(9)t(1;9)(q24 similar to q31;p23) = M5(two copies),der(14)t(14;? )(q10;?) = M17 in the majority of metaphases. These two derivative chromosomes were also observed a previous study. Our CGH analysis clearly showed that this deleted region in M1 is, in fact, translocated with derivative M5 and, in reality, is amplified. The cell lineestablished from nodule (SCID 5029 p11, showed a number of new changes, asdescribed; however, the most significant change was amplification of the 8q23 similar to qter region, harboring c-myc. This region was translocated with chromosomes 2, 4, and 16 as der(2) t(2;8)(q33;q23)=M12, der(4)t(4;8)(q34;q23)=M11, and der(16)t(8;16)(q24;q21)=M9. We deduce from our study that amplification of c-myc and other genes in the 8q23 similar to qter region were important in progression but did not lead to tumorigenicity. The population that became tumorigenic (SCID 5019 II) showed almost all of the same changes in the karyotype as observed in the nodular cell line; the only significant change was the appearance of der(11)t(4;11)(q32;q22)=M7 and the addition of another copy of t(3q;7p)=M2. These new changes lead to loss of chromosomes 3p, 4pter similar to q34, 6, 7q21 similar to qter, 11q22 similar toqter, and 18q, and gain of 3q, 7p, 8q23 similar to qter, and 11pter similar to q22, before the cell line became tumorigenic. The clonal selection of the population is proven by the presence of a number of the same derivativechromosomes in both the nodular and tumorigenic cell line. As it progressed to tumorigenicity, some of the same changes observed in the original study re-appear at different stages of malignancy, although it was absent in the nontumorigenic cell line. These are: der(16)t(8;1 6)(q24;q21)=M9 in the nodular cell line and der(11)t(4;11)(q32;q22)=M7 in the tumorigenic cell line. In our system, amplificafion of c-myc and other genes in der(2)t(2;8)(q33;q23) =M12, der(4) t(4;8)(q34;q23= M11 together with the presence of der(16)t(8;16)(q24;q21)=M9 and der(11)t(4;11)(q32;q22)=M5 makes the cell line tumorigenic. It is either nontumorigenic, with the presence of a marker equivalent to der(16)=M9 and der(11)=M7 observed in the original study, and onlynodular (SCIL) 5019 p11, present study), with the presence of number of markers with c-myc amplification (M9, M11, and M12). There is accumulation ofall the above-mentioned changes in the same cell before it becomes tumorigenic. (C) 2000 Elsevier Science Inc. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/01/20 alle ore 16:04:01