Table of Contents
1
UI - 11745676
AU - Evans MF; Herrington CS
TI -
Allelic imbalance is not restricted to numerically abnormal chromosomes
in epithelial ovarian tumours.
SO - J Pathol 2001 Nov;195(4):443-50
AD - Department of Pathology, Duncan Building, Royal Liverpool University
Hospital, Daulby Street, Liverpool L69 3GA, Merseyside, UK.
In this study, 23 low malignant potential (LMP) and 27 invasive
epithelial ovarian tumours have been examined by microdissection and
microsatellite polymerase chain reaction (PCR) for allelic imbalance
(AI) at loci on the p and q arms of chromosomes 1, 11, 17, and X, and
the data have been compared with interphase cytogenetics for numerical
abnormalities (aneusomy) of these chromosomes. AI was uncommon in LMP
tumours (5 of 23 at 9 of 146 informative loci) but was significantly
more common (p<0.001) in invasive carcinomas (21 of 27 at 47 of 168
informative loci). This difference remained when LMP tumours were
compared specifically with stage I carcinomas (p<0.001). A greater
number of loci were involved in AI amongst serous than amongst mucinous
carcinomas (p=0.015). AI was present at significantly more loci in
carcinomas showing aneusomy by interphase cytogenetics than in those
showing no numerical chromosome abnormalities (p<0.001). However,
amongst the carcinomas showing aneusomy, AI was as frequent at loci on
chromosomes with no numerical abnormality as at those with the numerical
changes. These data demonstrate that aneusomy and AI are interrelated
phenomena but that AI does not occur simply as a consequence of
numerical chromosome changes. Copyright 2001 John Wiley & Sons, Ltd.
2
UI - 11745677
AU - Piek JM; van Diest PJ; Zweemer RP; Jansen JW; Poort-Keesom RJ; Menko FH;
TI -
Gille JJ; Jongsma AP; Pals G; Kenemans P; Verheijen RH
Dysplastic changes in prophylactically removed Fallopian tubes of women
predisposed to developing ovarian cancer.
SO - J Pathol 2001 Nov;195(4):451-6
AD - Department of Obstetrics and Gynaecology, University Hospital Vrije
Universiteit, Amsterdam, The Netherlands.
The aim of this study was to investigate the occurrence of
(pre)neoplastic lesions in overtly normal Fallopian tubes from women
predisposed to developing ovarian carcinoma. The presence of
(pre)neoplastic lesions was scored in histological specimens from 12
women with a genetically determined predisposition for ovarian cancer,
of whom seven tested positive for a germline BRCA1 mutation. A control
group included 13 women. Immunohistochemistry was used to determine the
expression of p21, p27, p53, cyclin A, cyclin D1, bcl-2, Ki67,
HER-2/neu, and the oestrogen and progesterone receptors. Loss of
heterozygosity (LOH) analysis on the BRCA1 locus was also assessed on
dysplastic tissue by PCR studies. Of the 12 women with a predisposition
for ovarian cancer, six showed dysplasia, including one case of severe
dysplasia. Five harboured hyperplastic lesions and in one woman no
histological aberrations were found in the Fallopian tube. No
hyperplastic, dysplastic or neoplastic lesions were detected in the
Fallopian tubes of control subjects. In the cases studied,
morphologically normal tubal epithelium contained a higher proportion of
Ki67-expressing cells (p=0.005) and lower fractions of cells expressing
p21 (p<0.0001) and p27 (p=0.006) than in the control group. Even higher
fractions of proliferating cells were found in dysplastic areas (p=0.07)
and accumulation of p53 was observed in the severely dysplastic lesion.
Expression patterns of other proteins studied, including the hormone
receptors, were similar in cases and controls. One subject, a germline
BRCA1 mutation carrier, showed loss of the wild-type BRCA1 allele in the
severely dysplastic lesion. In conclusion, the Fallopian tubes of women
predisposed to developing ovarian cancer frequently harbour dysplastic
changes, accompanied by changes in cell-cycle and apoptosis-related
proteins, indicating an increased risk of developing tubal cancer.
Copyright 2001 John Wiley & Sons, Ltd.
3
UI - 11751427
AU - Riva F; Zuco V; Vink AA; Supino R; Prosperi E
TI -
UV-induced DNA incision and proliferating cell nuclear antigen
recruitment to repair sites occur independently of p53-replication
protein A interaction in p53 wild type and mutant ovarian carcinoma
cells.
SO - Carcinogenesis 2001 Dec;22(12):1971-8
AD - Centro di Studio per l'Istochimica del CNR, Piazza Botta 10, 27100
Pavia, Italy.
The tumour suppressor gene TP53 plays an important role in the
regulation of DNA repair, and particularly of nucleotide excision
repair. The influence of p53 status on the efficiency of the principal
steps of this repair pathway was investigated after UV-C irradiation in
the human ovarian carcinoma cell line IGROV-1 (expressing wild-type p53)
and in the derived clone IGROV-1/Pt1 (with p53 mutations at codons 270
and 282). Clonogenic survival after UV-C irradiation showed that
IGROV-1/Pt1 cells were approximately 2-fold more resistant to DNA damage
than parental cells. Modulation of p53 protein levels, cell cycle arrest
and apoptosis were induced in UV-irradiated IGROV-1 cells, but not in
the p53-mutant cell line. Exposure to UV or cisplatin induced
down-regulation of p53-replication protein A (RPA) interaction in
parental, but not in IGROV-1/Pt1 cells. However, persistent binding of
p53 to RPA did not affect the early steps of DNA repair. In fact, both
UV-induced DNA incision and the recruitment of proliferating cell
nuclear antigen (PCNA) to DNA repair sites occurred to a comparable
extent in p53-wild type and -mutant cell lines, although PCNA remained
associated with chromatin for a longer period of time in IGROV-1/Pt1
cells. Global genome repair, as detected by immunoblot analysis of
cyclobutane pyrimidine dimers, was not significantly different in the
two cell lines at 3 h after UV irradiation. In contrast, lesion removal
at 24 h was markedly reduced in IGROV-1/Pt1 cells, being approximately
25% of the initial amount of damage, as compared with approximately 50%
repair in parental cells. These results indicate that the presence of
mutant p53 protein and its persistent interaction with RPA do not affect
the early steps of nucleotide excision repair in IGROV-1/Pt1 cells.
Thus, repair defects in p53-mutant ovarian carcinoma cells may be
attributed to late events, possibly related to a reduced
removal/recycling of PCNA at repair sites.
4
UI - 11786728
AU - Hovig E; Rye PD; Warren DJ; Nustad K
TI -
CA 125: the end of the beginning.
SO - Tumour Biol 2001 Nov-Dec;22(6):345-7
AD - Central Laboratory, Norwegian Radium Hospital, Oslo, Norway.
CA 125, a high-molecular-weight mucin, was first defined in 1981 by the
monoclonal antibody OC125. Until recently, it has defied many attempts
to purify it from a variety of sources, although many research groups
have successfully raised antibodies that bind to CA 125. Nevertheless,
CA 125 has demonstrated its considerable value as a marker in monitoring
patients with ovarian cancer. This year, two research groups have
succeeded in cloning the high-molecular-weight mucin CA 125. Their
findings are summarized and the significance discussed in light of
existing data from the human genome. Copyright 2001 S. Karger AG, Basel
5
UI - 11786729
AU - O'Brien TJ; Beard JB; Underwood LJ; Dennis RA; Santin AD; York L
TI -
The CA 125 gene: an extracellular superstructure dominated by repeat
sequences.
SO - Tumour Biol 2001 Nov-Dec;22(6):348-66
AD - Department of Obstetrics and Gynecology, University of Arkansas for
Medical Sciences, Little Rock, AR 72205, USA. obrientimothyj@uams.edu
CA 125 has long presented problems to both clinicians and investigators
because there was no definitive information on its structure and
function. Here, we describe our work on cloning the CA 125 gene with the
anticipation that such information will provide the basis for
understanding its structure and its physiologic role in both normal and
malignant tissues. The CA 125 protein core is composed of a short
cytoplasmic tail, a transmembrane domain and an extraordinarily large
glycosylated extracellular structure. This structure is dominated by a
repeat domain composed of 156 amino acid repeat units which encompass
the epitope binding sites. The molecule also includes an amino terminal
domain of serine/threonine-rich sequences which would account for most
of the O-glycosylation known to be present in CA 125. CA 125 is an
unusually large transmembrane glycoprotein. Its release from the surface
of the cell is most probably dependent on cytoplasmic phosphorylation
followed by proteolytic cleavage. The extracellular domain is
characterized by a large number of repeat units (probably 60+) which
encompass an interactive disulfide bridged cysteine-loop and the site of
OC125 and M11 binding. Sequencing the gene provides us with the ability
to initiate the quest to understand the biological function of CA 125.
Copyright 2001 S. Karger AG, Basel
6
UI - 11780384
AU - Pan L; Tong Y; Jin Y; Zhou S; Zhang Y; Yang X; Mao N
TI -
Reversing drug resistance in the ovarian carcinoma cell line SKOV3/mdr1
in vitro by antisense oligodeoxynucleotides.
SO - Chin Med J (Engl) 2001 Sep;114(9):929-32
AD - Department of Obstetrics and Gynecology, Chinese Academy of Medical
Sciences, Peking Union Medical College Hospital, Beijing 100730, China.
OBJECTIVE: To investigate the effect of multidrug resistance gene 1
(mdr1) antisense oligodeoxynucleotides (ODNs) on reversing multidrug
resistance in the drug resistant ovarian carcinoma cell line SKOV3/mdr1.
METHODS: The ovarian carcinoma cell line SKOV3 transducted with a human
multidrug resistance gene (mdr1) served as the drug resistant model
(SKOV3/mdr1). The mdr1 antisense ODNs was transfected into SKOV3/mdr1
cells while mediated by lipofectamine. Reverse transcription-polymerase
chain reaction (RT-PCR) was used to measure the expression and the
amount of the mdr1 mRNA in the cells. The positive rate and function of
the mdr1 gene product P-glycoprotein (Pgp) in the mdr1 antisense ODNs
treated SKOV3/mdr1 cells were determined by flow cytometry and rhodamine
123 efflux. Drug resistance in the SKOV3/mdr1 cell line was observed by
MTT assay and cell colony culture. RESULTS: The mdr1 mRNA level was
decreased to about 60% of that of beta-actin after mdr1 antisense ODNs
treatment. The Pgp positive rate of mdr1 antisense ODNs treated
SKOV3/mdr1 cells decreased from 100% to 52.6% (P < 0.01). The
intracellular rhodamine 123 retention was increased from 9.1% to 33.8%
(P < 0.01). The chemoresistance to taxol decreased to 58% of SKOV3/mdr1
with mdr1 antisense ODN treatment. Compared with SKOV3/mdr1 cells in the
control group, under a certain range of drug concentrations, the number
of drug resistance colonies in mdr1 antisense ODNs treated SKOV3/mdr1
cells for taxol and doxorubicin decreased by 8.6 +/- 0.8 fold and 3.1
+/- 0.6 fold, respectively. Some non-specific functions during
oligodeoxyncleotide treatment was also detected. CONCLUSION: mdr1
expression in the SKOV1/mdr1 cell line was partially inhibited after
mdr1 antisense ODNs treatment at the mRNA and protein level, increasing
the chemotherapy sensitivity of this drug resistant ovarian carcinoma
cell line.
7
UI - 11554664
AU - Young RH
TI -
Guest editor's introduction. Ovarian tumors: perplexing patterns,
perspicacious pathologists.
SO - Semin Diagn Pathol 2001 Aug;18(3):155-60
AD - James Homer Wright Pathology Laboratories, Massachusetts General
Hospital, Harvard Medical School, Boston, USA.
8
UI - 11554665
AU - Young RH; Scully RE
TI -
Differential diagnosis of ovarian tumors based primarily on their
patterns and cell types.
SO - Semin Diagn Pathol 2001 Aug;18(3):161-235
AD - James Homer Wright Pathology Laboratories of the Massachusetts General
Hospital, Harvard Medical School, Boston, USA.
The differential diagnosis of ovarian tumors is reviewed based on their
patterns and cell types. This approach, which differs from the standard
textbook discussion of each neoplasm as an entity, has practical value
as differential diagnosis depends largely on the pattern or patterns and
cell type or types of tumors. Awareness of the broad range of lesions
that may exhibit particular patterns or contain one or more cell types
is crucial in formulating a differential diagnosis. The following
patterns are considered: moderate-to-large-glandular and hollow-tubular;
solid tubular and pseudotubular; cords and ribbons; insular; trabecular;
slit-like and reticular spaces; microglandular and microfollicular;
macrofollicular and pseudomacrofollicular; papillary; diffuse;
fibromatous-thecomatous; and biphasic and pseudobiphasic. The following
cell types are considered: small round cells; spindle cells; mucinous
cells, comprising columnar, goblet cell and signet ring cell subtypes;
clear cells; hobnail cells; oxyphil cells; and transitional cells. The
morphologic diversity of ovarian tumors poses many challenges; knowledge
of the occurrence and frequency of these patterns and cell types in
various tumors and tumor-like lesions is of paramount diagnostic
importance. A specific diagnosis can usually be made by evaluating
routinely stained slides, but much less often, special staining,
immunohistochemical staining or, very rarely, ultrastructural
examination is also required. Finally, clinical data, operative
findings, and gross features of the lesions may provide important, and
at times decisive diagnostic clues.
9
UI - 10885351
AU - Meijers-Heijboer EJ; Verhoog LC; Brekelmans CT; Seynaeve C;
TI -
Tilanus-Linthorst MM; Wagner A; Dukel L; Devilee P; van den Ouweland AM;
van Geel AN; Klijn JG
Presymptomatic DNA testing and prophylactic surgery in families with a
BRCA1 or BRCA2 mutation.
SO - Lancet 2000 Jun 10;355(9220):2015-20
AD - Department of Clinical Genetics, Erasmus University, Rotterdam, The
Netherlands.
BACKGROUND: Germline mutations in the BRCA1 and BRCA2 genes highly
predispose to breast and ovarian cancer. In families with BRCA1 or BRCA2
mutations, identification of mutation carriers is clinically relevant in
view of the options for surveillance and prevention. METHODS: We
assessed presymptomatic DNA testing and prophylactic surgery in 53
consecutive families presenting to the Rotterdam Family Cancer Clinic
with a known BRCA1 or BRCA2 mutation. We identified predictors for DNA
testing and prophylactic surgery with univariate and multivariate
analysis. FINDINGS: 682 unaffected individuals with a 50% risk (275
women and 271 men) or with a 25% risk (136 women) for carrying a
mutation were identified and offered a DNA test. Presymptomatic DNA
testing was requested by 48% (198 of 411) of women and 22% (59 of 271)
of men (odds ratio for difference between sexes 3.21 [95% CI 2.27-4.51];
p<0.001). In women, DNA testing was significantly more frequent at young
age, in the presence of children, and at high pre-test genetic risk for
a mutation. Of the unaffected women with an identified mutation who were
eligible for prophylactic surgery, 51% (35 of 68) opted for bilateral
mastectomy and 64% (29 of 45) for oophorectomy. Parenthood was a
predictor for prophylactic mastectomy but not for prophylactic
oophorectomy. Age was significantly associated with prophylactic
oophorectomy, but not with prophylactic mastectomy, although there was a
tendency towards mastectomy at younger ages. INTERPRETATION: In a
clinical setting, we show a high demand for BRCA1 and BRCA2 testing by
unaffected women at risk, and of prophylactic surgery by unaffected
women with the mutation. Young women with children especially opt for
DNA testing and prophylactic mastectomy.
10
UI - 11499060
AU - Frank TS; Critchfield GC
TI -
Identifying and managing hereditary risk of breast and ovarian cancer.
SO - Clin Perinatol 2001 Jun;28(2):395-406
AD - Myriad Genetic Laboratories, Salt Lake City, Utah, USA.
tfrank@myriad.com
In the past, all women with a family history of breast or ovarian cancer
were considered to be at increased risk of cancer themselves. The
discovery of BRCA1 and BRCA2 demonstrated that susceptibility to breast
and ovarian cancer can be inherited by women as a single-gene autosomal
dominant disorder. For such women, evaluation of family history is an
important screening tool to identify the possibility of hereditary
cancer risk but only genetic testing can provide definitive,
individualized risk assessment. Women who have inherited mutations in
BRCA1 or BRCA2 now have several medical management options to address
their increased risk of cancer. A well-educated community of health care
providers and patients can use hereditary risk assessment, including
genetic testing, to improve health care.
11
UI - 11775215
AU - Jiang C; Tan Y; Li E; Zhang D
TI -
Neuroendocrine differentiation in ovarian mucinous tumors.
SO - Chin Med J (Engl) 2000 Jan;113(1):70-4
AD - Department of Pathology, Tianjin Medical University, Tianjin 300070,
China.
OBJECTIVE: To investigate the relationship between neuroendocrine
differentiation in ovarian mucinous tumors and its genesis. METHODS: A
morphologic study of seventy-three cases of ovarian mucinous tumors (32
benign, 20 borderline, 21 malignant) using immunohistochemical and
immunohistochemical/histochemical double staining techniques. RESULTS:
The study showed that in tumors of benign, borderline and malignant
types, the incidence of chromogranin A (CgA) positive cells was 62.5%,
75%, 76% and that of 5-hydroxytryptamine (5-HT) positive cells was
31.3%, 40% and 39%, respectively. Neuroendocrine cells (NEC) were not
evenly distributed in any tumor. In four cases of the benign tumors, the
number of CgA positive cells was more than 30 percent, localizing
between the glandular basement membrane and the mucinous epithelial
cells, with many intermediate cells containing both CgA and periodic
acid-schiff (PAS) positive granules. CONCLUSION: The occurrence of both
neuroendocrine and exocrine granules within the same cell has been
previously described as "intermediate" in pancreatic hyperplasia,
pancreatic tumors and lung signet-ring cell carcinoids. This has not
previously been observed in benign ovarian mucinous tumors. Finding both
endocrine and exocrine granules within a single cell seems to indicate a
histogenetic relationship between the ovarian endocrine and exocrine
cells. The four cases of the benign tumors might be originated from a
common stem cell, such as the so-called amphocrine cell. The
relationship between these four tumors and neuroendocrine
differentiation in ovarian mucinous tumors needs to be further
clarified.
12
UI - 11791820
AU - McCann S; MacAuley D
TI -
Management of familial breast and ovarian cancer cases.
SO - Br J Gen Pract 2002 Jan;52(474):57
13
UI - 11808531
AU - Amso NN
TI -
Endometriosis. Clinicians and patients should be aware of association
between endometriosis and malignancies.
SO - BMJ 2002 Jan 12;324(7329):115
14
UI - 11506467
AU - Tuxen MK; Soletormos G; Petersen PH; Dombernowsky P
TI -
Interpretation of sequential measurements of cancer antigen 125 (CA
125), carcinoembryonic antigen (CEA), and tissue polypeptide antigen
(TPA) based on analytical imprecision and biological variation in the
monitoring of ovarian cancer.
SO - Clin Chem Lab Med 2001 Jun;39(6):531-8
AD - Department of Oncology and Clinical Chemistry, Herlev Hospital,
University of Copenhagen, Denmark.
The main objective with cancer antigen 125 (CA 125), carcinoembryonic
antigen (CEA), and tissue polypeptide antigen (TPA) monitoring of
ovarian cancer patients is to detect an early change of disease activity
with high reliability. We hypothesized that a monitoring scheme for
ovarian cancer patients with serological tumor markers should take into
account the stochastic variation, i.e. the probability that observed
increases and decreases may solely be due to analytical imprecision and
normal intra-individual biological variation. The aim of this study was
to provide a detailed characteristic of the within-subject mean steady
state concentrations and the associated variability in healthy
individuals with an age distribution representative for ovarian cancer
patients. Thirty-one healthy women with a median age of 55 years
comprised the study population. Sixteen blood samples were collected
from each subject in four series, with four samples per series, over a
period of approximately 1 year. We found that, i) natural
logarithmic-transformed concentrations were more homogeneously
distributed between individuals than the original concentrations, ii)
the within-subject mean steady state levels, the standard deviations,
and the coefficients of variation differed among subjects, and iii) the
steady state variability differed among the markers. In conclusion, our
data indicate that the assessment of sequential CA 125, CEA, and TPA
concentrations is more complex than hitherto recognized. We suggest that
it is necessary to adjust the assessment criteria to the type of marker,
and that assessment may be facilitated if based on natural logarithmic
transformed concentrations.
15
UI - 11807777
AU - Buchholz TA; Wu X; Hussain A; Tucker SL; Mills GB; Haffty B; Bergh S;
TI -
Story M; Geara FB; Brock WA
Evidence of haplotype insufficiency in human cells containing a germline
mutation in BRCA1 or BRCA2.
SO - Int J Cancer 2002 Feb 10;97(5):557-61
AD - Department of Radiation Oncology, The University of Texas M. D. Anderson
Cancer Center, Houston, TX 77030, USA. tbuchhol@notes.mdacc.tmc.edu
The BRCA1 and BRCA2 gene products are thought to play important roles in
the processing of DNA damage. To assess whether heterozygous mutations
in these genes are associated with cellular radiosensitivity, we
performed an in vitro radiation clonogenic survival assay on dermal
fibroblasts obtained from 8 sequence-proven BRCA heterozygotes (6 BRCA1,
2 BRCA2). These data were compared to results obtained from a previous
set of 17 prospectively studied cancer patients who had a negligible
risk for a BRCA mutation. In addition, results from radiation-induced
chromatid break assay performed on lymphocytes obtained from 9 BRCA
heterozygotes (8 BRCA1, 1 BRCA2) were compared to results from a control
group of 18 women with no cancer history. Results from both assays
suggested that cells containing a heterozygous mutation in BRCA1 or
BRCA2 were more radiosensitive than controls. For the fibroblast
studies, the mean surviving fraction at 2 Gy (SF2) for carriers was
0.279 vs. 0.348 for the control set (p = 0.007). For the lymphocyte
studies, the mean number of chromatid breaks after 125 cGy of radiation
was 0.79 breaks per cell for the carriers vs. 0.45 for the controls (p =
0.0005). There was no apparent difference in the radiosensitivity
between cells with BRCA1 vs. BRCA2 mutations (p = 0.769), although the
small sample size minimizes the certainty of this observation. These
preliminary results are consistent with a relationship between a
germline mutation in BRCA1 or BRCA2 and a hypersensitivity to radiation.
This phenotype could possibly predispose to an increased risk of
radiation-induced mutagenesis and carcinogenesis. Copyright 2001
Wiley-Liss, Inc.
16
UI - 11782386
AU - Shridhar V; Sen A; Chien J; Staub J; Avula R; Kovats S; Lee J; Lillie J;
TI -
Smith DI
Identification of underexpressed genes in early- and late-stage primary
ovarian tumors by suppression subtraction hybridization.
SO - Cancer Res 2002 Jan 1;62(1):262-70
AD - Department of Experimental Pathology, Division of Laboratory Medicine,
Mayo Clinic, Rochester, Minnesota 55905, USA. shridv@exrch.mayo.edu
To identify novel tumor suppressor genes involved in ovarian
carcinogenesis, we generated four down-regulated suppression subtraction
cDNA libraries from two early-stage (stage I/II) and two late-stage
(stage III) primary ovarian tumors, each subtracted against cDNAs
derived from normal ovarian epithelial cell brushings. Approximately
600-700 distinct clones were sequenced from each library. Comparison of
down-regulated clones obtained from early- and late-stage tumors
revealed genes that were unique to each library which suggested
tumor-specific differences. We found 45 down-regulated genes that were
common in all four libraries. We also identified several genes, the role
of which in tumor development has yet to be elucidated, in addition to
several under expressed genes, the potential role of which in
carcinogenesis has been described previously (Bagnoli et al., Oncogene,
19: 4754-4763, 2000; Yu et al., Proc. Natl. Acad. Sci. USA, 96: 214-219,
1999; Mok et al., Oncogene, 12: 1895-1901, 1996). The differential
expression of a subset of these genes was confirmed by semiquantitative
reverse transcription-PCR using glyceraldehyde-3-phosphate dehydrogenase
(GAPDH) as control in a panel of 15 stage I and 15 stage III tumors of
mixed histological subtypes. Chromosomal sorting of library sequences
revealed that several of the genes mapped to known regions of deletion
in ovarian cancer. Loss of heterozygosity (LOH) analysis revealed
multiple genomic regions with a high frequency of loss in both early-
and late-stage tumors. To determine whether loss of expression of some
of the genes corresponds to loss of an allele by LOH, we used a
microsatellite marker for one of the novel genes on 8q and have shown
that loss of expression of this novel gene correlates with loss of an
allele by LOH. In conclusion, our analysis has identified down-regulated
genes, which map to known as well as novel regions of deletions and may
represent potential candidate tumor suppressor genes involved in ovarian
cancer.
17
UI - 11826460
AU - Levin T; Reichelt J; Heimdal K; Moller P
TI -
[Information to families with hereditary breast and ovarian cancer]
SO - Tidsskr Nor Laegeforen 2001 Nov 20;121(28):3292-4
AD - Seksjon for genetisk veiledning Avdeling for kreftgenetikk Det Norske
Radiumhospital 0310 Oslo. pal.moller@klinmed.uio.no
BACKGROUND: Under Norwegian legislation, persons at risk should make the
initial contact with the proper health personnel, and not vice versa. It
may be argued that the physician should be allowed to make contact with
persons at risk of preventable or curable disorders. MATERIAL AND
METHODS: We identified all first-degree relatives of all 75 BRCA1
mutation carriers diagnosed within a given period of time and asked them
whether or not they had been informed by their relatives. RESULTS: After
two years, 60/63 (95%) adult sisters and daughters had made contact with
us; the remaining three (5%) had been informed. In comparison, 18/45
(40%) adult brothers and sons had contacted us. INTERPRETATION: The
legislation constituted no barrier to offering health services to the
target group. Information on our services had reached all close
relatives who could benefit from them. This may be representative for
curable inherited disorders. We examined inherited cancer limited to
females; similar studies on inherited cancers in males and on other
curable inherited disorders should be performed. Outside the framework
of the present study, we are aware of rare examples of distant cousins
who have not been properly informed through their families. One legally
acceptable way of identifying mutation carrier families is to test all
patients with breast or ovarian cancer for causative mutations. Health
services should be monitored to make future decisions based on empirical
evidence.
18
UI - 11810077
AU - Walker GR; Schlesselman JJ; Ness RB
TI -
Family history of cancer, oral contraceptive use, and ovarian cancer
risk.
SO - Am J Obstet Gynecol 2002 Jan;186(1):8-14
AD - Sylvester Comprehensive Cancer Center, University of Miami School of
Medicine, Florida, USA.
OBJECTIVE: The purpose of this study was to determine whether women with
a family history of ovarian cancer are at reduced risk of ovarian cancer
from the use of oral contraceptives and to compare their risk with that
of women with no family history of ovarian cancer. STUDY DESIGN: A
diagnosis of epithelial ovarian cancer were ascertained from 39
hospitals in 3 northeastern states. Personal interviews with the women
and 1367 control subjects provided data that allowed us to estimate the
relative risk of ovarian cancer in relation to a family history of
cancer and total duration of oral contraception. RESULTS: Among the 33
case patients and 24 control subjects with a first-degree family history
of ovarian cancer, risk of ovarian cancer declined with increasing
duration of oral contraception (P =.01). Risk reduction from short-term
use of oral contraceptives (< or = 48 months) did not differ
significantly by family history (combined estimate of odds ratio, 0.72;
90% CI, 0.59%-0.87%). Risk reduction from long-term use of oral
contraceptives (>48 months) was greater in women with a positive family
history of ovarian cancer (odds ratio, 0.12) than in women with a
negative family history of ovarian cancer (odds ratio, 0.51; test of
interaction, P =.04; 692 case patients, 1279 control subjects).
CONCLUSION: Four to 8 years of oral contraception may substantially
reduce the risk of ovarian cancer by age 70 years in women with a family
history of the disease, from approximately 4 women per 100 women who did
not use oral contraceptives to only 2 women per 100 women who did use
oral contraceptives.
19
UI - 11526704
AU - Rampone B; Rampone A; Tirabasso S; Panariello S; Rampone N
TI -
Immunological variations in women suffering from ovarian cancer.
Influence of radical surgical treatment.
SO - Minerva Ginecol 2001 Feb;53(1 Suppl 1):116-9
AD - Institute of Obstetrics and Gynaecology, Second University of Naples,
Italy.
BACKGROUND: The immune system includes all the innate or acquired
mechanisms, that the organism uses for protecting itself from the
aggression of external pathogens or neoplasia. About the control of the
tumor growth, the immune mechanisms implicated are quite a lot: the
cytotoxicity against the tumor cells by cytotoxic T lymphocyte,
macrophages, NK cells; simil-NK cells (ADCC). Tumors have generally
antigenic marked potential, for which numerous antigens have been
identified, but none of these has revealed a correlated specificity to
the neoplasia. Only a glycoprotein at elevated molecular weight, the
CA125, presents an elevated specificity and sensibility. The objective
of this study was to examine immunological variations in the peripheral
blood of patients with ovarian carcinoma before and after radical
surgical treatment. METHODS: In the Institute of Obstetrics and
Gynaecology of Second University of Studies of Naples the immunological
variations in 8 women (mean age: 59.5; range: 49-70 years) suffering
from ovarian cancer, have been evaluated before and after radical
surgical treatment (when the stage of the tumor made possible the
surgery) and compared to 8 normal volunteers of comparable age (control
in average for two years and subjected to a immunological screening with
blood drawings effected at the hospitalisation and later 1, 6, 12, 18,
24 months from surgical treatment. The immune evaluation were effected
with: proliferation tests on the monocytes of the peripheral blood,
evaluation of the production of Interleukin 1 and 2 with the leukocyte
phenotyping, evaluation of NK cells activity. The patients were followed
in average for two years. RESULTS: The radical surgery decidedly
improves the immune response. The ability to produce IL-1 by the
lymphocytes of the patients object of our study, appeared constantly
falling (with reduction of about 50%) before the surgery and it
meaningfully increases in the post-surgery period. The surgery doesn't
modify the lymphocytes T helper and T inducer. The surgery delays the
diminution of the NK cells in a little meaningful way. The periodic
dosage of the CA125 does not give the same results: in the 60% a
progressive increase was realised and in the 40% it remained constant.
CONCLUSIONS: The surgery constantly improved the physical state of the
patient, determining an increase of the immune response toward the
neoplasia, and therefore achieving a meaningful increase of survival.
20
UI - 11526705
AU - Catizone FA; Gesmundo G; Catizone C; Sena T; Mastrantonio P
TI -
[Limitations and expectations of Doppler color in the diagnosis of
ovarian cancer]
SO - Minerva Ginecol 2001 Feb;53(1 Suppl 1):12-7
AD - Istituto di Scienze Ginecologiche e Pediatriche, Universita Magna
Grecia, Catanzaro.
21
UI - 11526707
AU - Rampone B; Rampone A; Tirabasso S; Panariello S; Rampone N
TI -
Ovarian cancer screening by transvaginal color Doppler ultrasonography.
SO - Minerva Ginecol 2001 Feb;53(1 Suppl 1):125-8
AD - Institute of Obstetrics and Gynaecology, Second University of Naples,
Italy.
BACKGROUND: The need for the early detection of ovarian cancer continues
to be one of the most important issue in women's health care. The
ovarian neoplasia characteristically have a scarce symptomatology for
which it tries to create a sensitive and specific screening test so that
the diagnosis could precociously be made and, consequently, improve the
prognosis with a timely therapy. Our purpose was to assess the
performance of transvaginal color Doppler ultrasonography in ovarian
cancer screening. METHODS: In the Institute of Obstetrics and
Gynaecology of Second University of Studies of Naples, in the period
groups (the 1st group included 30 women in fertile age with standard
uterine dimensions, the 2nd group included 30 menopausal women), were
submitted to transvaginal color Doppler ultrasonography. Color Doppler
ultrasonography was performed with an ESAOTE ANSALDO AU5 HARMONIC
ultrasound machine provided with a 6.5 MHz real-time sector electronic
array endovaginal probe with a 5 MHz pulsed Doppler system and equipped
with the color velocity imaging system for the color blood flow
codification. The score used in the evaluation of the ovary are us
follows: volume of the adnexa (from 1 to 5); presence of papillas and
septa (from 1 to 5); wall thickness (from 1 to 5). An high score (> 12)
corresponds to probability of presence of neoplasia. For the flow
modifications the following parameters were considered: RI (Index of
resistance); PI (Pulse Index); Vmax (Maximum Speed). CD was considered
as suspicious when flow was detected and the lowest RI found was < or =
0.45, PI < or = 0.58 Vmax < or = 60. RESULTS: Sonographic morphology
evaluation and CD were suspicious in 11 cases and 9 of these were
positive on histopathological analysis (true positive = 15%, false
positive = 5%). All the women that had morphologically normal ovaries
observed on ultrasound examination and were not suspicious on CD
analysis, were also negative on histopathological analysis (true
negative = 80%). CONCLUSIONS: The color Doppler ultrasonography revealed
a decidedly valid method of screening of the first level, being
non-invasive examination, painless, therefore well accepted by the
patients, even if in some women, especially if in fertile age, the
physiological modifications calls for repeated investigations and
compare its parameters.
22
UI - 11526715
AU - Greggi S; Legge F; Mancuso S
TI -
[Familial ovarian carcinoma]
SO - Minerva Ginecol 2001 Feb;53(1 Suppl 1):3-5
AD - Istituto di Clinica Ostetrica e Ginecologica, Universita Cattolica del
Sacro Cuore, Roma.
23
UI - 11526717
AU - Amunni G; Susini T; Villanucci A; Massi GB
TI -
[Recurrence of malignant epithelial tumors of the ovary]
SO - Minerva Ginecol 2001 Feb;53(1 Suppl 1):37-9
AD - I Clinica Ginecologica e Ostetrica, Universita degli Studi, Firenze.
24
UI - 11526718
AU - Ferrandina G; Legge F; Fagotti A; Fanfani F; Mancuso S; Scambia G
TI -
[Biological factors with prognostic significance in ovarian cancer]
SO - Minerva Ginecol 2001 Feb;53(1 Suppl 1):40-5
AD - Istituto di Clinica Ostetrica e Ginecologica, Universita Cattolica del
Sacro Cuore, Roma.
25
UI - 11526719
AU - Imparato E; Parodi M
TI -
[Treatment of intestinal and urinary tract obstruction in patients with
advanced ovarian disease]
SO - Minerva Ginecol 2001 Feb;53(1 Suppl 1):46-7
AD - Divisione di Ginecologia e Ostetricia, E.O. Ospedali Galliera, Genova.
26
UI - 11526723
AU - Bolis PF; Zanaboni F; Crotti S
TI -
[Borderline ovarian tumors]
SO - Minerva Ginecol 2001 Feb;53(1 Suppl 1):6-9
AD - Clinica Ostetrica e Ginecologica, Universita dell'Insubria, Sede vi
Varese.
27
UI - 11526726
AU - Saponara R; Menditto A; Russo G; Musone R; Balbi GC; Balbi C
TI -
[Review of the literature on BRCA 1 and BRCA 2]
SO - Minerva Ginecol 2001 Feb;53(1 Suppl 1):72-4
AD - Istituto di Clinica Ostetrica e Ginecologica, Seconda Universita degli
Studi, Napoli.
28
UI - 11526732
AU - Iervolino P; Palmieri M; Rotondi M; D'Alessandro P; Iuliano R
TI -
[Borderline ovarian tumors. Retrospective analysis of 20 cases]
SO - Minerva Ginecol 2001 Feb;53(1 Suppl 1):97-9
AD - Divisione di Ostetricia e Ginecologia, Ospedale S. Maria di Loreto
Nuovo, Napoli.
BACKGROUND: To evaluate the clinical features, the surgical management
and outcome of 20 patients with stage-I borderline ovarian tumors.
METHODS: Twenty cases of FIGO stage-I ovarian tumors, aged from 31 to 58
years (mean 37 years) have been reviewed. All informations of clinical
stage, surgical intervention and prognosis were achieved by reviewing
hospital records. Minimal requirements for conservative management were
adequate staging and complete information about the therapeutic options.
Factors important in the choice of the treatment were, age, wish to
preserve fertility, histologic type and grade, and the stage of the
tumour. RESULTS: Eleven of the 20 patients (55%) were at stage IA, 6
cases (30%) were at stage IB, 3 cases (15%) were at stage IC. Thirteen
(65%) were with mucinous cystadenoma of borderline malignancy, 7 cases
(35%) were of serous type. Thirteen patients underwent total abdominal
hysterectomy and bilateral salpingo-oophorectomy (TAH and BSO). Seven
patients were treated with unilateral oophorectomy or unilateral
salpingo-oophorectomy (USO). One patient underwent enucleation of
ovarian tumor and biopsy of contralateral ovary. Any patient were
treated with chemotherapy after operation. With a median follow up of
two years, we observed no recurrence of carcinoma in women treated
conservatively or in those treated more radically. CONCLUSIONS:
Conservative surgery remains a therapeutic option in selected patients
with borderline ovarian tumors. Prolonged intensive follow-up is
required for women treated conservatively for borderline malignant
ovarian tumours.
29
UI - 11477127
AU - McCluggage WG
TI -
Clear cell carcinoma of the ovary arising in a mucinous cystadenoma.
SO - J Clin Pathol 2001 Aug;54(8):655-6
30
UI - 11714114
AU - Purdie DM; Bain CJ; Webb PM; Whiteman DC; Pirozzo S; Green AC
TI -
Body size and ovarian cancer: case-control study and systematic review
(Australia).
SO - Cancer Causes Control 2001 Nov;12(9):855-63
AD - Queensland Institute of Medical Research, Herston, Australia.
davidP@qimr.edu.au
OBJECTIVE: Although increased body mass is an established risk factor
for a variety of cancers, its relation with cancer of the ovary is
unclear. We therefore investigated the association between measures of
body mass index (BMI) and ovarian cancer risk. METHODS: Data from an
Australian case-control study of 775 ovarian cancer cases and 846
controls were used to examine the association with BMI. We have also
summarized the results from a number of other studies that have examined
this association. RESULTS: There was a significant increased risk of
ovarian cancer with increasing BMI, with women in the top 15% of the BMI
range having an odds ratio (OR) of 1.9 (95% confidence interval (CI),
1.3-2.6) compared with those in the middle 30%. Stratifying by physical
activity showed a stronger effect among inactive women (OR = 3.0, 95% CI
1.3-6.9). The overall effect was consistent with the findings of most
prior population-based case-control studies, while cohort studies
reported positive effects closer to the null. Hospital-based studies
gave variable results. CONCLUSIONS: Taken together, the evidence is in
favor of a small to moderate positive relation between high BMI and
occurrence of ovarian cancer.
31
UI - 11780319
AU - Ye D; Xie X; Lu W; Chen H; Cheng B
TI -
Growth inhibition of interleukin-2 receptor gene-transduced peripheral
blood lymphocytes on human ovarian cancer cells.
SO - Chin Med J (Engl) 2001 Mar;114(3):303-7
AD - Department of Oncology, Women's Hospital, School of Medicine, Zhejiang
University, Hangzhou 310006, China.
OBJECTIVE: To investigate the growth inhibition of interleukin-2
receptor (IL-2R) gene-transduced peripheral blood lymphocytes (PBLs) on
human ovarian cancer cells. METHODS: Interleukin-2 (IL-2) and IL-2R
genes were transfected into human ovarian cancer cell line 3AO and PBLs,
respectively, using the same Fugene vector. Twenty-four hours later
transfected and nontransfected PBLs were cocultured with transfected and
nontransfected 3AO for 48 hours. cytotoxicity of PBLs on 3AO was
detected by the MTT assay. RESULTS: The morphology of IL-2-transduced
3AO and IL-2R-transduced PBLs remained unchanged. 3AO cells could be
transfected with the IL-2 gene and expressed IL-2 mRNA, and PBLs could
be transfected with the IL-2R gene and expressed IL-2R mRNA. IL-2
transduced 3AO cells enhanced their response to the cytotoxicity of
PBLs. Furthermore, growth inhibition of PBLs to 3AO cells increased
significantly when the IL-2R was transfected into PBLs and when the IL-2
gene was transfected into 3AO cells and the two were combined.
CONCLUSIONS: IL-2R gene transduced PBLs are able to enhance their
cytotoxicity on IL-2 gene transduced ovarian cancer cells. This method
may be a new way to investigate IL-2 gene therapy for ovarian cancer.
32
UI - 11780192
AU - Wei F; Jiang Z; Yan C
TI -
Analysis of 20 mature ovarian cystic teratoma cases in postmenopausal
women.
SO - Chin Med J (Engl) 2001 Feb;114(2):137-8
AD - Department of Obstetrics and Gynecology, Beijing Hospital, Beijing
100730, China. weifenghua@263.net
OBJECTIVE: To study the incidence of malignant change, diagnosis and
management of mature cystic teratomas in postmenopausal women. METHODS:
Twenty cases of mature cystic teratoma in postmenopausal women admitted
retrospectively reviewed and evaluated. RESULTS: The number of
postmenopausal patients with mature cystic teratoma (20) accounted for
7.6% of the total number of patients with benign ovarian teratomas
(263). There were 3 cases of malignant change, which were squamous
carcinoma, carcinosarcoma, and digestive gland epithelial carcinoma. The
incidence of malignant change was 15%. CONCLUSION: In postmenopausal
women, mature ovarian cystic teratoma should be treated as lowly
malignant and should be paid much attention.
33
UI - 11779836
AU - Manderson EN; Mes-Masson AM; Novak J; Lee PD; Provencher D; Hudson TJ;
TI -
Tonin PN
Expression profiles of 290 ESTs mapped to chromosome 3 in human
epithelial ovarian cancer cell lines using DNA expression
oligonucleotide microarrays.
SO - Genome Res 2002 Jan;12(1):112-21
AD - Department of Human Genetics, McGill University, Montreal, Quebec H3A
1B1, Canada.
We have investigated previously the utility of oligonucleotide
expression microarray technology in an analysis of four spontaneously
transformed epithelial ovarian cancer (EOC) cell lines, TOV-21G,
TOV-81D, OV-90, and TOV-112D. Here, we examine the expression of 290
expressed sequence tags (ESTs) that map to human chromosome 3 in a
primary culture derived from normal ovarian surface epithelium (NOSE),
NOV-31, and the four spontaneously transformed EOC cell lines. One of
these cell lines, OV-90, harbors a deletion of an entire chromosome 3p
arm. Whereas the most aggressive cell lines (OV-90, TOV-112D, and
TOV-21G) exhibited the highest levels of expression, assessed by the
mean of expression values of all ESTs, OV-90 showed the lowest mean of
expression of ESTs that map to the 3p arm in comparison with TOV-112D
and TOV-21G. This difference in expression profile of 3p ESTs in OV-90
is also reflected in the ratio of expression of ESTs on 3p versus the 3q
arm and in that the expression values of ESTs that map to 3p were more
often lower than higher in OV-90 in two-way comparisons with NOV-31,
TOV-21G, and TOV-112D
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