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Abramson Cancer CenterNCI CANCERLIT® Search: Diagnosis-Histopathology-Pathogenesis of Ovarian Cancer - May 2002
National Cancer Institute®
Last Modified: May 1, 2002
Table of Contents
1
UI - 11920956
AU - Bharaj BB; Luo LY; Jung K; Stephan C; Diamandis EP
TI -
Identification of single nucleotide polymorphisms in the human
kallikrein 10 (KLK10) gene and their association with prostate, breast,
testicular, and ovarian cancers.
SO - Prostate 2002 Apr 1;51(1):35-41
AD - Department of Pathology and Laboratory Medicine, Mount Sinai Hospital,
Toronto, Ontario, Canada.
BACKGROUND: The KLK10 gene (also known as the normal epithelial
cell-specific 1 gene) is a member of the expanded human kallikrein gene
family. Recently, it has been reported that KLK10 is a tumor suppressor
gene and that its expression is downregulated in various forms of cancer
and cancer cell lines. KLK10 is also upregulated in ovarian cancer. We
thus hypothesized that the KLK10 gene may be a target for mutations in
various cancers. METHODS: We sequenced the five coding exons of the
KLK10 gene using genomic DNA from various tumors, normal tissues, and
blood, by PCR amplification and automated sequencing. RESULTS: In none
of the tumor-derived DNAs, we identified somatic mutations that could
inactivate this gene. However, we identified a prevalent germline single
nucleotide variation at codon 50 (exon 3) of this gene [GCC (alanine) to
TCC (serine)]. The GCC genotype was less prevalent in prostatic cancer
patients in comparison to control subjects (P = 0.027) but no
differences were seen with testicular, ovarian, and breast cancer. We
also identified four genetic variations in exon 4, at codons106 [GGC
(glycine) to GGA (glycine)], codon 112 [ACG (threonine) to ACC
(threonine)], codon 141 [CTA (leucine) to CTG (leucine)], and at codon
149 [CCG (proline) to CTG (leucine)]. None of these variations was
significantly different between normal subjects and cancer groups.
CONCLUSIONS: We found no evidence for somatic mutations of the KLK10
gene in cancers of the prostate, breast, ovary, and testis. The single
nucleotide variation at codon 50 appears to be associated with prostate
cancer risk. Copyright 2002 Wiley-Liss, Inc.
2
UI - 11588898
AU - McCann SE; Moysich KB; Mettlin C
TI -
Intakes of selected nutrients and food groups and risk of ovarian
cancer.
SO - Nutr Cancer 2001;39(1):19-28
AD - Department of Social and Preventive Medicine, University at Buffalo,
Buffalo, NY 14214, USA. mccann@acsu.buffalo.edu
In a hospital-based case-control study, we examined dietary intakes of
selected nutrients and food groups and ovarian cancer risk among 496
women with primary, histologically confirmed epithelial ovarian cancer
and 1,425 women with nonneoplastic diagnoses, ages 20-87 years, admitted
to Roswell Park Cancer Institute between 1982 and 1998. Data on diet and
other relevant risk factors in the few years before admission were
collected with a self-administered questionnaire. Odds ratios (OR) and
95% confidence intervals (CI) were estimated by unconditional logistic
regression adjusting for age, education, region of residence, regularity
of menstruation, family history of ovarian cancer, parity, age at
menarche, oral contraceptive use, and energy intake. Women in the
highest vs. the lowest quartile of total energy had a weak increase in
risk (OR = 1.25, 95% CI = 0.90-1.73). Significantly reduced risks were
associated with higher intakes of dietary fiber (OR = 0.57, 95% CI =
0.38-0.87), vitamin A (OR = 0.66, 95% CI = 0.45-0.98), carotenoid (OR =
0.64, 95% CI = 0.43-0.93), vitamin E (OR = 0.58, 95% CI = 0.38-0.88),
beta-carotene (OR = 0.68, 95% CI = 0.46-0.98), and total fruit and
vegetable intake (OR = 0.62, 95% CI = 0.42-0.92). Our findings suggest
that a diet high in plant foods may be important in reducing risk of
ovarian cancer.
3
UI - 11588899
AU - Tavani A; Gallus S; Dal Maso L; Franceschi S; Montella M; Conti E; La
TI -
Vecchia C
Coffee and alcohol intake and risk of ovarian cancer: an Italian
case-control study.
SO - Nutr Cancer 2001;39(1):29-34
AD - Istituto di Ricerche Farmacologiche Mario Negri, 20157 Milan, Italy.
tavani@marionegri.it
The relation between coffee and alcohol intake and ovarian cancer risk
was analyzed in a case-control study conducted in Italy between 1992 and
1999. Cases were 1,031 women, aged 18-79 years, with incident,
histologically confirmed invasive epithelial ovarian cancer, and
controls were 2,411 women, aged 17-79 years, admitted to the hospital
for acute nonneoplastic non-hormone-related diseases. Coffee intake
(mostly espresso and mocha) was not associated with ovarian cancer risk,
with an odds ratio (OR) of 0.93 [95% confidence interval (CI) =
0.69-1.27] in drinkers of > or = 4 cups/day compared with drinkers of <
1 cup/day. No meaningful relation was observed with cappuccino (OR =
1.06, 95% CI = 0.85-1.32 for drinkers compared with nondrinkers),
decaffeinated coffee (OR = 0.64, 95% CI 0.42-0.96), and tea intake (OR =
0.90, 95% CI = 0.75-1.08). Total alcohol intake was not associated with
ovarian cancer risk (OR = 1.09, 95% CI = 0.76-1.57 in drinkers of > or =
36 g/day compared with never drinkers). No relationship was found with
wine (OR = 1.03, 95% CI = 0.70-1.50 for > 39 g/day compared with never
drinkers), beer, amari, grappa, and spirits. No significant
heterogeneity was found for coffee or total alcohol intake across strata
of age, education, parity, oral contraceptive use, family history of
ovarian/breast cancer, body mass index, and calorie intake. This study,
based on a large data set; provides no support for a causal association
between invasive epithelial ovarian cancer risk and coffee and alcohol
intake.
4
UI - 11873549
AU - Fries MH; Holt C; Carpenter I; Carter CL; Daniels J; Flanagan J; Murphy
TI -
K; Hailey BJ; Martin L; Hume R; Hudson G; Cadman M; Weatherly R; Nunes
ME
Guidelines for evaluation of patients at risk for inherited breast and
ovarian cancer: recommendations of the Department of Defense Familial
Breast/Ovarian Cancer Research Project.
SO - Mil Med 2002 Feb;167(2):93-8
AD - Air Force Medical Genetics Center, Keesler Air Force Base, MS 39534,
USA.
Patients at high risk for inherited breast and/or ovarian cancer are
frequently encountered in all medical specialties. Department of
Defense, Health Affairs funding as part of the Breast Cancer Education
and Awareness Program was used to develop a comprehensive program for
the identification, counseling, genetic testing, and long-term follow-up
of such high-risk patients. This article reports the recommendations for
high-risk patient management based on 4 years of evaluation and care,
including discussions of the approach to counseling, indications for
genetic testing, post-testing counseling, patient surveillance with
examination, imagining, and laboratory testing, and suggested options
for surgical and chemoprophylaxis as well as lifestyle modifications.
5
UI - 11873550
AU - Fries MH; Holt C; Carpenter I; Carter CL; Daniels J; Flanagan J; Murphy
TI -
K; Hailey BJ; Martin L; Hume R; Hudson G; Cadman M; Weatherly R; Nunes
ME
Diagnostic criteria for testing for BRCA1 and BRCA2: the experience of
the Department of Defense Familial Breast/Ovarian Cancer Research
Project.
SO - Mil Med 2002 Feb;167(2):99-103
AD - Air Force Medical Genetics Center, Keesler Air Force Base, MS 39534,
USA.
The Department of Defense Familial Breast/Ovarian Cancer Research
Project has offered genetic counseling and testing for BRCA1 and BRCA2
on a research basis to patients meeting specific diagnostic criteria,
with risk for BRCA1 and BRCA2 mutations calculated based on the Couch
model. In 2.5 years, 250 patients were evaluated and 101 patients met
criteria requirements, including 33 who met criteria in more than one
category. Ninety patients elected to undergo DNA testing. In this group
of 90 patients, 14 mutations (15.5%) and 16 unclassified variants
(17.7%) were identified. The most common inclusion criteria were onset
of breast/ovarian cancer before age 45 years (n = 32) and onset of
breast/ovarian cancer before age 45 years with strong family history (n
= 21). However, when number of mutations and unclassified variants found
were compared separately across all diagnostic criteria (including those
of more than one capacity) using the chi 2 statistic, no significant
differences were seen among the categories to suggest that one criterion
was more predictive of mutations or variants than another. Couch risk
values for patients with mutations showed a mean of 14% and ranged from
3.2 to 43.5% (range for all patients, 1.2-69.7%). These findings
emphasize the importance of using multiple diagnostic criteria and
suggest that a Couch risk value of > 3% may be useful in selecting
patients for testing. The data also underscore the necessity of genetic
counseling in the testing process, particularly given the large number
of unclassified variants diagnosed and their uncertain status for
disease predisposition.
6
UI - 11883264
AU - Czekierdowski A; Bednarek W; Rogowska W; Kotarski J
TI -
[Difficulties in differential diagnosis of adnexal masses during
pregnancy: the role of greyscale and color doppler sonography]
SO - Ginekol Pol 2001 Dec;72(12A):1281-6
AD - I Katedry i Kliniki Ginekologii Operacyjnej AM w Lublinie.
We have attempted to determine the accuracy of greyscale and color
Doppler ultrasound in the differentiation of adnexal masses in
pregnancy. The studied group included 2245 pregnant women from low risk
population. Following criteria were evaluated: maximal diameter and
volume of the tumor, echogenicity, presence of septa and papillary
projections in grey scale sonography. Color Doppler analysis included
blood vessel presence and arrangement and blood flow characteristics
with the use of pulsatility (PI), resistive (RI) and systolic/diastolic
(S/D) indices. Preoperative CA-125 serum levels were available in 11
patients. In 66 (2.94%) patients adnexal tumors were detected during
routine ultrasound scan at the end of the first trimester. Twenty-seven
masses (1.2%) persisted beyond 16 weeks of gestation and were
subsequently surgically removed. Pathological diagnosis confirmed 19
serous cystadenomas, 4 endometriomas and 2 dermoids, one pedunculated
myoma and one fibrothecoma. Mean size of the tumors was 79 Jmm (range:
43-245 mm), mean volume 166. lml (range: 30-1320 ml). Doppler indices
values presented as mean, SD and range were as follows: PI = 1.26 +/-
0.71 (range: 0.57-3.84); RI = 0.61 +/- 0.15 (range: 0.33-0.89) and S/D =
2.62 +/- 0.98 (range: 1.17-4.91). Median serum concentration of CA-125
was 17 IU/ml (range: 8.4-1247 IU/ml). Only 3 of these women had elevated
(> 35 IU/ml) levels: 2 endometriomas (344 IU/ml and 1247 IU/ml) and one
myoma (37 IU/ml), respectively. Based on the sonographic findings two
solid tumors were incorrectly classified as probably malignant
(fibrothecoma and subserous myoma). Negative predictive value of
ultrasound diagnosis in the studied population was therefore 92.6% (25
of 27). We conclude that although prenatal sonography has the potential
to correctly classify most of adnexal masses, caution in risk assessment
is needed especially when persistent solid tumor is found.
7
UI - 11883294
AU - Nowak M; Szpakowski M; Malinowski A; Wieczorek A; Maciolek-Blewniewska
TI -
G; Wilczynski JR; Szpakowski A; Wierzbicka E; Malafiej E; Oszukowski P
[Serum cytokines in patients with ovarian cancer and benign ovarian
cysts]
SO - Ginekol Pol 2001 Dec;72(12A):1444-8
AD - Kliniki Chirurgii Ginekologicznej Instytutu Centrum Zdrowia Matki Polki
w Lodzi.
The aim of our study was to evaluate serum interleukin-6 (IL-6),
interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-alpha) and
interferon-gamma (IFN-gamma) as tumor markers--study based on the data
about tumor cytokines production and tumor-host interactions. METHODS:
We investigated 48 women: 17 with ovarian cancer untreated before, 16
with benign ovarian cysts and 15 healthy controls. Venous blood for
cytokines determinations were obtained before operations and during
routine screening tests. Titers of cytokines were measured by means of
ELISA technique. RESULTS: In the control group the upper limit of normal
IL-6 titers (95th percentile) was 5.5 pg/ml; the mean IL-8 concentration
was 9.6 +/- 15.1 pg/ml and the upper limit of normal was 37 pg/ml; serum
TNF-alpha and IFN-gamma were not detectable. In patients with benign
ovarian cysts the levels of all investigated cytokines didn't differ
significantly from healthy controls. Women with ovarian cancer had
significantly higher serum IL-8 levels (mean: 290.5 +/- 351 pg/ml) than
healthy controls or women with benign ovarian cysts; 88% of them had
IL-8 titers above the normal. The IL-6 titers in ovarian cancer were
also higher but didn't reach statistical significance, 53% of them had
IL-8 titers above the normal. TNF-alpha and IFN-gamma levels in ovarian
cancer were similar to patients with benign ovarian cysts. CONCLUSION:
Serum IL-8 levels in patients with ovarian cancer were significantly
higher when compared to healthy controls and benign ovarian cysts and in
almost 90% of ovarian cancers the titers of IL-8 were increased.
Additionally, 53% of women with ovarian cancer had elevated serum IL-6
levels.
8
UI - 11883295
AU - Bidzinski M; Krynicki R; Lindner B; Sobiczewski P; Panek G; Wierzba W;
TI -
Lewandowski Z
[Granulosa cell tumor--the assessment of some clinical and therapeutic
parameters as prognostic factors]
SO - Ginekol Pol 2001 Dec;72(12A):1449-54
AD - Kliniki Nowotworow Narzadow Plciowych Kobiecych Centrum Onkologii w
Warszawie.
The results of the clinical and therapeutic factors in prognostic mean
was presented. 48 cases of granulosa cell tumours treated from 1984 to
1994 in Oncology Centre in Warsaw were analysed. In investigated group
13 patients died, but only 8 because of relapse of the tumour. Among all
analysed patients, 79% have reached 5 years free survival period. Tumour
rupture, FIGO stage and incidence of irregular bleeding before
recognition of the tumour had significant prognostic value. There were
surprising that relative risk of relapse between patients stage I and II
were similar (1.0 vs 1.01). The relative risk between I and III stage
had strong prognostic difference. Additional operation after no radical
surgery did not influence on better prognosis, but followed radiotherapy
increase treatment results.
9
UI - 11925112
AU - Skates SJ
TI -
Screening for ovarian cancer-risk, education, worry: path to appropriate
use?
SO - Gynecol Oncol 2002 Apr;85(1):1-2
10
UI - 11925113
AU - Andersen MR; Peacock S; Nelson J; Wilson S; McIntosh M; Drescher C;
TI -
Urban N
Worry about ovarian cancer risk and use of ovarian cancer screening by
women at risk for ovarian cancer.
SO - Gynecol Oncol 2002 Apr;85(1):3-8
AD - Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA.
Rander@fhcrc.org
OBJECTIVE: This study examined reports of perceived risk of ovarian
cancer, worry, and screening use in a large sample of women. While
screening for asymptomatic women is not generally recommended, in 1994 a
consensus conference concluded that women with multiple affected
relatives are at high risk for ovarian cancer and should be encouraged
to participate in screening. The consensus report also suggested that
women with a single affected first-degree relative are at elevated risk
and while these women were not encouraged to get screening it was
suggested that they may choose to pursue screening outside of a
randomized trial [NIH Consensus Conference. JAMA 1995;273(6) 491-7].
METHODS: A total of 3257 women participated in this research by
completing a mailed survey on ovarian cancer risk, worry, and use of
screening. One hundred forty-two of these women were at high risk for
this disease due to a strong family history. An additional 144 women
were at elevated risk due to a single first-degree affected relative
with ovarian cancer. RESULTS: Family history did predict perceived risk,
difficulties due to worry, and use of ovarian cancer screening. However,
the group of women most likely to report high levels of perceived risk
and to have received screening for ovarian cancer were women with a
single affected relative rather than those at high risk, for whom
screening is recommended. CONCLUSIONS: These results suggest that many
women need additional education about ovarian cancer risk. Most women
overestimated their risk for this disease. Some average-risk women get
screening although it is not recommended outside of randomized trials,
and a significant percentage of women at high risk fail to get
recommended screening.
11
UI - 11925118
AU - Fei R; Shaoyang L
TI -
Combination antigene therapy targeting c-myc and c-erbB(2) in the
ovarian cancer COC(1) cell line.
SO - Gynecol Oncol 2002 Apr;85(1):40-4
AD - Department of Gynecologic Oncology, Zhongnan Hospital, Wuhan University,
169 Donghu Road, Wuhan, 430071, People's Republic of China.
OBJECTIVE: Antigene therapy targeting only one oncogene in ovarian
cancer has made much progress, although it still has some limitations.
To explore the potential for combination antigene therapy in ovarian
cancer, we examined the in vitro effects of liposmal antisense
phosphorothioate oligodeoxynucleotides targeting c-erbB(2) and c-myc
(LF-c-erbB(2)/c-myc AS-ODNs) in the human ovarian cancer COC(1) cell
line. METHODS: COC(1) cells were treated differently as follows: group A
with single LF-c-erbB(2) AS-ODNs; group B with single LF-c-myc AS-ODNs;
group C with combination LF-c-erbB(2)/c-myc AS-ODNs; and group D as
untreated control. Cell proliferation was studied by MTT assay and
clonal cultures. RT-PCR was used to measure gene expression of c-erbB(2)
and c-myc before and after transfection. Morphologic changes in the
COC(1) cells were observed with the electron microscope. RESULTS: Single
antigene therapy targeting c-erbB(2) or c-myc could reduce target gene
expression and inhibit COC(1) cell growth by 61.9 +/- 9.3 and 64.5 +/-
11.2%, respectively. However, combination antigene therapy could not
only suppress expression of c-erbB(2) and c-myc simultaneously, but also
inhibit COC(1) cell proliferation with a higher inhibitory rate of 82.6
+/- 12.1%. Apart from that, the combination agents could induce COC(1)
cell apoptosis. CONCLUSIONS: Our study suggests that combination
antigene therapy targeting c-erbB(2) and c-myc can inhibit COC(1) cell
proliferation and gene expression of c-erbB(2) and c-myc. Furthermore,
its effectiveness is much higher than that of individual antigene
therapy.
12
UI - 11925120
AU - Makhija S; Howden N; Edwards R; Kelley J; Townsend DW; Meltzer CC
TI -
Positron emission tomography/computed tomography imaging for the
detection of recurrent ovarian and fallopian tube carcinoma: a
retrospective review.
SO - Gynecol Oncol 2002 Apr;85(1):53-8
AD - Division of Gynecologic Oncology, University of Alabama at Birmingham,
35243, USA.
PURPOSE: Imaging modalities to evaluate ovarian/fallopian tube cancer
patients for recurrence are limited. Positron emission tomography (PET),
computed tomography (CT), magnetic resonance imaging (MRI), and
ultrasound lack the sensitivity to consistently detect recurrence or
measurable disease in these patients. A new technique combines PET and
CT (PET/CT) images to identify increased metabolic activity and to
locate that signal with improved anatomic specificity. The objective of
this study is to compare PET/CT, CT, and histologic findings in patients
with recurrent ovarian/fallopian tube cancers. METHODS: Retrospective
chart review of eight patients with primary ovarian (n = 6) or fallopian
tube (n = 2) cancer was performed. All eight patients underwent initial
cytoreductive surgery. Five patients initially received chemotherapy,
one received radioactive phosphorus ((32)P), one received tamoxifen, and
one received no therapy. Seven of eight patients had a suspected
recurrence based on clinical examination, elevated CA-125 level, and/or
abnormal CT findings; one patient requested a PET/CT. Histologic
findings from surgery were correlated with PET/CT and CT findings.
RESULTS: All eight patients had positive histology, and of these, seven
patients had a negative CT and five patients had lesions that were
correctly identified by PET/CT. CONCLUSIONS: Five of the eight (62%)
patients had recurrent disease based on correlative histology with a
positive PET/CT and a negative CT. These preliminary findings suggest
that combined PET/CT may be an effective means of identifying patients
with recurrent ovarian/fallopian tube cancer. Such patients could
potentially proceed to salvage treatment and avoid the morbidity and
expense of surgical assessment. Pilot studies comparing CT, PET, PET/CT,
and histologic findings are underway.
13
UI - 11925114
AU - Piver MS
TI -
Hereditary ovarian cancer. Lessons from the first twenty years of the
Gilda Radner Familial Ovarian Cancer Registry.
SO - Gynecol Oncol 2002 Apr;85(1):9-17
AD - Founder and Director of the Gilda Radner Familial Ovarian Cancer
Registry, Roswell Park Cancer Institute, Buffalo, New York 14263, USA.
mpiver@wnychs.org
14
UI - 11985374
AU - Anonymous
TI -
Management of advanced-stage ovarian cancer: median survival rate about
2-3 years.
SO - Prescrire Int 2002 Feb;11(57):24-5
(1) Most cases of ovarian cancer are diagnosed at an advanced stage
(peritoneal extension beyond the pelvis or distant metastases). (2) The
standard treatment is surgery followed by chemotherapy with paclitaxel +
platinum salt. Data favouring carboplatin over cisplatin in this setting
are of poor quality. (3) There is no standard second-line chemotherapy
regimen.
15
UI - 11966485
AU - Sayedur Rahman M; Al-Sibai MH; Rahman J; Al-Suleiman SA; El-Yahia AR;
TI -
Al-Mulhim AA; Al-Jama F
Ovarian carcinoma associated with pregnancy. A review of 9 cases.
SO - Acta Obstet Gynecol Scand 2002 Mar;81(3):260-4
AD - Department of Obstetrics, University of Garyounis, Benghazi, Libya.
paparahman@hotmail.com
BACKGROUND: The purpose of this study was to review patients with
ovarian cancer in pregnancy, the effectiveness of the available methods
of treatment and their prognosis. METHODS: A retrospective review of all
women diagnosed to have cancer of the ovary associated with pregnancy
diagnosis, treatment, pregnancy outcome and maternal survival were
noted. RESULTS: The incidence of ovarian carcinoma in pregnancy in the
series was 0.08/1000 deliveries. Of the 9 patients, 7 had epithelial
cancers; 4 serous cystadenocarcinoma, 2 mucinous cystadenocarcinomas and
one undifferentiated cancer. One patient each had dysgerminoma and
granulosa cell tumor. Six patients were in FIGO stage Ia, one Ic, one
IIa. One patient was in stage III. Five patients were treated by
unilateral salpingo-oophorectomy during pregnancy. Three patients had
total abdominal hysterectomy, bilateral salpingo-oophorectomy and
omentectomy followed by chemotherapy. Debulking of the tumor was done in
a patient in stage III with subsequent chemotherapy. This patient died
13 months from the time of diagnosis of the tumor. The overall 5-year
survival rate in the series was 78% and 100% for stage Ia. CONCLUSIONS:
Association of ovarian cancer with pregnancy is a rare occurrence. Early
diagnosis and appropriate treatment offers the best prognosis for the
patient. The higher survival rates in the series was attributed to a
larger number of patients in stage I of the disease and 2 patients with
a germ cell tumor and dysgerminoma which have the best prognosis.
Aggressive postoperative chemotherapy also contributed to the better
outcome.
16
UI - 11965550
AU - Bingle L; Singleton V; Bingle CD
TI -
The putative ovarian tumour marker gene HE4 (WFDC2), is expressed in
normal tissues and undergoes complex alternative splicing to yield
multiple protein isoforms.
SO - Oncogene 2002 Apr 18;21(17):2768-73
AD - Respiratory Medicine Unit, Division of Genomic Medicine, University of
Sheffield Medical School, Sheffield S10 2RX, UK.
The whey acidic protein (WAP) domain is a conserved motif, containing
eight cysteines found in a characteristic 4-disulphide core arrangement,
that is present in a number of otherwise unrelated proteins. WAP motifs
are present in SLPI and elafin, two antiproteinases located on
chromosome 20q12-13, in a locus rich in poorly characterized WAP domain
proteins. One of these proteins, which contains two WAP domains, is HE4
(also known as WFDC2), originally described as an epididymis specific
protein but more recently suggested to be a putative serum tumour marker
for ovarian cancer. We have shown that HE4 is expressed in a number of
normal human tissues outside of the male reproductive system, including
regions of the respiratory tract and nasopharynx, as well as in a subset
of lung tumour cell lines. Comparison of multiple HE4 cDNAs and RT-PCR
products with genomic sequence allowed the elucidation of the genomic
organization. These studies revealed that HE4 can undergo a complex
series of alternative splicing events that can potentially yield five
distinct WAP domain containing protein isoforms. These results cast
doubt on the potential role of HE4 as a serum tumour marker specific for
ovarian cancer and open the door to understanding the function of
multiple WAP domain containing protein isoforms arising from a single
gene.
17
UI - 11904463
AU - Nielsen B; Albregtsen F; Kildal W; Danielsen HE
TI -
Prognostic classification of early ovarian cancer based on very low
dimensionality adaptive texture feature vectors from cell nuclei from
monolayers and histological sections.
SO - Anal Cell Pathol 2001;23(2):75-88
AD - Department of Informatics, University of Oslo, P.O.Box 1080 Blindern,
N-0316 Oslo, Norway. birgitn@ifi.uio.no
In order to study the prognostic value of quantifying the chromatin
structure of cell nuclei from patients with early ovarian cancer, low
dimensionality adaptive fractal and Gray Level Cooccurrence Matrix
texture feature vectors were extracted from nuclei images of monolayers
and histological sections. Each light microscopy nucleus image was
divided into a peripheral and a central part, representing 30% and 70%
of the total area of the nucleus, respectively. Textural features were
then extracted from the peripheral and central parts of the nuclei
images.The adaptive feature extraction was based on Class Difference
Matrices and Class Distance Matrices. These matrices were useful to
illustrate the difference in chromatin texture between the good and bad
prognosis classes of ovarian samples. Class Difference and Distance
Matrices also clearly illustrated the difference in texture between the
peripheral and central parts of cell nuclei. Both when working with
nuclei images from monolayers and from histological sections it seems
useful to extract separate features from the peripheral and central
parts of the nuclei images.
18
UI - 11809533
AU - Baxter SW; Choong DY; Campbell IG
TI -
Microsomal epoxide hydrolase polymorphism and susceptibility to ovarian
cancer.
SO - Cancer Lett 2002 Mar 8;177(1):75-81
AD - VBCRC Cancer Genetics Laboratory, Peter MacCallum Cancer Institute,
Locked Bag No. 1 A'Beckett Street, Melbourne, Victoria, 8006, Australia.
Polymorphic variants of microsomal epoxide hydrolase (mEPHX) with
altered enzyme activity have been associated with an increased risk for
ovarian cancer. We assessed the frequency of exon 3 and exon 4 variants
of mEPHX among 291 ovarian cancers and 257 controls from a UK-based
population. The distribution of the exon 3 alleles among both the cancer
and control groups was significantly different from that expected under
Hardy-Weinberg equilibrium suggesting that the PCR restriction fragment
length polymorphism (PCR-RFLP) genotyping assay might be flawed. The
codon 113 polymorphism was reassessed using a two-color allele-specific
PCR-based assay. We found that a codon 119 G>A polymorphism, present in
20% of the British population and linked to the wild-type exon 3 allele,
resulted in some Tyr113/His113 heterozygotes being falsely classified as
His113/His113 homozygotes when using the PCR-RFLP assay. Consequently,
we reassessed all our codon 113 data using the new allele-specific
assay. We found no evidence of an association of ovarian cancer risk
with the exon 3 Tyr113>His113 variant. Similarly the frequencies of the
exon 4 His139>Arg139 genotypes were not significantly different between
cases and controls. Stratifying the genotyping data according to the
predicted mEPHX activity revealed a highly significant decrease in high
mEPHX activity among the serous ovarian cancers (P=0.01) suggesting that
high mEPHX activity may be protective for this histological sub-type.
Furthermore previous disease association studies of exon 3 alleles which
utilized the PCR-RFLP assay may be compromised by the existence of a
codon 119 G>A polymorphism which may be common in Caucasian populations.
19
UI - 11977628
AU - Yan C; Tian F; Xiao F; Li K; Li C
TI -
[Adhesion induces matrix metalloproteinase-9 gene expression in ovarian
cancer cells]
SO - Zhonghua Zhong Liu Za Zhi 2002 Jan;24(1):17-9
AD - Department of Tumor Molecular Biology, Reseach Clinic, Academy of
Military Medical Sciences, Beijing 100039, China.
OBJECTIVE: This work was conducted to investigate the expression of
matrix metalloproteinase 9 (MMP 9) gene in cancer cells by fibronectin
adhesion and the underlying mechanism of cell invasion. METHODS:
Following adhesion of ovarian cancer cells A2780 to fibronectin, mRNA
expression of MMP cells were assayed by reverse transcription-polymerase
chain reaction (RT-PCR). MMP9 promoter was cloned from genomic DNA of
HT1080 cells with PCR. The MMP-9-pGL2 reporter gene vector was
constructed and then transiently transfected into A2780 cells. RESULTS:
Adhesion induced the increase of cellular MMP9 mRNA content in A2780
cells, not affecting the expression of MMP2 or TIMP-1 gene. The
stimulation was enhanced with the increase adhesion time. When the
transfected cells were allowed to adhere and spread on FN-coated
surface, the promoter activity of MMP9 gene was also enhanced
dramatically. CONCLUSION: Cell-ECM adhesion may stimulate the expression
of MMP9 gene through stimulating the promoter activity, thereby
enhancing cancer cell invasion and metastasis.
20
UI - 11979089
AU - Slomovitz BM; Caputo TA; Gretz HF 3rd; Economos K; Tortoriello DV;
TI -
Schlosshauer PW; Baergen RN; Isacson C; Soslow RA
A comparative analysis of 57 serous borderline tumors with and without a
noninvasive micropapillary component.
SO - Am J Surg Pathol 2002 May;26(5):592-600
AD - Department of Obstetrics and Gynecology, New York Presbyterian
Hospital-Weill Medical College of Cornell University, New York, New
York, USA.
The literature concerning serous borderline tumors with a noninvasive
micropapillary component suggests an association with invasive implants.
We compared the clinicopathologic features of micropapillary serous
borderline tumors (MSBTs) with typical SBTs to determine the following:
1) the importance of focal micropapillary architecture in an otherwise
typical SBT, 2) the behavior of low-stage MSBTs, 3) whether high-stage
MSBTs are inherently more aggressive than high-stage SBTs, and 4)
whether invasive implants are prevalent in an MSBT cohort without
referral selection bias. The 57 borderline tumors studied were diagnosed
at a university hospital between 1981 and 1998; they included 14 MSBTs,
35 SBTs, and 8 SBTs with focal micropapillary features. None of the
specimens were referrals for expert pathologic consultation, thus
distinguishing our study group from most of those previously reported.
Neither MSBTs nor SBTs were associated with invasive implants at
diagnosis (0 of 14 and 0 of 43, respectively). They also did not differ
with respect to overall stage at diagnosis, but MSBTs were more
frequently bilateral than SBTs (71% versus 23%, p = 0.001). There was an
increased risk of recurrence in MSBT versus SBT (3 of 14 versus 1 of 43,
p = 0.035), but this was stage related; there was no difference between
groups when evaluating recurrence in stage I disease (0 of 8 versus 0 of
27). There was no difference in recurrence or stage at diagnosis between
SBTs with focal micropapillary features and other SBTs. There was 100%
survival in all groups. We conclude that high-stage MSBTs with
noninvasive implants should be considered a subtype of SBTs with an
increased risk of recurrence. Stage I MSBTs demonstrate clinical
features that are similar to low-stage SBTs. Focal micropapillary
architecture (<5 mm) has no bearing on outcome. MSBTs in the general
population are not strongly associated with invasive implants.
21
UI - 11774353
AU - Smith DI
TI -
Transcriptional profiling develops molecular signatures for ovarian
tumors.
SO - Cytometry 2002 Jan 1;47(1):60-2
AD - Mayo Clinic Cancer Center, Rochester, Minnesota 55905, USA.
smith.david@mayo.edu
Of the cancers unique to women, ovarian cancer has the highest mortality
rate. Over 26,000 women are diagnosed with this disease in the U.S.
annually, and 60% of those diagnosed will die of the disease. One of the
greatest problems with this disease is the lack of strong early warning
signs or symptoms resulting in advanced stage at presentation in most
women, followed by the outgrowth of chemotherapy-resistant disease in
the majority of patients. The 5-year survival for patients with early
stage disease ranges from 50-90%, but it is less than 25% for
advanced-stage disease. In collaboration with researchers at Millennium
Predictive Medicine (Cambridge, MA), the Ovarian Cancer Program of the
Mayo Clinic Cancer Center analyzed gene expression in over 50 primary
ovarian tumors, as compared with normal ovarian epithelial cells. The
technologies utilized included microarray analysis with nitrocellulose
filters containing 25,000 arrayed human cDNAs, as well as the
construction of subtraction suppression hybridization cDNA libraries and
their subsequent sequencing. Our specific focus has been on genes that
are underexpressed during the development of ovarian cancer, although
this analysis has revealed a large number of consistently up- and
down-regulated genes. There were more down-regulated genes in ovarian
tumors than up-regulated genes. In addition, the number of genes that
had altered expression levels was quite large. For example, we found 409
genes down-regulated at least 5-fold, and 72 genes up-regulated at least
5-fold in 33% of the tumors analyzed. We also observed that most of the
expression alterations observed in later stage (Stages III/IV) tumors
were also observed in early-stage tumors (Stages I/II). This was
corroborated using comparative genomic hybridization analysis on the
same tumors that were expression profiled. This analysis revealed that
the late-stage tumors had more gene amplification than early-stage
tumors, but most regions of change (either increases or decreases) were
in common between different stage tumors. We also have verified the
altered expression levels of several of these genes using several
complementary strategies. Finally, we are taking top candidate genes
that are consistently under-expressed in ovarian tumors and attempting
to determine their functional role in the development of ovarian cancer.
Copyright 2001 Wiley-Liss, Inc.
22
UI - 11992642
AU - Kolfschoten GM; Hulscher TM; Duyndam MC; Pinedo HM; Boven E
TI -
Variation in the kinetics of caspase-3 activation, Bcl-2 phosphorylation
and apoptotic morphology in unselected human ovarian cancer cell lines
as a response to docetaxel.
SO - Biochem Pharmacol 2002 Feb 15;63(4):733-43
AD - Department of Medical Oncology, Vrije Universiteit Medical Centre,
Amsterdam, The Netherlands.
Paclitaxel is able to cause cell death through the induction of
apoptosis. Cell death characteristics for docetaxel have not yet been
described in detail. We investigated four unselected human ovarian
cancer cell lines for the sensitivity to a 1hr exposure to docetaxel and
calculated the concentrations inhibiting 50% (IC(50)) and 90% (IC(90))
of cell growth. Of the cell lines A2780, H134, IGROV-1 (all wild-type
p53) and OVCAR-3 (mutant, mt p53) A2780 was most sensitive and OVCAR-3
least sensitive. Equitoxic drug concentrations representing IC(90)
values (25-510nM) were applied for 1hr to measure cell cycle
distribution, DNA degradation, and to count apoptotic cell bodies and
cells with multifragmented nuclei at various time-points after drug
exposure. H134, IGROV-1 and OVCAR-3 showed a continued mitotic block up
to at least 72hr and prolonged presence of cells with multifragmented
nuclei. High percentages of apoptosis were calculated at 48hr and at
later time-points. In contrast, A2780 cells accumulated in the S-phase
of the cell cycle and apoptosis was hardly present. The changes in the
expression levels of p53, p21/WAF1, Bax and Bcl-2, were not predictive
for docetaxel-induced apoptosis. Caspase-3 activation occurred only in
cells with accumulation in the G2/M phase starting as early as 8hr in
OVCAR-3. Prolonged Bcl-2 phosphorylation was evident in OVCAR-3, visible
at 24hr in H134 and IGROV-1, while this phenomenon did not occur in
A2780. The mitogen-activated protein kinase pathway (JNKs/SAPKs or c-Jun
N-terminal kinases/stress-activated protein kinases, JNK1/2;
extracellular response kinase, ERK1/2; p38) did not seem to be directly
involved in Bcl-2 phosphorylation or apoptosis. We conclude that
docetaxel is able to activate caspase-3, induce Bcl-2 phosphorylation
and apoptosis in cells that show a prolonged G2/M arrest, but cells may
also die by a caspase-3-independent cell death mechanism.
23
UI - 11570410
AU - Gjorgov AN
TI -
Tubal ligation and risk of ovarian cancer.
SO - Lancet 2001 Sep 8;358(9284):843-4; discussion 844
24
UI - 11799032
AU - Kirwan JM; Tincello DG; Herod JJ; Frost O; Kingston RE
TI -
Effect of delays in primary care referral on survival of women with
epithelial ovarian cancer: retrospective audit.
SO - BMJ 2002 Jan 19;324(7330):148-51
AD - Liverpool Women's Hospital. john.kirwan@lwh-tr.nwest.nhs.uk
OBJECTIVE: To examine referral pathways from primary care for patients
with epithelial ovarian cancer and to identify factors related to
survival at 18 months. DESIGN: Retrospective review of patient notes.
SETTING: General practices and receiving hospitals within Mersey region.
SUBJECTS: 135 patients with epithelial ovarian cancer identified from an
audit in the Mersey area between 1992 and 1994. MAIN OUTCOME MEASURES:
Delays between onset of symptoms and treatment attributable to patient,
general practitioner, and hospital. RESULTS: 105 (78%) women first
presented to their general practitioner within four weeks of the onset
of symptoms. 99 (73%) women were referred to hospital by their general
practitioners within four weeks of presentation, and 95 (70%) were seen
in hospital within two weeks of referral. Multivariate analysis with
survival as the dependent variable identified age (odds ratio 0.96, 95%
confidence interval 0.93 to 0.99) cancer stage III or more (0.15, 0.05
to 0.43), and non-specific symptoms (0.36, 0.14 to 0.89) as significant
variables. CONCLUSION: Most patients attended their general practitioner
within four weeks and were referred within two weeks. No evidence was
found that delays in referral or diagnosis adversely affected survival
at 18 months. Stage of disease at surgery was the most important adverse
factor. An effective screening programme is the most likely method to
improve survival.
25
UI - 11860053
AU - Benazon NR; Coyne JC; Calzone KA; Weber BL
TI -
Why not to screen high-risk women anticipating BRCA1/BRCA2 testing for
psychological distress.
SO - J Consult Clin Psychol 2002 Feb;70(1):258
26
UI - 11930570
AU - Seiser BV
TI -
Ovarian cancer strategies for nurse practitioners.
SO - J Am Acad Nurse Pract 2001 Aug;13(8):359-63
AD - Wausau Family Practice Center, Wausau, WI, USA.
bseiser@wausau.fammed.wisc.edu
PURPOSE: To review and outline practical strategies for the effective
detection and prevention of ovarian cancer. DATA SOURCES: Selected
scientific literature, government consensus findings, and the author's
experience. CONCLUSIONS: Ovarian cancer is the fourth most common cause
of cancer death in American women, ranking behind lung, breast, and
colorectal cancer. Seventy-five percent of ovarian cancers are currently
diagnosed at an advanced stage. IMPLICATIONS FOR PRACTICE: No
cost-effective screening methods are currently available. The battle to
beat ovarian cancer is based on four strategies: identification of risk
factors, appropriate screening methods, early detection, and prevention.
27
UI - 11995270
AU - Alexander-Sefre F; Menon U; Jacobs IJ
TI -
Ovarian cancer screening.
SO - Hosp Med 2002 Apr;63(4):210-3
AD - Department of Gynaecological Oncology, St Bartholomew's and the Royal
London Medical and Dental School, London EC1A 7BE.
Ovarian cancer is the fourth commonest cause of cancer deaths in women.
Multimodal screening with serum CA125 and transvaginal ultrasonography
have been shown to improve survival. However, the results so far do not
justify routine screening until the impact of screening on mortality has
been assessed in larger randomized trials.
28
UI - 11991929
AU - Elwood M
TI -
Study of effect of delays on ovarian cancer was weak.
SO - BMJ 2002 May 4;324(7345):1100
29
UI - 11932746
AU - Judson H; Hayward BE; Sheridan E; Bonthron DT
TI -
A global disorder of imprinting in the human female germ line.
SO - Nature 2002 Apr 4;416(6880):539-42
AD - University of Leeds, Molecular Medicine Unit, St. James's University
Hospital, UK.
Imprinted genes are expressed differently depending on whether they are
carried by a chromosome of maternal or paternal origin. Correct
imprinting is established by germline-specific modifications; failure of
this process underlies several inherited human syndromes. All these
imprinting control defects are cis-acting, disrupting establishment or
maintenance of allele-specific epigenetic modifications across one
contiguous segment of the genome. In contrast, we report here an
inherited global imprinting defect. This recessive maternal-effect
mutation disrupts the specification of imprints at multiple,
non-contiguous loci, with the result that genes normally carrying a
maternal methylation imprint assume a paternal epigenetic pattern on the
maternal allele. The resulting conception is phenotypically
indistinguishable from an androgenetic complete hydatidiform mole, in
which abnormal extra-embryonic tissue proliferates while development of
the embryo is absent or nearly so. This disorder offers a genetic route
to the identification of trans-acting oocyte factors that mediate
maternal imprint establishment.
30
UI - 11982262
AU - Cummings S
TI -
Weighing the risks. Genetic counseling for hereditary breast and ovarian
cancer.
SO - AWHONN Lifelines 2001 Jun-Jul;5(3):42-7
AD - Cancer Risk Clinic, University of Chicago, Chicago, IL, USA.
31
UI - 12023992
AU - Kauff ND; Satagopan JM; Robson ME; Scheuer L; Hensley M; Hudis CA; Ellis
TI -
NA; Boyd J; Borgen PI; Barakat RR; Norton L; Castiel M; Nafa K; Offit K
Risk-reducing salpingo-oophorectomy in women with a BRCA1 or BRCA2
mutation.
SO - N Engl J Med 2002 May 23;346(21):1609-15
AD - Clinical Genetics Service, Memorial Sloan-Kettering Cancer Center, New
York 10021, USA.
BACKGROUND: Risk-reducing salpingo-oophorectomy is often considered by
carriers of BRCA mutations who have completed childbearing. However,
there are limited data supporting the efficacy of this approach. We
prospectively compared the effect of risk-reducing salpingo-oophorectomy
with that of surveillance for ovarian cancer on the incidence of
subsequent breast cancer and BRCA-related gynecologic cancers in women
with BRCA mutations. METHODS: All women with BRCA1 or BRCA2 mutations
identified during a six-year period were offered enrollment in a
prospective follow-up study. A total of 170 women 35 years of age or
older who had not undergone bilateral oophorectomy chose to undergo
either surveillance for ovarian cancer or risk-reducing
salpingo-oophorectomy. Follow-up involved an annual questionnaire,
telephone contact, and reviews of medical records. The time to cancer in
the two groups was compared by Kaplan-Meier analysis and a Cox
proportional-hazards model. RESULTS: During a mean follow-up of 24.2
months, breast cancer was diagnosed in 3 of the 98 women who chose
risk-reducing salpingo-oophorectomy and peritoneal cancer was diagnosed
in 1 woman in this group. Among the 72 women who chose surveillance,
breast cancer was diagnosed in 8, ovarian cancer in 4, and peritoneal
cancer in 1. The time to breast cancer or BRCA-related gynecologic
cancer was longer in the salpingo-oophorectomy group, with a hazard
ratio for subsequent breast cancer or BRCA-related gynecologic cancer of
0.25 (95 percent confidence interval, 0.08 to 0.74). CONCLUSIONS:
Salpingo-oophorectomy in carriers of BRCA mutations can decrease the
risk of breast cancer and BRCA-related gynecologic cancer.
32
UI - 12023993
AU - Rebbeck TR; Lynch HT; Neuhausen SL; Narod SA; Van't Veer L; Garber JE;
TI -
Evans G; Isaacs C; Daly MB; Matloff E; Olopade OI; Weber BL; The
Prevention and Observation of Surgical End Points Study Group
Prophylactic oophorectomy in carriers of BRCA1 or BRCA2 mutations.
SO - N Engl J Med 2002 May 23;346(21):1616-22
AD - Center for Clinical Epidemiology and Biostatistics, University of
Pennsylvania School of Medicine, Philadelphia 19104-6021, USA.
trebbeck@cceb.med.upenn.edu
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