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Abramson Cancer CenterNCI CANCERLIT® Search: Diagnosis-Histopathology-Pathogenesis of Ovarian Cancer - July 2002
National Cancer Institute®
Last Modified: July 1, 2002
- Cultural basis for differences between US and French clinical recommendations for women at increased risk of breast and ovarian
- Expression of prostaglandin D synthase in ovarian cancer.
- Mutation screening analysis of the retinoblastoma related gene RB2/p130 in sporadic ovarian cancer and head and neck squamous cell cancer.
- Osteopontin as a biomarker for ovarian cancer.
- Clinical value of positron emission tomography with FDG for recurrent ovarian cancer.
- Psychosocial dimensions of BRCA testing: an overshadowed issue.
- Clinical value of positron emission tomography.
- Danazol linked to ovarian cancer.
- [The selection of taxol resistance associated genes in ovarian cancer cell line by mRNA DD]
- Development of a highly specialized cDNA array for the study and diagnosis of epithelial ovarian cancer.
- Asymptomatic adnexal masses: correlation of FDG PET and histopathologic findings.
- A current perspective on genetic testing for breast and ovarian cancer: the oral contraceptive decision.
- Hormonal replacement therapy and ovarian cancer.
- Ovarian tumor cell detection in peripheral blood progenitor cells harvests by RT-PCR.
- Genetics of synchronous uterine and ovarian endometrioid carcinoma: combined analyses of loss of heterozygosity, PTEN mutation, and
- Micronutrients and ovarian cancer: a case-control study in Italy.
- Polymorphisms of the estrogen-metabolizing genes CYP17 and catechol-O-methyltransferase and risk of epithelial ovarian cancer.
- [Borderline ovarian tumors]
- [Structure and function of epidermal growth factor receptors and their significance as a prognostic marker in ovarian carcinoma]
- [Tumor risk in Peutz-Jegher's syndrome]
- Parallel analysis of sporadic primary ovarian carcinomas by spectral karyotyping, comparative genomic hybridization, and expression
- Induction of apoptosis by the new anticancer drug XK469 in human ovarian cancer cell lines.
- [Risk factors for the development of ovarian carcinoma]
- Luteinizing hormone-releasing hormone induces JunD-DNA binding and extends cell cycle in human ovarian cancer cells.
- Allelic imbalance on chromosome 17p13 in borderline (low malignant potential) epithelial ovarian tumors.
- Prophylactic oophorectomy comes of age.
- Peritoneal lavage cytology: an assessment of its value during prophylactic oophorectomy.
- Cell proliferation and apoptosis in BRCA-associated hereditary ovarian cancer.
- Evaluation of prognostic factors and treatment modalities in ovarian cancer patients with brain metastases.
- Dietary fat intake and ovarian cancer in a cohort of US women.
- Gene expression profiling of hereditary and sporadic ovarian cancers reveals unique BRCA1 and BRCA2 signatures.
- Gene expression profiles of BRCA1-linked, BRCA2-linked, and sporadic ovarian cancers.
- Association of dairy products, lactose, and calcium with the risk of ovarian cancer.
- Menopausal hormone replacement therapy and risk of ovarian cancer.
- Estrogen replacement therapy and risk of ovarian cancer.
- Genetic counseling, testing, and screening for breast and ovarian cancer: practical and social considerations.
- Familial ovarian cancer.
- Contribution of BRCA2 germline mutations to hereditary breast/ovarian cancer in Germany.
- Clustering of individuals with both breast and ovarian cancer--a possible indicator of BRCA founder mutations.
- Micropapillary serous carcinoma of the ovary: cytomorphologic characteristics in peritoneal/pelvic washings.
- mRNA detection of tumor-rejection genes BAGE, GAGE, and MAGE in peritoneal fluid from patients with ovarian carcinoma as a potential
- Proteomic patterns in serum and identification of ovarian cancer.
- Stable karyotypes in epithelial cancer cell lines despite high rates of ongoing structural and numerical chromosomal instability.
- Comparative analysis of loss of heterozygosity of specific chromosome 3, 13, 17, and X loci and TP53 mutations in human epithelial ovarian
- Effect of fenretinide on ovarian carcinoma occurrence.
- Long-term survival and patterns of care in women with ovarian tumors of low malignant potential.
- Ovarian cancer p53 mutation is associated with tumor microvessel density.
- Assessment of gene expression profile by cDNA microarray analysis.
- Preoperative CA 125 levels: an independent prognostic factor for epithelial ovarian cancer.
Table of Contents
1
UI - 10094000
AU - Eisinger F; Geller G; Burke W; Holtzman NA
TI -
Cultural basis for differences between US and French clinical
recommendations for women at increased risk of breast and ovarian
cancer.
SO - Lancet 1999 Mar 13;353(9156):919-20
AD - Department of Cancer Control and INSERM CRI 9703, Paoli-Calmettes
Institute, Marseille, France.
2
UI - 11798075
AU - Su B; Guan M; Zhao R; Lu Y
TI -
Expression of prostaglandin D synthase in ovarian cancer.
SO - Clin Chem Lab Med 2001 Dec;39(12):1198-203
AD - Department of Laboratory Medicine, Hua Shan Hospital, Fudan University,
Shanghai, PR China.
Lipocalin-type prostaglandin D synthase (L-PGDS) has recently been shown
to be expressed in human brain tumors and breast tumors. However, L-PGDS
expression has not been investigated in ovarian cancer. The objective of
this study was to determine whether L-PGDS is expressed in human ovarian
cancer. Lipocalin prostaglandin D synthase mRNA was cloned and sequenced
by RT-PCR. Using in situ hybridization (ISH) technique, the expression
of L-PGDS mRNA in 54 ovarian cancer was investigated. Expression of
L-PGDS mRNA was found in tumor cells of all various types of ovarian
cancers. Patterns of staining of tumor cells varied among different
histological types of ovarian cancer. Significant discrepancy between
the intensity of the staining and histological types of ovarian cancer
could be established (p<0.01). It is reported for the first time that
the expression of mRNA of L-PGDS exists in the ovarian cancer, and is
related to the cancer type. This may have significance for the progress
of ovarian cancer.
3
UI - 12032225
AU - Alvi AJ; Hogg R; Rader JS; Kuo MJ; Maher ER; Latif F
TI -
Mutation screening analysis of the retinoblastoma related gene RB2/p130
in sporadic ovarian cancer and head and neck squamous cell cancer.
SO - Mol Pathol 2002 Jun;55(3):153-5
AD - Section of Medical and Molecular Genetics, Department of Paediatrics and
Child Health, University of Birmingham, Birmingham B15 2TT, UK.
AIMS: To investigate the involvement of the RB2/p130 gene in the
pathogenesis of sporadic ovarian cancer in addition to head and neck
squamous cell carcinoma (HNSCC). METHODS: Paired tumour and patient
matched normal DNA samples from 43 sporadic ovarian tumours and 39
normal/tumour HNSCC DNA samples were screened. The mutation screen used
polymerase chain reaction (PCR) amplification followed by single strand
conformation polymorphism analysis and direct sequencing of the PCR
products. Exons 19 and 20 (B domain) and exons 21 and 22 (C-terminus)
were analysed for mutations. These exons were chosen because most of the
point mutations in RB2/p130 are located in the C-terminal region and
mutations in these exons have been identified previously in
nasopharyngeal carcinomas and primary lung tumours. RESULTS: No abnormal
band shifts were seen in the samples analysed, and no bands directly
sequenced revealed the presence of mutations. CONCLUSIONS: Genetic
alterations in the RB2/p130 gene (exons 19-22) are unlikely to be
involved directly in the pathogenesis of sporadic ovarian cancer or
HNSCC.
4
UI - 12076210
AU - Seidman JD
TI -
Osteopontin as a biomarker for ovarian cancer.
SO - JAMA 2002 Jun 26;287(24):3209; discussion 3209-10
5
UI - 11373212
AU - Nakamoto Y; Saga T; Ishimori T; Mamede M; Togashi K; Higuchi T; Mandai
TI -
M; Fujii S; Sakahara H; Konishi J
Clinical value of positron emission tomography with FDG for recurrent
ovarian cancer.
SO - AJR Am J Roentgenol 2001 Jun;176(6):1449-54
AD - Department of Nuclear Medicine and Diagnostic Imaging, Graduate School
of Medicine, Kyoto University Hospital, 54 Shogoin-kawahara-cho,
Sakyo-Ku, Kyoto, 606-8507 Japan.
OBJECTIVE: Recurrence is often a major problem for patients who have
undergone surgery for ovarian cancer. This prospective study was
undertaken to evaluate the clinical contribution of positron emission
tomography (PET) using (18)F-fluorodeoxyglucose (FDG) for recurrent
ovarian cancer. SUBJECTS AND METHODS: Twenty-four women who had
undergone surgery or chemoradiotherapy for histopathologically proven
ovarian cancer were enrolled in this study. Ovarian cancer was thought
to have recurred in 12 of these women because of evidence on
conventional imaging modalities or tumor marker measurements (group A).
Clinical findings for the remaining 12 women showed them to be
disease-free (group B). PET findings for the women were compared with
the final diagnoses obtained by histopathology or by clinical follow-up.
The clinical contribution of PET was assessed by evaluating whether PET
yielded information complementing the findings of conventional
modalities and by examining its impact on treatment. RESULTS: PET gave
valuable information for seven of 12 patients in group A in addition to
the information obtained from findings on conventional imaging, and
treatment was affected in five patients. On the other hand, in group B,
additional information was obtained in only three of 12 patients, and
treatment of only one patient was affected. Overall sensitivity,
specificity, and accuracy of conventional imaging modalities were 72.7%,
75.0%, and 73.3%, respectively, and these rates improved to 92.3%,
100.0%, and 94.4%, respectively, by considering both conventional
imaging modalities and PET findings. CONCLUSION:Our preliminary data
suggest that whole-body PET with FDG can be a complementary modality for
following up patients who have had ovarian cancer, especially patients
believed to be at risk for recurrence.
6
UI - 11829055
AU - Bredart A; Autier P; Riccardo A; Audisio A; Geraghty JG
TI -
Psychosocial dimensions of BRCA testing: an overshadowed issue.
SO - Eur J Cancer Care (Engl) 2001 Jun;10(2):96-9
AD - Psycho-Oncology Research Unit, European Institute of Oncology, Milan,
Italy.
Routine cancer susceptibility testing will soon be feasible in clinical
practice. However, to date, this new technology has entailed many
limitations, including potential adverse psychosocial consequences.
Empirical studies examining these psychosocial aspects are strikingly
scarce, especially in continental European countries. Are we prepared
for managing the psychosocial problems that emerge from widespread
introduction of this practice? Current research do not take into account
cross-cultural variations in attitudes and reactions towards genetic
testing. This paper points to the urgent need for obtaining a more
accurate picture on the psychosocial aspects of breast cancer gene
testing and disclosure in order to design recommendations for
implementation in populations with highly variable cultural and legal
background.
7
UI - 11906897
AU - Laking GR; Price PM
TI -
Clinical value of positron emission tomography.
SO - AJR Am J Roentgenol 2002 Apr;178(4):1030
8
UI - 12067790
AU - Weideman M
TI -
Danazol linked to ovarian cancer.
SO - Lancet Oncol 2002 May;3(5):261
9
UI - 11798816
AU - Cheng G; Tian F; Li Y
TI -
[The selection of taxol resistance associated genes in ovarian cancer
cell line by mRNA DD]
SO - Zhonghua Yi Xue Za Zhi 2000 Jul;80(7):541-3
AD - Department of Obstetrics & Gynecology, Chinese PLA General Hospital,
Beijing, 100853, China.
OBJECTIVE: One of the main reasons of the treatment failure for ovarian
cancer is the emergence of drug resistance in which several genes
involved. The purpose of the study was to select the genes related to
Taxol resistance in ovarian cancer. METHODS: Resistant ovarian cancer
cell line, Skov3/Taxol-25, was established by interval exposure Skov3 to
Taxol. mRNA was compared between Skov3 and Skov3/Taxol-25 by mRNA DD.
RESULTS: Skov3/Taxol-25 showed 44 times increase resistance to Taxol
after 12 months of induction. There were 22 new differential bands
obtained from Skov3/Taxol-25 as compared with Skov3. 18 bands were
special by repeated PCR. In the 5 sub-clones, three clones were
homologous to the known gene. 105/106 base pair of clone 1 were
homologous to tPA (tissue plasminogen activator), 261/268 of clone 3 to
Kiaa 0372, and 406/409 of clone 18 to LDLC. The other 2 ESTs were new
gene segments, which were banked to Genbank with the number of AF120327
and AF120328. The identification by RT-PCR revealed that both tPA and
Kiaa0372 were special genes from Skov3/Taxol-25, while LDLC was
pseudopositive. CONCLUSION: Several genes were involved in the
resistance to Taxol in ovarian cancer. The enhanced expression of tPA
indicated the increased ability of metastasis after the acquisition of
resistance to taxol.
10
UI - 12019173
AU - Sawiris GP; Sherman-Baust CA; Becker KG; Cheadle C; Teichberg D; Morin
TI -
PJ
Development of a highly specialized cDNA array for the study and
diagnosis of epithelial ovarian cancer.
SO - Cancer Res 2002 May 15;62(10):2923-8
AD - Laboratory of Cellular and Molecular Biology, Gerontology Research
Center, National Institute on Aging/NIH, 5600 Nathan Shock Drive,
Baltimore, MD 21224, USA.
Ovarian cancer is a major cause of cancer death in women. Unfortunately,
the molecular pathways underlying ovarian cancer progression are poorly
understood, making the development of novel diagnostic and therapeutic
strategies difficult. On the basis of our previous observations obtained
from serial analysis of gene expression, we have constructed a
specialized cDNA array for the study of ovarian cancer. Small,
specialized arrays have several practical advantages and can reveal
information that is lost in the "noise" generated by irrelevant genes
present in larger arrays. The array, which we named Ovachip, contains
516 cDNAs chosen from our serial analysis of gene expression and cDNA
array studies for their relevance to ovarian cancer. The gene expression
patterns revealed with the Ovachip are highly reproducible and extremely
consistent among the different ovarian specimens tested. This array was
extremely sensitive at differentiating ovarian cancer from colon cancer
based on expression profiles. The Ovachip revealed clusters of
coordinately expressed genes in ovarian cancer. One such cluster, the
IGF2 cluster, is particularly striking and includes the insulin-like
growth factor II, the cisplatin resistance-associated protein, the
checkpoint suppressor 1, the cyclin-dependent kinase 6, and a protein
tyrosine phosphatase receptor. We also identified a cluster of
down-regulated genes that included the cyclin-dependent kinase 7 and
cyclin H. Thus, the Ovachip allowed us to identify previously
unidentified clusters of differentially expressed genes that may provide
new paradigms for molecular pathways important in ovarian malignancies.
Because of the relevance of the arrayed genes, the Ovachip may become a
powerful tool for investigators in the field of ovarian cancer and may
facilitate progress in understanding the etiology of this disease and in
its clinical management.
11
UI - 12034950
AU - Fenchel S; Grab D; Nuessle K; Kotzerke J; Rieber A; Kreienberg R; Brambs
TI -
HJ; Reske SN
Asymptomatic adnexal masses: correlation of FDG PET and histopathologic
findings.
SO - Radiology 2002 Jun;223(3):780-8
AD - Department of Nuclear Medicine, University of Ulm, Steinhovelstrasse 9,
89075 Ulm, Germany. sabine.fenchel@medizin.uni-ulm.de
PURPOSE: To analyze asymptomatic adnexal masses at positron emission
tomography (PET) with fluorodeoxyglucose (FDG) in correlation with
histopathologic findings and evaluate FDG PET for assessing malignancy
in comparison with transvaginal B-mode and Doppler ultrasonography (US)
and magnetic resonance (MR) imaging. MATERIALS AND METHODS: Ninety-nine
patients underwent static FDG PET of the abdomen. US scans were
evaluated according to sonomorphologic scoring systems. Resistance index
of tumor blood vessels was calculated. Transverse and sagittal
T1-weighted MR images obtained before and after intravenous
administration of gadopentetate dimeglumine with a fat-saturation
technique and T2-weighted MR images were acquired at 1.5 T. Adnexal mass
malignancy was first assessed with each modality and then with a
combination of the three techniques. Final diagnosis was made with
histopathologic evaluation. RESULTS: FDG PET depicted seven of 12
malignant and 66 of 87 benign asymptomatic adnexal tumors.
False-negative PET results were obtained in five of seven stage pT1a
cystadenocarcinomas and tumors of low malignant potential but not in
advanced-stage ovarian carcinomas. Small moderately intense FDG
accumulations in the lower pelvis were caused by benign adnexal tumors
or gastrointestinal activity in 21 of 27 cases. The overall
sensitivities and specificities were 58% (95% CI: 27.7, 84.8) and 76%
(95% CI: 65.5, 84.4), respectively, for FDG PET; 92% (95% CI: 61.5,
99.8) and 60% (95% CI: 48.7, 70.1), respectively, for US; 83% (95% CI:
51.6, 97.7) and 84% (95% CI: 74.5, 90.9), respectively, for MR imaging;
and 92% (95% CI: 61.5, 99.8) and 85% (95% CI: 75.8, 91.8), respectively,
for the combination of three modalities. CONCLUSION: Since the
sensitivity of US is as high as that of PET, MR imaging, and the
combination of three modalities, it remains the method of choice for
diagnosis and assessment of asymptomatic adnexal masses.
12
UI - 11965197
AU - Friedenson B
TI -
A current perspective on genetic testing for breast and ovarian cancer:
the oral contraceptive decision.
SO - MedGenMed 2001 Nov 2;3(6):2
AD - Department of Biochemistry and Molecular Biology at the University of
Illinois at Chicago, Chicago, Illinois, USA. molmeddoc@Yahoo.com.
A clinician faces a problem in how best to counsel the woman with a
family history of breast or ovarian cancer about her options for
pregnancy prevention. The physician must guide her as she makes new and
complex decisions. Recent data strongly support an amplified effect of
the estrogens in oral contraceptives for the woman with a genetic risk
for breast cancer. Nonetheless, a woman's immediate need to prevent
pregnancy may be much more important to her than worrying about the
long-term risk of breast cancer. Another factor is that oral
contraceptives prevent ovarian cancer, so the physician may wish to
prescribe them to protect her from ovarian cancer. In some genetic
backgrounds, however, oral contraceptives not only do not prevent
ovarian cancer, but they may raise the risk of breast cancer so
significantly that they should not be taken. With other genetic
backgrounds, oral contraceptives will protect the woman from ovarian
cancer without much effect on her breast cancer risk. When does each of
these cancer risks or benefits become significant? The clinician can
provide an important benefit to a woman who must prevent pregnancy yet
worries about her cancer risk. The physician can help her evaluate the
evidence, with its gaps and uncertainties, in the context of her own
preferences. To assist in this evaluation, this decision aid provides
base-line estimates of the cancer risk that accompanies each of a
woman's options. In some cases, genetic testing is likely to provide
valuable information as she makes choices about contraception and the
risks vs. benefits of different alternatives available to her.
13
UI - 12047299
AU - Tiitinen A
TI -
Hormonal replacement therapy and ovarian cancer.
SO - Acta Obstet Gynecol Scand 2002 Jun;81(6):479-81
AD - Helsinki University Central Hospital, Hus, Finland. aila.tiitinen@hus.fi
14
UI - 12047311
AU - Kurata H; Takakuwa K; Tsuneki I; Aoki Y; Tanaka K
TI -
Ovarian tumor cell detection in peripheral blood progenitor cells
harvests by RT-PCR.
SO - Acta Obstet Gynecol Scand 2002 Jun;81(6):555-9
AD - Department of Obstetrics and Gynecology, Faculty of Medicine, Niigata
University, Japan. tounin@med.niigata-u.ac.jp
BACKGROUND: To evaluate the frequency of tumor cell contamination in
autologous peripheral-blood progenitor cells from patients with ovarian
cancer, and to determine the impact of infusing such cells on relapses
after high-dose chemotherapy. METHODS: Seventy-three samples of
peripheral-blood progenitor cells from 24 ovarian cancer patients were
studied for contaminated tumor cells by cytokeratin 7 and cytokeratin 20
reverse transcriptase polymerase chain reaction. RESULTS: Tumor cell
contamination in peripheral-blood progenitor cells was detected in 11 of
24 patients (46%) and, among these, in four of 11 patients who received
transplantations of peripheral-blood progenitor cells. There was no
trend towards longer relapse-free survival in patients infused with
cytokeratin-negative peripheral-blood progenitor cells as compared with
positive ones. Interestingly, two of four patients who received
transplantations of peripheral-blood progenitor cells containing tumor
cells were free from progression at 20 and 41 months after
transplantation. CONCLUSION: Tumor cell contamination of
peripheral-blood progenitor cells was frequently noted by transcriptase
polymerase chain reaction in patients with ovarian cancer. The
biological and clinical significance of this finding remains to be
elucidated.
15
UI - 12055677
AU - Fujii H; Matsumoto T; Yoshida M; Furugen Y; Takagaki T; Iwabuchi K;
TI -
Nakata Y; Takagi Y; Moriya T; Ohtsuji N; Ohtsuji M; Hirose S; Shirai T
Genetics of synchronous uterine and ovarian endometrioid carcinoma:
combined analyses of loss of heterozygosity, PTEN mutation, and
microsatellite instability.
SO - Hum Pathol 2002 Apr;33(4):421-8
AD - Department of Pathology, Juntendo University School of Medicine, Tokyo,
Japan.
Synchronous development of carcinomas in the endometrium and ovaries is
a fairly common phenomenon, but distinction of a single clonal tumor
with metastasis from 2 independent primary tumors may present diagnostic
problems. To determine clonality and the occurrence of progression, we
microdissected multiple foci from 17 cases of synchronous endometrioid
carcinomas and studied loss of heterozygosity (LOH), microsatellite
instability (MI), and PTEN mutations. In 14 of the 17 cases, genetic
alterations were either homogeneous or found in only some of the foci.
LOH was detected for 10q (4 cases), 17p (2 cases), and 2p, 5q, 6q, 9p,
11q, 13q, and 16q (1 case each). Four cases had the MI phenotype with
discordant MI patterns between both tumor sites, thus indicating a
biclonal or triple clonal process. In 3 of 6 cases with PTEN mutations,
identical mutations in both tumor sites indicated a single clonal
neoplasm. Altogether, 14 synchronous tumors were genetically diagnosed
as follows: single clonal tumor, characterized by concordant genetic
alterations in both tumor sites, including identical LOH, identical PTEN
mutations, and/or identical sporadic allelic instability patterns (4
cases); single clonal tumor with genetic progression, homogeneous LOH or
identical PTEN mutations in both tumor sites and progressive LOH in
ovarian metastatic foci (2 cases); and double (7 cases) or triple clonal
tumors (1 case), determined by discordant PTEN mutations, heterogeneous
LOH, and/or discordant MI patterns. Thus, 35% of synchronous tumors were
monoclonal, 47% were polyclonal, and 18% were undetermined. The
favorable prognosis of synchronous endometrioid carcinomas may be due to
the occurrence of PTEN mutations in both independent and metastatic
tumors, the MI-positive independent primary tumors, and the low
frequency of LOH. Copyright 2002, Elsevier Science (USA). All rights
reserved.
16
UI - 11822759
AU - Bidoli E; Lavecchia C; Talamini R; Negri E; Parpinel M; Conti E;
TI -
Montella M; Carbone MA; Franceschi S
Micronutrients and ovarian cancer: a case-control study in Italy.
SO - Ann Oncol 2001 Nov;12(11):1589-93
AD - Servizio di Epidemiologia, Centro di Riferimento Oncologico, Aviano
Italy. epidemiology@cro.it
BACKGROUND: The role of selected micronutrients, vitamins and minerals
in the aetiology of epithelial ovarian cancer was investigated using
data from a case-control study conducted between 1992 and 1999 in five
Italian areas. PATIENTS AND METHODS: Cases were 1,031 patients with
histologically confirmed incident epithelial ovarian cancer. Controls
were 2,411 subjects admitted for acute, non-neoplastic diseases to major
hospitals in the same catchment areas. Dietary habits were elicited
using a validated food frequency questionnaire including 78 food groups
and recipes. Odds ratios (OR) and 95% confidence intervals (95% CI) were
computed by quintiles of intake of nutrients. RESULTS: Inverse
associations emerged for vitamin E (OR = 0.6; 95% CI: 0.5-0.8),
beta-carotene (OR = 0.8; 95% CI: 0.6-1.0), lutein/zeaxanthin (OR = 0.6;
95% CI: 0.5-0.8 for the highest vs. the lowest quintile of intake), and
calcium intake (OR = 0.7; 95% CI: 0.6-1.0). When the combined effect of
calcium and vitamin E was considered, the OR reached 0.4 (95% CI:
0.3-0.7) for subjects in the highest compared to those in the lowest
intake tertile of both micronutrients. Results were consistent across
strata of menopausal status, parity and family history of ovarian or
breast cancer. CONCLUSIONS: The intake of selected micronutrients, which
were positively correlated to a diet rich in vegetables and fruits, was
inversely associated with ovarian cancer.
17
UI - 12036914
AU - Garner EI; Stokes EE; Berkowitz RS; Mok SC; Cramer DW
TI -
Polymorphisms of the estrogen-metabolizing genes CYP17 and
catechol-O-methyltransferase and risk of epithelial ovarian cancer.
SO - Cancer Res 2002 Jun 1;62(11):3058-62
AD - Department of Obstetrics, Gynecology, and Reproductive Biology, Brigham
and Women's Hospital, Harvard Medical School, 75 Francis Street, Boston,
MA 02115, USA.
Because some studies have linked polymorphic variants of the
estrogen-metabolizing genes CYP17 and catechol O-methyl transferase
(COMT) with risk for hormonally related cancers, we sought to determine
whether selected polymorphisms of these genes differed between women
with and without ovarian cancer. From a population-based study of
ovarian cancer, we analyzed DNA from a total of 480 cases and controls.
PCR amplification was performed using primers that amplify restriction
sites for MspAI (A2 polymorphism-CYP17) and NlaIII (Val/Met
polymorphism-COMT). Digestion of the PCR products was performed.
Genotypes identified by gel electrophoresis were assigned as homozygous
wild type (WW), heterozygous variant (Wv), and homozygous variant (vv).
Frequencies were compared using chi(2) or Fisher's exact tests. Logistic
regression was used to calculate crude and adjusted relative risks (RRs)
for ovarian cancer associated with possession of any variant allele
overall, and within demographic, weight, and smoking history categories,
and by histological subtype of ovarian cancer. A portion (68.9%) of
cases either carried or was homozygous for the A2 variant of CYP17
compared with 53.9% of controls, for a RR (and 95% confidence interval)
of 1.86 (1.26, 2.75; P = 0.003), adjusted for age, parity, oral
contraceptive use, site of study, and family history of breast or
ovarian cancer. The increased risk was most apparent for women >50 and
women with invasive serous cancers. A portion (71.9%) of cases either
carried or was homozygous for the Val/Met variant of COMT, compared with
76.9% of controls (P = 0.27). Although the inverse association of
ovarian cancer with possession of a Val/Met variant was not significant
overall, it was for mucinous tumors of the ovary, with an adjusted RR of
0.28 (0.13, 0.61; P = 0.0012). Possession of the A2 variant of CYP17
appears to increase risk for ovarian cancer, whereas possession of the
Val/Met variant of COMT decreases the risk for mucinous tumors.
Confirmation in other populations and further exploration of potential
pathogenetic mechanisms will be necessary.
18
UI - 11935694
AU - Ivanov S
TI -
[Borderline ovarian tumors]
SO - Akush Ginekol (Sofiia) 2002;42(1):23-5
AD - Gynaecological Clinic, SBALAG-EAD, Sofia.
Forty three patients with borderline ovarian tumours were examined from
1987 till 2000. 28 patients (65.1%) were serous tumours and 15 patients
(35%) were mucinous. The median age was 42.2 +/- 15.4 years. The
follow-up period was 5.4 +/- 3.2 years. Preoperatively Ca125 were 52.5
+/- 50.3 and of Ca19.9-42.4 +/- 46.8 IU. 83% of the patients were in
stage I and 17% in stage III. There was no significant difference in the
tumour volumes. Ca125 were significantly increased in the serous tumours
and Ca19.9 were increased in the mucinous tumours. All the patients were
followed up and are in good health or remission with exception of 2 who
developed recurrence.
19
UI - 11935696
AU - Tomov S; Gorchev G; Tsingilev D; Kurlov A; Kolnova S
TI -
[Structure and function of epidermal growth factor receptors and their
significance as a prognostic marker in ovarian carcinoma]
SO - Akush Ginekol (Sofiia) 2002;42(1):28-31
20
UI - 12053288
AU - Nguyen HN
TI -
[Tumor risk in Peutz-Jegher's syndrome]
SO - Dtsch Med Wochenschr 2002 Jun 7;127(23):1272-3
AD - Schwerpunkt Gastroenterologie und Stoffwechselkrankheiten, Hubertusstr,
Germany.
21
UI - 12067990
AU - Bayani J; Brenton JD; Macgregor PF; Beheshti B; Albert M; Nallainathan
TI -
D; Karaskova J; Rosen B; Murphy J; Laframboise S; Zanke B; Squire JA
Parallel analysis of sporadic primary ovarian carcinomas by spectral
karyotyping, comparative genomic hybridization, and expression
microarrays.
SO - Cancer Res 2002 Jun 15;62(12):3466-76
AD - Ontario Cancer Institute, Princess Margaret Hospital, University Health
Network, Toronto, Ontario, Canada.
Analysis of ovarian carcinomas has shown that karyotypes are often
highly abnormal and cannot be identified with certainty by conventional
cytogenetic methods. In this study, 17 tumors derived from 13 patients
were analyzed by a combination of spectral karyotyping (SKY),
comparative genomic hybridization (CGH), and expression microarrays.
Within the study group, a total of 396 chromosomal rearrangements could
be identified by SKY and CGH analysis. When the distribution of
aberrations was normalized with respect to relative genomic length,
chromosomes 3, 8, 11, 17, and 21 had the highest frequencies. Parallel
microarray expression studies of 1718 human cDNAs were used to analyze
expression profiles and to determine whether correlating gene expression
with chromosomal rearrangement would identify smaller subsets of
differentially expressed genes. Within the entire set of samples,
microarray expression analysis grouped together poorly differentiated
tumors irrespective of histological subtype. For three patients, a
comparison between genomic alterations and gene expression pattern was
performed on samples of primary and metastatic tumors. Their common
origin was demonstrated by the close relationship of both the SKY and
CGH karyotypes and the observed profiles of gene expression. In
agreement with the pattern of genomic imbalance observed for chromosome
3 in ovarian cancer, the relative expression profile with respect to a
normal ovary exhibited a contiguous pattern of reduced expression of
genes mapping to the 3p25.5-3p21.31 and increased expression of genes
from 3q13.33-3q28. This study demonstrates that SKY, CGH, and microarray
analysis can in combination identify significantly smaller subsets of
differentially expressed genes for future studies.
22
UI - 12085231
AU - Ding Z; Zhou JY; Wei WZ; Baker VV; Wu GS
TI -
Induction of apoptosis by the new anticancer drug XK469 in human ovarian
cancer cell lines.
SO - Oncogene 2002 Jul 4;21(29):4530-8
AD - Department of Pathology, Karmanos Cancer Institute, Wayne State
University School of Medicine, Detroit 48201, USA.
XK469, a synthetic quinoxaline phenoxypropionic acid derivative, has
been found to have selective activity against a broad panel of solid
tumors including several drug-resistant cell lines and has been approved
for phase I clinical evaluation. Recent studies suggested that XK469 is
a selective topoisomerase IIbeta inhibitor, but the mechanism of
XK469-induced cell death remains unknown. Here we investigate the
ability of XK469 to induce apoptosis of human cancer cells. In the human
ovarian cancer cell line PA1, XK469 caused the release of cytochrome c,
activation of caspases including caspases 9, 7 and 3, cleavage of PARP,
and subsequently cell death. Moreover, Bcl2 and Bax were cleaved in
XK469 treated cells. PA1 cells expressing the dominant negative-caspase
9 were less sensitive to XK469. Importantly, in these PA1 cells
expressing DN-casp 9, the activation of caspases including caspases 3, 7
and 9, and cleavage of Bax and Bcl2 were inhibited, suggesting that the
activation of the mitochondrial pathway is required for XK469-induced
anticancer activity. These results indicate that the induction of
apoptosis by XK469 may account for its anti-tumor activity and such
activity is required for the activation of the mitochondrial pathway.
Thus, our study defines a possible mechanism, at least in part,
underlying XK469-induced anti-cancer activity.
23
UI - 11965725
AU - Malinova M
TI -
[Risk factors for the development of ovarian carcinoma]
SO - Akush Ginekol (Sofiia) 1999;38(1):57-60
24
UI - 12054733
AU - Gunthert AR; Grundker C; Hollmann K; Emons G
TI -
Luteinizing hormone-releasing hormone induces JunD-DNA binding and
extends cell cycle in human ovarian cancer cells.
SO - Biochem Biophys Res Commun 2002 May 31;294(1):11-5
AD - Department of Gynecology and Obstetrics, Georg-August-University,
Robert-Koch-Street 40, D-37075 Gottingen, Germany.
Expression of luteinizing hormone-releasing hormone (LHRH) and its
receptor as part of an autocrine regulatory system of cell proliferation
has been demonstrated in a number of human malignant tumors, including
cancers of the ovary. This study was conducted to investigate whether
LHRH induces activation of JunD and affects cell cycle regulation and
DNA synthesis. Treatment of primary human ovarian cancer cells and human
ovarian cancer cell lines EFO-21 and EFO-27 with LHRH agonist
triptorelin (100 nM) resulted in an increase in G(0/1) phase and a
decrease in G(2/S) phase of cell cycle. Treatment of quiescent EFO-21 or
EFO-27 cells with triptorelin (100 nM) resulted in a 46.7 or 44.2-fold
increase of AP-1 activation, respectively (p<0.001). Maximal binding of
JunD on DNA consensus sequence was found after 4 h of treatment of
quiescent EFO-21 or EFO-27 cells with triptorelin (100 nM). DNA
synthesis was significantly decreased to 45.5+/-11.4% (day
0=control=100%; p<0.001) after 3 days of triptorelin (1 nM) treatment.
These results suggest that LHRH agonist triptorelin induces JunD-DNA
binding, resulting in reduced proliferation as indicated by increased
G(0/1) phase of cell cycle and decreased DNA synthesis. Since LHRH
activates nucleus factor kappa B (NF kappa B) and protects ovarian
cancer cells from doxorubicin-induced apoptosis and JunD is shown to
decrease cell cycle and cell proliferation, we propose that JunD
activated by LHRH acts as a modulator of cell proliferation and
cooperates with the anti-apoptotic and anti-mitogenic functions of LHRH.
25
UI - 12090593
AU - Zanotti KM; Hart WR; Kennedy AW; Belinson JL; Casey G
TI -
Allelic imbalance on chromosome 17p13 in borderline (low malignant
potential) epithelial ovarian tumors.
SO - Int J Gynecol Pathol 1999 Jul;18(3):247-53
AD - Department of Obstetrics and Gynecology, The Cleveland Clinic
Foundation, Ohio 44195, USA.
Borderline epithelial ovarian tumors (BEOTs) possess clinical and
pathologic features intermediate between cystadenomas and
cystadenocarcinomas. Although the clinical and pathologic
characteristics of BEOTs are well described, the molecular aspects are
poorly understood. Three regions of loss of heterozygosity (often
referred to as allelic imbalance [AI] when identified by polymerase
chain reaction) on chromosome 17p13, one of which includes the p53 gene,
have been implicated in the development of ovarian and breast cancers.
To provide evidence that genes in these regions also may be involved in
the development of BEOTs, we undertook a detailed analysis of AI at all
three loci in BEOTs from 21 patients. Seventeen of the BEOTs were serous
and four were mucinous. Five of 21 tumors (24%) had AI at one or more
loci. Four tumors had AI using the D17S695 marker, two of which showed
AI only at this locus. In addition, three tumors exhibited AI at the
D17S654 locus, one of which showed AI only at this locus. These data
suggest that there may be two tumor suppressor genes distal to p53
involved in the development of at least a subset of BEOTs. Peritoneal
implants from a subset of serous BEOTs also were evaluated for AI and
were found to be concordant with the primary tumor in all cases. Their
genetic similarity is consistent with the implantation theory of
peritoneal spread of serous BEOTs in these cases.
26
UI - 12051864
AU - Rubin SC
TI -
Prophylactic oophorectomy comes of age.
SO - Gynecol Oncol 2002 Jun;85(3):395-6
27
UI - 12051865
AU - Colgan TJ; Boerner SL; Murphy J; Cole DE; Narod S; Rosen B
TI -
Peritoneal lavage cytology: an assessment of its value during
prophylactic oophorectomy.
SO - Gynecol Oncol 2002 Jun;85(3):397-403
AD - Department of Laboratory Medicine and Pathology, Mount Sinai Hospital,
Toronto, Canada. tcolgan@mtsinai.on.ca
OBJECTIVE: Prophylactic oophorectomy (PO) is an accepted treatment
strategy for women who are at high risk for the development of ovarian
carcinoma, particularly women who are BRCA mutation-positive. This study
sought to assess the utility of peritoneal lavage cytology at the time
of PO in detecting occult malignancy in this group of patients. METHODS:
Thirty-five high-risk women, who were not suspected of having any
malignancy or ovarian mass, underwent peritoneal lavage at the time of
PO. Thirty-one of the thirty-five women had undergone BRCA mutation
analysis (BRCA1+, 18; BRCA2+, 10; BRCA-, 3). Intensive histopathologic
examination was used in all 35 cases to identify occult carcinoma.
Lavage specimens were reviewed for the presence of malignant cells and
endosalpingiosis. The cytologic review was conducted without knowledge
of either the histopathologic or BRCA results. RESULTS: In 32 of the 35
lavage specimens no malignancy was detected. In the remaining three
cases malignant cells were detected; in two of these cases
histopathologic examination confirmed an ovarian/tubal occult carcinoma.
Two of these women were BRCA1 mutation positive. Endosalpingiosis was
detected in the peritoneal lavage specimens of 7 of the 32 cases showing
no evidence of malignancy. All of these 7 women were BRCA mutation
positive or unknown. CONCLUSION: Peritoneal lavage cytology can detect
occult carcinoma at the time of PO and should be performed at PO. The
significance of occult carcinoma detected by either histopathologic or
cytopathologic examination is uncertain. Whether the prevalence of
endosalpingiosis detectable by lavage cytology is increased in BRCA
mutation-positive patients requires further study.
28
UI - 12051869
AU - Levine DA; Federici MG; Reuter VE; Boyd J
TI -
Cell proliferation and apoptosis in BRCA-associated hereditary ovarian
cancer.
SO - Gynecol Oncol 2002 Jun;85(3):431-4
AD - Gynecology and Breast Research Laboratory, Memorial Sloan-Kettering
Cancer Center, New York, New York 10021, USA.
OBJECTIVE: The goal was to test the hypothesis that cellular growth
properties differ between hereditary and sporadic ovarian cancers.
METHODS: Cell proliferation and apoptosis were assessed in 67 tumors
associated with deleterious germline BRCA mutations (hereditary) and 69
tumors without BRCA mutations (sporadic). Cell proliferation was
evaluated by immunohistochemical analysis of Ki-67 expression, and
apoptosis was assessed using a TUNEL assay. RESULTS: The mean number of
Ki-67-immunopositive nuclei was significantly higher in ovarian cancers
from the hereditary group compared with those from the sporadic group (P
= 0.017). Cell proliferation did not differ significantly between BRCA1-
and BRCA2-associated hereditary tumors, and apoptosis did not differ
significantly between the hereditary and sporadic tumors. CONCLUSION:
These data indicate that ovarian carcinomas associated with germline
BRCA mutations have a significantly higher growth fraction than sporadic
cancers. This property may contribute to an improved response to
cytotoxic chemotherapy, partially accounting for the longer
recurrence-free interval and overall survival observed in the hereditary
group.
29
UI - 12051879
AU - Anupol N; Ghamande S; Odunsi K; Driscoll D; Lele S
TI -
Evaluation of prognostic factors and treatment modalities in ovarian
cancer patients with brain metastases.
SO - Gynecol Oncol 2002 Jun;85(3):487-92
AD - Division of Gynecologic Oncology, Department of Surgery, Roswell Park
Cancer Institute, Elm & Carlton Streets, Buffalo, New York 14263, USA.
OBJECTIVE: The objective of this study is to evaluate the impact of
different clinical variables and treatment modalities on survival in
patients with brain metastases from ovarian carcinoma. METHODS: Methods
included: (1) retrospective chart review of all patients with ovarian
cancer and brain metastases from 1986 to 2000 at Roswell Park Cancer
Institute and (2) Medline search was performed to extract data from all
published reports with three or more cases of ovarian cancer with brain
metastases. Cox regression analysis, Kaplan-Meier test, and log rank
test were used to calculate survival and compare the impacts of clinical
variables and treatment modalities. RESULTS: Fifteen patients with brain
metastases out of 1042 women with ovarian carcinoma were identified from
our institution, an incidence of 1.4%. The median time from initial
diagnosis to detection of brain metastases was 22 months. Patients who
were not treated after brain metastasis had a median survival of 0.5
month versus 6 months with therapy. In the subgroup of patients treated
with a combination of radiation, surgery, and chemotherapy, the median
survival was 22 months. Literature analysis combined with our data
generated 124 patients. The only clinically significant variable
impacting survival was the presence or absence of additional distant
recurrence with median survivals of 3 and 8 months, respectively (P =
0.005). Among patients who received treatment, the combination of
radiation and surgery with or without chemotherapy appears to be
beneficial, with a median survival of 20 months (P < 0.001). CONCLUSION:
Patients with brain metastases from ovarian cancer without any evidence
of disease in other sites appear to benefit from aggressive combined
treatment with external radiation and surgery with or without
chemotherapy with a median survival of 20 months.
30
UI - 12076885
AU - Bertone ER; Rosner BA; Hunter DJ; Stampfer MJ; Speizer FE; Colditz GA;
TI -
Willett WC; Hankinson SE
Dietary fat intake and ovarian cancer in a cohort of US women.
SO - Am J Epidemiol 2002 Jul 1;156(1):22-31
AD - Channing Laboratory, Department of Medicine, Brigham and Women's
Hospital and Harvard Medical School, Boston, MA, USA.
eberstone@schoolph.umass.edu
Several studies have suggested that high intake of fats and fat-rich
foods may increase the risk of ovarian cancer. The authors examined
these relations in the Nurses' Health Study cohort. Dietary intake was
assessed in 1980, 1984, 1986, and 1990 by using a self-administered food
frequency questionnaire. Food data were used to calculate intake of
various fats and fatty acids. For best reflection of long-term intake,
an updated, cumulative, averaged measure of fat intake was used to
predict incidence of ovarian cancer. Between 1980 and 1996, 301 incident
cases of invasive epithelial ovarian cancer were confirmed among the
80,258 participants who completed the baseline food frequency
questionnaire. There was no evidence of a positive association between
intake of any type of fat and ovarian cancer risk, even after adjustment
of fat subtypes for one another. Women in the highest quintile of total
fat intake were not at increased risk compared with those in the lowest
quintile (multivariate relative risk = 1.03, 95 percent confidence
interval: 0.72, 1.45, p for trend = 0.97). Intakes of fat-rich foods
were also not appreciably associated with ovarian cancer risk, although
an increase in risk with frequent intake of eggs was observed. Overall,
results suggest no association between intake of any type of fat and
ovarian cancer.
31
UI - 12096075
AU - Hedenfalk IA
TI -
Gene expression profiling of hereditary and sporadic ovarian cancers
reveals unique BRCA1 and BRCA2 signatures.
SO - J Natl Cancer Inst 2002 Jul 3;94(13):960-1
32
UI - 12096084
AU - Jazaeri AA; Yee CJ; Sotiriou C; Brantley KR; Boyd J; Liu ET
TI -
Gene expression profiles of BRCA1-linked, BRCA2-linked, and sporadic
ovarian cancers.
SO - J Natl Cancer Inst 2002 Jul 3;94(13):990-1000
AD - Division of Clinical Sciences of the National Cancer Institute,
Gaithersburg, MD,USA.
BACKGROUND: Germline mutations in BRCA1 and BRCA2 are responsible for
5%-10% of epithelial ovarian cancers, but the molecular pathways
affected by these mutations are unknown. We used complementary DNA
(cDNA) microarrays to compare gene expression patterns in ovarian
cancers associated with BRCA1 or BRCA2 mutations with gene expression
patterns in sporadic epithelial ovarian cancers and to identify patterns
common to both hereditary and sporadic tumors. METHODS: Tumor samples
from 61 patients with pathologically confirmed epithelial ovarian
adenocarcinoma with matched clinicopathologic features were studied,
including 18 with BRCA1 founder mutations, 16 with BRCA2 founder
mutations, and 27 without either founder mutation (termed sporadic
cancers). The cDNA microarrays contained 7651 sequence-verified
features. Gene expression data were analyzed with a modified two-sided F
test, with P<.0001 considered statistically significant. The expression
level of six genes was also studied with reverse
transcription-polymerase chain reaction. RESULTS: The greatest contrast
in gene expression was observed between tumors with BRCA1 mutations and
those with BRCA2 mutations; 110 genes showed statistically significantly
different expression levels (P<.0001). This group of genes could
segregate sporadic tumors into two subgroups, "BRCA1-like" and
"BRCA2-like," suggesting that BRCA1-related and BRCA2-related pathways
are also involved in sporadic ovarian cancers. Fifty-three genes were
differentially expressed between tumors with BRCA1 mutations and
sporadic tumors; six of the 53 mapped to Xp11.23 and were expressed at
higher levels in tumors with BRCA1 mutations than in sporadic tumors.
Compared with the immortalized ovarian surface epithelial cells used as
reference, several interferon-inducible genes were overexpressed in the
majority of tumors with a BRCA mutation and in sporadic tumors.
CONCLUSIONS: Mutations in BRCA1 and BRCA2 may lead to carcinogenesis
through distinct molecular pathways that also appear to be involved in
sporadic cancers. Sporadic carcinogenic pathways may result from
epigenetic aberrations of BRCA1 and BRCA2 or their downstream effectors.
33
UI - 12117706
AU - Goodman MT; Wu AH; Tung KH; McDuffie K; Kolonel LN; Nomura AM; Terada K;
TI -
Wilkens LR; Murphy S; Hankin JH
Association of dairy products, lactose, and calcium with the risk of
ovarian cancer.
SO - Am J Epidemiol 2002 Jul 15;156(2):148-57
AD - Cancer Etiology Program, Cancer Research Center of Hawaii, University of
Hawaii, Honolulu, HI 96813, USA. marc@crch.hawaii.edu
Epidemiologic findings have been inconsistent regarding the association
of dietary fat, dairy products, and lactose with risk of ovarian cancer.
The authors conducted a case-control study in Hawaii and Los Angeles,
California, to examine several dietary hypotheses regarding the etiology
of ovarian cancer in a population with a broad range of dietary intakes.
A total of 558 patients with ovarian cancer diagnosed in 1993-1999 and
607 controls were interviewed regarding their diet. Consumption of all
dairy products, all types of milk, and low-fat milk, but not consumption
of whole milk, was significantly inversely related to the odds of
ovarian cancer. Similar inverse gradients in the odds ratios were
obtained for intakes of lactose and calcium, although these nutrients
were highly correlated (r = 0.77). The odds ratio for ovarian cancer was
0.46 (95% confidence interval: 0.27, 0.76) among women in the highest
quartile of dietary calcium intake versus the lowest (p for trend =
0.0006). The significant dietary association was limited to dairy
sources of calcium (p for trend = 0.003), although a nonsignificant
inverse gradient in risk was also found in relation to calcium
supplement intake. These results suggest that intake of low-fat milk,
calcium, or lactose may reduce the risk of ovarian cancer.
34
UI - 12117398
AU - Lacey JV Jr; Mink PJ; Lubin JH; Sherman ME; Troisi R; Hartge P;
TI -
Schatzkin A; Schairer C
Menopausal hormone replacement therapy and risk of ovarian cancer.
SO - JAMA
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