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Abramson Cancer CenterNCI CANCERLIT® Search: Diagnosis-Histopathology-Pathogenesis of Ovarian Cancer - June 2002
National Cancer Institute®
Last Modified: June 1, 2002
- Effect of prevention strategies on survival and quality-adjusted survival of women with BRCA1/2 mutations: an updated decision analysis.
- [CA-125 antigen]
- Contribution of BRCA1 and BRCA2 to familial ovarian cancer: a gynecologic oncology group study.
- Enhancement of the adenoviral sensitivity of human ovarian cancer cells by transient expression of coxsackievirus and adenovirus receptor (CAR).
- The benefits of comprehensive surgical staging in the management of early-stage epithelial ovarian carcinoma.
- The effect of raloxifene on the incidence of ovarian cancer in postmenopausal women.
- The use of PET scanning in ovarian cancer.
- [Hormone replacement therapy and ovarian tumors]
- Molecular events associated with dysplastic morphologic transformation and initiation of ovarian tumorigenicity.
- Tumor vaccine for ovarian carcinoma targeting sperm protein 17.
- Peritoneal metastases: detection with spiral CT in patients with ovarian cancer.
- Tumour suppressor genes in sporadic epithelial ovarian cancer.
- Inactivation of p16/CDKN2 and p15/MTS2 is associated with prognosis and response to chemotherapy in ovarian cancer.
- Body mass index in relation to ovarian cancer: a multi-centre nested case-control study.
- [Hereditary ovarian cancer]
- Prophylactic surgery in patients with inherited risk of ovarian cancer.
- Diagnostic value of US and CT in the assessment of ovarian teratomas and their qualifications for surgical treatment with laparoscopic method.
- Recreational physical activity and ovarian cancer in a population-based case-control study.
- BRCAPRO validation, sensitivity of genetic testing of BRCA1/BRCA2, and prevalence of other breast cancer susceptibility genes.
- A molecular blueprint for targeting cancer?
- Secondary cytoreductive surgery for recurrent epithelial ovarian cancer.
- Distinct lymphatic spread of endometrial carcinoma in comparison with cervical and ovarian carcinomas.
- CD40 activation in epithelial ovarian carcinoma cells modulates growth, apoptosis, and cytokine secretion.
- Loss of heterozygosity at chromosome 3p in epithelial ovarian cancer in China.
- In vitro testing of platinum-based drugs on a panel of human ovarian tumour cell lines.
- Cancer studies explore targeted therapy, researchers seek new prevention strategies.
- The effects of abdominal and bimanual pelvic examination and transvaginal ultrasonography on serum CA-125 levels.
- Resistance to p53-mediated growth suppression in human ovarian cancer cells retain endogenous wild-type p53.
- Frequent LOH at hMLH1, a highly variable SNP in hMSH3, and negligible coding instability in ovarian cancer.
- [Structural and functional features of the ovaries as a risk factor for ovarian cancer in infertile women]
Table of Contents
1
UI - 12011131
AU - Grann VR; Jacobson JS; Thomason D; Hershman D; Heitjan DF; Neugut AI
TI -
Effect of prevention strategies on survival and quality-adjusted
survival of women with BRCA1/2 mutations: an updated decision analysis.
SO - J Clin Oncol 2002 May 15;20(10):2520-9
AD - Herbert Irving Comprehensive Cancer Center, Department of Medicine,
College of Physicians and Surgeons, Columbia University, 630 W 168th
Street, New York, NY 10032, USA.
PURPOSE: This study updates findings regarding the effects of
prophylactic surgery, chemoprevention, and surveillance on the survival
and quality-adjusted survival of women who test positive for BRCA1/2
mutations. MATERIALS AND METHODS: Markov modeling of outcomes was
performed in a simulated cohort of 30-year-old women who tested positive
for BRCA1/2 mutations. The model incorporated breast and ovarian cancer
incidence rates from the literature and mortality rates from the
Surveillance, Epidemiology, and End Results Program. Quality adjustment
of survival estimates were obtained from a survey of women aged 33 to 50
years. Sensitivity analyses were performed of varied assumptions
regarding timing and effects of preventive measures on cancer incidence
and adverse effects. RESULTS: A 30-year-old woman could prolong her
survival beyond that associated with surveillance alone by use of
preventive measures: 1.8 years with tamoxifen, 2.6 years with
prophylactic oophorectomy, 4.6 years with both tamoxifen and
prophylactic oophorectomy, 3.5 years with prophylactic mastectomy, and
4.9 years with both surgeries. She could prolong her quality-adjusted
survival by 2.8 years with tamoxifen, 4.4 years with prophylactic
oophorectomy, 6.3 years with tamoxifen and oophorectomy, and 2.6 years
with mastectomy, or with both surgeries. The benefits of all of these
strategies would decrease if they were initiated at later ages.
CONCLUSION: Women who test positive for BRCA1/2 mutations may derive
greater survival and quality adjusted survival benefits than previously
reported from chemoprevention, prophylactic surgery, or a combination.
Observational studies and clinical trials are needed to verify the
results of this analysis of the long-term benefits of preventive
strategies among BRCA1/2-positive women.
2
UI - 11987487
AU - Zakrzewska I
TI -
[CA-125 antigen]
SO - Postepy Hig Med Dosw 2002;56(1):29-38
AD - Zaklad Laboratoryjnej Diagnostyki Klinicznej Akademii Medycznej w
Bialymstoku.
This review describes the physicochemical and biological properties of
antigen CA125 and clinical utility of antigen in oncologic diagnostic.
CA125 is the most reliable marker for ovarian cancer in clinical
practice. Analysis of CA125 values performed by many authors revealed
its highest concentrations in serous and endrometrioid histological
type. Serial measurements of CA125 are useful in monitoring the response
to chemotherapy and follow-up the early detection of recurrent disease
of patients with ovarian cancer.
3
UI - 11972384
AU - Reedy M; Gallion H; Fowler JM; Kryscio R; Smith SA
TI -
Contribution of BRCA1 and BRCA2 to familial ovarian cancer: a
gynecologic oncology group study.
SO - Gynecol Oncol 2002 May;85(2):255-9
AD - Division of Gynecologic Oncology, University of Kentucky, Lexington, KY
40536, USA.
OBJECTIVES: The aim of the study was to determine the prevalence of
BRCA1 and BRCA2 germline mutations among ovarian cancer patients
ascertained to have a family history of ovarian cancer. METHODS: Ovarian
cancer patients were eligible if they had a family history of cancer
that met any one of the following criteria: (1) a first-degree relative
with ovarian cancer; (2) a second-degree relative with ovarian cancer
plus a first-degree relative with breast cancer (diagnosed younger than
50 years of age); or (3) a first- and a second-degree relative with
breast cancer (diagnosed younger than 50 years of age). The entire
coding sequence of BRCA1 and exon 11 of BRCA2 were screened for germline
alterations by single-strand conformation polymorphism analysis.
RESULTS: Of 26 eligible patients screened for mutations, 12 had
deleterious alterations, 8 in BRCA1 and 4 in BRCA2. A correlation was
noted between the presence of a BRCA1 mutation and the strength of
family history of breast ovarian cancer, with the likelihood of a
mutation increasing with the number of affected relatives (P = 0.0002).
No association was detected between the location of mutations in BRCA1
and the ratio of ovarian cancer cases relative to breast cancer (P =
0.28). CONCLUSIONS: Mutations in BRCA1 or BRCA2 are present in about 50%
of ovarian cancer patients with at least one first-degree relative with
disease, and in 70% of patients with two or more relatives with ovarian
cancer. (c) 2002 Elsevier Science (USA).
4
UI - 11972385
AU - Kim JS; Lee SH; Cho YS; Choi JJ; Kim YH; Lee JH
TI -
Enhancement of the adenoviral sensitivity of human ovarian cancer cells
by transient expression of coxsackievirus and adenovirus receptor (CAR).
SO - Gynecol Oncol 2002 May;85(2):260-5
AD - Clinical Research Center, Samsung Biomedical Research Institute, Seoul
135-710, Korea.
OBJECTIVE: The coxsackievirus and adenovirus receptor (CAR) is known to
be a primary receptor for attachment during adenovirus infection of
target cells and thus is closely related to adenoviral infection
efficiency. To extend this notion to human ovarian cancer, we
investigated the difference in expression levels of CAR in human ovarian
cancer cell lines and whether their adenoviral sensitivities are
enhanced by transient transfection of the CAR gene. METHODS: Adenoviral
infection efficiency was examined by flow cytometry analysis,
beta-galactosidase staining, and beta-galactosidase activity assay.
Expression of the CAR-specific mRNA and protein was analyzed by reverse
transcription polymerase chain reaction and flow cytometry,
respectively. RESULTS: Expression of CAR in human ovarian cancer cell
lines (SKOV3, 2774, PA-1, and OVCAR3) appeared to be correlated with
their susceptibilities to adenovirus-mediated gene delivery. The 2774
and PA-1 cells expressing an easily detectable level of CAR on the cell
surface showed a higher susceptibility to infection with both AdCMVGFP
and AdRSVbetagal than SKOV3 and OVCAR3 cells, both of which had hardly
detectable levels of CAR. Ectopic expression of the CAR gene by
transient transfection of these ovarian cancer cells resulted in a
dramatic increase in their adenoviral sensitivities. CONCLUSION: These
data show that the expression of CAR is closely related to
susceptibility to adenovirus infection in human ovarian cancer cells.
These results indicate that the CAR gene can be a useful tool in
boosting the efficiency of adenoviral vector-mediated gene therapy
against human ovarian cancer. (c) 2002 Elsevier Science (USA).
5
UI - 11972399
AU - Le T; Adolph A; Krepart GV; Lotocki R; Heywood MS
TI -
The benefits of comprehensive surgical staging in the management of
early-stage epithelial ovarian carcinoma.
SO - Gynecol Oncol 2002 May;85(2):351-5
AD - Division of Gynecologic Oncology, Dept. of Obstetrics, Gynecology, and
Reproductive Sciences, University of Saskatchewan, Royal University
Hospital, 103 Hospital Drive, Saskatoon, Saskatchewan, Canada S7N 0W8.
letien@duke.usask.ca
OBJECTIVE: The management of understaged patients with apparent
clinically early ovarian cancer is difficult. Options include offering
chemotherapy based on histopathologic factors or reoperation to obtain
the necessary information needed to assign an accurate surgical stage.
This study aims to compare these two approaches and to define the role
of staging surgery in this common patient population. METHODS:
Retrospective chart reviews were carried out at the Universities of
Manitoba and Saskatchewan over the period 1975 to 1999. Demographic data
and surgical findings were abstracted and entered into a computerized
database for analysis. Patients not having surgical staging procedures
were offered platinum-based chemotherapy based on high tumor grades,
dense adhesions, and presence of surface excrescences or large necrotic
areas. Patients with surgically proven stage I disease were treated with
no further therapy regardless of histopathologic factors. Descriptive
statistics are used to summarize the data. Logistic and Cox regression
models are used to identify significant predicting factors for
recurrences and progression-free intervals. RESULTS: One hundred and
thirty-eight patients presented with tumor macroscopically confined to
the ovary at the time of laparotomy. The median age at presentation is
56.5 (18-90). The histology distribution was serous tumor in 28.3%,
mucinous in 26.1%, endometrioid in 23.2%, clear cell in 14.5%,
anaplastic in 2.2%, and mixed types in 5.8%. The grade distribution was
47.1% grade 1, 27.5% Grade 2, and 25.4% Grade 3. Sixty-eight percent of
the patients had a comprehensive surgical staging procedure initially.
Thirty-six percent of these patients were found to have extraovarian
metastases and were subsequently treated with adjuvant chemotherapy.
Forty-three percent of those not having staging laparotomy were offered
chemotherapy based on high risk factors only. At a median follow-up of
58 months. 77% of patients remained disease-free and 23% had recurrent
disease. Of 60 patients with surgically proven stage I treated
expectantly, 6 (10%) recurred, whereas of 25 unstaged patients treated
expectantly due to lack of risk factors 7 (28%) recurred (P = 0.036). In
patients treated expectantly, a significant survival advantage was noted
in the staged group. Logistic regression showed age (OR 1.032, P =
0.043), high grade (OR 4.16, P = 0.003), and lack of a proper staging
surgery (OR 2.62, P = 0.032) to be important factors predicting
recurrence. In terms of progression-free interval, only age (OR 1.027, P
= 0.048) and tumor grade (OR 3.62, P = 0.05) are significant predictors.
CONCLUSION: Absence of surgical pathologic high-risk factors is inferior
to comprehensive staging laparotomy findings in guiding recommendations
for subsequent adjuvant therapy. Patients who have not been properly
staged stand a significant risk of recurrent disease despite more
frequent use of chemotherapy. All clinically early-stage ovarian cancer
patients should be considered for comprehensive staging surgery prior to
further treatment recommendations. (c) 2002 Elsevier Science (USA).
6
UI - 11972407
AU - Neven P; Goldstein SR; Ciaccia AV; Zhou L; Silfen SL; Muram D
TI -
The effect of raloxifene on the incidence of ovarian cancer in
postmenopausal women.
SO - Gynecol Oncol 2002 May;85(2):388-90
AD - Department of Obstetrics and Gynecology, Algemene Kliniek St.-Jan,
Broekstraat 114, B-1000 Brussels, Belgium.
Patrick.neven@uz.kuleuven.ac.be
OBJECTIVE: The aim of this study was to determine the incidence of
ovarian cancer in postmenopausal women treated with raloxifene compared
with placebo. METHODS: This analysis comprises integrated data from
seven randomized, placebo-controlled trials of raloxifene (N = 9837).
Ovarian cancer cases were identified from the safety database and
reviewed by a gynecologic adjudication review board. RESULTS: Sixteen
cases of ovarian cancer were reported: 8 women (79.4/100,000
patient-years) on placebo and 8 (37.4/100,000 patient-years) on pooled
raloxifene doses. The relative risk of ovarian cancer associated with
raloxifene therapy was 0.50 (95% confidence interval, 0.19-1.35).
CONCLUSION: Raloxifene use was not associated with an increased risk for
ovarian cancer. (c) 2002 Elsevier Science (USA).
7
UI - 11972408
AU - Markman M
TI -
The use of PET scanning in ovarian cancer.
SO - Gynecol Oncol 2002 May;85(2):391; discussion 391-2
8
UI - 11987569
AU - Sevcik L; Klat J; Koliba P
TI -
[Hormone replacement therapy and ovarian tumors]
SO - Ceska Gynekol 2002 Mar;67(2):55-8
AD - Porodnicko-gynekologicka klinika, FNsP Ostrava.
OBJECTIVE: Analysis of risk and protective factors and hormone
replacement therapy in the aethiology and pathogenesis of ovarian
cancer. The role of hormone replacement therapy in the complex treatment
in women with ovarian cancer is discussed. DESIGN: Reviewed article.
SETTING: Department of Obstetrics and Gynaecology, University Hospital
Ostrava. METHODS: Analysis of epidemiological studies. CONCLUSION: The
role of hormone replacement therapy as a risk factor of ovarian cancer
has not been confirmed. Hormone replacement therapy as a part of
supportive and symptomatic therapy has been acceptable in a great deal
of patients with ovarian cancer.
9
UI - 12015763
AU - Yang DH; Smith ER; Cohen C; Wu H; Patriotis C; Godwin AK; Hamilton TC;
TI -
Xu XX
Molecular events associated with dysplastic morphologic transformation
and initiation of ovarian tumorigenicity.
SO - Cancer 2002 May 1;94(9):2380-92
AD - Ovarian Cancer Program, Fox Chase Cancer Center, Philadelphia,
Pennsylvania 19111, USA.
BACKGROUND: Disabled-2 (Dab2), a candidate tumor suppressor of ovarian
carcinoma, frequently (around 80%) loses its expression in ovarian
tumors. Expression of exogenous Dab2 in tumor cell lines negatively
regulates growth and suppresses the downstream signal of the Ras/mitogen
activated protein kinase mitogenic pathway. The inactivation of Dab2 is
believed to be an early event in ovarian tumorigenicity. METHODS: The
authors analyzed the correlation among expression of Dab2, presence of
basement membrane (collagen IV and laminin), morphologic alteration of
the surface epithelial cells, and expression of the mitotic index marker
Mib-1 in 50 archived ovarian tumors by an immunohistochemical approach.
The stainings of Dab2, Mib-1, collagen IV, and laminin in premalignant
lesions bordering both normal and neoplastic ovarian surface epithelium
from adjacent slides were analyzed in 50 ovarian tumors. RESULTS: In
these 50 ovarian tumors, the percentage of Mib-1 positive tumor cells
distributed in a wide range, from 1% to 75%, and there has no strong
correlation with the expression of Dab2. However, in the premalignant
regions bordering tumor and normal ovarian surface epithelium, the loss
of Dab2 expression closely correlated with the dysplastic morphologic
transition and Mib-1 expression of the ovarian surface epithelial cells.
In 20 foci in 12 out of the 50 tumors, a transition from normal to
neoplastic morphology within a contiguous epithelium was observed, and
in all cases the morphologic change correlated with the loss of Dab2
staining. In addition, the collagen and laminin staining of the basement
membrane were absent or weakened in pre-malignant epithelium prior to
loss of Dab2 expression in all these 20 cases. Nevertheless, collagen IV
and laminin were detectable in established adenomas on the same tumor
slides. CONCLUSIONS: The loss of Dab2 is closely associated with the
transition of ovarian surface epithelial cells to premalignant states
and is likely involved in the initiation of ovarian tumorigenicity.
Transient loss of collagen IV and laminin in the basement membrane of
the premalignant epithelium and subsequent inactivation of Dab2 are
common early events associated with tumorigenicity of the ovarian
surface epithelium. Copyright 2002 American Cancer Society.DOI
10.1002/cncr.10497
10
UI - 12015770
AU - Chiriva-Internati M; Wang Z; Salati E; Timmins P; Lim SH
TI -
Tumor vaccine for ovarian carcinoma targeting sperm protein 17.
SO - Cancer 2002 May 1;94(9):2447-53
AD - Division of Hematology and Oncology, Texas Tech University School of
Medicine at Amarillo, USA.
BACKGROUND: The authors previously identified sperm protein 17 (Sp17) as
being expressed in patients with multiple myeloma. The restricted
expression of Sp17 in normal tissue makes it an ideal target for tumor
vaccine. In the current study, the authors extended their research to
include ovarian carcinoma. METHODS: A pair of sequence specific primers
was used in reverse transcriptase-polymerase chain reaction to determine
the gene expression of Sp17. A recombinant Sp17 protein was used with
monocyte-derived dendritic cells and autologous peripheral blood
mononuclear cells to generate Sp17 specific cytotoxic T-lymphocytes
(CTLs). The successful generation of Sp17 specific CTLs was confirmed
using standard (51)chromium-release assays. RESULTS: Sp17 was found to
be expressed in the primary tumor cells from 70% of the patients with
ovarian carcinoma. Human leukocyte antigen (HLA) class I- restricted
Sp17 specific CTLs were generated successfully from the peripheral blood
of three patients with ovarian carcinoma at the time of disease
presentation. These CTLs were able to lyse autologous Epstein-Barr
virus-transformed lymphoblastoid cells in a Sp17-dependent manner.
Target lysis was HLA class I-dependent and could be blocked by
antibodies against monomorphic HLA class I but not HLA class II
molecules. The CTLs also lysed Sp17-positive autologous tumor cells,
suggesting that Sp17 is processed and presented in association with the
HLA class I molecules in Sp17- positive tumor cells in a concentration
and configuration that could be recognized by recombinant protein-primed
CTLs. Tumor cell killing by the CTLs appeared to be mediated through the
perforin pathway. Flow cytometric analysis of the CTLs indicated that
they predominantly were CD8 in phenotype and produced interferon-gamma
and scant amounts of interleukin-4. CONCLUSIONS: The results of the
current study suggest the potential of Sp17 as a target for
immunotherapy in patients with ovarian carcinoma. Copyright 2002
American Cancer Society.DOI 10.1002/cncr.10506
11
UI - 11997559
AU - Coakley FV; Choi PH; Gougoutas CA; Pothuri B; Venkatraman E; Chi D;
TI -
Bergman A; Hricak H
Peritoneal metastases: detection with spiral CT in patients with ovarian
cancer.
SO - Radiology 2002 May;223(2):495-9
AD - Department of Radiology, Memorial Sloan-Kettering Cancer Center, New
York, NY, USA. fergus.coakley@radiology.ucsf.edu
PURPOSE: To determine the accuracy of spiral computed tomography (CT) in
the depiction of peritoneal metastases by using surgical findings in
patients with ovarian cancer as the standard of reference. MATERIALS AND
METHODS: Three independent readers reviewed the preoperative CT scans
obtained in 64 patients who underwent primary surgery for ovarian
cancer. Readers rated the likelihood of peritoneal metastases on a
five-point scale and recorded the presence or absence of ascites,
parietal peritoneal thickening or enhancement, and small-bowel wall
thickening or distortion. Peritoneal metastases were identified as
nodular, plaquelike, or infiltrative soft-tissue lesions in the
peritoneal fat or on the peritoneal surface. Area under the receiver
operating characteristic curve was calculated for each reader.
Interreader agreement was evaluated with the kappa statistic.
Descriptive statistical data were determined with dichotomized ratings
(1-3 = absent; 4-5 = present). RESULTS: Areas under the receiver
operating characteristic curves for the three readers were 0.95, 0.93,
and 0.89. Paired kappa values ranged from 0.75 to 0.91. Reader
sensitivity for metastases 1 cm or smaller in maximum diameter (25%-50%)
was significantly (P <.05) lower than overall sensitivity (85%-93%).
Ascites, parietal peritoneal thickening or enhancement, and small-bowel
wall thickening or distortion demonstrated positive predictive values of
72%-93%, with kappa values of 0.12-0.80. CONCLUSION: Spiral CT is
accurate in the depiction of peritoneal metastases from ovarian cancer,
although sensitivity is reduced in patients with tumor implants 1 cm or
smaller. Ancillary signs of peritoneal malignancy are limited by low
interobserver agreement. Copyright RSNA, 2002
12
UI - 11882011
AU - Liu Y; Ganesan TS
TI -
Tumour suppressor genes in sporadic epithelial ovarian cancer.
SO - Reproduction 2002 Mar;123(3):341-53
AD - ICRF Molecular Oncology Laboratories, Institute of Molecular Medicine,
John Radcliffe Hospital, Headington, Oxford OX3 9DS, UK.
Ovarian cancer is the most frequent cause of death from gynaecological
malignancies in the western world, and sporadic epithelial ovarian
cancer is its most predominant form. The aetiology of sporadic ovarian
cancer remains unknown. Genetic studies have enabled a better
understanding of the evolution of tumour progression. A major focus of
research has been to identify tumour suppressor genes implicated in
sporadic ovarian cancer over the past decade. Several tumour suppressor
genes have been identified by strategies such as positional cloning and
differential expression display. Further research is warranted to
understand fully their contribution to the pathogenesis of sporadic
ovarian cancer.
13
UI - 11992549
AU - Kudoh K; Ichikawa Y; Yoshida S; Hirai M; Kikuchi Y; Nagata I; Miwa M;
TI -
Uchida K
Inactivation of p16/CDKN2 and p15/MTS2 is associated with prognosis and
response to chemotherapy in ovarian cancer.
SO - Int J Cancer 2002 Jun 1;99(4):579-82
AD - Department of Obstetrics and Gynecology, Self Defense Force Sendai
Hospital, Miyagi 983-8580, Japan. k2-kudoh@xa2.so-net.ne.jp
To define the involvement of p16/CDKN2 and p15/MTS2 tumor-suppressor
genes for response to chemotherapy in primary epithelial ovarian cancer,
we analyzed alterations of the gene in 45 patients who were treated with
primary cytoreductive surgery followed by 6 courses of
cis-diamminedichloroplatinum (II) (cisplatin)-based combination
chemotherapy. Homozygous deletion of p16/CDKN2 and p15/MTS2 genes was
found in 8 (18%) and 15 (33%) cases, respectively. Response to the
chemotherapy was confirmed by finding at second surgery after the
chemotherapy in 26 patients, resulting in 17 responders and 9
nonresponders. The abundance of gene deletion in nonresponders (56%) was
significantly higher (p = 0.0463) when compared to that in responders
(18%). Moreover, the deletion of genes was a significant poor prognostic
factor (p = 0.0441) in advanced ovarian cancer. These results suggest
that deletion of p16/CDKN2 and/or p15/MTS2 is a potential indicator for
poor chemotherapy response and adverse prognosis in ovarian cancer
patients. Copyright 2002 Wiley-Liss, Inc.
14
UI - 11992553
AU - Lukanova A; Toniolo P; Lundin E; Micheli A; Akhmedkhanov A; Muti P;
TI -
Zeleniuch-Jacquotte A; Biessy C; Lenner P; Krogh V; Berrino F; Hallmans
G; Riboli E; Kaaks R
Body mass index in relation to ovarian cancer: a multi-centre nested
case-control study.
SO - Int J Cancer 2002 Jun 1;99(4):603-8
AD - Department of Nutrition and Cancer, International Agency for Research on
Cancer, 150 Cours Albert Thomas, 69372 Lyon, France. lukanova@iarc.fr
The incidence of ovarian cancer is up to 10 times higher in Western
countries than in rural Asia and Africa. One common consequence of a
Western lifestyle is the development of excessive body weight and
obesity. A multi-centre prospective study was conducted to investigate
the association between body mass index (BMI) and ovarian cancer risk. A
case-control study was nested within 3 prospective cohorts in New York
(USA), Umea (Sweden) and Milan (Italy). Information on anthropometry,
demographic characteristics, medical history and lifestyle was obtained
at the time of subjects' recruitment in each cohort. Women diagnosed
with primary, invasive epithelial ovarian cancer from the 3 cohorts (n =
122) diagnosed 12 months or later after recruitment into the respective
cohort served as case subjects. For each case subject, 2 control
subjects that matched the case subject on cohort, menopausal status, age
and date of recruitment were randomly identified. Data were analyzed by
conditional logistic regression. There was an inverse association
between BMI and ovarian cancer risk. For increasing quartiles of BMI
above the lowest, the ORs were 0.62 (0.32-1.21), 0.59 (0.30-1.17) and
0.46 (0.23-0.92), p = 0.03. Analyses limited to women diagnosed 3 or
more years after recruitment into the cohorts did not alter these
findings. When obese women (BMI > 30) were compared to lean women (BMI <
or = 23), the inverse association became stronger, with an OR of 0.38
(0.17-0.85), p < 0.02. There was some evidence of direct association of
ovarian cancer with height, which was limited to cancers diagnosed
before age 55. Our data suggest that increasing body weight may confer a
protection against ovarian cancer. Copyright 2002 Wiley-Liss, Inc.
15
UI - 11519321
AU - Trifonov I; Todorova M; Uzunova Zh
TI -
[Hereditary ovarian cancer]
SO - Akush Ginekol (Sofiia) 2001;41 Suppl 4():3-7
16
UI - 11606116
AU - Morice P; Pautier P; Delaloge S
TI -
Prophylactic surgery in patients with inherited risk of ovarian cancer.
SO - Gynecol Oncol 2001 Nov;83(2):445-7
17
UI - 11977327
AU - Krupski W; Jakiel G; Zlomaniec J
TI -
Diagnostic value of US and CT in the assessment of ovarian teratomas and
their qualifications for surgical treatment with laparoscopic method.
SO - Ann Univ Mariae Curie Sklodowska [Med] 2001;56():285-93
AD - 2nd Department of Radiology, Medical University of Lublin.
In the group of 17 women after surgery with histopathologically
confirmed diagnosis of teratomas diagnostic usefulness of US and CT was
analysed. Differentiated echostructure of tumours was correlated with
different densities of pathologic tissues in CT examination, also after
their contrast enhancement. In 2 patients teratomas of both ovaries were
recognised, in the remaining 15 women tumours were unilateral. In total
morphologic pictures of 19 teratomas were assessed, 9 times tumours with
prevailing liquid component had the picture of a thick-walled cyst, 7
times these were hyperechogenic fatty foci and in 3 cases had the
character of solid tumours. Teratomas had different morphologic
pictures, but it was possible to show the prevalence of one element and
classify the tumour to one of the three types of teratomas. It was found
that US examination, due to its high frequency, lets early diagnose
teratomas before they are accessible in the clinical exam, in the
symptomless period or when they give indirect symptoms, usually dysuric
ones. CT examination, due to its high sensitivity in recognising fatty
tissue and calcifications, is necessary before laparoscopic operation
requiring fragmentation of big tumours to determine their character.
18
UI - 11992414
AU - Bertone ER; Newcomb PA; Willett WC; Stampfer MJ; Egan KM
TI -
Recreational physical activity and ovarian cancer in a population-based
case-control study.
SO - Int J Cancer 2002 May 20;99(3):431-6
AD - Department of Biostatistics and Epidemiology, School of Public Health
and Health Sciences, University of Massachusetts, Amherst, MA
01003-9304, USA. ebertone@schoolph.umass.edu
Results from epidemiologic studies of physical activity and ovarian
cancer have been inconsistent, with 2 prospective studies reporting a
modest positive association. We evaluated this relationship in a
population-based case-control study conducted in Massachusetts and
Wisconsin. Incident cases diagnosed between 1991 and 1994 were
identified through statewide tumor registries. Community controls were
selected randomly from lists of licensed drivers and Medicare
recipients. Participation in moderate and vigorous recreational physical
activity at age 12, age 20 and 5 years prior to diagnosis was assessed
by telephone interview. Data were available for 327 cases and 3,129
controls. Results were adjusted for age, parity and other ovarian cancer
risk factors. Total and vigorous physical activity were not associated
with a substantial decrease in ovarian cancer risk at any age. The
relative risk (RR) for women reporting > or = 7 vs. 0 hr/week of recent
vigorous activity was 0.85 [95% confidence interval (CI) = 0.39-1.86; p
for trend = 0.31]. When metabolic equivalent task (MET) hours of
activity were estimated, only women in the highest category had any
reduction in risk (RR for > 42 MET-hours/week at the reference age =
0.70; 95% CI = 0.36-1.35; p for trend = 0.41). Overall, our results
provide only limited support for an inverse association between
recreational physical activity and risk of ovarian cancer. Copyright
2002 Wiley-Liss, Inc.
19
UI - 12039933
AU - Berry DA; Iversen ES Jr; Gudbjartsson DF; Hiller EH; Garber JE; Peshkin
TI -
BN; Lerman C; Watson P; Lynch HT; Hilsenbeck SG; Rubinstein WS; Hughes
KS; Parmigiani G
BRCAPRO validation, sensitivity of genetic testing of BRCA1/BRCA2, and
prevalence of other breast cancer susceptibility genes.
SO - J Clin Oncol 2002 Jun 1;20(11):2701-12
AD - Department of Biostatistics, University of Texas M.D. Anderson Cancer
Center, Houston, TX 77030-4009, USA. dberry@mdanderson.org
PURPOSE: To compare genetic test results for deleterious mutations of
BRCA1 and BRCA2 with estimated probabilities of carrying such mutations;
to assess sensitivity of genetic testing; and to assess the relevance of
other susceptibility genes in familial breast and ovarian cancer.
PATIENTS AND METHODS: Data analyzed were from six high-risk genetic
counseling clinics and concern individuals from families for which at
least one member was tested for mutations at BRCA1 and BRCA2.
Predictions of genetic predisposition to breast and ovarian cancer for
301 individuals were made using BRCAPRO, a statistical model and
software using Mendelian genetics and Bayesian updating. Model
predictions were compared with the results of genetic testing. RESULTS:
Among the test individuals, 126 were Ashkenazi Jewish, three were male
subjects, 243 had breast cancer, 49 had ovarian cancer, 34 were
unaffected, and 139 tested positive for BRCA1 mutations and 29 for BRCA2
mutations. BRCAPRO performed well: for the 150 probands with the
smallest BRCAPRO carrier probabilities (average, 29.0%), the proportion
testing positive was 32.7%; for the 151 probands with the largest
carrier probabilities (average, 95.2%), 78.8% tested positive. Genetic
testing sensitivity was estimated to be at least 85%, with
false-negatives including mutations of susceptibility genes heretofore
unknown. CONCLUSION: BRCAPRO is an accurate counseling tool for
determining the probability of carrying mutations of BRCA1 and BRCA2.
Genetic testing for BRCA1 and BRCA2 is highly sensitive, missing an
estimated 15% of mutations. In the populations studied, breast cancer
susceptibility genes other than BRCA1 and BRCA2 either do not exist, are
rare, or are associated with low disease penetrance.
20
UI - 9916789
AU - Tlsty TD
TI -
A molecular blueprint for targeting cancer?
SO - Nat Genet 1999 Jan;21(1):64-5
21
UI - 12052591
AU - Tay EH; Grant PT; Gebski V; Hacker NF
TI -
Secondary cytoreductive surgery for recurrent epithelial ovarian cancer.
SO - Obstet Gynecol 2002 Jun;99(6):1008-13
AD - Gynaecological Cancer Centre, Royal Hospital for Women, Department of
Obstetrics and Gynaecology, University of New South Wales, Sydney,
Australia.
OBJECTIVE: To review our experience with secondary cytoreductive surgery
for recurrent epithelial ovarian cancer with regard to its feasibility,
morbidity, mortality, patient selection, and survival. METHODS:
Forty-six patients who underwent secondary cytoreductive surgery at the
were retrospectively reviewed. The mean age at surgery was 50.3 years,
and the median disease-free interval was 26 months. Eighty-nine percent
of patients had a disease-free interval of at least 12 months.
Twenty-five patients (54%) had localized disease at the time of surgery.
Univariate survival outcomes were analyzed using the log rank test, and
survival curves were calculated using the method of Kaplan-Meier.
RESULTS: Two patients (4%) were inoperable and 19 patients (41%) were
cytoreduced to no macroscopic disease. There was one postoperative death
(2%), and four patients (8.7%) had significant postoperative morbidity.
With a median follow-up of 88 months, the overall median survival was
22.5 months. Patients with a disease-free interval of less than 12
months after their initial treatment had a median survival of 6 months,
compared with 11 months if the disease-free interval was 12-24 months
and 39 months for those with a disease-free interval of 24 months or
more (P =.001, log rank). Patients who had any residual disease had a
median survival of 11 months, whereas those with no residual disease had
a median survival of 38 months (P =.002, log rank). CONCLUSION: For
carefully selected patients with recurrent epithelial ovarian cancer: 1)
complete surgical resection is feasible more commonly than with primary
cytoreduction, 2) serious morbidity and mortality are acceptable, and 3)
significant survival benefit accrues when a) all macroscopic disease can
be resected, or b) the disease-free interval is 24 months or more.
22
UI - 11911974
AU - Matsumoto K; Yoshikawa H; Yasugi T; Onda T; Nakagawa S; Yamada M; Kawana
TI -
K; Minaguchi T; Oda K; Hasumi Y; Taketani Y
Distinct lymphatic spread of endometrial carcinoma in comparison with
cervical and ovarian carcinomas.
SO - Cancer Lett 2002 Jun 6;180(1):83-9
AD - Department of Obstetrics and Gynecology, Faculty of Medicine, University
of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo, Japan.
The distribution of metastatic pelvic lymph nodes (PLNs) and aortic
lymph nodes (ALNs) in 27 node-positive endometrial carcinomas (ECs) was
analyzed in comparison with that in 25 node-positive cervical carcinomas
(CCs) and 58 node-positive ovarian carcinomas (OCs). All patients
underwent systematic pelvic and aortic lymphadenectomy. Lymph nodes were
classified into the five subgroups: ALN above the inferior mesenteric
artery (IMA; A1), ALN below the IMA (A2), the common iliac and sacral
LNs (P1), the internal and external iliac LNs and obturator LNs (P2) and
the suprainguinal LNs (P3). EC was similar to CC in that metastases to
P2 were more frequent compared to A1 or A2, whereas EC and OC shared a
common feature in that A1, A2 and P2 were involved at high rates. ALN
metastases were significantly associated with P1 positivity in both EC
and CC (P<0.05), but not in OC. However, the incidence of both ALN and
PLN metastases in EC (67%) was similar to that in OC (61%), being much
higher than that in CC (36%). ALN involvement alone was observed in 7%
for EC, 0% for CC and 21% for OC. Based on the distribution of LN
metastases, it appears that CC metastasizes primarily to PLN, whereas OC
metastasizes almost equally to both PLN and ALN. Interestingly, EC can
directly metastasize to both PLN and ALN with PLN metastases being
dominant, a distinct lymphatic spread pattern better viewed as being
somewhere between CC and OC.
23
UI - 11950960
AU - Gallagher NJ; Eliopoulos AG; Agathangelo A; Oates J; Crocker J; Young LS
TI -
CD40 activation in epithelial ovarian carcinoma cells modulates growth,
apoptosis, and cytokine secretion.
SO - Mol Pathol 2002 Apr;55(2):110-20
AD - CRC Institute for Cancer Studies, University of Birmingham Medical
School, Birmingham B15 2TA, UK.
BACKGROUND/AIMS: CD40, a member of the tumour necrosis factor (TNF)
receptor family, is expressed on a variety of haematopoietic cells and
is crucial in orchestrating both humoral and cellular immune responses.
CD40 is also expressed on some carcinoma cells, where its function
remains largely unknown. This study investigated the effects of CD40
ligation on ovarian carcinoma cell growth and apoptosis and on cytokine
production, in addition to the role of the NF-kappa B and JNK signalling
pathways. METHODS: CD40 expression was measured in epithelial ovarian
carcinoma (EOC) biopsies by immunohistochemistry and in EOC cell lines
by flow cytometry. To examine the effects of CD40 ligation on cell
growth recombinant soluble CD40 ligand was used to stimulate EOC cell
lines and growth was measured by MMT assays. Cytokine production was
measured by enzyme linked immunosorbent assays interleukin 8 (IL-8) gene
transcription was estimated by means of reverse transcription polymerase
chain reaction. The integrity of the CD40 signalling pathway in those
cell lines that did not produce cytokines in response to CD40 ligation
was assessed by the detection of the transcription factor NF-kappa B by
an electrophoretic mobility shift assay. To investigate the defect in
the NF-kappa B pathway the phosphorylation status of I kappa B alpha was
determined by an antibody specific to phosphorylated I kappa B alpha and
dissociation of the I kappa B alpha-p65 complex was assessed by
co-immunoprecipitation. RESULTS: CD40 is expressed in primary ovarian
carcinoma biopsies and EOC cell lines. CD40 ligation resulted in growth
inhibition in most of these carcinoma cell lines and was also found to
promote apoptosis, with this last effect only being evident in early
passage EOC cells. CD40 ligation also induced significant IL-6 and IL-8
production in most of the EOC cell lines examined and it was confirmed
for IL-8 that this effect was regulated at the transcriptional level.
NF-kappa B activation in response to CD40 ligation was found in three of
the EOC cell lines and specific defects in the CD40 induced NF-kappa B
pathway were identified in two cell lines. However, CD40 engagement
induced JNK activation in all the EOC cell lines. CONCLUSIONS: These
data suggest that the CD40 pathway is functional in ovarian carcinoma
cells and highlight the need for further studies to provide insight into
the role of CD40 in the carcinogenic process and the possible
exploitation of this pathway for novel therapeutic approaches.
24
UI - 11975680
AU - Zhang GL; Xu KL
TI -
Loss of heterozygosity at chromosome 3p in epithelial ovarian cancer in
China.
SO - Int J Gynecol Cancer 2002 Mar-Apr;12(2):198-201
AD - Department of Gynecological Oncology, Shanghai Cancer Hospital, Fu Da
University, Shanghai, China.
The aim of this investigation was to determine the relationship between
3p loss of heterozygosity (LOH) and the pathogenesis of ovarian cancer.
Fifty cases of epithelial ovarian tumor, including 40 cases with
malignant tumors and 10 cases with benign tumors, were examined by
polymerase chain reaction (PCR) with D3s1228 and D3s1038 microsatellite
polymorphism markers at 3p. Thirty-two of the 40 cases (80%) with
ovarian cancer showed LOH at 3p14 or 3p25, but only 1 of 10 cases
(10.0%) with benign ovarian tumor showed 3p LOH. Among them, 24 cases
(60.0%) had LOH at 3p14 and 16 cases (40.0%) at 3p25, as well as 8 cases
(20.0%) with codeletion on both 3p14 and 3p25. According to FIGO
staging, the frequency of LOH at 3p in ovarian cancer patients with
stage IIIa or IIIb was higher than that in patients with stage I or II
(P < 0.05), but there was no relationship between 3p LOH and the
pathologic types in epithelial ovarian cancer (P > 0.05). Since 3p LOH
commonly occurs in epithelial ovarian cancer and LOH at 3p14 and 3p25
correlates to the staging of ovarian cancer, it is suggested that there
are some candidate ovarian TSGs harbored in the 3p region and that the
detection of 3p LOHs may be used as a genetic marker for monitoring the
development of ovarian cancer.
25
UI - 12000179
AU - Garner CM; Hubbold LM; Chakraborti PR
TI -
In vitro testing of platinum-based drugs on a panel of human ovarian
tumour cell lines.
SO - Br J Biomed Sci 2002;59(1):15-9
AD - Oncology Research Laboratory, Derby Cancer Centre, Derby City General
Hospital. briannation@ibms.org
Much improvement in the treatment of ovarian cancer has been achieved
since the introduction of platinum compounds in the 1980s, with the
result that single-agent platinum-based therapy following primary
surgery is now the standard treatment for advanced ovarian cancer. The
main therapeutic effect of chemotherapy is based on the sensitivity of
the patient's tumour to the drug. However, testing a new chemical
compound on humans requires much care, time and resources, whereas prior
testing of drugs on cancer cell lines may indicate those drugs
particularly suited to treatment of a specific disease. This study
investigates the actions of two established platinum-based
chemotherapeutic agents (cisplatin and carboplatin) on a panel of 10
human ovarian cancer cell lines. Each cell line was plated onto 96-well
tissue culture plates, incubated for 72 hours with the drug,
formalin-fixed and then assessed using the methylene blue colorimetric
microassay to detect viable cells. The IC50 values for each cell line
were calculated in order to assess the toxicity of each drug, and a wide
range of responses were observed across the 10 cell lines investigated.
This suggests that the panel reflected the heterogeneous nature of
ovarian cancer, a malignancy in which a huge range of drug sensitivities
can be seen even among tumours of the same histological type. The
results indicate that the panel could be of use either as a primary
screen to test new drugs against ovarian cancer or to investigate the
drug resistance that is so common in this disease.
26
UI - 12069652
AU - Stephenson J
TI -
Cancer studies explore targeted therapy, researchers seek new prevention
strategies.
SO - JAMA 2002 Jun 19;287(23):3063-7
27
UI - 10758808
AU - Sari R; Buyukberber S; Sevinc A; Ates M; Balat O; Hascalik S; Turk M
TI -
The effects of abdominal and bimanual pelvic examination and
transvaginal ultrasonography on serum CA-125 levels.
SO - Clin Exp Obstet Gynecol 2000;27(1):69-71
AD - Inonu University, School of Medicine, Department of Internal Medicine,
Turgut Ozal Medical Center, Malatya, Turkey.
The need for the early detection of ovarian cancer continues to be one
of the most important issues in women's health care. The three most
extensively evaluated screening methods for ovarian cancer are pelvic
examination, transvaginal ultrasonography, and serum CA-125 levels. The
answers to questions such as should the levels of CA-125 be measured
before bimanual pelvic examination or transvaginal ultrasonography or do
abdominal examinations effect the levels of CA-125 are obscure.
Fifty-four otherwise healthy female volunteers at the preovulatory phase
of the menstrual cycle complaining of vaginal candidiasis were divided
into 3 groups. Abdominal (group 1), bimanual pelvic (group 2), and
transvaginal ultrasonography (group 3) examination was performed and
serum CA-125 levels were evaluated prior to examination and 10 minutes,
6 hours, and 24 hours after the examination. As a result, serum CA-125
levels (U/ml) were found to be 8.13 +/- 4.76, 8.23 +/- 5.05, 8.32 +/-
4.88, and 8.33 +/- 4.94 in the group of abdominal examination,
respectively, 8.23 +/- 4.89, 8.45 +/- 5.15, 8.77 +/- 4.96, and 8.79 +/-
5.50 in the group of bimanual pelvic examination, respectively, and 8.19
+/- 4.56, 8.30 +/- 5.10, 8.81 +/- 5.56, and 8.88 +/- 5.71 in the group
of transvaginal ultrasonography, respectively. The serum CA-125 levels
detected prior to examinations were statistically insignificant when
compared with the results obtained at 10 minutes, 6 hours, and 24 hours
later in all three groups. We concluded that physical examination,
either abdominal or pelvic, and transvaginal ultrasonography do not
change the serum levels of CA-125.
28
UI - 12014634
AU - Jin X; Burke W; Rothman K; Lin J
TI -
Resistance to p53-mediated growth suppression in human ovarian cancer
cells retain endogenous wild-type p53.
SO - Anticancer Res 2002 Mar-Apr;22(2A):659-64
AD - Department of Obstetrics and Gynecology, University of Michigan
Comprehensive Cancer Center, Ann Arbor 48109-0936, USA.
Cancer cells containing mutated p53 are sensitive to the re-introduction
of the wild-type (wt) p53. We sought to determine whether ovarian cancer
cells that retain wt p53 are sensitive to the re-introduction of wt p53.
Our results demonstrated that A2780 and PA-1 cells, which retain wt p53,
are more resistant to apoptosis and growth suppression induced by
exogenous expression of wt p53 than SKOV-3 and Caov-3 cells that contain
mutated p53. All cell lines, except PA-1, showed induction of the
p53-targeted genes. Further, inhibitors of p53-dependent apoptosis, mdm2
and Bcl-xL were not overexpressed in A2780 and PA-1 cells. These results
suggest that one major defect in PA-1 cells is due to abrogation of
induction of the p53-targets which is independent of mdm2 and Bcl-xL.
Although A2780 cells showed induction of the p53-targeted genes, the
cleavage of caspase-9 was undetectable. Therefore, p53-dependent
apoptosis may be blocked upstream or at the caspase-9 level in A2780
cells.
29
UI - 12014680
AU - Arzimanoglou II; Hansen LL; Chong D; Li Z; Psaroudi MC; Dimitrakakis C;
TI -
Jacovina AT; Shevchuk M; Reid L; Hajjar KA; Vassilaros S; Michalas S;
Gilbert F; Chervenak FA; Barber HR
Frequent LOH at hMLH1, a highly variable SNP in hMSH3, and negligible
coding instability in ovarian cancer.
SO - Anticancer Res 2002 Mar-Apr;22(2A):969-75
AD - Department of Obstetrics-Gynecology, Weill Medical College of Cornell
University, New York, NY 10021, USA. Arziman@lycosmail.com
BACKGROUND: Molecular alterations such as DNA microsatellite instability
(MSI/RER), single nucleotide polymorphism (SNP) and loss of
heterozygosity (LOH) can occur throughout the genome and be associated
with different types of cancer. In the present study, we aimed at
detecting molecular alterations within the mismatch DNA repair genes in
ovarian cancer (OC), using a sensitive, accurate and reliable protocol
we have developed. MATERIALS AND METHODS: A combination of
high-resolution GeneScan software analysis and automated DNA cycle
sequencing was used. RESULTS: Negligible coding MSI was observed in
selected sequences of mismatch DNA repair genes in our series of
sixty-two ovarian tumors and matched blood DNAs. Unlike MSI, loss of one
hMLH1 allele was scored in almost half (47%) of the informative cases.
In addition, an SNP in hMSH3/intron 5 was found to be highly variable in
OC patients. CONCLUSION: 1) Coding DNA instability is likely to be a
very rare event in OC and, therefore, may not significantly contribute
to the development of OC, and 2) the high frequency of LOH at hMLH1
observed in our ovarian tumors suggests that further investigation is
needed to determine if such a trend exists in other mismatch DNA repair
and/or critical genes.
30
UI - 11881387
AU - Iakimova TP; Dudnichenko AS; Kartashov SM
TI -
[Structural and functional features of the ovaries as a risk factor for
ovarian cancer in infertile women]
SO - Lik Sprava 2001 Sep-Dec;(5-6):73-6
In examining 502 female patients with cancer of the ovaries (OC)
infertility was identified in 21.9 percent of cases. The prevalent form
of infertility was tubal infertility (92.7%), there were but a few
instances of the endocrine form (1.8%). The infertile women were studied
for their hormonal and receptorial status (receptors of estradiol and
progesterone). It has been established that women with the endocrine
variant of infertility present with more prominent hormonal inadequacies
in the hypophysis-ovaries system and manifest changes in the receptorial
status of the ovaries than those with tubal infertility; the findings in
the latter have not been shown to be different from controls. In
endocrine infertility OC is in fact not encountered, which fact can be
related to morphological features of the ovaries giving origin to
endocrine disturbances, and to a decline in the receptorial status and
absence of ovulation.
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