ICANCER RESEARCH 58. 2278-2281. June I. IWK]
Advances in Brief
Genomic Changes in Endometrial Polyps Associated with Tamoxifen Show No
Evidence for Its Action as an External Carcinogen1
Paola Dal Cin, Dirk Timmerman, Ivo Van den Berghe, Sylke Wanschura, Bernd Kazmierczak, Ignace Vergole,
Jan Deprest, Patrick Neven, Philippe Moerman, JörnBullerdiek, and Herman Van den Berghe2
Center fur Human Genetics IP. D. C.. H. V. d. B.I and Departments of Obstetrics and Gynecology ¡D.T.. I. V.. J. D.I and Pathology ¡I.V.d. B„P. M.¡.University of Leuven,
MKK) Leuven. Belgium; Department of Obstetrics and Gynecology, St. Jans-iekenhuis, B-IÃoeOOBrussels, Belgium ¡P.NJ; and Center for Human Genetics and Genetic Coniiseli
University of Bremen, D-28359 Bremen. Germany ¡S.W.. B. K., J. B.I
B-
Abstract
Eighty-eight cndometrial specimens from 36 postmenopausal breast
cancer patients treated with tamoxifen were investigated cytogenetically
and molecularly using fluorescence in situ hybridization with appropriate
probes for the HMGIC and HMCIY senes. Twenty control specimens, 10
endometrial polyps, and 10 endometrial biopsy specimens were investi
gated in the same way. Of the 88 specimens, 44 were from endometrial
polyps; 3 were from endocervical polyps; 7 were from cystic endome-
trium; 30 were from normal or atrophie endometrium, normal endocer-
vix, or myonietrium; and 4 were from endometrial carcinomas. Chromo
some investigation of the endometrial polyps showed the nature of the
chromosome changes in tamoxifen-induced polyps to be the same as that
in the controls and in sporadic endometrial polyps described in the
literature. HMGIC and HMGIY gene rearrangements in both groups were
identical as shown by fluorescence in situ hybridization, which also al
lowed for the detection of seven hidden paracentric inversions involving
I2ql5, one of which occurred in a cystic endometrium. The carcinomas
did not exhibit any of these changes. Because abnormal expression of
HMGIC or IlMtïn as a consequence of structural chromosome changes in
12ql5 or 6p21, respectively, is invariably associated with benign neoplasia,
tamoxifen-associated endometrial polyps are unlikely to undergo further
malignant transformation, and a mode of action of tamoxifen as an
external carcinogen is unlikely.
Introduction
Tamoxifen is a nonsteroidal triphenylethylene derivative that has
been widely used in the treatment of breast cancer since the 1970s. It
blocks the growth-promoting effects of estrogens in breast tissue,
mainly through competitive inhibition of the estrogen receptor mech
anism ( 1).
In addition, an estrogenic effect on the endometrium has been
described, resulting in a variety of endometrial changes ranging from
endometrial hyperplasia to polyps and endometrial cancer (2-4).
Most sporadic endometrial polyps present discernable genomic
changes. Cytogenetic investigations demonstrated that different spe
cific chromosome rearrangements can be observed despite a seem
ingly identical clinical and morphological appearance. Besides a nu
merically important group with a normal karyotype, three major
cytogenetically abnormal subgroups have been identified involving
the 6p21, I2ql5, and 7q22 regions (5). These chromosome abnormal
ities led to the discovery of underlying molecular rearrangements and
to partial elucidation of the mechanisms of tumorigenesis by abnormal
Received 2/17/98; accepted 4/17/98.
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1This article presents research results of the Belgian program on Interuniversity Poles
of Attraction initiated by the Belgian Stale, Prime Minister's Office. Science Policy
Programming. The scientific responsibility is assumed hy its authors.
" To whom requests for reprints should be addressed, at Center for Human Genetics.
University of Leuven. Herestraat 49. B-3000 Leuven. Belgium. Phone: 32-16-34-58-78:
Fax: 32-16-34-59-92.
expression of the HMGIC and HMGIY genes in endometrial polyps
with 12q and 6p anomalies, respectively (6-8).
Because the frequency of endometrial polyps significantly in
creases among tamoxifen-treated patients (9, 10), we investigated
these endometrial changes cytogenetically and molecularly to exam
ine whether the same genomic changes were present in the tamoxifen-
related tumors as those known to occur in endometrial changes
unrelated to tamoxifen.
Materials and Methods
Patients and Clinical Data. Transvaginal ultrasonography combined with
sonohysterography. when necessary, was the technique used in our monitoring
of the uterus in 36 tamoxifen-treated postmenopausal breast cancer patients
(some clinical data are summarized in Table 1; Ref. 11).
Suspected endometrial lesions were resected together with a randomly taken
endometrial biopsy. Part of each specimen was processed for pathological
investigations, and the remaining tissue was used for cytogenetic analysis.
For the purpose of this study, endometrial polyps as well as normal-looking
endometrium from 10 patients who were not treated with tamoxifen were
resected and used as controls. A total of 88 specimens from tamoxifen-treated
patients were studied cytogenetically (Table 2) in addition to 20 specimens
from the control population.
Cytogenetic and Molecular Cytogenetic Investigations. G-banded met-
aphases were obtained after short-term culture of an overnight disaggregated
specimen of each sample according to routine methods. At least 20 metaphases
were analyzed in each tissue sample.
FISH' was performed after GTG-banding of the same metaphase spreads
according to the procedure described by Kievits et al. (12). Metaphases were
hybridized with a pool of cosmids 27EI2 and 142HI flanking the third intron
of the HMGIC gene mapped at 12ql5 (6) and a PAC clone containing the
HMGIY gene located at 6p21.2 (13), respectively. Slides were analyzed using
a Zeiss Axioplan fluorescence microscope (Zeiss, Oberkochen, Germany).
Results were processed and recorded with the Power Gene Karyotyping
System (Perceptive Scientific Instruments; Halleddale, United Kingdom). In
translocations affecting HMGIC or HMGIY. split signals were observed on the
derivative chromosome 12 or 6, respectively, and on the translocation chro
mosome partners. In the case of pericentric or paracentric inversion of chro
mosome 12 or 6. split signals on the short and the long arm or a double signal
on one arm, respectively, were observed on those chromosomes. In cases
without an intragenic break in the HMGIC or HMGIY genes, the signal was not
found to be split in its original site or on the translocation partner.
Results
Pathology Findings. Of the resected endometrial lesions from
tamoxifen-treated patients (88 specimens), 44 specimens were diag
nosed as endometrial polyps, whereas 3 specimens were endocervical
polyps. Results of the histológica! investigation of the 41 other spec
imens are found in Table 2.
Ten samples of normal-looking endometrium from control patients
'The abbreviations used are: FISH, fluorescence in situ hybridization; PAC, PI
artificial chromosome.
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Research.
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