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Abramson Cancer CenterNCI CANCERLIT® Search: Endometrial Cancer - July 2002
National Cancer Institute®
Last Modified: July 1, 2002
- Pathological findings of gynecologic organs obtained at female radical cystectomy.
- Distinct PTEN mutational spectra in hereditary non-polyposis colon cancer syndrome-related endometrial carcinomas compared to sporadic
- Diagnosis of premalignant endometrial disease.
- Transforming growth factor beta signaling is disabled early in human endometrial carcinogenesis concomitant with loss of growth inhibition.
- Anti-Yo antibody-positive cerebellar degeneration associated with endometrial carcinoma: case report and review of the literature.
- Relationship between p53 pathway and estrogen receptor status in endometrioid-type endometrial cancer.
- Considerations when analyzing the methylation status of PTEN tumor suppressor gene.
- Endometrial and colorectal tumors from patients with hereditary nonpolyposis colon cancer display different patterns of microsatellite
- Influence of omental biopsy on adjuvant treatment field in clinical Stage I endometrial carcinoma.
- [Magnetic resonance (MR) in endometrial carcinoma preoperative evaluation]
- Predicting atypia inside endometrial polyps.
- Clinical implications of the expression of estrogen receptor-alpha and -beta in primary and metastatic lesions of uterine endometrial cancers.
- Acceleration of invasive activity via matrix metalloproteinases by transfection of the estrogen receptor-alpha gene in endometrial
- Grade of endometrial carcinoma.
- Increased myeloperoxidase and lipid peroxide-modified protein in gynecological malignancies.
- [Primary hormone treatment of early endometrial cancer]
- Immunohistochemical comparison of uterine papillary serous and papillary endometrioid carcinoma: clues to pathogenesis.
- Interleukin-1 system and sex steroid receptor gene expression in human endometrial cancer.
- Intraoperative gross examination of myometrial invasion and cervical infiltration in patients with endometrial cancer: decision-making
- Who needs an endometrial biopsy?
- Staging quality is related to the survival of women with endometrial cancer: a Scottish population based study. Deficient surgical staging
- Medically inoperable stage I endometrial carcinoma: a few dilemmas in radiotherapeutic management.
- Frequent frameshift mutations of RIZ in sporadic gastrointestinal and endometrial carcinomas with microsatellite instability.
- Expression of matrix metalloproteinases in ovarian endometriomas: immunohistochemical study and enzyme immunoassay.
- MSI in endometrial carcinoma: absence of MLH1 promoter methylation is associated with increased familial risk for cancers.
- DNA ploidy and S-phase fraction analyses of hyperplastic, atypical and cancerous endometrium using flow cytometry from paraffin-embedded
- Intravaginal high-dose-rate brachytherapy for Stage IB (FIGO Grade 1, 2) endometrial cancer.
- Pathologic quiz case. An incidental endometrial tumor masked by large leiomyoma.
- Tamoxifen and toremifene treatment of breast cancer and risk of subsequent endometrial cancer: a population-based case-control study.
- Microsatellite instability and mutation analysis of candidate genes in unselected sardinian patients with endometrial carcinoma.
- Paradoxical expression of cell cycle inhibitor p27 in endometrioid adenocarcinoma of the uterine corpus - correlation with proliferation
- Estrogen and cancer.
- Can a preoperative CA 125 level be a criterion for full pelvic lymphadenectomy in surgical staging of endometrial cancer?
- Assessment of prognostic factors in stage IIIA endometrial cancer.
- Microsatellite instability, MLH1 promoter methylation, and loss of mismatch repair in endometrial cancer and concomitant atypical
- Ribosomal DNA methylation in patients with endometrial carcinoma: an independent prognostic marker.
- To block estrogen's synthesis or action: that is the question.
- Abdominal hysterectomy after insertion of tension-free vaginal tape.
Table of Contents
1
UI - 12050510
AU - Chang SS; Cole E; Smith JA Jr; Cookson MS
TI -
Pathological findings of gynecologic organs obtained at female radical
cystectomy.
SO - J Urol 2002 Jul;168(1):147-9
AD - Department of Urologic Surgery, Vanderbilt University Medical Center,
Nashville, Tennessee, USA.
PURPOSE: Historically anterior pelvic exenteration has been the
recommended treatment for invasive urothelial carcinoma in women
undergoing radical cystectomy. We evaluated the pathological features of
reproductive organs removed during exenteration to determine the
incidence of malignant pathology in these organs and the need for
removal. MATERIALS AND METHODS: We reviewed the records of all patients
Of these 382 patients, we identified 68 females who underwent radical
cystectomy for urothelial carcinoma. We reviewed preoperative, operative
and pathological findings, including bladder, lymph nodes, uterine and
adnexal pathology, in these female patients. RESULTS: Median patient age
was 64 years (range 35 to 86). Gynecologic organs were present in 40 of
the 68 surgical specimens (59%). The reasons for absent gynecologic
pathology were previous hysterectomy in 26 cases and the preservation of
organs during orthotopic urinary diversion creation in 2. Malignancy was
identified in 3 specimens, including invasive urothelial carcinoma in 2
(5%). In these 2 cases invasion was clearly identified intraoperatively.
Low grade stromal sarcoma of the uterus was present in 1 specimen (2%).
CONCLUSIONS: In the absence of clinical suspicion radical hysterectomy
at cystectomy rarely improves cancer control. Furthermore, secondary
malignancies are rare. The functional impact of preserving gynecologic
organs is a subject of ongoing study.
2
UI - 11854177
AU - Zhou XP; Kuismanen S; Nystrom-Lahti M; Peltomaki P; Eng C
TI -
Distinct PTEN mutational spectra in hereditary non-polyposis colon
cancer syndrome-related endometrial carcinomas compared to sporadic
microsatellite unstable tumors.
SO - Hum Mol Genet 2002 Feb 15;11(4):445-50
AD - Clinical Cancer Genetics Program and Human Cancer Genetics Program,
Comprehensive Cancer Center and Division of Human Genetics, Department
of Internal Medicine, The Ohio State University, Columbus, OH 43210,
USA.
Germline PTEN mutations cause Cowden syndrome (CS) and
Bannayan-Riley-Ruvalcaba syndrome (BRR), two hamartoma-tumor syndromes
with an increased risk of breast, thyroid and endometrial cancers.
Somatic genetic and epigenetic inactivation of PTEN is involved in as
high as 93% of sporadic endometrial carcinomas (EC), irrespective of
microsatellite status, and can occur in the earliest precancers. EC is
the most frequent extra-colonic cancer in patients with hereditary
non-polyposis colon cancer syndrome (HNPCC), characterized by germline
mutations in the mismatch repair (MMR) genes and by microsatellite
instability (MSI) in component tumors. To determine whether PTEN is
involved in the pathogenesis of EC arising in HNPCC cases, and whether
PTEN inactivation precedes MMR deficiency, we obtained 41 ECs from 29
MLH1 or MSH2 mutation positive HNPCC families and subjected them to PTEN
expression and mutation analysis. Immunohistochemical analysis revealed
68% (28/41) of the HNPCC-related ECs with absent or weak PTEN
expression. The remaining 27% (11/41) of tumors had normal expression
and 5% (2/41) with mixed populations showing weak/absent as well as
normal expression. Mutation analysis of 20 aberrant PTEN-expressing
tumors revealed that 17 (85%) harbored 18 somatic PTEN mutations. All
mutations were frameshift, 10 (56%) of which involved the 6(A) tracts in
exon 7 or 8. These results suggest that PTEN plays a significant
pathogenic role in both HNPCC and sporadic endometrial carcinogenesis,
unlike the scenarios for colorectal cancer. Furthermore, we have shown
that somatic PTEN mutation, especially frameshift, is a consequence of
profound MMR deficiency in HNPCC-related ECs. In contrast, among 60
previously reported MSI+ sporadic ECs with 70 somatic mutations in PTEN,
39 (56%) were frameshift, of which only eight (21%) were affecting the
6(A) tracts in exon 7 or 8 (P = 0.01), suggesting that PTEN mutations
may precede MMR deficiency.
3
UI - 11986334
AU - Mutter GL
TI -
Diagnosis of premalignant endometrial disease.
SO - J Clin Pathol 2002 May;55(5):326-31
AD - Department of Pathology, Harvard Medical School, Brigham and Women's
Hospital, Boston, MA 02115, USA. gmutter@rics.bwh.harvard.edu
Modern molecular methods for precancer diagnosis have expanded the range
of detectable disease to a preclinical level and provided material for
histopathological correlation. The precancer scenario begins with
sporadic acquisition of rare PTEN mutation bearing glands, which are
morphologically unremarkable, and progresses to discrete foci of
cytologically altered glands, readily visible on routinely stained
sections. Clinical outcome studies of women with endometrial lesions
have established threshold diagnostic features that confer increased
cancer risk. This class of high risk lesions has been designated
endometrial intraepithelial neoplasia (EIN). EIN is diagnosed by
presence of cytological demarcation, crowded gland architecture, minimum
size of 1mm, and careful exclusion of mimics. Most EIN lesions have been
diagnosed as atypical endometrial hyperplasias in the World Health
Organisation system. Specialised molecular and morphometric analyses
have been extremely useful in redefining clinically relevant
premalignant endometrial disease, but translation to improved patient
care requires the informed participation of pathologists.
4
UI - 12019154
AU - Parekh TV; Gama P; Wen X; Demopoulos R; Munger JS; Carcangiu ML; Reiss
TI -
M; Gold LI
Transforming growth factor beta signaling is disabled early in human
endometrial carcinogenesis concomitant with loss of growth inhibition.
SO - Cancer Res 2002 May 15;62(10):2778-90
AD - Department of Pathology, Kaplan Comprehensive Cancer Center, New York
University School of Medicine, 550 First Avenue, New York, NY 10016,
USA.
Transforming growth factor beta (TGF-beta), a potent ubiquitous
endogenous inhibitor of epithelial cell growth, is secreted as a latent
molecule (LTGF-beta)requiring activation for function. TGF-beta signals
through the type I(TbetaRI) and type II (TbetaRII) receptors, which
cooperate to phosphorylate/activate Smad2/3, the transcriptional
regulators of genes that induce cell cycle arrest. That carcinomas grow
in vivo suggests that they are refractory to TGF-beta. However, this has
been difficult to prove because of an inability to analyze the
functional status of TGF-beta in vivo as well as lack of close
physiological paradigms for carcinoma cells in vitro. The current
studies demonstrate that whereas primary cultures of endometrial
epithelial cells derived from normal proliferative endometrium (PE; n =
10) were dose-dependently and maximally growth inhibited by 55% +/- 5.3%
with 10 pM TGF-beta1, endometrial epithelial cells derived from
endometrial carcinomas (ECAs; n = 10) were unresponsive (P < or =
0.0066). To determine the mechanism of TGF-beta resistance in ECAs, we
analyzed the TGF-beta signaling pathway in vivo by immunohistochemistry
using specific antibodies to TbetaRI and TbetaRII, Smads, and to the
phosphorylated form of Smad2 (Smad2P), an indicator of cells responding
to bioactive TGF-beta. Smad2P was expressed in all of the normal
endometria (n = 25), and was localized to the cytoplasm and nucleus in
PE, and only nuclear in the secretory endometrium. In marked contrast,
Smad2P immunostaining was weak or undetectable in ECA (n = 22; P < or =
0.001) and reduced in glandular hyperplasia (n = 25) compared with
normal endometrium. However, total Smad2 and Smad7 (which inhibits Smad2
activation) levels were identical in ECA and normal tissue. Consistent
with loss of downstream signaling, both TbetaRI (n = 19) and TbetaRII (n
= 22) protein expression were significantly reduced in ECA compared with
PE (n = 11; P < or = 0.05). By in situ hybridization, the mRNA levels of
TbetaRI and TbetaRII were decreased in the carcinoma cells compared with
normal PE glands, suggesting that receptor down-regulation occurs at the
transcriptional level. Furthermore, a somatic frameshift mutation in the
polyadenine tract at the 5' end of the TbetaR-II gene was detected in
two of six cases examined. Finally, the ability of explants of ECA to
activate endogenous LTGF-beta was deficient compared with normal tissue
(23.5% versus 7.4%). Therefore, our results suggest that loss of Smad2
signaling in ECA may be because of down-regulation of TbetaRI and
TbetaRII, and/or decreased activation of LTGF-beta. Because disruption
of TGF-beta signaling occurred independent of grade or degree of
invasion and was evident in premalignant hyperplasia, we conclude that
inactivation of TGF-beta signaling leading to escape from normal growth
control occurs at an early stage in endometrial carcinogenesis, thereby
defining novel molecular targets for cancer prevention.
5
UI - 11824891
AU - Brock S; Ellison D; Frankel J; Davis C; Illidge T
TI -
Anti-Yo antibody-positive cerebellar degeneration associated with
endometrial carcinoma: case report and review of the literature.
SO - Clin Oncol (R Coll Radiol) 2001;13(6):476-9
AD - Wessex Cancer Centre, Southampton, UK.
Paraneoplastic cerebellar degeneration (PCD) is a rare, severely
debilitating disease, often with a rapid onset and progression, which
predate the diagnosis of malignancy. Despite characteristic features,
diagnosis is commonly difficult and successful therapy, which relies on
early instigation of treatment, is rare. Here we present a patient in
whom anti-Yo antibody-positive PCD was associated with endometrial
carcinoma and an extensive review of the literature outlining the
clinical features, pathogenesis and treatment of PCD.
6
UI - 12055672
AU - Maeda K; Tsuda H; Hashiguchi Y; Yamamoto K; Inoue T; Ishiko O; Ogita S
TI -
Relationship between p53 pathway and estrogen receptor status in
endometrioid-type endometrial cancer.
SO - Hum Pathol 2002 Apr;33(4):386-91
AD - Department of Obstetrics and Gynecology, Osaka City University Graduate
School of Medicine, Japan.
We analyzed the mechanism of estrogen receptor (ER) loss and status of
the p53 pathway in 64 cases of endometrial cancer. 26.6% (17 of 64) of
endometrial cancers lost ER. Methylation of the ER CpG island was
significantly related to ER status (P = 0.0074). However, the
methylation site of the ER CpG island differed between breast and
endometrial cancers. The abnormal expression rate of p14ARF, MDM2, p53,
and the p53 pathway were 7.8% (5 of 64), 32.8% (21 of 64), 25.0% (16 of
64) and 53.1% (34 of 64), respectively. There was no significant
difference in the overexpression of MDM2 between p53-positive cases
(43.8%: 7 of 16) and p53-negative cases (29.2%; 14 of 48) (P = 0.3595).
Abnormal p53 was higher in grade 3 tumors (55.6%; 5 of 9) than in grade
1 and 2 tumors (20.0%; 11 of 55) (P = 0.0364). The abnormality of the
p53 pathway was higher in grade 3 tumors (88.9%; 8 of 9) than in grade 1
and 2 tumors (47.3%; 26 of 55) (P = 0.0294). However, there was no
significant difference in abnormal p53 pathway between ER-negative and
ER-positive cases. In endometrial cancer, ER CpG island methylation was
the important mechanism of ER loss. However, there was no significant
relationship between the p53 pathway and ER status. Copyright 2002,
Elsevier Science (USA). All rights reserved.
7
UI - 11891178
AU - Zysman MA; Chapman WB; Bapat B
TI -
Considerations when analyzing the methylation status of PTEN tumor
suppressor gene.
SO - Am J Pathol 2002 Mar;160(3):795-800
AD - Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto,
Ontario, Canada.
Epigenetic mechanisms of gene silencing, including promoter
hypermethylation of tumor suppressor genes, have been shown to
contribute to tumorigenesis. PTEN is an important tumor suppressor
implicated in the pathogenesis of a number of familial and sporadic
cancers. Germline mutations of PTEN predispose to dominantly inherited
hamartomatous disorders Cowden syndrome and Bannayan-Zonana syndrome.
Somatic PTEN mutations commonly occur in endometrial, breast, prostate,
and thyroid tumors. Several investigators have speculated on PTEN
promoter hypermethylation as a possible mechanism of PTEN inactivation
but data supporting such observations is not forthcoming. The genomic
sequence of PTEN is 98% identical to a highly conserved processed PTEN
pseudogene (psiPTEN) and this sequence identity extends 841 base pairs
into the promoter region. This high degree of homology has made analysis
of the methylation status of the PTEN promoter quite challenging. We
have investigated the methylation profiles of the promoter region of
PTEN in endometrial, breast, and colon cancer cell lines, as well as in
a panel of primary endometrial tumors using a combination of
methylation-specific polymerase chain reaction, methylation-sensitive
restriction analysis, and bisulfite sequencing. Our results show that
the pseudogene, and not PTEN, is predominantly methylated in cell lines
and tumors. Without careful consideration of the critical nucleotide
differences between the two sequences, results obtained from PTEN
analysis may not necessarily represent the methylation status of PTEN.
8
UI - 12057899
AU - Kuismanen SA; Moisio AL; Schweizer P; Truninger K; Salovaara R; Arola J;
TI -
Butzow R; Jiricny J; Nystrom-Lahti M; Peltomaki P
Endometrial and colorectal tumors from patients with hereditary
nonpolyposis colon cancer display different patterns of microsatellite
instability.
SO - Am J Pathol 2002 Jun;160(6):1953-8
AD - Department of Medical Genetics, University of Helsinki, Helsinki,
Finland.
The colorectum and uterine endometrium are the two most commonly
affected organs in hereditary nonpolyposis colon cancer (HNPCC), but the
genetic basis of organ selection is poorly understood. As tumorigenesis
in HNPCC is driven by deficient DNA mismatch repair (MMR), we compared
its typical consequence, instability at microsatellite sequences, in
colorectal and endometrial cancers from patients with identical
predisposing mutations in the MMR genes MLH1 or MSH2. Analysis of
non-coding (BAT25, BAT26, and BAT40) and coding mononucleotide repeats
(MSH6, MSH3, MLH3, BAX, IGF2R, TGF beta RII, and PTEN), as well as MLH1-
and MSH2-linked dinucleotide repeats (D3S1611 and CA7) revealed
significant differences, both quantitative and qualitative, between the
two tumor types. Whereas colorectal cancers displayed a predominant
pattern consisting of instability at the BAT loci (in 89% of tumors),
TGF beta RII (73%), dinucleotide repeats (70%), MSH3 (43%), and BAX
(30%), no such single pattern was discernible in endometrial cancers.
Instead, the pattern was more heterogeneous and involved a lower
proportion of unstable markers per tumor (mean 0.27 for endometrial
cancers versus 0.45 for colorectal cancers, P < 0.001) and shorter
allelic shifts for BAT markers (average 5.1 bp for unstable endometrial
cancers versus 9.3 bp for colorectal cancers, P < 0.001). Among the
individual putative "target" loci, PTEN instability was associated with
endometrial cancers and TGF beta RII instability with colon cancers. The
different instability profiles in endometrial and colorectal cancers
despite identical genetic predisposition underlines organ-specific
differences that may be important determinants of the HNPCC tumor
spectrum.
9
UI - 12066951
AU - Nieto JJ; Gornall R; Toms E; Clarkson S; Hogston P; Woolas RP
TI -
Influence of omental biopsy on adjuvant treatment field in clinical
Stage I endometrial carcinoma.
SO - BJOG 2002 May;109(5):576-8
AD - Department of Gynaecological Oncology, St Mary's Hospital, Portsmouth,
UK.
In this study to assess the role of omental biopsy in the diagnosis of
extrapelvic disease, data from 100 consecutive women with clinical Stage
I endometrial cancer undergoing primary surgical treatment in our
institution were analysed: 80 women had an omental biopsy, 20 did not,
and six had adenocarcinoma in the omentum. No obvious morbidity
attributable to this rapid and easily performed surgical procedure was
recorded. We conclude that visual inspection and palpation of the
omentum at the time of abdominal surgery for endometrial carcinoma is
worthwhile and advisable. In addition, adopting a protocol of
histological assessment upstaged a further two cases of this series.
These data suggest that this technique might influence the prescription
of adjuvant pelvic radiation in approximately one in 10 women currently
considered for such therapy, as disease can be easily documented as
having extended beyond the conventional radiotherapy field.
10
UI - 11549999
AU - Wiesenfeld U; Cova M; De Lazslo P; Tinelli A; Mangino F; Grimaldi E;
TI -
Guaschino S
[Magnetic resonance (MR) in endometrial carcinoma preoperative
evaluation]
SO - Minerva Ginecol 2001 Oct;53(5):341-6
AD - Clinica Ginecologica ed Ostetrica, IRCCS Burlo Garofolo, Universita
degli Studi, Trieste, Italy. wiesenfe@burlo.trieste.it
BACKGROUND: Myometrial invasion of endometrial carcinoma is an important
prognostic factor because the degree of myometrial invasion is
correlated with the rate of lymphnode metastases and of recurrences. The
aim of the study was a preoperative evaluation of endometrial carcinoma
by Magnetic Resonance (MR). METHODS: The authors present a prospective
study performed on 54 cases of endometrial carcinoma collected at the
Department of Gynecology and Obstetrics of the University of Trieste
(Italy). All the patients were considered as Stage I after hysteroscopy
and endocervical curettage. Prior to surgery all the patients underwent
MR at the Department of Radiology of the University of Trieste (Italy)
in order to evaluate the depth of myometrial invasion. The surgical
procedure included total abdominal hysterectomy, bilateral
salpingo-oophorectomy and pelvic and lomboaortic lymphadenectomy in high
risk cases. Statistical evaluation was performed by Fischer's exact
test. RESULTS: Statistically significant positive correlation was found
(p<0.001) between MR staging and surgical staging. The sensitivity
reported in our series for distinguishing between superficial disease
(Stage IA and IB) and deep myometrial invasion (Stage IC) was 92%.
CONCLUSIONS: Preoperative MR is helpful in selecting patients at high
risk of nodal involvement and it is suggested that, although MR is
considered an expensive examination, its use should be always considered
before surgical treatment of patients with high surgical risk.
11
UI - 11833867
AU - Perez-Medina T; Bajo J; Huertas MA; Rubio A
TI -
Predicting atypia inside endometrial polyps.
SO - J Ultrasound Med 2002 Feb;21(2):125-8
AD - Department of Obstetrics and Gynecology, Santa Cristina University
Hospital, Madrid, Spain.
OBJECTIVE: To evaluate the efficacy of color Doppler exploration for
assessing atypia inside endometrial polyps. METHODS: A prospective study
was conducted in a tertiary university hospital. Eight hundred six
patients with endometrial polyps were studied with color Doppler
sonography, and the resistive index inside the polyp stalk was obtained.
The patients were then referred for hysteroscopic resection, and
pathologic analysis was performed. RESULTS: Thirty-five polyps with
sonographic indications of atypia were pathologically confirmed.
Sonographic indications of atypia inside 16 polyps were not confirmed.
Three nonquestionable endometrial polyps had atypia inside them.
CONCLUSIONS: Low Doppler resistance is highly predictive of atypia
inside endometrial polyps.
12
UI - 12065875
AU - Fujimoto J; Sakaguchi H; Aoki I; Toyoki H; Tamaya T
TI -
Clinical implications of the expression of estrogen receptor-alpha and
-beta in primary and metastatic lesions of uterine endometrial cancers.
SO - Oncology 2002;62(3):269-77
AD - Department of Obstetrics and Gynecology, Gifu University School of
Medicine, Japan.
Novel human estrogen receptor (ER)-beta was identified in cDNA libraries
from human testes. ER-beta specifically expresses in the testis, ovary,
thymus, spleen, osteoblasts, fetus and uterine endometrium. ER-beta
might not conserve the same physiological functions as does ER-alpha.
Therefore, expressions of ER-alpha and ER-beta mRNAs in primary and
metastatic lesions of uterine endometrial cancers were investigated. The
levels of ER-beta mRNA were significantly lower than those of ER-alpha
mRNA in uterine endometrial cancers and in normal uterine endometria.
The ratio of ER-beta to ER-alpha mRNA in most primary uterine
endometrial cancers was similar to that in normal uterine endometria
(<0.4% of ER-beta mRNA to ER-alpha mRNA). On the other hand, in 14 of
the 20 lymph node metastasis-positive cases of uterine endometrial
cancers, the ratio in the metastatic lesion was significantly higher
than that in the primary lesion of the corresponding case, and patient
prognosis in these cases was extremely poor. Therefore, it is suggested
that the intact synchronized expression of ER-beta interacting with
ER-alpha might be disrupted, especially in most metastases of uterine
endometrial cancers, leading to poor patient prognosis related to
estrogen refractoriness. Copyright 2002 S. Karger AG, Basel
13
UI - 12115520
AU - Mizumoto H; Saito T; Ashihara K; Nishimura M; Tanaka R; Kudo R
TI -
Acceleration of invasive activity via matrix metalloproteinases by
transfection of the estrogen receptor-alpha gene in endometrial
carcinoma cells.
SO - Int J Cancer 2002 Aug 1;100(4):401-6
AD - Department of Obstetrics and Gynecology, Sapporo Medical University
School of Medicine, Sapporo, Japan.
It is well known that the functions of reproductive organs are regulated
by sex steroids and their receptors and it is hypothesized that the
progression of neoplasms that originate from the reproductive organs is
influenced by them. However, the correlation between sex steroids and
tumor progression, especially tumor invasion, is not well known in
endometrial carcinoma. In our study, we focused on the influence of
estrogen and its receptor in invasion and matrix metalloproteinases
(MMPs), which are known to be important in tumor invasion, as well as on
endometrial carcinoma cells. The growth of Ishikawa cells, to which an
estrogen receptor-alpha expressing vector was transfected, was
accelerated by 17 beta-estradiol as was the acceleration of the
expression of cyclin D1. By invasion assay, in conditions with 17
beta-estradiol, the invasiveness of Ishikawa cells was enhanced.
Furthermore, according to the accelerated invasiveness, the expression
of MMP-1, -7 and -9 and Ets-1 was enhanced. These results suggest that
activation of ER-alpha by estrogen results in tumor progression by
stimulating cell growth and invasiveness via acceleration of the
expression of MMPs. Copyright 2002 Wiley-Liss, Inc.
14
UI - 11717548
AU - Alameda F; Serrano S; Peiro R; Exposito M; Fuste P; Carreras R
TI -
Grade of endometrial carcinoma.
SO - Am J Surg Pathol 2001 Dec;25(12):1556
15
UI - 11813987
AU - Song M; Santanam N
TI -
Increased myeloperoxidase and lipid peroxide-modified protein in
gynecological malignancies.
SO - Antioxid Redox Signal 2001 Dec;3(6):1139-46
AD - Department of Gynecology and Obstetrics, Emory University, School of
Medicine, Atlanta, GA 30322, USA.
Oxidative stress has been implicated in several diseases, including
cancer. Oxidants induce oncogenes and their products associated with
cell growth. Even though epidemiological studies implicate oxidants in
promoting cancer, there is still a lack of in vivo evidence for the
same. In this study, we measured the levels of myeloperoxidase (MPO), an
enzyme associated with oxidation and autoantibodies to lipid
peroxide-modified protein (LOOH-RSA), in the plasma of subjects with
gynecological cancers. The gynecological cancer subjects (n = 201) had
higher plasma MPO and LOOH-RSA levels compared with control subjects (n
= 60). Immunohistochemical analysis of tissues revealed that
immunostaining for MPO and LOOH-RSA was higher in cancer tissues
compared with controls. The staining was specific to cell types and not
ubiquitously present. Neutrophils, monocytes/macrophages, and natural
killer cells have been proposed to play a role in cancer promotion and
progression. This study proposes a role for oxidative stress and
especially MPO in cancer.
16
UI - 11965713
AU - Ivanov S; Ivanov S; Kurlov T; Milev A; Kulander S; Ivanov V
TI -
[Primary hormone treatment of early endometrial cancer]
SO - Akush Ginekol (Sofiia) 1999;38(1):20-3
Six cases of primary treated endometrial cancer are included in this
research work. Five of these women ended with tumour regression and 2
with pregnancies and deliveries of children. All of the women are still
alive without having disease with mean follow-up period of 36.5 months
(from 16 to 80 months). We consider that this is very promising method
of treatment to offer y conservative treatment with high level of
survival and possibility for having y child. Diagnostic and therapeutic
data for the patients who are with early endometrial cancer and wish to
have y child are analyised in this study. Four of the women were treated
with GnRh-analogs-Zoladex and 2 with progestins-high doses.
17
UI - 12092593
AU - Demopoulos RI; Mesia AF; Mittal K; Vamvakas E
TI -
Immunohistochemical comparison of uterine papillary serous and papillary
endometrioid carcinoma: clues to pathogenesis.
SO - Int J Gynecol Pathol 1999 Jul;18(3):233-7
AD - Department of Pathology, New York University Medical Center, New York,
10016, USA.
Twenty-four predominantly papillary carcinomas of the endometrium, 10
serous and 14 endometrioid, were compared using a variety of
immunohistochemical antibodies, including p53, estrogen and progesterone
receptors, carcinoembryonic antigen, and E-cadherin. These were selected
to attempt to find clues to explain the disparate behavior of these two
tumor subtypes. We found that 6 of 8 (75%) serous carcinomas had a p53
reactivity score of 300, whereas 90% of endometrioid tumors had a p53
reactivity score of less than 20 (p = 0.0008). Combined estrogen and
progesterone hormone reactivity was positive in 13 (100%) of
endometrioid lesions compared with 4 of 8 (50%) of serous lesions (p =
0.0117). The significantly greater p53 expression and its significantly
diminished hormone receptor expression indicate that papillary serous
carcinomas belong to the type II group of endometrial carcinomas that
occur in a background of atrophic endometrium, are high grade, present
with high stage disease, and have a poor prognosis. In contrast,
papillary endometrioid carcinomas, which belong to type I carcinomas,
often arise in a background of estrogen-stimulated endometrial
hyperplasia, are usually well-differentiated, and have a good prognosis.
Early p53 mutations in papillary serous carcinoma as well as in
endometrial intraepithelial serous carcinoma may partially explain their
proclivity for early intra-abdominal dissemination. Carcinoembryonic
antigen expression was similar in both groups and therefore is not
useful to characterize possible differences in the cell of origin. The
reactivity scores for E-cadherin were also similar in the two tumor
subtypes, thus not supporting the hypothesis that decreased cell to cell
adhesion molecules might contribute to early dissemination of serous
lesions.
18
UI - 12051868
AU - Singer CF; Kronsteiner N; Marton E; Walter I; Kubista M; Czerwenka K;
TI -
Schreiber M; Tschugguel W; Wieser F; Kubista E
Interleukin-1 system and sex steroid receptor gene expression in human
endometrial cancer.
SO - Gynecol Oncol 2002 Jun;85(3):423-30
AD - Division of Special Gynecology, Department of Pathology, Division of
Endocrinology, University of Vienna Medical Center, Waehringer Guertel
18-20, Vienna, Austria. Christian.Singer@univie.ac.at
OBJECTIVES: The interleukin-1 system is known to play a pivotal role in
human physiology and reproduction. In the cycling endometrium,
interleukin-1alpha activity is controlled by sex steroids and is
confined to the perimenstrual phase, where it is involved in the events
leading to tissue lysis and menstruation. Since local tissue degradation
is also a feature of malignant tumors, our goal was to analyze the gene
expression of interleukin-1alpha and other interleukin-1 family members
and compare it with estrogen receptor alpha, estrogen receptor beta, and
progesterone receptor mRNA expression in 27 endometrial carcinomas and
13 normal endometria. METHODS: Endometrial tumor tissues were obtained
during hysterectomy for endometrial cancer, and normal endometrium was
sampled in women undergoing surgical procedures for nonendometrial
pathologies. Gene expression was analyzed by reverse transcription
polymerase chain reaction. Protein expression was detected and localized
by immunohistochemical staining. RESULTS: A strong gene expression of
interleukin-1 type I receptor, estrogen recptor alpha, and progesterone
receptor was detected in all tumor tissues and in the majority of benign
endometrial tissues. However, in contrast to nonmalignant endometria,
variable amounts of interleukin-1beta and interleukin-1 receptor
antagonist mRNA were also detected in most of the tumor samples. Gene
expression of interleukin-1alpha and estrogen receptor beta was
considerably less frequent, with interleukin-1alpha being absent in all
peri- and postmenopausal endometria and in all but one of the
well-differentiated tumors. With decreasing differentiation
interleukin-1alpha gene expression became more frequent. In these cases,
interleukin-1alpha protein was detected predominantly in epithelial
tumor cells of lower-grade tumors. CONCLUSION: We have demonstrated the
presence of the interleukin-1 system in endometrial malignancies, and
found a negative correlation between interleukin-1alpha and tumor
differentiation. We hypothesize that the nonphysiological expression of
interleukin-1alpha in less differentiated tumors might contribute to
their invasiveness and malignant behavior.
19
UI - 12051878
AU - Vorgias G; Hintipas E; Katsoulis M; Kalinoglou N; Dertimas B; Akrivos T
TI -
Intraoperative gross examination of myometrial invasion and cervical
infiltration in patients with endometrial cancer: decision-making
accuracy.
SO - Gynecol Oncol 2002 Jun;85(3):483-6
AD - Department of Gynaecology, Piraeus, Greece. vorgiasgeorge@yahoo.gr
OBJECTIVES: We sought to determine the accuracy of gross evaluation of
the depth of myometrial invasion and the involvement of the cervix, and
its value in determining the need for extensive surgery in patients with
endometrial carcinoma. METHODS: The intraoperative records of 256
patients operated for endometrial cancer were used to compare the gross
evaluations with the final microscopic histopathological findings. In
the theater, the uterus was opened and inspected after its removal. The
depth of myometrial invasion was noted as less or greater than 50% using
a full-thickness incision through the tumor, while cervical involvement
was noted as positive or negative, based on extension of the tumor below
the internal cervical os. Standard statistical calculations were used to
determine accuracy, sensitivity, specificity, positive and negative
predictive values, and false-positive and false-negative rates of the
method. RESULTS: Regarding the depth of myometrial invasion, gross
evaluation could accurately predict the final result in 88.2% of
patients. Sensitivity, specificity, positive, and negative predictive
values were 83.7, 90.6, 82.8, and 91.1%, respectively. False-positive
results were noted in 9.4% of cases and false-negative in 16.3%.
Analysis of the characteristics of the false-negative patients showed
that they had aggressive variant tumors, tumors of advanced grade, and
tumors that more frequently had developed from an atrophic endometrium.
With respect to cervical involvement, gross evaluation had an overall
accuracy of 98.5%, 0% false-positive rate, 11.5% false-negative rate,
88.5% sensitivity, 100% specificity, 100% positive predictive value, and
98.3% negative predictive value. CONCLUSION: Our data suggest that
visual gross examination of the uterus provides safe and reliable
estimates of both myometrial invasion and cervical infiltration. So, the
surgeon can rely on the procedure to decide the need for further
operative manipulations.
20
UI - 12053633
AU - Samson SL; Gilmour D
TI -
Who needs an endometrial biopsy?
SO - Can Fam Physician 2002 May;48():885-7
AD - Dalhousie University, Halifax, NS.
21
UI - 12085172
AU - Crawford SC; De Caestecker L; Gillis CR; Hole D; Davis JA; Penney G;
TI -
Siddiqui NA
Staging quality is related to the survival of women with endometrial
cancer: a Scottish population based study. Deficient surgical staging
and omission of adjuvant radiotherapy is associated with poorer survival
of women diagnosed with endometrial cancer in Scotland during 1996 and
1997.
SO - Br J Cancer 2002 Jun 17;86(12):1837-42
AD - Department of Gynaecological Oncology, Stobhill Hospital Glasgow G21
3UW, UK. s.c.crawford@btinternet.com
The association between treatment variation and survival of women with
endometrial cancer was investigated. A retrospective cohort based upon
the complete Scottish population registered on in-patient and day-case
hospital discharge data (Scottish Morbidity Record-1) and cancer
registration (Scottish Morbidity Record-6) coded C54 and C55 in ICD10,
hundred and three patients who underwent surgical treatment out of 781
patients that were diagnosed with endometrial cancer in Scotland during
1996 and 1997. The overall quality of surgical staging was poor. The
quality of staging was related to both the year that the surgeon passed
the Member of the Royal College of Obstetricians and Gynaecologists
examination and also to 'specialist' status but was not related to
surgeon caseload. Two clinically important prognostic factors were found
to be associated with survival; whether the International Federation of
Obstetrics and Gynaecology stage was documented, RHR=2.0 (95% CI=1.3 to
3.1) and also to the use of adjuvant radiotherapy, RHR=2.2 (95% CI=1.5
to 3.5). The associations with survival were strongest in patients with
advanced disease, International Federation of Obstetrics and Gynaecology
stages 1C through to stage 3. Deficiencies in staging and variations in
the use of adjuvant radiotherapy represent a possible source of
avoidable mortality in patients with endometrial cancer. Consequently,
there should be a greater emphasis on improving the overall quality of
surgical staging in endometrial cancer. Copyright 2002 Cancer Research
UK
22
UI - 12118561
AU - Chao CK; Grigsby PW; Perez CA; Mutch DG; Herzog T; Camel HM
TI -
Medically inoperable stage I endometrial carcinoma: a few dilemmas in
radiotherapeutic management.
SO - Int J Radiat Oncol Biol Phys 1996 Jan 1;34(1):27-31
AD - Radiation Oncology Center, Mallinckrodt Institute of Radiology,
Washington University School of Medicine, St Louis, MO 63110, USA.
PURPOSE: The aggressiveness of radiation therapy for patients with
medically inoperable endometrial carcinoma is controversial. Patients
may die of their underlining medical disease before succumbing to
cancer. We try to identify certain subgroup of patients who might
benefit most from an aggressive approach and also investigate the impact
of residual tumor present in dilatation and curettage (D&C) specimen
obtained in second intracavitary implant (ICI). METHODS AND MATERIALS:
From 1965 to 1990, 101 patients were treated for clinical clinical Stage
I endometrial carcinoma with RT alone due to medical problems. Ages
ranged from 39 to 94 years (median 71 years). There were 18 patients
with clinical Stage IA and 83 with clinical Stage IB disease. Histology
included 44 well-differentiated, 37 moderately differentiated, and 20
poorly differentiated tumors. Radiation therapy consisted of external
beam only in 3 patients, ICI alone in 26, whole pelvis plus ICI in 10,
and whole pelvis plus split field plus ICI in 62. A second D&C was
performed on 26 patients at the time of the second ICI. Minimum
follow-up was 2 years (median, 6.3 years). RESULTS: The 5-year actuarial
disease-free survival (DFS) for the studied cohort is comparable to the
expected survival of an age-matched population. Pelvic control was 100%
for Stage IA and 88% for Stage IB with 5-year disease-free survivals of
80 and 84%, respectively. We also observed a greater disassociation of
DFS and overall survial among patients older than 75 years (84 and 55%,
respectively) than in younger patients (84 and 78%, respectively). This
is mainly because older patients succumbed to their medical illness.
Well-differentiated disease demonstrated the trend toward a better
outcome than moderately or poorly differentiated lesions in Stage IB
patients (p = 0.05), but not in Stage IA patients. Aggressive radiation
therapy approach showed the trend toward a better result in Stage IB
patients 75 years of age or younger. There were two failures among 19
patients with no tumor found in the D&C specimen at the time of second
implant. In contrast, seven patients with residual tumor seen in the
endometrial sample at the time of second implant remain disease free.
CONCLUSIONS: Radiation therapy alone is an effective treatment modality
for medically inoperable Stage I endometrial carcinoma. Disease-free
survival can be translated into longer overall survival in the younger
age group, but not in older patients. The latter tend to die of their
underlining medical illness. Tumor differentiation influenced the
prognosis of Stage IB disease. No tumor seen in the endometrial sampling
at the time of second implant did not correlate with a better disease
control, and the treatment plan should not be modified on such
information.
23
UI - 10987271
AU - Piao Z; Fang W; Malkhosyan S; Kim H; Horii A; Perucho M; Huang S
TI -
Frequent frameshift mutations of RIZ in sporadic gastrointestinal and
endometrial carcinomas with microsatellite instability.
SO - Cancer Res 2000 Sep 1;60(17):4701-4
AD - The Burnham Institute, La Jolla, California 92037, USA.
Many lines of evidence suggest that the retinoblastoma protein
interacting zinc finger gene RIZ is a strong candidate for the tumor
suppressor locus on 1p36, a region commonly deleted in many human
cancers with chromosomal instability. In addition, a role for RIZ in
tumors of the microsatellite instability pathway is suggested by
frequent frameshift mutations in hereditary non-polyposis colorectal
carcinomas. Here we studied RIZ mutations in sporadic cancers with
microsatellite instability. Frameshift mutations in the two coding
polyadenosine tracks of RIZ were found in 19 (48%) of 40 gastric
carcinomas, 6 (33%) of 18 endometrial carcinomas, 14 (26%) of 51 of
colorectal carcinomas, and 7 (54%) of 13 cell lines. Eleven tumor
tissues showed biallelic inactivation of RIZ. In contrast, no frameshift
mutations were found in 70 microsatellite stable tumors. These results
suggest an important role for RIZ in sporadic cancers with
microsatellite instability.
24
UI - 12034345
AU - Mizumoto H; Saito T; Ashihara K; Nishimura M; Takehara M; Tanaka R; Ito
TI -
E; Kudo R
Expression of matrix metalloproteinases in ovarian endometriomas:
immunohistochemical study and enzyme immunoassay.
SO - Life Sci 2002 Jun 7;71(3):259-73
AD - Department of Obstetrics and Gynecology, Sapporo Medical University
School of Medicine, S-1, W-16, Chuo-ku, Sapporo 060-0061, Japan.
Like carcinoma, endometriosis has the unique characteristics, of
invasion and metastasis, though pathologically, it is a benign tumor.
However, the mechanism of destruction of the surrounding tissue in
endometriosis is still unclear. In this study, the expression and
localization of matrix metalloproteinases (MMP)-1, -2, -3, -7, -9 and
tissue inhibitors of metalloproteinases-1 (TIMP-1) were evaluated by
immunohistochemistry for 20 cases and the amounts of MMP-1, TIMP-1 and
MMP-1/TIMP-1 complex in the fluid of endometrioma, were analyzed by
ELISA and western blotting for 20 cases, which were analyzed by
immunohistochemical study. MMP-1, -2 and -9 were detected strongly in
both stromal and epithelial cells and MMP-7 in the epithelial cells in
the menstrual period. MMP-3 was mainly expressed in macrophage
containing hemosiderin but the change of expression was not clear.
TIMP-1 was intensively detected in both stromal and epithelial cells in
the menstrual period but the expression decreased in other stages of the
menstrual cycle. ELISA for MMP-1 also showed results similar to
immunohistochemistry, suggesting that it was released to the cyst in the
menstrual period when it was released to the extracellular space from
the cytoplasm. The expression of TIMP-1 was not clearly changed during
the menstrual cycle. From these results, it was suggested that the
destruction of the surrounding matrix by endometriosis might be caused
by various MMPs, which are mainly produced in stromal cells.
25
UI - 12115503
AU - Whelan AJ; Babb S; Mutch DG; Rader J; Herzog TJ; Todd C; Ivanovich JL;
TI -
Goodfellow PJ
MSI in endometrial carcinoma: absence of MLH1 promoter methylation is
associated with increased familial risk for cancers.
SO - Int J Cancer 2002 Jun 10;99(5):697-704
AD - Department of Internal Medicine, Washington University School of
Medicine, St. Louis, MO, USA.
Loss of DNA mismatch repair occurs in a variety of malignancies and is
associated with genome-wide instability of microsatellite repeats, a
molecular phenotype referred to as microsatellite instability (MSI). MSI
is a consistent feature of colorectal and endometrial tumors from
patients with hereditary non-polyposis colorectal cancer (HNPCC).
Sporadic colorectal and endometrial cancers that exhibit MSI frequently
have methylation of the MLH1 promoter. We undertook a detailed family
and medical history study to compare family cancer risk for women with
MSI-positive and -negative endometrial cancers. The MLH1 promoter
methylation status was determined for all cancers. Family histories were
developed for 80 probands (40 with MSI-positive and 40 with MSI-negative
tumors). The numbers of reported cancers in first- and second-degree
relatives of the 2 groups were similar. There was a modest increase in
familial cancer clustering for MSI-positive probands. When MSI-positive
tumors were subclassified according to MLH1 promoter methylation, a
clear association between methylation status and familial cancer risk
was evident. Women with MSI-positive endometrial cancers in which the
MLH1 promoter was unmethylated had a 7-fold relative risk (RR) of
demonstrating familial clustering of cancers [RR 7.07 (95% confidence
interval 2.29-21.81)]. The women with MSI-positive, MLH1-unmethylated
tumors were significantly younger than the rest of the study population
(56.1 years vs. 65.4, p < or = 0.01). Age of onset and tumor MSI not
associated with MLH1 promoter methylation may point to women with a
genetic susceptibility to malignancies. Copyright 2002 Wiley-Liss, Inc.
26
UI - 11866205
AU - Pervez S; Hitchcock A; Sinton TM; Mani A; Smith JL
TI -
DNA ploidy and S-phase fraction analyses of hyperplastic, atypical and
cancerous endometrium using flow cytometry from paraffin-embedded
tissues.
SO - Pathol Res Pract 2002;198(1):13-7
AD - Department of Pathology, The Aga Khan University Hospital Karachi,
Pakistan. shahid.pervez@aku.edu
Atypical hyperplasia of the endometrium is an entity that needs to be
clearly distinguished from other florid hyperplastic states on the one
hand and from well-differentiated adenocarcinomas on the other. This may
at times be difficult on pure morphological grounds. In this study, DNA
ploidy and S-phase fraction of hyperplastic, atypical and cancerous
endometrium were evaluated using flow cytometry from paraffin-embedded
tissues. In total, 72 cases (24 hyperplastic, 24 atypical and 24
adenocarcinomas) were selected. All hyperplastic endometria showed a
diploid stemline, while 2/24 atypical hyperplasias showed aneuploid
(Near-diploid) peaks. Both of these cases were severely atypical and one
of these, on hysterectomy, showed early invasive carcinoma. There was no
significant difference in mean S-phase fractions of hyperplastic vs.
atypical endometria. DNA aneuploidy was significantly more common with
much higher S-phase fractions in poorly and moderately differentiated
carcinomas than in well-differentiated ones. It was concluded that
aneuploid (near-diploid) peaks, if ever present in atypical
hyperplasias, may indicate an aggressive disease/neoplastic
transformation.
27
UI - 12062616
AU - Alektiar KM; McKee A; Venkatraman E; McKee B; Zelefsky MJ; Mychalczak
TI -
BR; Hoskins WJ; Barakat RR
Intravaginal high-dose-rate brachytherapy for Stage IB (FIGO Grade 1, 2)
endometrial cancer.
SO - Int J Radiat Oncol Biol Phys 2002 Jul 1;53(3):707-13
AD - Department of Radiation Oncology, Memorial Sloan-Kettering Cancer
Center, 1275 York Avenue, New York, NY 10021, USA. alektiak@mskcc.org
PURPOSE: To evaluate the outcome of patients with Stage IB Grades 1 and
2 endometrial cancer treated with adjuvant high-dose-rate intravaginal
1999, 233 patients with Stage IB FIGO Grades 1 and 2 were treated with
postoperative adjuvant high-dose-rate intravaginal brachytherapy. The
median dose was 21 Gy in 7 Gy/fraction given at 2-week intervals. The
mean age was 60 years. All patients underwent simple hysterectomy.
Comprehensive surgical staging, defined as pelvic washing and pelvic and
paraaortic lymph nodes sampling, was done in 9% of patients. Patients
with FIGO Grade 3, papillary serous cancer, or clear-cell cancer were
excluded from this analysis. Complications were assessed in terms of
late Radiation Therapy Oncology Group toxicity (Grade > or =3) of the
gastrointestinal tract, genitourinary tract, and vagina. RESULTS: With a
median follow-up of 57 months, the 5-year vaginal/pelvic control,
disease-free survival, and overall survival rate was 96% (95% confidence
interval [CI] 94-99%), 94% (95% CI 91-98%), and 94% (95% CI 91-98%),
respectively. The influence on outcome of age, grade (1 vs. 2), depth of
invasion (one-third or less or greater than one-third), capillary
space-like invasion, lower uterine segment involvement, and
comprehensive surgical staging was evaluated. None of these factors
significantly affected the rate of vaginal/pelvic control. Only age > or
=60 years influenced the outcome for disease-free and overall survival.
The 5-year rate for both disease-free and overall survival was 90% (95%
CI 84-97%) for patients > or =60 years old compared with 99% (95% CI
96-100%) for those <60 years (p = 0.03 and 0.005, respectively). Of 233
patients, 3 (1%) developed Grade 3 or greater complications, with a
5-year actuarial rate of 2% (95% CI 0-5%). Two patients developed Grade
3 genitourinary toxicity, and 1 Grade 4 vaginal toxicity. CONCLUSION: On
the basis of this retrospective study, adjuvant postoperative
high-dose-rate intravagin
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