Four cytogenetic subgroups can be identified in endometrial polyps

Four cytogenetic subgroups can be identified in endometrial polyps

153 Abstracts B8 FLUORESCENCE IN SITU HYBRIDIZATION OF PAP SMEARS IN MANAGEMENT OF A NEW TECHNIQUE. CERVICAL CANCER: Kristtne L. Kingsley’. Aurelia...

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153

Abstracts

B8

FLUORESCENCE IN SITU HYBRIDIZATION OF PAP SMEARS IN MANAGEMENT OF A NEW TECHNIQUE. CERVICAL CANCER: Kristtne L. Kingsley’. Aurelia’ M. Mclonil. Lisa A. Michael T. Medchil12, Angelica M. Zaid2. Avery U’Ren’. A. Sandbcrg * (1) Southwest Biomedical Research Institute and Genetrix. Inc.. Scottsdale. AZ (2)

B7

St.

Joseph’s Hospital. Phoenix. Despite major advances in the

Koole, w. Andrie. E. Valdes, J. Bergha, w. Van do Van Canter for Human Genetics (P.D.C., P.K., H.V.D.B.), Department of Pathology (Ph.M.) and Department of Obstetrics and Gynecology (J.D.), University of Lauven, Belgium; Istituto di Biologia Cemrsle (R.V., S.U.). Divisione Ostetrica e Cinecologice USL21 @.A) and Servisio di Anatomia, Istologia e Citologia (E.V.), University of Cegliari, Italy.

Hoerman. Dcprest,

AZ. early

diagnosis

and

tretument of cervtcal cancer. an estnnated 15.000 new cases and 4600 deaths from cervical cancer will occur in

the

United

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cases.

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States m characterized

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course

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hybridization

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new

approach

cancer

uhhzing

(FISH)

methodology

of

m

wluch some

We have cytogenetically investigated a total of 33 solitary endometrial polyps, seven of which have Clonal previously. chromosome been reported rearrangements were found in 19 out of 33 tumors cytogenetically abnormal major (57%). Three those be distinguished: a) with subgroups can b) those rearrangements of the 6p21-p22 region, the 12q13-15 region, c) with rearrangements of those with rearrangements of the lq22 region. A normal karyotype is found in a fourth subgroup. Recombinations of the 6~21-22 region with 2935 and lOq22 have not been described before, as well as rearrangements of 7q22. Thus, endometrial polyps, like several other benign mesenchymal tumors, present several cytogenetically different subgroups despite a seemingly identical appearance. It is clinical and morphological look for a indicated, therefore, to common denominator of these tumors at molecular level.

vaI,es widely Cylogenetic

disease be

one

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fluorescence to

early m detect

numerical chromosomal changes III Pap smear slides. Cytogenetic analysts of cervical tumors has revealed abnormalities most commonly involving recurrent chromosomes 1.3.11. and 17; therefore. we chose IO centromerlc probes for these chromosomes !n utke non-fixed Pap smear slides are our study. In brief. treated with 0.8% NaCttrate, dried over a low flame. and Slides are then air dried and transferred to 70% ETOH. briefly treated with proteinase K. Hybridization IS performed accordrng to standard procedures. Based on our preliminary findings in normal controls and cancer patients with varying degrees of cervical neoplasia. we believe that FISH analysis of cervical smear slides could represent a powerful tool m The technique the early diagnosis of cervical cancer. is appealing due to easy collection of samples. potential use as a diagnoslic tool in ambiguous cases. and easy monitormg

B9

of

patients

at

risk

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CHARACTERIZATION OF A LETHAL HUMAN ENDOMETRIAL CARCINOMA CELL-LINE (NOU-I) WITH 46, XX GENOME

JS Noumoffl, Faruqil lCrozer-Chester

VA LiVolsi2,

P.

Il. Van den

epithelial

problems

pathologically.

Insight

cervical

the

is

of

dysplastic

diagnostic

predicted

Inwoduce

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patho+eteples

present

molecular and prognosuc value.

Cervical

1994.

FOUR CYTOCENETIC SUBGROUPS CAN BE IDENTIFIED IN ENDONETRIAL POLYPS Dal Cin, B. Vanni. S. llarras, Ph. P.

PG Satyaswaroop3.

RB Degerl,

CYTOGENETIC ASSOCIATIONS JR Sawyer’,

SA

Medical Center, Upland, PA, ZHospital University of Pennsylvania, Philadelphia, PA, 3Hershey Medical Center, Hershey, PA Immortal gynecologic cell lines, especially of endometrial origin. are few and diverse. Those cell lines of epitheiial origin currently available have multiple chromosomal alterations, making the study of origin and molecular genetic characteristics of such neoplasms difficult, if not impossible. We have established a new epithelial, poorly differentiated adenocarcinoma cell line (NOU-I) witi 46, XX chromosomal complement. To confirm the character of the tumor grown in vitro, this cell line was injected intraperitoneally in the nude mouse. The tumor grown in vivo had the identical histology and chromosomally the same 46, XX complement. The cells from the original tumor and those in the nude mouse shared the same characteristics with respect to histopathology. immunohistochemistry. steroid hormone receptor content and growth characteristics. We report the only cell line of a highly aggressive epithelial, endometrial adenocarcinoma with 46. XX genomic complement. This presents an ideal opporhmity for further molecular genetic studies to evaluate early gene abnormalities in endometrial cancer.

PROGRESSION IN PEDIATRIC JM Bell’.

WM ChadduckP. Sciences’ Center2.

, Little Rock Washington

1, C

Tee', FA

of Arkansas

for Medial

JR Thomas

Umversity AR

OF TELOMERIC SOLID TUMORS

and Children’s

National

~oopl Medical

D C.

Tebmeric associations (tas) are a rare phenomenon m which the tebmeres of a smgle chromosome or hvo distnxt chromosomes are associated or pined with mwmal or no loss of material from either chromosome end. Dicentric chromosomes caused bv tar tend to pull apstl during mitosis and result in a deletion in o& daughter cell and a partial duplication in the other. We have studii five pediatric tumors including an anaptastlc astrocytoms (AA), two gliobtastomas (GBM). an undifferentiated (embryonsl) sarcoma of the lwer (UESL). and a neurilemona by in-situ cutture and G-banding techmques. All five tumors showed dicentrlc and/or mutticentric chromosomes resutta-tg from fusion events involving segments of different chromosomes Four of the fwe tumors showed the progression of clonst tas resulting II-I either the gain or toss of chrcmosome segments. The AA karyoyipe of 56-57 chromosomes with ksryotypic evoluhon resunmg in clonal tas of the tetomere of 20q. which subsequently woked ctonal tas of 4p. 1 lp. 21q and 22q. One GEM showed a ksryotype with 82-90 chromxomes. with ISO 17q. and showed ctonal fusron of 8q and 19q. and 21p to 21~. A second GEM showed a complex unstable ksryotype wth 73-89 chromosomes and tas of 1 lp. which apparently served as the precursor lestion to the progresswe loss of 1 lp. The UESL showed a chromosome range of 43-53. with iso 17q. and cbnal tas of 4p and 22q. The neunlemoma showed clonal tas of lq and 16q resutting in the subsequent toss of lq The frequent wolvement of lip m tas III gaunt cell tumora of bone (Cancer, 6452697.1991). and III two of the fwe tumors presented here (AA. GBM). suggests Ihat this regton may be a ‘hot spot” for telomenc fusions. In addition. the progresswe loss of 1 lp an one of these tumors (GBM). and the recent report of the progresswe loss of 1 lp by tas in a Wtims’ tumor (Cancer. 74:767.1994) suaaests telomerlc fusion and loss of

, showed a

chromosome segmenis ci; wolve regions known to contain tumor suppressor genes. The findmgs in these tumors prowdes further evidence that tas is a chromoaomal mechanism occurrmg dunng the cytogenetlc progression of some solid tumors which can be responsible for the loss of chromosome segments contammg tumor suppressor gene*