Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 61
Filtrar
Mais filtros








Base de dados
Intervalo de ano de publicação
2.
Histopathology ; 39(5): 447-54, 2001 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-11737301

RESUMO

AIMS: To describe the clinical and histological features of a series of cases of placentas originally diagnosed as partial moles in which the final diagnosis was that of placental stem villous hydrops, mesenchymal dysplasia or Beckwith-Wiedemann syndrome. METHODS AND RESULTS: We searched a computerized database containing cases of suspected or proven trophoblastic disease examined at the Trophoblastic Disease Unit at Charing Cross Hospital, London, to identify cases in which stem vessel hydrops was present without other histological features of partial mole. For each case, histological sections were examined and the histological features present recorded. There were 15 cases identified. Placental weight was above the 95th centile of the normal for gestation in all cases in which this information was documented. In an additional five cases the placenta was described as 'large'. All cases had marked stem vessel hydropic change with cyst formation and in the majority of cases some terminal villous hydrops was also present. In 13 of the 15 cases there was marked aneurysmal dilatation of stem villous vessels. Nine had focal chorioangiomatoid change and in four of these extramedullary haematopoiesis was focally present in these areas. No excessive trophoblast proliferation was noted in any case and no trophoblastic inclusions typical of partial mole were identified. CONCLUSIONS: This study has identified cases of stem villous hydrops, mesenchymal dysplasia or Beckwith-Wiedemann spectrum in pregnancies initially diagnosed as partial hydatidiform mole in the second half of pregnancy and has highlighted the need for detailed pathological examination and clinicopathological correlation in all such cases.


Assuntos
Mola Hidatiforme/patologia , Placenta/patologia , Neoplasias Uterinas/patologia , Adolescente , Adulto , Síndrome de Beckwith-Wiedemann/patologia , Diagnóstico Diferencial , Feminino , Humanos , Doenças Placentárias/patologia , Gravidez
4.
Mol Hum Reprod ; 7(3): 279-85, 2001 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-11228248

RESUMO

Zonula occludens-1 (ZO-1) and occludin are key molecules in cell-cell contacts. They are tight junction constituents and therefore play a pivotal role in tissue differentiation and organogenesis. In the present report we have investigated the expression of ZO-1 and occludin in normal human placentae and in hydatidiform moles using immunohistochemical and Western blot analyses. In normal placentae, ZO-1 and occludin were mainly localized in the apical part of the syncytium, in cell-cell contacts between syncytium and villous cytotrophoblastic cells as well as between the latter. Extravillous cytotrophoblast of cell islands and cell columns was positive for ZO-1 and occludin in the cell layers proximally located to the villous stroma whereas the cytotrophoblastic cells, distally located from the villous stroma, were totally negative. Furthermore, fetal vessels showed a positive staining pattern for ZO-1 throughout gestation, whereas a positive reaction for occludin was produced mainly at term. A striking result was the altered expression of ZO-1 and occludin in partial and complete moles. In 11 moles, these two molecules were not expressed at all, while in the other nine, their expression was only cytoplasmic in syncytium and villous cytotrophoblastic cells. These findings suggest that ZO-1 and occludin participate in normal placental development, maintaining the organization and functions of different tissue components. The down-regulation and/or dysregulation of these two molecules may be related to phenotypic changes associated with epithelial cell transformation of the chorionic villi in partial and complete moles.


Assuntos
Mola Hidatiforme/metabolismo , Proteínas de Membrana/biossíntese , Fosfoproteínas/biossíntese , Placenta/metabolismo , Complicações Neoplásicas na Gravidez/metabolismo , Neoplasias Uterinas/metabolismo , Western Blotting , Células Cultivadas , Endotélio Vascular/citologia , Feminino , Humanos , Mola Hidatiforme/patologia , Imuno-Histoquímica/métodos , Ocludina , Placenta/patologia , Gravidez , Complicações Neoplásicas na Gravidez/patologia , Terceiro Trimestre da Gravidez , Células Tumorais Cultivadas , Neoplasias Uterinas/patologia , Proteína da Zônula de Oclusão-1
6.
Lancet ; 356(9223): 36-9, 2000 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-10892763

RESUMO

BACKGROUND: Partial hydatidiform moles (PMs) rarely require chemotherapy and have never previously been proven to transform into choriocarcinoma, the most malignant form of gestational trophoblastic disease (GTD). Consequently, some have questioned whether women with PMs need human chorionic gonadotropin (hCG) follow-up. Here, we investigate whether PMs can transform into choriocarcinomas. METHODS: Patients with a PM who developed a subsequent choriocarcinoma were identified from our GTD database. The histology of both PM and ensuing choriocarcinoma was reviewed and flow cytometry used to verify the triploid status of the PMs. To determine whether the choriocarcinoma arose from the PM, DNA from the PM and choriocarcinoma in each patient was compared using microsatellite polymorphisms. FINDINGS: Of the 3000 patients with PM, 15 required chemotherapy for persisting GTD. This was identified as choriocarcinoma in three cases. In one patient, the local pathologist could not differentiate between a PM or a hydropic abortion and neither central histological review nor hCG follow-up were obtained. This patient nearly died before the diagnosis of choriocarcinoma was made. Fortunately, the local pathologists correctly diagnosed PM in the two other patients who were then registered for hCG follow-up. Some months later, the hCG was rising and repeat uterine evacuation revealed choriocarcinoma. The PM was confirmed to be triploid in all three cases and genetic analysis showed that the subsequent choriocarcinomas contained identical single maternal and two paternal alleles at several independent loci. INTERPRETATION: Our results show that PMs can transform into choriocarcinoma. All patients with suspected PM should be reviewed centrally and, if confirmed, need hCG follow-up.


Assuntos
Transformação Celular Neoplásica/patologia , Coriocarcinoma/diagnóstico , Mola Hidatiforme/diagnóstico , Neoplasias Uterinas/diagnóstico , Adulto , Alelos , Coriocarcinoma/terapia , Gonadotropina Coriônica/sangue , Feminino , Citometria de Fluxo , Humanos , Mola Hidatiforme/terapia , Neoplasias Pulmonares/diagnóstico , Neoplasias Pulmonares/secundário , Neoplasias Pulmonares/terapia , Masculino , Repetições de Microssatélites , Poliploidia , Gravidez , Neoplasias Uterinas/terapia
7.
J Pathol ; 191(1): 67-70, 2000 May.
Artigo em Inglês | MEDLINE | ID: mdl-10767721

RESUMO

The purpose of this study was to determine whether amniotic tissue found associated with cases of complete hydatidiform mole (CM) was genetically identical to the CM, and therefore part of the molar pregnancy, or genetically dissimilar to the CM, suggesting derivation from a twin pregnancy. DNA was prepared from formalin-fixed, paraffin-embedded blocks of tissue containing both CM and amnion. Maternal DNA was prepared from decidual tissue in the same blocks, or from a maternal blood sample. Fluorescent microsatellite genotyping was carried out to determine the origin of both the CM and the amniotic tissue. In one of six cases examined, the amniotic tissue was genetically different from the CM and was therefore likely to be derived from a twin pregnancy. In the five remaining cases, the amniotic tissue was genetically identical to the CM and was likely to be derived from the same conceptus. It is concluded that androgenetic CM can support the development of amniotic tissue and that some early embryonic development may occur in CM. The presence of amnion, or other fetal tissues, associated with molar tissue should not therefore always be considered indicative of a diagnosis of partial mole (PM).


Assuntos
Âmnio/patologia , Mola Hidatiforme/genética , Mola Hidatiforme/patologia , Gravidez Múltipla , Alelos , Feminino , Genótipo , Humanos , Repetições de Microssatélites , Reação em Cadeia da Polimerase , Polimorfismo Genético , Gravidez
8.
Hum Reprod ; 15(3): 594-8, 2000 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-10686202

RESUMO

Complete hydatidiform mole (CHM) is an abnormality in pregnancy due to a diploid conception which is generally androgenetic in origin, i. e. all 46 chromosomes are paternally derived. We have examined the genetic origin of repetitive hydatidiform moles in a patient having three CHM by two different partners, and no normal pregnancies. Using fluorescent microsatellite genotyping, we have shown all three CHM to be biparental, rather than androgenetic, in origin. Examination of informative markers for each homologous pair of chromosomes, in two of the CHM, failed to reveal any evidence of unipaternal disomy, suggesting that the molar phenotype might result from disruption of normal imprinting patterns due to a defect in the maternal genome. It has been suggested that intracytoplasmic sperm injection (ICSI), followed by selection of male embryos, can prevent repetitive CHM; but examination of sex chromosome-specific sequences in the three CHM described here, showed that, while two were female, the first CHM was male. Selection of male embryos is therefore unlikely to prevent repetitive CHM in this patient. Our results suggest that the genetic origin of repetitive CHM should be determined prior to in-vitro fertilization (IVF) and that current strategies for the prevention of repetitive CHM may not be appropriate where the CHM are of biparental origin.


Assuntos
Mola Hidatiforme/genética , Neoplasias Uterinas/genética , Adulto , Feminino , Humanos , Masculino , Repetições de Microssatélites , Polimorfismo Genético , Gravidez , Recidiva , Cromossomo X , Cromossomo Y
9.
Int J Gynecol Cancer ; 10(1): 76-81, 2000 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-11240655

RESUMO

Multiple pregnancies with hydatidiform mole are rare. We describe here a patient who delivered a male fetus and a female fetus together with molar tissue following treatment for infertility. comparing microsatellite polymorphisms in the DNA from the patient, her partner, the two normal placentas and the molar tissue, we were able to show that this was a triplet pregnancy with two normal conceptions and a complete hydatidiform mole of monospermic origin.

10.
Hematol Oncol Clin North Am ; 13(1): 225-44, x, 1999 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-10080078

RESUMO

Advances in the last 20 years have led to a better understanding of the process of gestational trophoblastic disease (GTD), and consequently, to improved diagnosis, management, and prognosis. Patients with GTD should be registered at a trophoblastic disease center for follow-up, and those with persistent disease should receive chemotherapy, methotrexate, and folinic acid for low-risk disease, and EMACO (etoposide, actinomycin-D, methotrexate, vincristine, and cyclophosphamide) for high-risk disease, without loss of fertility. Most patients with relapsing or resistant disease can be treated effectively with surgery and/or cisplatin in EP/EMA (etoposide, platinum-etoposide, methotrexate, actinomycin-D) combination.


Assuntos
Neoplasias Trofoblásticas , Neoplasias Uterinas , Feminino , Humanos , Mola Hidatiforme/genética , Mola Hidatiforme/patologia , Mola Hidatiforme/terapia , Gravidez , Neoplasias Trofoblásticas/genética , Neoplasias Trofoblásticas/patologia , Neoplasias Trofoblásticas/terapia , Tumor Trofoblástico de Localização Placentária/genética , Tumor Trofoblástico de Localização Placentária/patologia , Tumor Trofoblástico de Localização Placentária/terapia , Neoplasias Uterinas/genética , Neoplasias Uterinas/patologia , Neoplasias Uterinas/terapia
11.
J Pathol ; 189(4): 600-8, 1999 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-10629564

RESUMO

Syndecans (syn-1, -2, -3, -4) and glypican-1 are proteoglycans expressed during development in association with changes in tissue organization and differentiation. They participate in the modulation of growth factor actions and in cell-cell and cell-matrix adhesion. The expression of syn-1, -2, -3, -4, and glypican-1 has been studied in normal human placenta and in gestational trophoblastic disease such as hydatidiform mole, invasive mole, and choriocarcinoma, using immunohistochemistry and western blots. Syndecan-3 was not expressed in normal or pathological tissues. During normal gestation, the other proteoglycans showed a specific staining pattern, which for some was modified during pregnancy. For instance, syn-1 was only expressed in syncytiotrophoblast; syn-4 was mainly localized in the villous and extravillous cytotrophoblast in the first trimester, whereas at term it was expressed in the syncytiotrophoblast. The most striking results are the altered expression patterns of syndecans and glypican-1 in pathological tissues. These proteoglycans showed a progressive decrease of immunostaining related to the increase of severity of trophoblastic disease, in particular in invasive mole and choriocarcinoma. In addition, dysregulation in the localization of the expression patterns was observed for syn-2 and -4. Because changes in syndecan expression enable cells to become more or less responsive to their micro-environment, the down-regulation and/or dysregulation of syndecans in relation to the degree of severity of trophoblastic diseases provides new insights into the progression of these pathologies.


Assuntos
Mola Hidatiforme/metabolismo , Proteoglicanas/análise , Trofoblastos/metabolismo , Western Blotting , Coriocarcinoma/metabolismo , Coriocarcinoma/patologia , Feminino , Heparina/análogos & derivados , Heparina/análise , Humanos , Mola Hidatiforme/patologia , Mola Hidatiforme Invasiva/metabolismo , Mola Hidatiforme Invasiva/patologia , Imuno-Histoquímica , Glicoproteínas de Membrana/análise , Proteínas de Neoplasias/análise , Gravidez , Primeiro Trimestre da Gravidez , Terceiro Trimestre da Gravidez , Sindecana-4 , Sindecanas , Trofoblastos/patologia , Neoplasias Uterinas/metabolismo , Neoplasias Uterinas/patologia
12.
Int J Gynaecol Obstet ; 60 Suppl 1: S57-64, 1998 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-9833616

RESUMO

Since 1973, hCG follow up and treatment of patients with hydatidiform moles in the UK has been centralised. Registrations of moles have increased from 475 to 1248 in 2 years but histological review shows that first trimester non-molar hydropic abortions (HAs) and complete moles (CMs) are often called partial moles (PMs) by pathologists. The introduction and widespread acceptance of the term PM in 1977, coincided with improvements in ultrasound which brought forward 6 weeks the average time of evacuation of CMs, when hydrops is not yet complete but partial and when vessels are present in most CMs, leading to erroneous diagnoses of PM. Many true PMs are dismissed as HAs and often, HAs are called PMs. Valid diagnostic criteria for younger CMs and for PMs have been available for over 10 years and when used, PM is overwhelmingly associated with triploidy. Reported diploid PMs are partly explained by misdiagnosed HAs, rare cases of Beckwith-Widemann syndrome, CMs with partially developed hydrops, twin pregnancies and rare androgenetic CMs with fetal red cells in villi. A rare mole with "normal" diploid biparental karyotype probably exists but morphologically resembles CM. CM and PM have widely different prognosis but the present diagnostic confusion means much of the published epidemiological, clinical and genetic information on PM based on suspect diagnostic criteria ia also suspect.


Assuntos
Mola Hidatiforme/diagnóstico , Neoplasias Uterinas/diagnóstico , Feminino , Idade Gestacional , Humanos , Mola Hidatiforme/epidemiologia , Londres/epidemiologia , Ploidias , Gravidez , Prognóstico , Neoplasias Uterinas/epidemiologia
13.
J Reprod Med ; 43(1): 53-9, 1998 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-9475150

RESUMO

OBJECTIVE: To analyze the genetic background of tumors in patients with placental site trophoblastic tumors (PSTTs) and clinical outcome in patients treated for this rare variant of trophoblastic disease at a single center. STUDY DESIGN: Analysis of all patients with PSTTs treated at the Charing Cross Hospital between 1975 and 1995. RESULTS: We studied the molecular genetics of a group of PSTTs using polymerase chain reaction allelotyping and GeneScan software. We were able to show, in the seven cases in which detailed molecular analysis was successful, that four of these PSTTs were from diploid, bi-parental pregnancies and three were androgenetic tumors following monospermic complete hydatidiform moles. For patients with PSTT localized to the uterus, the treatment of choice is hysterectomy. The sensitivity of PSTT to current cytotoxic chemotherapy is variable. Several patients have been cured using the etoposide, methotrexate, actinomycin D/cyclophosphamide, vincristine schedule, but clinical impressions suggest that cisplatinum probably should be introduced into the chemotherapy schedule from the outset in a schedule such as etoposide, cisplatin/etoposide, methotrexate, actinomycin D. CONCLUSION: PSTT is a very rare variant of gestational trophoblastic tumor, and its biologic behavior is clearly heterogeneous. The treatment of choice for patients whose disease is limited to the uterus is hysterectomy; for patients with more extensive or metastatic disease, chemotherapy is indicated, but the clinical outcome is variable. A long interval from the antecedent pregnancy to clinical presentation is a major adverse prognostic variable, and the outcome in patients whose last known pregnancy was > 2 years prior to presentation with PSTT is poor.


Assuntos
Placenta/patologia , Tumor Trofoblástico de Localização Placentária/terapia , Neoplasias Uterinas/terapia , Adulto , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Quimioterapia Adjuvante , DNA de Neoplasias/análise , Feminino , Humanos , Histerectomia , Pessoa de Meia-Idade , Reação em Cadeia da Polimerase , Gravidez , Prognóstico , Estudos Retrospectivos , Taxa de Sobrevida , Fatores de Tempo , Tumor Trofoblástico de Localização Placentária/genética , Tumor Trofoblástico de Localização Placentária/patologia , Neoplasias Uterinas/genética , Neoplasias Uterinas/patologia
14.
15.
Int J Gynaecol Obstet ; 60 Suppl 1: S57-S64, 1998 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-29645239

RESUMO

Since 1973, hCG follow up and treatment of patients with hydatidiform moles in the UK has been centralised. Registrations of moles have increased from 475 to 1248 in 2 years but histological review shows that first trimester non-molar hydropic abortions (HAs) and complete moles (CMs) are often called partial moles (PMs) by pathologists. The introduction and widespread acceptance of the term PM in 1977, coincided with improvements in ultrasound which brought forward 6 weeks the average time of evacuation of CMs, when hydrops is not yet complete but partial and when vessels are present in most CMs, leading to erroneous diagnoses of PM. Many true PMs are dismissed as HAs and often, HAs are called PMs. Valid diagnostic criteria for younger CMs and for PMs have been available for over 10 years and when used, PM is overwhelmingly associated with triploidy. Reported diploid PMs are partly explained by misdiagnosed HAs, rare cases of Beckwith-Widemann syndrome, CMs with partially developed hydrops, twin pregnancies and rare androgenetic CMs with fetal red cells in villi. A rare mole with "normal" diploid biparental karyotype probably exists but morphologically resembles CM. CM and PM have widely different prognosis but the present diagnostic confusion means much of the published epidemiological, clinical and genetic information on PM based on suspect diagnostic criteria ia also suspect.

16.
J Pathol ; 181(2): 183-8, 1997 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-9120723

RESUMO

It is believed that fetal development does not occur in complete mole (CM); when present, it is usually interpreted as proof of partial mole (PM), in most cases a triploid conception with a low incidence of persistent trophoblastic disease (PTD). However, histological examination of 3180 moles in 8 years showed 60 moles (1.8 per cent) with features of CM and either embryonic tissues or amnion in the sample. Flow cytometry (FC) in 40 showed diploid complement in all. In ten of the 40, there was evidence of a twin; in 17, there was only amnion, which could belong to a twin; in the remaining 13, there was no evidence of a twin and nucleated fetal red blood cells (FRCs) were seen within molar vessels in ten (0.3 per cent). Seven of the 40 patients (17.5 per cent) and one of the ten with FRCs in villi (10 per cent) developed PTD, an incidence comparable to that of CM. Genetic studies in seven of these tea are reported separately. Finding fetal tissues with a mole or FRCs in molar vessels is not enough to classify it as PM, since it can be a CM with a twin, fetal development CM, or possibly a third type of mole. These rare diploid moles with fetal tissues have histological appearances and prognosis similar to those of CM.


Assuntos
Diploide , Embrião de Mamíferos/patologia , Eritrócitos/patologia , Mola Hidatiforme/patologia , Neoplasias Uterinas/patologia , Adulto , Âmnio/patologia , Desenvolvimento Embrionário e Fetal , Feminino , Citometria de Fluxo , Humanos , Pessoa de Meia-Idade , Gravidez , Gravidez Múltipla , Prognóstico
17.
J Pathol ; 181(2): 189-95, 1997 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-9120724

RESUMO

The purpose of this study was to determine the genetic origin of a series of seven diploid hydatidiform moles with fetal red blood cells in the molar villi, normally a characteristic feature of triploid, partial hydatidiform moles. DNA was prepared from formalin-fixed, paraffin-embedded blocks of molar tissue and blood from the patient and her partner. The genetic origin of molar tissue was determined by comparing microsatellite polymorphisms in molar and parental tissue following polymerase chain reaction (PCR) amplification of DNA. In six cases, the hydatidiform mole was shown to be androgenetic in origin and therefore genetically to be a complete hydatidiform mole. In one case, the hydatidiform mole was of biparental origin, having both a maternal and a paternal contribution to the genome. We conclude that fetal red blood cells may be observed in the villi of complete hydatidiform moles. In cases where the degree of trophoblastic hyperplasia and ploidy is suggestive of a complete hydatidiform mole, the presence of fetal red blood cells alone should not be considered indicative of a diagnosis of partial hydatidiform mole.


Assuntos
Diploide , Embrião de Mamíferos/patologia , Eritrócitos/patologia , Mola Hidatiforme/genética , Neoplasias Uterinas/genética , DNA de Neoplasias/genética , Diagnóstico Diferencial , Feminino , Humanos , Mola Hidatiforme/patologia , Repetições de Microssatélites , Reação em Cadeia da Polimerase , Polimorfismo Genético , Gravidez , Neoplasias Uterinas/patologia
19.
Clin Cancer Res ; 2(5): 897-902, 1996 May.
Artigo em Inglês | MEDLINE | ID: mdl-9816247

RESUMO

Placental site trophoblastic tumor is a very rare variant of gestational trophoblastic disease which differs histologically and immunocytochemically from gestational choriocarcinoma. The English language literature includes only 74 reported cases. Seventeen patients have been managed at Charing Cross Hospital with this diagnosis. The median follow-up is 4.6 years, and the 5-year overall survival is 80% (95% confidence interval, 55-93%). Multivariate regression analysis identified an interval of >2 years since the preceding pregnancy as an independent adverse prognostic factor. Genotypic analysis by PCR allelotyping has confirmed the gestational origin of all 11 tumors successfully studied. More detailed molecular analysis has identified the causative pregnancy for eight tumors. Five were diploid biparental tumors following term pregnancies, and three were androgenetic tumors following monospermic complete hydatidiform moles.


Assuntos
Neoplasias Trofoblásticas/genética , Neoplasias Uterinas/genética , Adulto , Gonadotropina Coriônica/sangue , Feminino , Genótipo , Humanos , Pessoa de Meia-Idade , Gravidez , Prognóstico , Taxa de Sobrevida , Resultado do Tratamento , Neoplasias Trofoblásticas/mortalidade , Neoplasias Trofoblásticas/terapia , Neoplasias Uterinas/mortalidade , Neoplasias Uterinas/terapia
20.
Eur J Cancer ; 32A(4): 593-7, 1996 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-8695258

RESUMO

59 patients were treated for newly diagnosed metastatic ovarian germ cell tumours with POMB/ACE chemotherapy (which contains cisplatinum, vincristine, methotrexate, bleomycin, actinomycin D, cyclophosphamide and etoposide). The median follow-up was 7.7 years. The 3 year survival is 87.8% (95% confidence interval 76.9-93.9%) and no relapses occurred more than 3 years after treatment. 4 (7%) patients had primary drug resistance to POMB/ACE and 4 (7%) have relapsed. One patient in complete remission developed secondary acute myeloid leukaemia after receiving a total of 1.3 g/m2 etoposide. 6 of 12 (50%) patients referred at relapse were salvaged by POMB/ACE. 14 of 33 (42%) women (> 18 years old) have had successful pregnancies after fertility conserving surgery and chemotherapy with no congenital abnormalities reported. The POMB/ACE regimen is as efficacious as other published regimens for ovarian germ cell tumours (OGCT) and balances a low incidence of life-threatening toxicity with a high success rate.


Assuntos
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Germinoma/tratamento farmacológico , Neoplasias Ovarianas/tratamento farmacológico , Adolescente , Adulto , Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos , Bleomicina/administração & dosagem , Criança , Pré-Escolar , Cisplatino/administração & dosagem , Cisplatino/efeitos adversos , Ciclofosfamida/administração & dosagem , Ciclofosfamida/efeitos adversos , Dactinomicina/administração & dosagem , Dactinomicina/efeitos adversos , Etoposídeo/administração & dosagem , Etoposídeo/efeitos adversos , Feminino , Germinoma/mortalidade , Germinoma/cirurgia , Humanos , Leucovorina/administração & dosagem , Leucovorina/efeitos adversos , Metotrexato/administração & dosagem , Pessoa de Meia-Idade , Recidiva Local de Neoplasia , Neoplasias Ovarianas/mortalidade , Neoplasias Ovarianas/cirurgia , Gravidez , Complicações Neoplásicas na Gravidez , Indução de Remissão , Terapia de Salvação , Taxa de Sobrevida , Vincristina/administração & dosagem
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA