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Abramson Cancer CenterNCI CANCERLIT® Search: Gestational Trophoblastic Neoplasms - October 2002
National Cancer Institute®
Last Modified: October 1, 2002
- Oral contraceptive use and gestational choriocarcinoma.
- [Use of sulprostone in the evacuation of molar pregnancies]
- Termination of molar pregnancy by intramuscular administration of 15(S)-15-methyl-prostaglandin F2 alpha.
- Choriocarcinoma presenting as a complication of elective first trimester abortion.
- Failure of contraceptive steroids to modify human chorionic gonadotrophin secretion by hydatidiform mole tissue and choriocarcinoma
- The influence of oral contraceptives on the postmolar human chorionic gonadotropin regression curve.
- Risk factors for gestational trophoblastic disease in Italy.
- Reproductive patterns and the risk of gestational trophoblastic disease.
- Relationship of oral contraceptives and the intrauterine contraceptive devices to the regression of concentrations of the beta subunit of human
- Cervical choriocarcinoma associated with an intrauterine contraceptive device: a case report.
- Epidemiology of hydatidiform mole and choriocarcinoma.
- Oral contraceptives and post-molar trophoblastic tumours.
- Postmolar contraception.
- Don't ignore a positive pregnancy test.
- Identification of choriocarcinoma by the hCG beta-to-hCG proportion in patients with delayed diagnosis caused by contraceptive use.
- Inhibition of antigen transport by expression of infected cell peptide 47 (ICP47) prevents cell surface expression of HLA in choriocarcinoma
- Doppler ultrasonography of the uterine artery and the response to chemotherapy in patients with gestational trophoblastic tumors.
- [Trophoblastic diseases--a group of rare diseases]
- Growth-associated gene expression profiles by microarray analysis of trophoblast of molar pregnancies and normal villi.
- [Massive fetomaternal bleeding--an insidious and serious pregnancy complication]
- Expression of nm23-H1 protein in relation to myometrial invasion in complete hydatidiform moles.
- [The clinical analysis and results of treatment of the patients with gestational trophoblastic disease]
- [Choriocarcinoma with atypical clinical course. Case report]
- Gestational trophoblastic disease.
- Expression of the p53 gene and apoptosis in gestational trophoblastic disease.
- The molar vesicle fluid contains the beta-core fragment of human chorionic gonadotropin.
- Lack of membrane transport of l-thyroxine sulphate in the human choriocarcinoma cell line, JAr.
- Production of interleukin (IL)-6 and IL-8 by a choriocarcinoma cell line, BeWo.
- Altered mitochondrial gene expression in human gestational trophoblastic diseases.
- Upregulation of neutral endopeptidase expression and enzymatic activity during the differentiation of human choriocarcinoma cells.
- Extravillus endovascular implantation site trophoblast invasion is abnormal in complete versus partial molar pregnancies.
- Progesterone stimulates the expression of aminopeptidase A/angiotensinase in human choriocarcinoma cells.
- Immunohistochemical demonstration of placental protein 5 in trophoblastic tumours.
- The expression of major histocompatibility antigens in the chorionic villi of molar placentae.
- Purine re-utilization in normal and malignant cells of human placental origin.
- Linkage of human chorionic gonadotrophin and placental lactogen biosynthesis to trophoblast differentiation and tumorigenesis.
- Hydatidiform mole in Nottingham: a 12-year retrospective epidemiological and morphological study.
- Identification of triploidy by DA/DAPI staining of trophoblastic interphase nuclei.
- Serum proteins in vesicular fluid of hydatidiform moles: a lack of selectivity of molar trophoblast in the transfer of maternal serum
- Genetic studies in hydatidiform mole with clinical correlations.
- HLA expression by trophoblast of invasive moles.
- Immunogenicity of hydatidiform mole.
- Expression of HLA-DR molecules in human gestational choriocarcinoma cell lines and malignant cell lines.
- The propensity to malignancy of dispermic heterozygous moles.
- Detection of oncomodulin, an oncodevelopmental protein in human placenta and choriocarcinoma cell lines.
- Direct chromosomal preparation for studying hydatidiform moles.
- Immunohistochemical studies of fetal trophoblast and maternal decidua in hydatidiform mole and choriocarcinoma.
- Receptor-mediated endocytosis of 125I-labelled transferrin by human choriocarcinoma (JAR) cells.
- Chorangiocarcinoma: an unusual tumour of the placenta. The missing link?
- Flow cytometry in persistent trophoblastic disease.
- Hydatidiform mole: an ultrastructural analysis of syncytiotrophoblast surface organization.
- A new approach using DNA fingerprinting for the determination of androgenesis as a cause of hydatidiform mole.
- Intraplacental choriocarcinoma: a case report.
- Re-evaluation of hydatidiform mole by DNA fingerprint method: the discrepancy in the diagnoses by pathological finding and the DNA
- Regulation by interleukin-1 beta of growth and collagenase production by choriocarcinoma cells.
- Functional characterization of L-alanine transport in a placental choriocarcinoma cell line (BeWo).
- Basal and interferon-induced 2',5'-oligoadenylate synthetase activity in human placental trophoblast and trophoblast-derived malignant cell
- Placental isoferritin levels during first trimester of normal and complete molar gestations.
- Expression of G proteins in human placentae from molar pregnancies.
- Dome formation induced by v-H-ras oncogene in a human choriocarcinoma cell line.
- Characterization of a sodium-dependent vitamin transporter mediating the uptake of pantothenate, biotin and lipoate in human placental
- Hypoxia downregulates continuous and interleukin-1-induced expression of human chorionic gonadotropin in choriocarcinoma cells.
- Cellular specificity of fibroblastic proMMP-3 downregulation by normal or cancer trophoblastic cells.
- Suppression by beta-mercaptoethanol of the intracellular hormonal dynamics of human chorionic gonadotropin-beta subunit (hCG-beta) in BeWo
- Sodium-independent lysine uptake by the BeWo choriocarcinoma cell line.
- p53, Bax and Bcl-2 expression, and apoptosis in gestational trophoblast of complete hydatidiform mole.
- Uptake of reverse T3 in the human choriocarcinoma cell line, JAr.
- Uptake of L-triiodothyronine sulphate by human choriocarcinoma cell line, JAr.
- Expression of telomerase subunits and localization of telomerase activation in hydatidiform mole.
- Human choriocarcinoma cell line JEG-3 produces and secretes active retinoids from retinol.
- Color Doppler imaging in the sonohysterographic diagnosis of residual trophoblastic tissue.
Table of Contents
1
UI - 2044074
AU - Palmer JR
TI -
Oral contraceptive use and gestational choriocarcinoma.
SO - Cancer Detect Prev 1991;15(1):45-8
AD - Slone Epidemiology Unit, Boston University School of Medicine,
Brookline, MA 02146.
Substantial advances have occurred in the treatment of gestational
trophoblastic disease, but little is known about the etiology. Routine
screening of data from a case-control study of several diseases revealed
an association between gestational choriocarcinoma and oral
contraceptive (OC) use. A detailed analysis of 23 cases of gestational
choriocarcinoma, 34 of invasive hydatidiform mole, and 49 of
hydatidiform mole, each matched on age and geographic area to 4 controls
who had been pregnant at least once, was carried out. Relative to women
who had never used oral contraceptives, the estimated relative risk of
choriocarcinoma for women who had used oral contraceptives for at least
5 years was 6.0 (95% CI, 1.3 to 28); for invasive mole and hydatidiform
mole, the relative risks were elevated but not statistically
significant. Oral contraceptive use has also been associated with an
increased risk of gestational choriocarcinoma in a recent study
conducted in the western U.S. These findings raise the hypothesis that
long-term oral contraceptive use, or a correlate of use such as exposure
to sexually transmitted infections, increases the risk of one or more of
the manifestations of gestational trophoblastic disease.
2
UI - 2068488
AU - Pinet C; Colau JC
TI -
[Use of sulprostone in the evacuation of molar pregnancies]
SO - Rev Fr Gynecol Obstet 1991 Jan;86(1):53-5
AD - Service de Gynecologie-Obstetrique, Hopital Foch, Suresnes.
The diagnosis of molar pregnancy is now easy based upon a triple
clinical, laboratory and ultrasonographic approach. Histology provides
final confirmation. However treatment is more difficult since uterine
evacuation may be very hemorrhagic or traumatic. A clinical case forms
the basis here for a review of the main features concerning the
diagnosis and treatment of hydatidiform mole.
3
UI - 7403332
AU - Keirse MJ
TI -
Termination of molar pregnancy by intramuscular administration of
15(S)-15-methyl-prostaglandin F2 alpha.
SO - Prostaglandins Med 1980 May;4(5):333-9
Eleven patients entered a multicentre trial of repeated intramuscular
injections of 15(S)-15-methyl-prostaglandin F2 alpha (15-me-PGF2 alpha)
for terminating molar pregnancy. Duration of pregnancy ranged from 9 to
24 (median: 16) weeks and uterine size from 15 to 24 (median: 19) weeks.
Complete (n=5) or incomplete (n=4) expulsion of molar tissue occurred in
9 patients (82%) after a median duration of 15.7 hours. In the remaining
2 patients treatment was interrupted after 8 hours at a cervical
dilatation of 1 cm or more. Gastro-intestinal side effects were
prominent in 64%. The use of prostaglandins in the management of
hydatidiform mole is discussed.
4
UI - 7219391
AU - Lyon FA; Adcock LL
TI -
Choriocarcinoma presenting as a complication of elective first trimester
abortion.
SO - Minn Med 1980 Oct;63(10):733-5
5
UI - 7027540
AU - Gal D; Simpson ER; Porter JC; MacDonald PC; Buchsbaum HJ
TI -
Failure of contraceptive steroids to modify human chorionic
gonadotrophin secretion by hydatidiform mole tissue and choriocarcinoma
cells in culture.
SO - Steroids 1981 Jun;37(6):663-71
The effect of steroids contained in oral contraceptives, namely
ethinylestradiol:17 alpha-ethinyl-1,3,5,(10)-estratriene-3, 17-diol (E)
and norethindrone acetate:17 beta-acetoxy-17-ethinyl-4-estren-3-one (N),
on cell replication and human chorionic gonadotropin (hCG) secretion by
choriocarcinoma cells in monolayer culture and by hydatidiform mole
tissue maintained in organ culture were studied. The steroids were added
to the culture medium individually or in combination to achieve a range
of concentrations (10-10 to 10-4), within and beyond the presumed
concentration of these substances in the blood of women taking oral
contraceptives. The effect of luteinizing hormone releasing hormone
(LHRH) on hCG secretion by choriocarcinoma cells in monolayer culture
also was investigated. The rate of hCG production by either
choriocarcinoma cells in monolayer culture or by hydatidiform mole
tissue maintained in organ culture was not affected by the hormones used
in this study; indeed hCG secretion remained reasonably unchanged even
with high concentrations of steroids (up to 10-4 M) or LHRH (up to 10-4
mg x ml-1). Cell replication, as measured by increase in amount of
cellular protein and DNA, was not stimulated by either of these
compounds.
6
UI - 2580438
AU - Morrow P; Nakamura R; Schlaerth J; Gaddis O Jr; Eddy G
TI -
The influence of oral contraceptives on the postmolar human chorionic
gonadotropin regression curve.
SO - Am J Obstet Gynecol 1985 Apr 1;151(7):906-14
This article reports a retrospective analysis of 149 evaluable cases of
molar pregnancy managed at Women's Hospital, Los Angeles
County/University of Southern California Medical Center, from January
1977, through June, 1983. In the 84 cases prior to 1981, the patients
received estrogen-progestogen oral contraceptives after evacuation while
the 55 patients seen after that used nonhormonal contraceptives. The
frequency of abnormal regression of the serum beta-subunit of human
chorionic gonadotropin in the two groups was not significantly different
(22.6% in the hormonal contraception group versus 34.5% in the
nonhormonal contraception group). The groups were compared for known and
potential risk factors and were nearly identical with respect to patient
age, parity, maternal blood type, and race. There were also no
significant differences with respect to uterine size, preevacuation
beta-subunit of human chorionic gonadotropin serum titer greater than
100,000 mIU/ml, and frequency of theca-lutein cysts. Gestational age was
significantly shorter and the frequency of cases with a preevacuation
beta-subunit of human chorionic gonadotropin serum titer greater than
250,000 mIU/ml significantly higher in the nonhormonal contraception
group, indicating that the nonhormonal contraception group had a higher
risk for abnormal human chorionic gonadotropin regression than the
hormonal contraception group. We conclude that this study provides no
evidence that the use of estrogen-progestogen oral contraceptives prior
to human chorionic gonadotropin remission increases the risk for
invasive mole or choriocarcinoma following molar pregnancy.
7
UI - 2990199
AU - La Vecchia C; Franceschi S; Parazzini F; Fasoli M; Decarli A; Gallus G;
TI -
Tognoni G
Risk factors for gestational trophoblastic disease in Italy.
SO - Am J Epidemiol 1985 Mar;121(3):457-64
factors for gestational trophoblastic disease in a case-control study of
100 women with trophoblastic tumors (17 partial hydatidiform moles, 63
complete moles, and 20 choriocarcinomas) and 200 age-matched controls
admitted for normal deliveries to university or general hospitals in
Lombardy, Northern Italy. Questions were asked about each patient's
general life-style, and medical, obstetric, menstrual, contraceptive,
and social history. The risk of trophoblastic disease increased with
increasing paternal age: women whose husbands were aged 40-44 years and
45 years or more had a relative risk of 2.4 and 4.2, respectively,
compared to women married to men aged under 40 years. This association
was independent of maternal age. Cigarette smoking was associated with
trophoblastic tumors (relative risk estimate for smokers vs. never
smokers = 2.0, 95% confidence interval = 1.2-3.2), the risk being
greater for women who smoked more cigarettes and for longer. The effect
of cigarette smoking was not explained by any other identified potential
distorting factor. A positive history of fertility problems or
difficulties in conception and a personal or family history of
gestational trophoblastic disease were more common among the cases. Past
use of oral contraceptives was not related to the risk of trophoblastic
tumors, but use of an intrauterine device was significantly more common
among the cases. The findings give epidemiologic support to the evidence
of an androgenetic role in the origin of hydatidiform mole; moreover,
they provide new hypotheses on the risk factors for gestational
trophoblastic disease in developed countries. Further exploration of
these factors may lead to a more coherent body of evidence on the
etiology of these diseases.
8
UI - 2992274
AU - Parazzini F; La Vecchia C; Pampallona S; Franceschi S
TI -
Reproductive patterns and the risk of gestational trophoblastic disease.
SO - Am J Obstet Gynecol 1985 Aug 1;152(7 Pt 1):866-70
The relation between reproductive pattern and the risk of gestational
trophoblastic disease was evaluated in a case-control study conducted in
Northern Italy on 310 women with histologically confirmed gestational
trophoblastic disease and two control groups consisting of 290 obstetric
subjects and 394 patients in hospital for acute, nonobstetric,
nongynecologic conditions. Compared to that for nulliparous women, the
estimated age-adjusted relative risk of trophoblastic disease for parous
women was 0.6 (90% confidence limit = 0.4 to 0.9) when obstetric
controls were used as a comparison group and 0.4 (95% confidence limit =
0.2 to 0.6) compared with other controls. Conversely, a history of
spontaneous abortions was associated with elevated risk of gestational
trophoblastic disease, and the risk increased significantly with
increasing number of spontaneous abortions. When the combined effect of
parity and spontaneous abortions was considered, the major factor
influencing the risk of gestational trophoblastic disease was the
existence of one or more previous term pregnancies.
9
UI - 6849356
AU - Ho Yuen B; Burch P
TI -
Relationship of oral contraceptives and the intrauterine contraceptive
devices to the regression of concentrations of the beta subunit of human
chorionic gonadotropin and invasive complications after molar pregnancy.
SO - Am J Obstet Gynecol 1983 Jan 15;145(2):214-7
One hundred ninety-four patients with pathologically confirmed molar
pregnancy and intact uteri were studied prospectively. Group A included
177 patients in whom the beta subunit of human chorionic gonadotropin
(hCG-beta) declined to normal (less than 5 mlU/ml) without chemotherapy,
whereas group B included 17 patients with invasive complications in the
postmolar phase which necessitated the use of chemotherapy. Only women
with intact uteri were included in the study. In group A, there were no
significant differences in the human chorionic gonadotropin (hCG)
positive interval between women who used intrauterine contraceptive
devices, barrier and other methods, and those who used oral
contraceptives. Differences in the proportions of women in groups A and
B who used the oral contraceptives and intrauterine contraceptive
devices were not observed. However, the mean dosage of estrogen and the
proportion of women who ingested more than 50 micrograms of estrogen
were higher in group B. These data suggest that (1) the oral
contraceptives with less than 50 micrograms of estrogen and the
intrauterine contraceptive devices do not prolong the hCG-beta positive
interval nor increase the risk of invasive complications in the
postmolar phase which requires the use of chemotherapy; and (2) the dose
of estrogen (in formulations that contain more than 50 micrograms)
rather than the oral contraceptives per se may influence the risk of
these postmolar complications.
10
UI - 6684883
AU - Martin BR 3rd; Orr JW Jr; Austin JM Jr
TI -
Cervical choriocarcinoma associated with an intrauterine contraceptive
device: a case report.
SO - Am J Obstet Gynecol 1983 Oct 1;147(3):343-4
11
UI - 6386504
AU - Bracken MB; Brinton LA; Hayashi K
TI -
Epidemiology of hydatidiform mole and choriocarcinoma.
SO - Epidemiol Rev 1984;6():52-75
12
UI - 6106866
AU - Berkowitz RS; Marean AR; Goldstein DP; Bernstein MR
TI -
Oral contraceptives and post-molar trophoblastic tumours.
SO - Lancet 1980 Oct 4;2(8197):752
13
UI - 3287245
AU - Pandiyan N; Jequier AM
TI -
Postmolar contraception.
SO - Obstet Gynecol Surv 1988 May;43(5):258-62
AD - Department of Obstetrics & Gynaecology, University of Nottingham,
University Hospital, Queen's Medical Centre, U.K.
Recent studies on the etiology and the cytogenetics of trophoblastic
tumors suggest that hydatidiform mole and choriocarcinoma may be
conditions with no causal relationship. With the advent of newer
diagnostic methods which aid in the early diagnosis of pregnancy and
help to differentiate it from abnormal pregnancy together with the
increasing concern over the safety of use of the contraceptive measures
following a hydatidiform mole, it is suggested that a period of
postmolar contraception may no longer be necessary. The follow-up of
these patients should include serial sonography in association with
other currently available methods. Pregnancy should also be allowed to
occur naturally if the patient so desires.
14
UI - 2848605
AU - Smith DB; Rustin GJ; Bagshawe KD
TI -
Don't ignore a positive pregnancy test.
SO - BMJ 1988 Oct 29;297(6656):1119-20
AD - Department of Medical Oncology, Charing Cross Hospital, London.
15
UI - 9649918
AU - Vartiainen J; Alfthan H; Lehtovirta P; Stenman UH
TI -
Identification of choriocarcinoma by the hCG beta-to-hCG proportion in
patients with delayed diagnosis caused by contraceptive use.
SO - Contraception 1998 Apr;57(4):257-60
AD - Department of Obstetrics, Helsinki University Central Hospital, Finland.
The use of contraceptives, especially subdermal implants and
levonorgestrel-containing intrauterine device (IUD), often cause
irregular bleeding. Thus, they may mask unsuspected choriocarcinoma,
which also often presents with abnormal bleeding. Choriocarcinoma is
mostly curable with combination chemotherapy, but delayed diagnosis can
lead to treatment failure. Two cases of choriocarcinoma with
considerable delay in diagnosis, due partly to contraceptive use, are
reported. The proportion of human chorionic gonadotropin-beta (hCG beta)
and total hCG immunoreactivity showed that the proportion of hCG beta
was elevated at presentation in both cases.
16
UI - 11254939
AU - Easterfield AJ; Austen BM; Westwood OM
TI -
Inhibition of antigen transport by expression of infected cell peptide
47 (ICP47) prevents cell surface expression of HLA in choriocarcinoma
cell lines.
SO - J Reprod Immunol 2001 Apr;50(1):19-40
AD - Division of Immunology, St. George's Hospital Medical School, Cranmer
Terrace, London SW17 ORE, UK.
Cell surface expression of HLA class I (including non-classical HLA-G)
in JEG3 (choriocarcinoma cell line) was blocked by stable transfection
with the sequence encoding the Herpes simplex virus protein, infected
cell peptide 47 (ICP47) inserted into a vector pCEP4. Intracellular
expression of ICP47 protein in ICP47-transfected cells was demonstrated.
The lack of HLA cell surface expression was likely to be due to blockage
of peptide transport from the cytoplasm into the endoplasmic reticulum
by ICP47. ICP47 is known to block the heterodimeric transporter
associated with antigen processing (formed from TAP1 and TAP2). Western
blotting with a polyclonal antibody to the C-terminus of TAP1 showed
high expression of TAP1 in BeWo and JEG3, but not JAR cells, expression
that was strongly upregulated by gamma-interferon. Gamma-interferon also
upregulated the cell surface expression of HLA class I. TAP1 was
strongly expressed in MC2 and MC3 extravillous cytotrophoblast cell
lines immortalised with the SV40 large T antigen. The results suggest a
role for non-classical HLA in the presentation of antigenic peptides to
the immune system.
17
UI - 12006530
AU - Agarwal R; Strickland S; McNeish IA; Patel DC; Foskett M; Boultbee JE;
TI -
Newlands ES; Seckl MJ
Doppler ultrasonography of the uterine artery and the response to
chemotherapy in patients with gestational trophoblastic tumors.
SO - Clin Cancer Res 2002 May;8(5):1142-7
AD - Department of Health Gestational Trophoblastic Disease Unit, Charing
Cross Hospital Campus, Imperial College, London W6 8RF, United Kingdom.
PURPOSE: Increasing new blood vessel formation (neoangiogenesis) within
tumors is an adverse prognostic factor for survival in several cancers.
Neoangiogenesis is usually determined histopathologically and not in
vivo. To assess neoangiogenesis in vivo, we have used Doppler
ultrasonography (US) to measure the uterine artery pulsatility index
(UAPI) in patients with gestational trophoblastic tumors (GTTs). Here,
we assess whether the UAPI can provide independent prognostic
information predictive of methotrexate resistance (MTX-R), a drug
central to the management of GTT. EXPERIMENTAL DESIGN: All patients
reviewed to determine their pretreatment Charing Cross Hospital (CXH)
prognostic score, uterine volume, the lowest UAPI of either uterine
artery, number of metastases, and human chorionic gonadotropin (hCG)
concentration. Of the 164 patients for whom all data were available, 47
subsequently developed MTX-R, defined as a plateaued or rising hCG in
two consecutive samples. RESULTS: UAPI, hCG, uterine volume, presence of
metastases, and the overall CXH prognostic score were all predictive of
MTX-R on univariate analysis. Moreover, the UAPI remained a significant
independent predictor of MTX-R on multiple logistic regression analysis.
After adjustment for the CXH prognostic score, the odds ratio for the
risk of MTX-R in patients with a UAPI < or =1 compared with those with a
UAPI >1 was 2.68 (95% confidence interval, 1.25-5.74; P = 0.01). The
unadjusted odds ratio for the above comparison was 2.32 (95% confidence
interval, 1.14-4.7; P = 0.02). CONCLUSIONS: The UAPI, as an indirect in
vivo measure of functional tumor vascularity, independently predicts the
response to chemotherapy in GTTs.
18
UI - 12183814
AU - Loukovaara M; Lehtovirta P
TI -
[Trophoblastic diseases--a group of rare diseases]
SO - Duodecim 2001;117(24):2539-46; quiz 2546, 2571
AD - HUS:n naistensairaala Haartmaninkatu 2, 00290 Helsinki.
pentti.lehtovirta@hus.fi
19
UI - 12068171
AU - Kato HD; Terao Y; Ogawa M; Matsuda T; Arima T; Kato K; Yong Z; Wake N
TI -
Growth-associated gene expression profiles by microarray analysis of
trophoblast of molar pregnancies and normal villi.
SO - Int J Gynecol Pathol 2002 Jul;21(3):255-60
AD - Division of Molecular and Cell Therapeutics, Department of Molecular
Genetics, Medical Institute of Bioregulation, Kyushu University, Beppu
City, Oita, Japan.
We used microarray analysis to investigate expression profiles of 589
known genes committed to cell growth control to characterize regulatory
circuitry for cell proliferation in complete moles (CMs). CMs are
characterized by hyperplastic trophoblast and have a high propensity to
give rise to choriocarcinoma. Characteristic alterations in gene
expression profiles were observed when compared with normal villi.
Fifty-seven genes were significantly up-regulated in CMs and involved
the Ras-Map kinase 3, Jak-STAT5, and Wnt signal pathways, implicating
growth factor or cytokine-mediated signal pathways in the trophoblastic
hyperplasia of CMs. Several genes associated with anti-apoptosis, cell
structuring, and/or cell attachment were also up-regulated in CMs. In
contrast, relatively fewer genes were down-regulated and these involved
IGFBPs, versican, interleukin-1, tumor necrosis factor receptor, CD44,
and RAD52. Genes identified in this study may elucidate regulation
mechanisms of trophoblastic proliferation and mechanisms causing a
pathological phenotype in CMs.
20
UI - 12233006
AU - Ulander VM; Ammala P; Sjoberg J; Lehtovirta P
TI -
[Massive fetomaternal bleeding--an insidious and serious pregnancy
complication]
SO - Duodecim 2002;118(6):621-4
AD - HUS:n naistenklinikka PL 140, 00029 HUS.
21
UI - 11963831
AU - Alex S; Panikkar B; Devi C; Balaram P
TI -
Expression of nm23-H1 protein in relation to myometrial invasion in
complete hydatidiform moles.
SO - J Soc Gynecol Investig 2002 Mar-Apr;9(2):111-5
AD - Division of Cancer Research, Regional Cancer Centre, Trivandrum, Kerala,
India-695011.
OBJECTIVE: Although nm23-H1 protein expression has been related to
invasion in many cancers, its expression and prognostic significance in
complete hydatidiform moles has not yet been investigated. The search
for biologic parameters in molar placentas, which are useful for
identifying patients who show myometrial invasion of the tumor, is
crucial. We examined the clinical significance of nm23-H1 expression in
complete hydatidiform mole. METHODS: Sections of 105 cases of complete
hydatidiform moles (including 25 cases of invasive mole) and 95 cases of
gestational age--matched normal placentas were immunohistochemically
stained with anti-nm23-H1 antibody, which recognizes the nm23-H1/NDP
kinase A gene product. RESULTS: Expression of nm23-H1 was detected in
the cytotrophoblasts and syncytiotrophoblasts of molar placentas and
normal placentas, whereas it was not detected in stromal tissue.
Expression of nm23-H1 showed a negative relation to invasion, suggesting
its use as a potential marker of myometrial invasion in complete
hydatidiform moles. CONCLUSION: nm23-H1 expression could be used as a
marker for accurate evaluation of myometrial invasion in complete
hydatidiform mole.
22
UI - 12152292
AU - Pietrzak K; Drabik M; Ziolkowska-Seta I; Bidzinski M; Tulimowski J
TI -
[The clinical analysis and results of treatment of the patients with
gestational trophoblastic disease]
SO - Ginekol Pol 2002 Apr;73(4):390-5
AD - Kliniki Nowotworow Narzadow Plciowych Kobiecych Centrum Onkologii
Instytutu im. M. Sklodowskiej-Curie w Warszawie.
OBJECTIVES: The aim of this work was to establish the dependence between
the results of treatment and clinical stage and prognostic factors of
the patients with gestational trophoblastic disease. MATERIALS AND
METHODS: The retrospective analysis of 1259 patients with Gestational
Trophoblastic Disease (GTD) observed in years of 1977-1995 in the Maria
Sklodowska-Curie Memorial Cancer and Institute of Oncology in Warsaw,
Poland was made. Out of them 281 had recommendation for treatment. The
mean age of the examined women was 34.5 years and treated patient 38.0
years. The clinical structure of the treated patients according to
clinical stages: I--202 (72.1%), II low risk--17(6.1%), II high risk--4
(1.4%), III low risk--22 (7.9%), III high risk--26 (9.3%), IV--9 (3.2%).
The clinical structure of the treated patients by histopathological
type: hydatidiform mole 148 (52.7%), invasive mole 34 (12.1%),
choriocarcinoma 93 (33.1%), without histopathological diagnosis 6
(2.1%). The distribution of the treated patients by antecedent
pregnancy: hydatidifrom mole 166 (59.1%), spontaneous abortion 47
(16.7%), ectopic pregnancy 9 (3.2%) term delivery 59 (21%). RESULTS:
Among 281 patients who received chemotherapy 79 of them underwent
surgery. In the group of 281 treated patients, 267 (95%) are alive
without the signs of disease, 11 (3.9%) died, 1 (0.4%) is alive with the
symptoms of disease, 2 (0.7%) were lost of observation. CONCLUSIONS: 1.
Among the observed patients with GTD 23% needed treatment. 2. The most
common histopathological type of observed patients was hydatidiform
mole. 3. General treatment of patients with GTD consists of
chemotherapy. 4. The results of treatment should be seen as successful
since 96.5% of patients survived 5 years. 5. Survival of patients with
GTD depends on clinical stage and risk factors.
23
UI - 12152293
AU - Popiela A; Panszczyk M; Gabrys M
TI -
[Choriocarcinoma with atypical clinical course. Case report]
SO - Ginekol Pol 2002 Apr;73(4):396-9
AD - II Kliniki Ginekologii AM we Wroclawiu.
Authors describe a case of choriocarcinoma with an atypical clinical
course in 28-year old woman nine months after a normal pregnancy and
labour. Diagnosis of the disease was very hard because endometrial
biopsy did not show any suspected cells and two performed pregnancy
tests were not positive. Diagnosis was confirmed after a hysterectomy.
Authors conclude that every unclear vaginal bleeding during woman's
reproductive years should be considered with a beta-HCG level
measurement.
24
UI - 12196865
AU - Gerulath AH; Ehlen TG; Bessette P; Jolicoeur L; Savoie R; Society of
TI -
Obstetricians and Gynaecologists of Canada; Gynaecologic Oncologists of
Canada; Society of Canadian Colposcopists
Gestational trophoblastic disease.
SO - J Obstet Gynaecol Can 2002 May;24(5):434-46
AD - Toronto, Ontario, Canada.
OBJECTIVE: To provide standards for the diagnosis and treatment of
patients with hydatidiform mole and gestational trophoblastic tumours
(GTT).OPTIONS: Prognostic factors useful for treatment decisions in GTT
are defined with patients classified as low-, medium-, and high-risk
groups.OUTCOMES: Improved mortality and morbidity.EVIDENCE: Evidence was
gathered using Medline for relevant studies and articles from 1980 to
2001 with specific reference to diagnosis, treatment options, and
outcomes. The quality of evidence of Recommendations has been described
using the Evaluation of Evidence criteria outlined in the Report of the
Canadian Task Force on the Periodic Health Exam. RECOMMENDATIONS:1.
Suction curettage is the preferred method of evacuation of the
hydatidiform mole (III-C). Post-operative surveillance with hCG assays
is essential (II-3B). 2. Low-risk patients with both non-metastatic and
metastatic disease should be treated with single-agent chemotherapy,
either methotrexate or dactinomycin (II-3B). 3. Medium-risk patients
should usually be treated with multi-agent chemotherapy, either MAC or
EMA (III-C); single-agent chemotherapy may also be used (III-C). 4.
High-risk patients should be treated with multi-agent chemotherapy
EMA/CO, with selective use of surgery and radiotherapy (II-3B). Salvage
chemotherapy with EP/EMA and surgery should be employed in resistant
disease (III-C). 5. Placental site trophoblastic tumour that is
non-metastatic should be treated with hysterectomy (III-C). Metastatic
disease should be treated with chemotherapy, most commonly EMA/CO
(III-C).6. Women should be advised to avoid pregnancy until hCG levels
have been normal for six months following evacuation of a molar
pregnancy and for one year following chemotherapy for gestational
trophoblastic tumour. The combined oral contraceptive pill is safe for
use by women with GTT (III-C).VALIDATION: These guidelines have been
reviewed and approved by the Policy and Practice Guidelines Committee of
the Society of Obstetricians and Gynaecologists of Canada (SOGC), the
Gynaecologic Oncologists of Canada (GOC), the Society of Canadian
Colposcopists (SCC), and by Executive and Council of the SOGC.SPONSOR:
The Society of Obstetricians and Gynaecologists of Canada.
25
UI - 10692252
AU - Halperin R; Peller S; Sandbank J; Bukovsky I; Schneider D
TI -
Expression of the p53 gene and apoptosis in gestational trophoblastic
disease.
SO - Placenta 2000 Jan;21(1):58-62
AD - Department of Obstetrics and Gynecology, Assaf Harofeh Medical Center,
Zerifin, Israel.
In order to understand the involvement of the p53 tumour suppressor gene
in the pathogenesis of gestational trophoblastic disease (GTD), we
investigated its genetic status, protein expression and its role in
apoptosis in samples of complete and partial hydatidiform mole as
compared with those of normal placenta. Direct sequencing of polymerase
chain reaction (PCR) products of the coding and non-coding regions of
the p53 gene demonstrated no mutations in any of the studied samples.
Immunohistochemical studies revealed increased expression of the p53
protein predominantly in the nuclei of villous cytotrophoblasts. This
over-expression of p53 was found in all samples of complete mole, in 50
per cent of partial mole samples and in about 30 per cent of normal
placenta cases, although no significant difference in the staining
intensity and pattern was observed. An in situ detection of DNA nicking
(TUNEL) staining, demonstrating apoptosis, was also detected
predominantly in villous cytotrophoblasts and in stromal areas. The per
centage of apoptotic cells in all studied samples, determined by flow
cytometry, demonstrated a significant increase in apoptotic cells in
samples of complete and partial hydatidiform mole compared with those of
normal placenta (P< 0.0003 and P< 0.004, respectively).In conclusion,
the current study may provide a possible explanation to the pathogenesis
of GTD, probably associated with extensive p53-dependent apoptosis to
modulate excessive trophoblastic proliferation. Copyright 2000 Harcourt
Publishers Ltd.
26
UI - 10692255
AU - Khan S; Katabuchi H; Araki M; Ohba T; Koizumi T; Okamura H; Nishimura R
TI -
The molar vesicle fluid contains the beta-core fragment of human
chorionic gonadotropin.
SO - Placenta 2000 Jan;21(1):79-87
AD - Department of Obstetrics and Gynecology, Kumamoto University School of
Medicine, Honjo 1-1-1, Kumamoto-City, 860-8556, Japan.
The human chorionic gonadotropin (hCG) beta-core fragment (beta-CF) is a
major molecular form of hCG beta subunit (hCGbeta) immunoreactivity in
the urine of pregnant women and patients with trophoblastic disease. The
majority of evidence supports the fact that the beta-CF is a degradative
product of intact hCG and free hCGbeta in the kidneys. We found a
beta-CF-like substance in the fluid of molar vesicles from a patient
with complete hydatidiform mole. The molar fluid beta-CF (mbeta-CF) was
indistinguishable from the beta-CF in the patient's urine (ubeta-CF) by
immunoreactivity and by elution profile on gel chromatography. The
binding study to lectins, however, showed that mbeta-CF contains a
carbohydrate moiety that differs from that of
ubeta-CF.Immunohistochemistry with anti-beta-CF antibody demonstrated a
strong immunoreactivity in a large number of macrophages in the molar
villous stroma. In vitro incubation of intact hCG with peritoneal
macrophages showed a slow increase of intact hCG in the cell cytosol
with the appearance of beta-CF-like substance in the cell supernatant.
In conclusion, the source of beta-CF in molar fluid is likely to be
macrophages existing in the villous stroma. Thus macrophages may ingest
intact hCG and act as a local regulator of gonadotropic hormones.
Copyright 2000 Harcourt Publishers Ltd.
27
UI - 10736255
AU - Bernus I; Mitchell AM; Manley SW; Mortimer RH
TI -
Lack of membrane transport of l-thyroxine sulphate in the human
choriocarcinoma cell line, JAr.
SO - Placenta 2000 Mar-Apr;21(2-3):283-5
AD - Conjoint Endocrine Laboratory, Clinical Research Centre, RBH Research
Foundation and Division of Chemical Pathology, Queensland Health
Pathology Service, Royal Brisbane Hospital Campus, Brisbane, Queensland,
Australia. irenB@qimr.edu.au
We examined uptake of l -thyroxine sulphate (T(4)S) and possible
interactions between T(4)S and thyroxine (T(4)) uptake in the
choriocarcinoma cell line JAr. Cells were incubated with 50 p
m(125)I-T(4)S in the absence (total uptake) and in the presence
(non-specific uptake) of 10 microm T(4)S. Cells were also incubated at
37 degrees C for 2 min with 50 p m(125)I-T(4)in the presence of an
increasing amount of unlabelled T(4)(0-10 microm) or T(4)S (0-30
microm). There was negligible total uptake of(125)I-T(4)S (1.14+/-0. 05
fmol/mg cellular protein, mean+/-sem) and no specific uptake after 120
min incubation. Minor inhibition of(125)I-T(4)uptake by T(4)S could be
explained entirely by a low level of residual T(4)(0. 2 per cent) in the
T(4)S preparation. These findings indicate that T(4)S does not share the
T(4)membrane transporter. Copyright 2000 Harcourt Publishers Ltd.
28
UI - 10833370
AU - Fujisawa K; Nasu K; Arima K; Sugano T; Narahara H; Miyakawa I
TI -
Production of interleukin (IL)-6 and IL-8 by a choriocarcinoma cell
line, BeWo.
SO - Placenta 2000 May;21(4):354-60
AD - Department of Obstetrics and Gynecology, Oita Medical University,
Hasama-machi, Oita, 879-5593, Japan.
To clarify the biological and pathological features of choriocarcinoma,
we evaluated the in vitro production of cytokines by a choriocarcinoma
cell line, BeWo. We measured the concentration of interleukin (IL)-6 and
IL-8 in the culture media of BeWo cells after stimulation with various
modulatory agents of cytokine expression by enzyme-linked immunosorbent
assays. Northern blot analysis was used to examine the expression of
IL-6 and IL-8 mRNA in these cells. A weak expression of IL-6 and IL-8
was detected in unstimulated BeWo cells by both methods. IL-6
transcription and secretion were dose-dependently enhanced by
stimulation with IL-1beta, tumour necrosis factor (TNF)-alpha,
transforming growth factor (TGF)-beta1 and 12-O-tetradecanoyl
phorbol-13-acetate (TPA). Forskolin, lipopolysaccharide and
interferon-gamma had no effect on these cytokines production. The
TNF-alpha-induced secretion of IL-6 was inhibited by dexamethasone. The
TPA-induced production of IL-6 was inhibited by
1-(5-isoquinolinylsulfonyl)-2-methylpiperazine and sphyngosine,
suggesting the involvement of a protein kinase C-dependent pathway.
Levels of IL-8 mRNA and protein were also dose-dependently increased by
stimulation with IL-1beta, TNF-alpha and TPA. In contrast to IL-6, the
expression of IL-8 was not affected by TGF-beta1. It is suggested that,
in addition to the production of steroidal and non-steroidal hormones,
these cytokines may serve as part of a cytokine network that modulates
the proliferation and angiogenesis of choriocarcinomas. Copyright 2000
Harcourt Publishers Ltd.
29
UI - 11170827
AU - Durand S; Dumur C; Flury A; Abadie P; Patrito L; Podhajcer O;
TI -
Genti-Raimondi S
Altered mitochondrial gene expression in human gestational trophoblastic
diseases.
SO - Placenta 2001 Feb-Mar;22(2-3):220-6
AD - Departamento de Bioquimica Clinica, Facultad de Ciencias Quimicas,
Universidad Nacional de Cordoba, Pabellon Argentina, Ala Oeste, Ciudad
Universitaria, 5000 Cordoba, Argentina.
To assess the molecular basis of phenotypic alterations present in the
gestational trophoblastic diseases (GTDs) and to identify genes whose
expression is specifically associated with these placental proliferative
disorders we performed differential display (DD) techniques. This
strategy resulted in the isolation of four mitochondrial transcripts
downregulated in benign, as well as in malignant, trophoblastic diseases
encoding the cytochrome oxidase subunit I (COX I), the ATPase subunit 6,
the 12S ribosomal RNA (12S rRNA) and the transfer RNA for phenylalanine
(tRNA(Phe)).This expression pattern was confirmed by Northern blot in
normal early placenta (NEP), complete hydatidiform mole (CHM),
persistent gestational trophoblastic disease (PGTD) and the human
choriocarcinoma derived cell line JEG-3. Quantification of mitochondrial
DNA by dot blot indicated that these changes in expression were not
associated with a significant alteration in the number of mitochondrial
genome. In addition, a reduction in the mitochondrial transcription
factor A (mtTFA) mRNA level was observed in benign as well as in
malignant trophoblastic diseases in correlation with the decrease in the
mitochondrial transcript levels. Furthermore, Western blot analysis for
COX-I showed a close parallelism with the expression level of the
cognate RNA. Taken together, these data demonstrate that a significant
change in mitochondrial transcription is associated with the phenotypic
alteration present in GTDs. Copyright 2001 Harcourt Publishers Ltd.
30
UI - 11440542
AU - Uehara C; Ino K; Suzuki T; Kajiyama H; Kikkawa F; Nagasaka T; Mizutani S
TI -
Upregulation of neutral endopeptidase expression and enzymatic activity
during the differentiation of human choriocarcinoma cells.
SO - Placenta 2001 Jul;22(6):540-9
AD - Department of Obstetrics and Gynecology, Nagoya University School of
Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan.
Neutral endopeptidase (NEP)/CD10, a cell-surface peptidase degrading
various bioactive peptides, is mainly present in syncytiotrophoblasts in
the human placenta. However, the change in NEP expression upon
trophoblast differentiation remains to be clarified. In the present
study, we examined the expression of NEP in the differentiating
trophoblast using the BeWo choriocarcinoma cell line as a model system.
Under the normal culture conditions, NEP was very weakly expressed on
most proliferating cytotrophoblastic BeWo cells, while a minority of the
cell population (less than 5 per cent ), consisting of giant,
multinucleated cells, clearly expressed NEP at the cell membrane.
Treatment of BeWo cells with forskolin (FSK) for 48-72 h resulted in an
11- to 44-fold increase in the level of hCG secretion and induced cell
fusion leading to the formation of multinucleated syncytiotrophoblasts,
indicating functional and morphological differentiation.
Fluorescence-activated cell sorting (FACS) analysis revealed that
treatment with FSK significantly increased the cell-surface protein
expression of NEP on differentiating BeWo cells. Consistently, there was
a significant increase in the NEP enzymatic activity after FSK
treatment. The level of hCG secretion from the FSK-treated cells was
further enhanced when the cells were treated in the presence of the NEP
inhibitor phosphoramidon. Immunohistochemical analysis of normal
chorionic villi and choriocarcinoma tissues revealed the localization of
NEP in syncytiotrophoblastic cells, as opposed to weak or negative
staining in cytotrophoblastic cells. These data demonstrate that
induction of choriocarcinoma cell differentiation is associated with an
increase of NEP/CD10 expression at the cell surface, suggesting a role
of this enzyme in regulating differentiated trophoblast functions such
as hCG secretion. NEP/CD10 may also be a new cellular differentiation
marker of both the normal and neoplastic trophoblast. Copyright 2001
Harcourt Publishers Ltd.
31
UI - 11597192
AU - Sebire NJ; Rees H; Paradinas F; Fisher R; Foskett M; Seckl M; Newlands E
TI -
Extravillus endovascular implantation site trophoblast invasion is
abnormal in complete versus partial molar pregnancies.
SO - Placenta 2001 Sep-Oct;22(8-9):725-8
AD - Department of Histopathology, Trophoblastic Disease Surveillance Unit,
Charing Ross Hospital, London, UK. njs@fetalpathology.co.uk
This study examines endovascular trophoblast invasion in pregnancies
complicated by complete hydatidiform mole (CM), partial hydatidiform
mole (PM) and non-molar abortions (HA). Two hundred consecutive cases
from a supra-regional referral centre for suspected trophoblastic
disease were examined histologically with particular regard to the
presence or absence of endovascular trophoblast invasion of decidual
vessels. There were 57 CM, 75 PM and 68 HA. The prevalence of normal
endovascular invasion of decidual vessels was significantly lower in CM
compared to all other clinical groups, amongst which there were no
significant differences. Endovascular trophoblast was identified in
about 80 per cent of HA and PM moles, compared to only around 25 per
cent of CM (Z = -4.0, P< 0.0001). The majority of cases of complete mole
demonstrated a similar appearance, of implantation site showing florid
interstitial extravascular trophoblast invasion with surrounding of
decidual vessels but without normal endovascular trophoblast invasion or
'plugging' seen. In many cases, there also appeared to be destruction of
decidual vessels with interstitial haemorrhage and extensive fresh blood
clot present in the histological sections. These findings may provide
some explanation regarding the mechanism of clinical findings in molar
pregnancy. Copyright 2001 Harcourt Publishers Ltd.
32
UI - 11718570
AU - Katsumata Y; Nomura S; Ino K; Iwanaga K; Kurosawa N; Ito T; Okada M;
TI -
Tsujimoto M; Kikkawa F; Mizutani S
Progesterone stimulates the expression of aminopeptidase
A/angiotensinase in human choriocarcinoma cells.
SO - Placenta 2001 Nov;22(10):831-6
AD - Department of Obstetrics and Gynecology, Nagoya University School of
Medicine, Nagoya 466-8550, Japan.
In human placenta aminopeptidase A (APA), a principal enzyme that
converts angiotensin II to angiotensin III, seems to be involved in
angiotensin II metabolism during pregnancy. In this study, we
investigated the possible effects of progesterone and estrogen on APA
mRNA and protein levels in choriocarcinoma cells as a model for
placenta. By RNase protection assay, progesterone induced higher APA
mRNA levels than estrogen at the same concentration. Progesterone
exhibited dose-dependent stimulation of APA mRNA, 1.8-fold increase at
10(-6) m for 24 h treatment. Progesterone at 10(-6) m increased APA mRNA
levels within 12 h and in time-dependent fashion up to 24 h.
Fluorescence-activated cell sorting analysis and measurements of APA
activities revealed the induction of APA protein by progesterone.
Expression of progesterone receptors (PR) and glucocorticoid receptors
(GR) were determined in these cells by RT-PCR, which suggested that the
progesterone's actions might be displayed through PR and/or GR. These
findings may serve as a useful model to study the effects of
progesterone on angiotensin II metabolism in placenta, although the
physiological validity of these studies remains to be clarified.
Copyright 2001 Harcourt Publishers Ltd.
33
UI - 6281754
AU - Lee JN; Wahlstrom T; Seppala M; Salem HT; Ouyang PC; Chard T
TI -
Immunohistochemical demonstration of placental protein 5 in
trophoblastic tumours.
SO - Placenta 1982 Jan-Mar;3(1):67-70
An immunoperoxidase technique was used for the detection of placental
protein 5 (PP5) in tissue specimens from trophoblastic tumours. PP5 was
detected in all of 15 cases of hydatidiform mole, in two out of six
destructive moles and in one of seven choriocarcinomas. Though the
biological importance of PP5 is not clear, its association with
inactivation of plasmin suggests a role in the control of placental
invasiveness.
34
UI - 6390422
AU - Fisher RA; Lawler SD
TI -
The expression of major histocompatibility antigens in the chorionic
villi of molar placentae.
SO - Placenta 1984 May-Jun;5(3):237-42
Frozen sections of chorionic villi from molar placentae, ranging in
menstrual age from 9 to 19 weeks, were studied by an immunoperoxidase
technique using the monoclonal antibody to HLA-A,-B,-C antigens W6/32.
The distribution of class I HLA antigens in molar placentae was compared
with that in normal placental tissue of comparable menstrual age. The
results showed that the distribution of these antigens in molar
placentae is similar to that seen in normal placentae. In both tissues,
class I HLA antigens were absent from the syncytiotrophoblast and the
cy
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