National Cancer Institute®
Last Modified: March 1, 2002
1
UI - 11830871
AU - Paavonen J; Saikku P
TI -
[Chlamydiaceae and cancer]
SO - Duodecim 1999;115(3):265-9
AD - HYKS:n naistenklinikka Haartmaninkatu 2 00290 Helsinki.
jorma.paavonen@helsinki.fi
2
UI - 10995813
AU - Vergote I; Rustin GJ; Eisenhauer EA; Kristensen GB; Pujade-Lauraine E;
TI -
Parmar MK; Friedlander M; Jakobsen A; Vermorken JB
Re: new guidelines to evaluate the response to treatment in solid tumors
[ovarian cancer]. Gynecologic Cancer Intergroup.
SO - J Natl Cancer Inst 2000 Sep 20;92(18):1534-5
3
UI - 11805587
AU - Harlap S; Olson SH; Curtin JP; Caputo TA; Nakraseive C; Sanchez D; Xue X
TI -
Epithelial ovarian carcinoma and fertility of parents.
SO - Epidemiology 2002 Jan;13(1):59-65
AD - Department of Obstetrics and Gynecology, New York University School of
Medicine, NY 10016, USA harlas01@popmail.med.nyu.edu.
We studied the fertility of the parents of 163 women with epithelial
ovarian carcinoma in two hospitals in New York City, compared with the
parents of 159 controls from similar neighborhoods. We used
unconditional logistic regression to control for covariates, including
parity, oral contraceptive use, age at menarche, and Jewish ancestry.
Compared with women with zero or one sibling, those with two, three or
four or more siblings had adjusted odds ratios (95% confidence
intervals) of 0.91 (0.47-1.77), 0.61 (0.28-1.37), and 0.50 (0.26-0.98).
On average, each additional sibling was associated with a risk reduction
to 0.80 (0.66-0.98). These findings support the hypothesis that
heritable conditions associated with reduced fertility of the subjects'
parents may contribute to risk and may explain some of the effects of
parity on the risk of this carcinoma. Alternatively, they may reflect
some unidentified aspect of the environment experienced by girls growing
up in small families. If confirmed in other data sets, these findings
imply that sibship size might have confounded previous estimates of risk
associated with a family history of cancer or with Jewish ethnicity.
4
UI - 11805588
AU - Vachon CM; Mink PJ; Janney CA; Sellers TA; Cerhan JR; Hartmann L; Folsom
TI -
AR
Association of parity and ovarian cancer risk by family history of
breast or ovarian cancer in a population-based study of postmenopausal
women.
SO - Epidemiology 2002 Jan;13(1):66-71
AD - Department of Health Sciences Research, Mayo Clinic and Mayo Foundation,
Rochester, MN 55905, USA. vachon@mayo.edu
Although parity is associated with a decreased risk of ovarian cancer in
the general population, this association among women with a family
history is less clear. We examined this question in a prospective cohort
of 31,377 Iowa women 55-69 years of age at baseline. Relative risks
(RRs) and 95% confidence intervals (CIs) were estimated through Cox
regression. We identified 181 incident epithelial ovarian cancers
through 13 years of follow-up. At baseline, 14% of the women reported
breast or ovarian cancer in a first-degree relative, and an additional
12% reported a family history in a second-degree relative. Among women
without a family history of breast or ovarian cancer in a first-degree
relative, nulliparous women were at slightly increased risk of ovarian
cancer (RR = 1.4, 95% CI = 0.9-2.4) compared with parous women, whereas
among women with a family history, nulliparous women were at a much
higher risk (RR = 2.7, 95% CI = 1.1-6.6) than parous women. Similar
results were seen when family history included first- or second-degree
relatives with breast or ovarian cancer or a first- or second-degree
relative with ovarian cancer only. Nulliparity may be more strongly
associated with an increased risk of ovarian cancer among women with a
family history of breast or ovarian cancer, compared with women who do
not have a family history of those cancers.
5
UI - 11830553
AU - Liu JR; Opipari AW; Tan L; Jiang Y; Zhang Y; Tang H; Nunez G
TI -
Dysfunctional apoptosome activation in ovarian cancer: implications for
chemoresistance.
SO - Cancer Res 2002 Feb 1;62(3):924-31
AD - Department of Obstetrics and Gynecology, University of Michigan Medical
School, L4000 Women's Hospital, 1500 East Medical Center Drive, Ann
Arbor, MI 48109, USA. rliu@umich.edu
Alterations in the regulation of apoptosis may contribute to the
pathogenesis of cancer and resistance of tumor cells to chemotherapy. In
mammalian cells, nonreceptor-mediated apoptosis occurs predominantly via
assembly of a cytochrome c-dependent apoptosome complex containing
caspase-9 and apoptotic protease-activating factor-1 (Apaf-1). We show
here that cytosolic extracts from human ovarian carcinoma cell lines and
primary ovarian tumor samples are deficient in their ability to activate
procaspase-9 in the presence of cytochrome c and dATP when compared with
control extracts. SKOV3, a human ovarian carcinoma cell line with
diminished apoptosome activity, was significantly more resistant to
chemotherapy-induced apoptosis than cell lines with functional Apaf-1
activity. This dysfunctional apoptosome activity was not explained by
reduced expression levels of caspase-9 or Apaf-1. Moreover, expression
levels of known inhibitors of the apoptosome, including heat shock
protein 70, heat shock protein 90, or X-linked inhibitor of apoptosis,
did not correlate with functional activity of the apoptosome. SKOV3, an
ovarian cancer cell line with dysfunctional apoptosome activity, retains
the ability to form the Apaf-1 oligomer; however, there is a diminished
amount of caspase-9 in the apoptosome. The reduction in the amount of
caspase-9 in the apoptosome in the SKOV3 cell line was associated with
diminished caspase-3 activity. Dysfunctional apoptosome activation may
contribute both to the pathogenesis of ovarian carcinoma and to
chemoresistance.
6
UI - 11748848
AU - Machackova E; Damborsky J; Valik D; Foretova L
TI -
Novel germline BRCA1 and BRCA2 mutations in breast and breast/ovarian
cancer families from the Czech Republic.
SO - Hum Mutat 2001 Dec;18(6):545
AD - Department of Cancer Epidemiology and Genetics, Masaryk Memorial Cancer
Institute, Zluty kopec 7, Brno 656 53, Czech Republic.
Germline mutations in breast cancer susceptibility genes, BRCA1 and
BRCA2, are responsible for a substantial proportion of high-risk breast
and breast/ovarian cancer families. To characterize the spectrum of
BRCA1 and BRCA2 mutations, we screened Czech families with
breast/ovarian cancer using the non-radioactive protein truncation test,
heteroduplex analysis and direct sequencing. In a group of 100 high-risk
breast and breast/ovarian cancer families, four novel frame shift
mutations were identified in BRCA1 and BRCA2 genes. In BRCA1, two novel
frame shift mutations were identified as 3761-3762delGA and
2616-2617ins10; in BRCA2, two novel frame shift mutations were
identified as 5073-5074delCT and 6866delC. Furthermore, a novel missense
substitution M18K in BRCA1 gene in a breast/ovarian cancer family was
identified which lies adjacent just upstream of the most highly
conserved C3HC4 RING zinc finger motif. To examine the tertiary
structure of the RING zinc finger domain and possible effects of M18K
substitution on its stability, we used threading techniques according to
the crystal structure of RAG1 dimerization domain of the DNA-binding
protein. Copyright 2000 Wiley-Liss, Inc.
7
UI - 11773280
AU - Schildkraut JM; Calingaert B; Marchbanks PA; Moorman PG; Rodriguez GC
TI -
Impact of progestin and estrogen potency in oral contraceptives on
ovarian cancer risk.
SO - J Natl Cancer Inst 2002 Jan 2;94(1):32-8
AD - Department of Community and Family Medicine, Duke Comprehensive Cancer
Center, Duke University Medical Center, Durham, NC 27710, USA.
schil001@mc.duke.edu
BACKGROUND: Oral contraceptive (OC) use is associated with a reduced
risk of developing ovarian cancer, but the mechanism for the risk
reduction has not been well defined. In this study, we investigate the
relationship between the progestin and estrogen potency in combination
OCs and the risk of developing ovarian cancer. METHODS: The study
included 390 case subjects with epithelial ovarian cancer and 2865
control subjects, between 20 and 54 years of age, identified from the
Cancer and Steroid Hormone Study. Logistic regression was used to
calculate odds ratios (ORs) and 95% confidence intervals (CIs) for the
associations between ovarian cancer risk and combination OC formulations
while controlling for potential confounders. All statistical tests were
two-sided. RESULTS: With users of high-progestin/high-estrogen potency
OC as the referent group, users of low-progestin/high-estrogen potency
formulations (adjusted OR = 2.1; 95% CI = 1.2 to 3.7) and
low-progestin/low-estrogen potency formulations (adjusted OR = 1.6; 95%
CI = 0.9 to 3.0) had a higher risk of ovarian cancer than users of
high-progestin/high-estrogen potency formulation. Low-progestin potency
OC formulations were associated with a statistically significant higher
risk than high-progestin potency formulations (adjusted OR = 2.2; 95% CI
= 1.3 to 3.9). This association was seen even among users of short
duration. CONCLUSION: The combination OC formulations with
high-progestin potency appear to be associated with a greater reduction
in ovarian cancer risk than those with low-progestin potency. Mechanisms
underlying this reduction may include inhibition of ovulation and/or
some direct biologic effects of the progestin.
8
UI - 11773283
AU - Geisler JP; Hatterman-Zogg MA; Rathe JA; Buller RE
TI -
Frequency of BRCA1 dysfunction in ovarian cancer.
SO - J Natl Cancer Inst 2002 Jan 2;94(1):61-7
AD - Division of Gynecologic Oncology, Department of Obstetrics and
Gynecology, Holden Comprehensive Cancer Center, University of Iowa, Iowa
City 52242, USA.
BACKGROUND: Ovarian cancer is one of the most common hereditary cancers
in women. Mutations in the BRCA1 gene increase a woman's risk of ovarian
cancer. Testing for BRCA1 mutations is cumbersome and impractical for
large populations. Therefore, we developed an efficient strategy to
detect various types of BRCA1 dysfunction and also determined the
relative frequency of BRCA1 dysfunction in ovarian cancer. METHODS:
Tumors from 221 patients with epithelial ovarian cancer were screened
for loss of heterozygosity (LOH) at the BRCA1 locus. BRCA1 complementary
DNA (cDNA) and genomic DNA from all cancers with BRCA1 LOH (106 tumors)
or noninformative status (15 tumors) were polymerase chain reaction
(PCR) amplified and analyzed for protein truncation in a coupled
transcription/translation test. When truncated BRCA1 protein was
detected, the BRCA1 gene from both the tumor and a paired blood sample
was sequenced. When BRCA1 expression in tumor cDNA was not detected with
a protein truncation test, a methylation-specific PCR was used to
determine whether the promoter region of BRCA1 was methylated and thus
inactivated. All statistical tests were two-sided. RESULTS: Fifty-one
(23.1%) of 221 tumors had BRCA1 dysfunction, including 18 with germline
mutations, 15 with somatic mutations, and 18 with monoallelic or
biallelic hypermethylated promoters. By the consideration of only tumors
with LOH or that were noninformative, the efficiency for detecting BRCA1
dysfunction improved to 45 (37.2%) of 121 tumors. Therefore,
LOH/noninformative was a strong predictor of mutation status (Fisher's
exact test, P<.001). However, this subset of tumors did not include
those with BRCA1 missense mutations (estimated at six [2.7%] of 221 not
detected by our method) or biallelic promoter methylation (estimated at
six [2.7%] of 221). CONCLUSIONS: BRCA1 dysfunction in ovarian cancer is
common and occurs via multiple mechanisms. The use of LOH, rather than a
family history of ovarian cancer, as a first step in a screening
strategy, followed by protein truncation testing, appears to increase
the chance of identifying tumors with BRCA1 dysfunction.
9
UI - 11848020
AU - Czupkallo G; Jakowicki JA; Baranowski W
TI -
[Stromal leydig cell tumor coexisting with ascites]
SO - Ginekol Pol 2001 Oct;72(10):825-8
AD - Oddzial Ginekologiczno-Polozniczy Szpitala SP ZOZ w Belzycach.
The stromal Leydig cell tumour (SLCT), a very rare, benign neoplasm was
described in 75-year old woman. The patient presented the typical signs
of virilisation (hirsutism, masculine alopecia, moderate clitoris
enlargement, deep voice) as well as hypertension and insulin independent
type of diabetes mellitus (IIDM). Additionally, she had marked ascites
(3400 ml as established during surgery). The serum concentration of
testosterone before the surgery was elevated up to 7.6 ng/ml. FSH and LH
were at very low range (2.5 mIU/ml, 3.4 mIU/ml, respectively) whereas 17
beta-oestradiol was elevated (56 pg/ml). Total abdominal hysterectomy
with salpingo-oophorectomy (TAH/BSO) and omentectomy were performed. The
histopathological findings revealed stromal Leydig cell tumour with
Reinke crystalloids. The postoperative follow-up was complicated by
venous thrombosis. Five weeks after the surgery only slight regression
of the signs of virilisation was observed. Hormonal findings were
adequate to the patient age range (FSH--16.7 mIU/ml, LH--21.1 mIU/ml,
testosterone--0.19 ng/ml, 17 beta-oestradiol concentration below 10
pg/ml).
10
UI - 11852993
AU - Pieretti M; Hopenhayn-Rich C; Khattar NH; Cao Y; Huang B; Tucker TC
TI -
Heterogeneity of ovarian cancer: relationships among histological group,
stage of disease, tumor markers, patient characteristics, and survival.
SO - Cancer Invest 2002;20(1):11-23
AD - Department of Pathology and Laboratory Medicine, University of Kentucky
Medical Center, Lexington, USA. mpieretti@usouthal.edu
Epidemiological studies have established associations between various
reproductive factors and risk of ovarian cancer; it has also been
observed that some of these risk factors are only associated with
specific histological subgroups. To investigate the correlation of
genetic alterations with these risk factors, we examined a consecutive
series of 158 ovarian cancer cases treated at the University of Kentucky
(1990-96). Common molecular genetic alterations (LOH on chromosome 17,
P53 alterations, K-RAS mutations), histological and clinical
characteristics of the disease, demographic patient information and
survival were evaluated. These latter data were from the Kentucky Cancer
Registry. Univariate analysis showed higher frequencies of chromosome 17
loss and P53 mutations in tumors of advanced stage and grade, and in
older and post-menopausal women. Non-mucinous tumors were more likely to
be classified as late stage, high-grade cancers, and to have chromosome
17 loss and P53 mutations. Survival analysis indicated that stage was
the only independent significant variable. When stage was the outcome
variable in multiple logistic regression analysis, histology and
chromosome 17 loss were significantly associated with poor survival.
This case-case study provides evidence that ovarian cancers of mucinous
and non-mucinous histology are significantly different with respect to
clinical characteristics, survival and molecular alterations. It also
lends support to the hypothesis that ovarian cancer is a heterogeneous
disease with distinct etiological factors and clinical outcomes, which
may require different approaches to treatment.
11
UI - 11857303
AU - Marth C; Kisic J; Kaern J; Trope C; Fodstad O
TI -
Circulating tumor cells in the peripheral blood and bone marrow of
patients with ovarian carcinoma do not predict prognosis.
SO - Cancer 2002 Feb 1;94(3):707-12
AD - Department of Obstetrics and Gynecology, Innsbruck University Hospital,
Innsbruck, Austria. christian.marth@uibk.ac.at
BACKGROUND: Ovarian carcinoma is apparently restricted for a long time
to the peritoneal cavity. However, about 50% of patients with a
surgically documented complete intraabdominal response experience later
recurrence. Occult hematogenous micrometastases are common to most
epithelial malignancies and have recently been found in 30% of bone
marrow samples of ovarian carcinoma patients, as examined by
immunocytochemistry. Moreover, these findings were associated with poor
progression-free and overall survival. The aim of the current study was
to evaluate the possible prognostic significance of tumor cells detected
in the peripheral blood and bone marrow of ovarian carcinoma patients by
an immunomagnetic method. METHODS: In a total of 90 patients with
histologically proven epithelial ovarian carcinoma, blood and (in 73
cases) bone marrow samples were taken. Tumor cells were identified by a
microbead coated with the antibody MOC-31, which recognizes an epitope
regularly expressed on ovarian carcinoma cells. RESULTS: The authors
detected carcinoma cells in the bone marrow in 21% of ovarian carcinoma
patients, and in the peripheral blood in 12% of patients. Mean overall
survival was 25 and 28 months for patients with or without circulating
tumor cells, respectively. CONCLUSIONS: Ovarian carcinoma cells seem to
reach peripheral circulation more frequently than expected. However, in
contrast to an earlier report, detection of tumor cells in the bone
marrow and/or blood was not associated with poor prognosis in ovarian
carcinoma patients. This discrepancy remains unexplained, but
characterization of circulating ovarian carcinoma cells for their
malignant and metastatic capacity is clearly warranted. Copyright 2002
American Cancer Society. DOI 10.1002/cncr.10250
12
UI - 11859985
AU - Mogren I; Stenlund H; Hogberg U
TI -
Long-term impact of reproductive factors on the risk of cervical,
endometrial, ovarian and breast cancer.
SO - Acta Oncol 2001;40(7):849-54
AD - Department of Clinical Science, Umea University, Sweden.
ingrid.mogren@obstgyn.umu.se
The influence of maternal age, parity, low or high birthweight, multiple
births, and pre-eclampsia on the risk of cervical, endometrial, ovarian
and breast cancers was studied. Data on 40951 women and the outcomes of
their deliveries between 1955 and 1995 were obtained from birth
registers. For the mothers, data from the Swedish Cancer Registry and
the Cause of Death Register were added. The sample was evaluated using
Cox's regression in univariate and bivariate analyses where the relative
risk and its 95% confidence interval were calculated. Increasing
maternal age at first birth was associated with an increasing relative
risk of endometrial, ovarian, and breast cancers, and with a decreased
risk of cervical cancer. Multiparity was a protective factor for all
gynaecological cancers, including cervical and breast cancers. Multiple
births were associated with an increased risk of endometrial cancer.
13
UI - 11808141
AU - Niimi S; Tanaka T
TI -
[Malignant ovarian tumor]
SO - Nippon Rinsho 2001 Nov;59 Suppl 7():347-63
AD - Department of Obstetrics & Gynecology, Jikei University School of
Medicine.
14
UI - 11812079
AU - Bao R; Selvakumaran M; Hamilton TC
TI -
Targeted gene therapy of ovarian cancer using an ovarian-specific
promoter.
SO - Gynecol Oncol 2002 Feb;84(2):228-34
AD - Ovarian Cancer Program, Fox Chase Cancer Center, Philadelphia,
Pennsylvania 19111, USA.
OBJECTIVES: The "suicide" gene therapy of cancer using promoters such as
cytomegalovirus could cause severe toxicity to normal tissues due to a
lack of specificity of prodrug activation. Therefore, we investigated
gene therapy of ovarian cancer using ovarian-specific promoter (OSP1) to
limit the synthesis of the prodrug activating enzyme HSVtk to ovarian
cancer cells. METHODS: The HSVtk expressing plasmid pOSP1-HSVtk was
created and transfected into an ovarian cancer cell line OVCAR3. The
ganciclovir (GCV) sensitivity of the stable transfectants was evaluated
with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide
method. Tissue specificity of this promoter was evaluated by comparing
the sensitivity to GCV between ovarian and nonovarian cancer cell lines
after they were transfected with pOSP1-HSVtk. One transfectant sensitive
to GCV was implanted intraperitoneally to immunocompromised mice which
were treated subsequently with GCV. Furthermore, this ovarian cancer
survival model was used to evaluate the in vivo efficacy of cationic
lipid mediated pOSP1-HSVtk gene delivery followed by GCV treatment.
RESULTS: Stable transfectants of OVCAR3 cells bearing OSP1-HSVtk became
more sensitive to GCV treatment compared to the parental cell line and
vector transfected OVCAR3 cell line. OSP1-HSVtk could specifically
sensitize the OVCAR3 ovarian cancer cell line to GCV. SCID mice
transplanted with the OVCAR3 transfectant and treated with GCV survived
longer than the mice without GCV treatment (P = 0.032). In vivo gene
delivery mediated by a cationic lipid (GL67) followed by GCV treatment
yielded a longer survival in the OVCAR3 survival model (P = 0.016).
CONCLUSIONS: The OSP1 promoter can selectively direct suicide gene
therapy of ovarian cancer and the in vivo efficacy is improved by using
a cationic lipid GL67 as delivery vehicle as opposed to the direct
injection of plasmid. B)2001 Elsevier Science.
15
UI - 11812090
AU - Schiffenbauer YS; Meir G; Maoz M; Even-Ram SC; Bar-Shavit R; Neeman M
TI -
Gonadotropin stimulation of MLS human epithelial ovarian carcinoma cells
augments cell adhesion mediated by CD44 and by alpha(v)-integrin.
SO - Gynecol Oncol 2002 Feb;84(2):296-302
AD - Department of Biological Regulation, Weizmann Institute of Science,
Rehovot 76100, Israel.
OBJECTIVE: The goal of this work was to evaluate the involvement of
gonadotropins in the regulation of adhesion of human epithelial ovarian
carcinoma. We studied two pathways that were previously implicated in
the metastatic implantation of ovarian carcinoma to the peritoneum,
namely hyaluronan-CD44 and RGD-integrin mediated adhesion. METHODS: Two
cell lines derived from human epithelial ovarian carcinoma (MLS and
OC238) were stimulated with luteinizing hormone (LH) and/or follicle
stimulating hormone (FSH). Expression of CD44 was evaluated by Western
blotting. Expression of alpha(v)-integrins was studied by RT-PCR and
Northern blot. Integrin and CD44 mediated adhesion of the cells was
analyzed using culture plates coated either with a thrombin derived RGD
containing peptide or fibronectin for integrin mediated adhesion or with
hyaluronan for CD44 mediated adhesion. RESULTS: MLS cells stimulated
with either LH or FSH showed increased adhesion to culture plates coated
with hyaluronan, as well as to culture plates coated with fibronectin or
with a thrombin derived RGD containing peptide. In these cells,
gonadotropin stimulation led to induced expression of the integrin
subunit alpha(v) and CD44, the cell surface hyaluronan receptor. On the
other hand, OC238 cells showed no expression of the integrin subunit
alpha(v) and no hormonal effect on the expression of CD44. Accordingly,
adhesion of OC238 cells on either RGD or CD44 was not affected by
hormonal stimulation. CONCLUSION: Elevated levels of gonadotropins may
in some cases facilitate peritoneal metastatic dissemination of ovarian
cancer by increasing cell adhesion, the first essential step in the
invasion process. B)2002 Elsevier Science.
16
UI - 11812093
AU - Eisenkop SM
TI -
Thoracoscopy for the management of advanced epithelial ovarian cancer--a
preliminary report.
SO - Gynecol Oncol 2002 Feb;84(2):315-20
AD - Women's Cancer Center, Encino-Tarzana, 5525 Etiwanda Ave., Suite 311,
Tarzana, California 91356, USA. dobsnccats@earthlink.net
OBJECTIVE: To determine possible benefits of thoracoscopy for the
management of patients with Stage IIIC and IV epithelial ovarian cancer.
METHODS: Thirty patients underwent thoracoscopy at the time of primary
cytoreduction to determine the presence and extent of intrathoracic
disease and the feasibility of cytoreduction. Survival of patients with
Stage IV disease undergoing thoracoscopy was compared to that of
historical controls (Stage IV on the basis of positive pleural effusion
cytology and/or pleural involvement by contiguous diaphragmatic
metastases) who did not undergo thoracoscopy (log-rank analysis).
RESULTS: Among the 24 patients with Stage IV disease having
thoracoscopy, 11 (45.8%) did not have macroscopic intrathoracic disease,
10 (41.7%) underwent pleural implant ablation and/or excision as well as
nodal excision that influenced the final cytoreductive outcome, and 3
(12.5%) had efforts to achieve complete intra-abdominal cytoreduction
abbreviated after unresectable intrathoracic disease was found. The 24
patients who had thoracoscopy and the historical controls were not
significantly different with respect to median age, performance status,
extent of intra-abdominal disease, amount of ascites, and
intra-abdominal cytoreductive outcome. The median and estimated 5-year
survival for the entire cohort were 28.9 months and 42%, respectively.
Log-rank analysis revealed the probability of survival to be improved by
the performance of thoracoscopy (performed vs not performed, P = 0.05).
CONCLUSIONS: Thoracoscopy quantifies the volume of intrathoracic
disease, may allow abbreviation of the abdominal phase of cytoreduction
for patients with unresectable pleural disease, and permits complete
cytoreduction for some patients who might otherwise have unrecognized
macroscopic residual intrathoracic disease. A multi-institutional
prospective study may better define the role of this procedure in
clinical practice. B)2002 Elsevier Science.
17
UI - 11812103
AU - Guerriero S; Ajossa S; Melis G
TI -
Is three-dimensional power Doppler ultrasound better than
two-dimensional power Doppler?
SO - Gynecol Oncol 2002 Feb;84(2):352-3
18
UI - 11848544
AU - Yen RF; Sun SS; Shen YY; Changlai SP; Kao A
TI -
Whole body positron emission tomography with 18F-fluoro-2-deoxyglucose
for the detection of recurrent ovarian cancer.
SO - Anticancer Res 2001 Sep-Oct;21(5):3691-4
AD - Department of Nuclear Medicine and PET Center National Taiwan University
Hospital, Taipei.
Although many cancers can be detected by whole-body positron emission
tomography (PET) with 18F-fluoro-2-deoxyglucose (FDG), there has been
limited clinical experience with FDG-PET for the detection of recurrent
ovarian cancers. Therefore, the aim of this study was to evaluate the
clinical value of FDG-PET in the detection of recurrent ovarian cancer.
Whole body FDG-PET scans were performed on 24 women who had previous
histories of ovarian cancer and treatment with surgery and chemotherapy.
All patients also underwent physical examination, laboratory testing of
serum CA-125 level and pelvic-abdominal-chest computed tomography (CT)
or magnetic resonance imaging (MRI). The results of FDG-PET scans were
correlated with serum CA-125 level, CT/MRI and operative pathology
results. The diagnostic sensitivity was 90.9%, 90.9% and 90.9%,
specificity was 92.3%, 76.9% and 46.2% and accuracy was 91.7%, 83.3% and
66.7% for FDG-PET, serum tumor marker of CA-125 level and CT/MRI in
detecting recurrent ovarian cancer, respectively. FDG-PET is a useful
diagnostic tool in detecting recurrent ovarian cancers with high
specificity as compared with the serum tumor marker CA-125 level and the
conventional CT/MRI morphological imaging methods.
19
UI - 11848553
AU - Scholz HS; Benedicic C; Haas J; Tamussino K; Petru E
TI -
Stage IV ovarian cancer: prognostic factors and survival beyond 5 years.
SO - Anticancer Res 2001 Sep-Oct;21(5):3729-32
AD - Department of Obstetrics and Gynecology, University of Graz, Austria.
scholzhs@kfunigraz.ac.at
BACKGROUND: Ovarian cancer continues to be the leading cause of death
due to gynecologic malignancies and most patients still present with
advanced disease. In the present study we evaluated long-term survival
and prognostic factors in patients with stage IV ovarian cancer.
PATIENTS AND METHODS: The charts of 62 consecutive women with FIGO stage
IV epithelial ovarian cancer were reviewed. RESULTS: Chemotherapy was
the only factor associated with longer survival. Three patients (5%)
survived for longer than 5 years. One died of disease at 6.3 years and
two are alive without evidence of disease at 12.4 and 14.9 years,
respectively. CONCLUSION: Survival seemed to correlate with the
possibility of administering chemotherapy. Patients with verified stage
IV ovarian cancer, in whom due to the initial tumor load, operative
extent and concomitant illness, the possibility of postoperative
chemotherapy administration seems questionable, might be considered for
primary chemotherapy followed by surgery.
20
UI - 11870520
AU - O'Doherty AM; Church SW; Russell SE; Nelson J; Hickey I
TI -
Methylation status of oestrogen receptor-alpha gene promoter sequences
in human ovarian epithelial cell lines.
SO - Br J Cancer 2002 Jan 21;86(2):282-4
AD - School of Biology and Biochemistry, The Queen's University of Belfast,
Lisburn Road, Belfast, Northern Ireland, UK.
We have determined the methylation status of the CpG island of the
oestrogen receptor alpha gene in seven human ovarian cell lines. Cell
lines expressing oestrogen receptor alpha showed no evidence of
hypermethylation. In three of four cell lines that produced no
detectable oestrogen receptor alpha protein, hypermethylation was
observed at the NotI site of the CpG island. These results indicate that
aberrant hypermethylation may be responsible for a significant
proportion of epithelial ovarian tumours in which oestrogen receptor
alpha expression is lost. Copyright 2002 The Cancer Research Campaign
21
UI - 11845216
AU - Dibble SL; Roberts SA; Robertson PA; Paul SM
TI -
Risk factors for ovarian cancer: lesbian and heterosexual women.
SO - Oncol Nurs Forum 2002 Jan-Feb;29(1):E1-7
AD - Institute for Health and Aging in the School of Nursing, University of
California, San Francisco, CA, USA. sdibble@itsa.ucsf.edu
PURPOSE/OBJECTIVES: To compare the distribution of risk factors for
developing ovarian cancer in lesbian and heterosexual women. DESIGN:
Secondary analysis of a retrospective medical record review. SETTING:
Urban health clinic with special outreach to lesbians. SAMPLE: Typical
participant (N = 1,019) was 42.9 years old and white (70%). Most were
without health insurance, and 99% were poor (< $15,780 annual income).
The majority (58%, n = 586) described themselves as heterosexual; 42% (n
= 433) said they were lesbian. METHODS: Data were collected from medical
records and analyzed using analysis of covariance and logistic
regression techniques. MAIN RESEARCH VARIABLES: Ovarian cancer risk
factors (parity, exogenous hormone use, smoking, body mass index [BMI],
and tubal ligation/hysterectomy). FINDINGS: Lesbians had a higher BMI;
heterosexual women had higher rates of current smoking and a higher
incidence of the protective factors of pregnancy, children,
miscarriages, abortions, and use of birth control pills. CONCLUSIONS:
The results of this study indicate that lesbians may have an increased
risk for developing ovarian cancer. A study designed specifically to
explore the risk factors of lesbian and heterosexual women for
developing ovarian cancer must be undertaken to confirm these findings.
IMPLICATIONS FOR NURSING PRACTICE: Differences in risk levels may exist
for lesbians; therefore, healthcare providers must become comfortable
asking questions about sexual orientation and behavior.
22
UI - 11815406
AU - Bonadona V; Saltel P; Desseigne F; Mignotte H; Saurin JC; Wang Q;
TI -
Sinilnikova O; Giraud S; Freyer G; Plauchu H; Puisieux A; Lasset C
Cancer patients who experienced diagnostic genetic testing for cancer
susceptibility: reactions and behavior after the disclosure of a
positive test result.
SO - Cancer Epidemiol Biomarkers Prev 2002 Jan;11(1):97-104
AD - Unit of Prevention and Genetic Epidemiology, Comprehensive Cancer Center
Leon Berard, 28 rue Laennec, 69008 Lyon, France.
The aim of this prospective study was to evaluate the consequences of
the disclosure of a positive genetic test result to patients affected
with cancer. Personal repercussions and patients' behavior with the
transmission of their results to relatives were considered. We conducted
semistructured interviews with 23 cancer patients identified as carriers
of a cancer-predisposing mutation for hereditary breast ovarian or
nonpolyposis colorectal cancers, 1 month after the disclosure of the
test result. Eight patients spontaneously expressed distressed reactions
("you no longer feel cured"), and 14 patients reported at least one
negative feeling (dissatisfied, discouraged, unhappy, or worried),
despite expecting to be a carrier. Sixteen patients expressed concerns
about the risk of developing another cancer, and 18 were concerned for
their children's future, in that they may carry the mutation and develop
a cancer. Although 8 patients found that disadvantages of knowing their
genetic status outweighed the advantages, all but 1 did not regret
having undergone genetic testing. All of the patients transmitted their
results to at least one close relative. Although 6 of them expressed
difficulties in being the only person who could transmit the information
and 9 said it was a heavy responsibility, all except 1 did not want
someone else to have to inform their families. Our results illustrate
the potential negative impact of diagnostic genetic testing in patients
with cancer. This includes distressed reactions and difficulties in
transmitting their results to relatives. Future large-scale studies are
warranted to confirm our findings.
23
UI - 11821091
AU - Dor J; Lerner-Geva L; Rabinovici J; Chetrit A; Levran D; Lunenfeld B;
TI -
Mashiach S; Modan B
Cancer incidence in a cohort of infertile women who underwent in vitro
fertilization.
SO - Fertil Steril 2002 Feb;77(2):324-7
AD - Department of Obstetrics and Gynecology, Chaim Sheba Medical Center, Tel
Hashomer 52621, Israel.
OBJECTIVE: To assess whether ovarian hyperstimulation and IVF increase
the risk for cancer. DESIGN: Historical cohort analysis. SETTING; IVF
units of two medical centers in Israel. PATIENT(S): Five thousand
twenty-six women who underwent IVF between 1981 and 1992.
INTERVENTION(S); Cancer incidence rates were determined through linkage
to the National Cancer Registry and were compared with expected rates
with respect to age, sex, and place of birth. MAIN OUTCOME MEASURE(S):
Development of cancer. RESULT(S): Twenty-seven cases of cancer were
observed, and 35.6 were expected (standardized incidence ratio, 0.76
[95% CI, 0.50-1.10]). Eleven cases of breast cancer were observed,
whereas 15.86 were expected (standardized incidence ratio, 0.69 [95% CI,
0.46-1.66]). One case of ovarian cancer and 1 case of cervical cancer
were observed, compared with 1.74 and 1.73 cases expected, respectively.
The type of infertility, number of IVF cycles, and treatment outcome did
not significantly affect risk for cancer. CONCLUSION(S): In a cohort of
women treated with IVF, no excess risk for cancer was noted.
24
UI - 11786575
AU - Ben David Y; Chetrit A; Hirsh-Yechezkel G; Friedman E; Beck BD; Beller
TI -
U; Ben-Baruch G; Fishman A; Levavi H; Lubin F; Menczer J; Piura B;
Struewing JP; Modan B; National Israeli Study of Ovarian Cancer
Effect of BRCA mutations on the length of survival in epithelial ovarian
tumors.
SO - J Clin Oncol 2002 Jan 15;20(2):463-6
AD - Department of Gynecology, Haemek Medical Center, Afula.
PURPOSE: To study the role of BRCA mutations in ovarian cancer survival.
PATIENTS AND METHODS: Blood samples and specimens of ovarian tumors
(whenever blood samples were not available) at the time of the primary
surgery were obtained in the course of a nationwide case-control study
of women with ovarian cancer in Israel. The three common BRCA mutations
in Israel (185delAG, 5382insC, and 6174delT) were analyzed with a
multiplex polymerase chain reaction to amplify the exons containing the
three mutations using fluor-labeled primers in a single reaction.
Because each mutation is a small insertion or deletion, they can be
detected as length polymorphisms. Patients were followed for up to 5
years (range, 20 to 64 months). Statistical analysis was performed using
the Kaplan-Meier method and the log-rank test. Stepwise Cox regression
analysis was used for determination of independent prognostic factors.
RESULTS: This report is based on 896 blood or tumor specimens analyzed
for the presence of the BRCA mutations. Of these, 234 women (26.1%) were
found to be positive. A significant difference in survival pattern was
found between BRCA1/BRCA2 carriers and noncarriers among the women with
invasive ovarian cancer (median survival, 53.4 months v. 37.8 months;
3-year survival, 65.8% v. 51.9%, respectively). These differences were
independent of age at diagnosis or stage of the disease. CONCLUSION: Our
data indicate that the survival of patients with ovarian cancer is
affected by BRCA germline mutation, at least in the early years after
diagnosis.
25
UI - 11829379
AU - Leeson S; Iredale R; Stansfield K; Evans A; Gray J
TI -
Developing a cancer genetics service in Wales: opinions of
gynaecologists on the management of women at risk of familial ovarian
cancer.
SO - Eur J Cancer Care (Engl) 2001 Sep;10(3):172-8
AD - Department of Obstetrics and Gynaecology, Ysbyty Gwynedd, North Wales,
UK.
In Wales, a cancer genetics service has been developing since 1998.
Gynaecologists play an integral role in the management of women with a
family history of ovarian cancer and we were interested in investigating
referral practice and management for relatives of patients with ovarian
cancer among gynaecologists in Wales. In 1999, a postal questionnaire
was sent to all gynaecologists. The response rate was 51%. The
questionnaire contained structured questions about current provision and
a number of hypothetical scenarios to explore referral patterns to the
cancer genetics service. The results of this study showed that referrals
varied widely among specialists, as did the numbers who required onward
referral to cancer genetics. The offer of screening to women at high
risk of ovarian cancer was consistent, although there were variations in
how often it was offered and the age at which it was offered. Most
gynaecologists were easily able to establish when it was appropriate to
refer onwards to cancer genetics, differentiating between women at high
or low risk. There was some confusion about women at moderate risk of
ovarian cancer. This study demonstrated the need for clear referral
guidelines in Wales. Guidelines have since been distributed to all
general practitioners and specialists; however, continued monitoring and
further evaluation of referral practices will be necessary.
26
UI - 11844820
AU - Kolomainen DF; Larkin JM; Badran M; A'Hern RP; King DM; Fisher C;
TI -
Bridges JE; Blake PR; Barton DP; Shepherd JH; Kaye SB; Gore ME
Epithelial ovarian cancer metastasizing to the brain: a late
manifestation of the disease with an increasing incidence.
SO - J Clin Oncol 2002 Feb 15;20(4):982-6
AD - Gynaecology Unit, Royal Marsden Hospital, London, United Kingdom.
PURPOSE: We present the Royal Marsden Hospital experience of cerebral
metastases from primary epithelial ovarian carcinoma (EOC) over the last
20 years and examine the evidence for an increasing incidence of EOC
metastasizing to this site. PATIENTS AND METHODS: A total of 3,690 women
with EOC were seen at the Royal Marsden Hospital from 1980 to 2000.
Eighteen of these patients developed cerebral metastases. RESULTS:
Median age at diagnosis of EOC was 52 years (range, 39 to 67). All
patients received at least one line of platinum-based chemotherapy; 56%
(10 of 18) received more than one line of treatment; 17% (three of 18),
two lines; 11% (two of 18), three lines; and 28% (five of 18), four
lines. The median treatment interval between each line of chemotherapy
was 12, 18, and 4 months. The median interval between diagnosis and CNS
relapse was 46 months (range, 12 to 113), in comparison with 5 and 7.5
months for hematogenous relapse in lung or liver, respectively (P
<.001). The incidence of CNS metastases in our population from 1980 to
1984 was 0.2%; from 1985 to 1989, 0%; from 1990 to 1994, 0.3%; and from
1995 to 1999, 1.3% (P <.001). An analysis of data from the literature
also suggests that the incidence of cerebral metastases from EOC has
increased over time. CONCLUSION: CNS metastases in EOC are a rare and
late manifestation of the disease, occurring in patients with a
prolonged survival caused by repeated chemosensitive relapses. An
analysis of our data and the data from the literature suggests that the
incidence of metastasis at this site in patients with EOC is increasing.
27
UI - 11855877
AU - McGuire V; Jesser CA; Whittemore AS
TI -
Survival among U.S. women with invasive epithelial ovarian cancer.
SO - Gynecol Oncol 2002 Mar;84(3):399-403
AD - Department of Health Research and Policy, Stanford University School of
Medicine, Stanford, California 94305-5405, USA.
vmcguire@leland.stanford.edu
OBJECTIVE: Invasive epithelial ovarian cancer is a highly fatal disease,
diagnosed at advanced stages when survival is poor. Relatively little is
known about the variation in survival across U.S. women of different
race/ethnicities. To investigate this issue, we evaluated pathological
characteristics and death rates due to invasive epithelial ovarian
cancer in a population-based sample of patients from six racial/ethnic
groups. METHODS: The analysis included 38,012 women diagnosed with
primary invasive epithelial ovarian cancer between 1973 and 1997 in the
Surveillance, Epidemiology and End Results Program of the National
Cancer Institute. RESULTS: Filipina patients were younger at diagnosis,
more likely to have localized disease, and had more mucinous cancers
than whites. African-Americans were more likely than whites to be
diagnosed at older ages, with distant disease and with
undifferentiated/unclassified cancers. After adjusting for age at
diagnosis, stage of disease at diagnosis, and cancer histology, we found
that, compared to whites, death rates were significantly elevated among
African-Americans and significantly reduced among Hispanics and
Filipina. We also found that death rates declined significantly with
time since diagnosis among women with advanced disease. CONCLUSION: The
declining death rates in women with advanced disease suggest the
presence of considerable prognostic heterogeneity among these women,
which could reflect differences in quality of care. This issue, as well
as the survival disadvantage for African-American women and survival
advantages for Hispanic and Filipina women, needs investigation.
28
UI - 11855878
AU - Kolfschoten GM; Hulscher TM; Schrier SM; van Houten VM; Pinedo HM; Boven
TI -
E
Time-dependent changes in factors involved in the apoptotic process in
human ovarian cancer cells as a response to cisplatin.
SO - Gynecol Oncol 2002 Mar;84(3):404-12
AD - Department of Medical Oncology, Vrije Universiteit Medical Centre,
Amsterdam, the Netherlands.
OBJECTIVES: Apoptosis is believed to be a major mechanism of
cisplatin-induced cell death. We investigated the kinetics of apoptosis
in four human ovarian cancer cell lines treated with cisplatin to obtain
insight into the role and the behavior of a variety of factors involved
in this process. METHODS: The cell lines A2780, H134, and IGROV-1 (all
wild-type p53) and OVCAR-3 (mutant p53) were exposed to cisplatin for 1
h and the antiproliferative effects were measured after 96 h. At various
time points up to 96 h after the 1-h exposure to the individual 90%
growth-inhibiting cisplatin concentrations, FACS analysis and
May-Grunwald Giemsa staining were carried out to determine the extent of
apoptosis. At the same time points protein expression levels of p53,
p21/WAF1, Bax, and Bcl-2 and the activity of caspase-3 were measured.
FACS analysis was also carried out to determine changes in cell cycle
distribution as a response to cisplatin. RESULTS: The four cell lines
differed in sensitivity to cisplatin. A2780 was the most sensitive and
IGROV-1 was the least sensitive. In contrast, IGROV-1 cells showed the
highest percentage of apoptosis (30-40%), while A2780 had the lowest
percentage (6-14%) (r = 0.99). The occurrence of apoptosis was not
dependent on functional p53. Of interest, caspase-3 activity was in line
with the percentage of apoptosis and preceded DNA fragmentation and the
visualization of condensed nuclei. Wild-type p53 cells accumulated in
the S phase, while OVCAR-3 arrested in the G2/M phase. The protein
expression levels of p53, p21/WAF1, Bax, and Bcl-2 varied in time, but
were not related to the apoptotic behavior of the cells. Upregulation of
p53 was already evident before activation of caspase-3. CONCLUSIONS:
Time-dependent changes in the various factors involved in the apoptotic
process induced by equitoxic doses of cisplatin vary strongly among the
cell lines. Caspase-3 activation plays an important role in
cisplatin-induced apoptosis and this precedes morphological changes. The
ability of cells to enter apoptosis, however, does not seem to predict
sensitivity to cisplatin.
29
UI - 11855879
AU - Leitao M; Boyd J
TI -
Preoperative CA-125 levels in patients with hereditary compared to
sporadic epithelial ovarian carcinoma.
SO - Gynecol Oncol 2002 Mar;84(3):413-5
AD - Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York,
New York 10021, USA.
OBJECTIVE: The aim of this study was to determine whether a significant
difference in preoperative CA-125 levels exists between patients with
BRCA-associated hereditary ovarian carcinoma and those with sporadic
ovarian carcinoma and whether the CA-125 level predicts the probability
of optimal cytoreductive surgery. METHODS: From a retrospective cohort
of 189 consecutive ovarian cancer patients genotyped for BRCA mutation
status, data on preoperative CA-125 levels were available for 49/88
(56%) hereditary cases and 43/101 (43%) sporadic cases. Data on the
extent of surgical cytoreduction were obtained for all 92 patients with
available CA-125 data. Comparison of preoperative CA-125 levels between
hereditary and sporadic groups was assessed using the Kruskal-Wallis
chi(2) test. Correlation of surgical cytoreduction with preoperative
CA-125 level was assessed using Fisher's exact test. RESULTS: Mean
preoperative CA-125 levels were not significantly different among BRCA1
(2289 U/ml), BRCA2 (2586 U/ml), and sporadic (3307 U/ml) cases (P =
0.5). For hereditary cases, optimal cytoreduction was achieved in 59% of
patients with preoperative CA-125 levels of <500 U/ml