RESUMO
Excitement about the dramatic increase in potential successful anticancer medicines in recent years is hampered by the high costs involved as well as the length of time traditional pathways take for regulatory approval. The translation of experimental clinical data into real-world evidence is also problematic. While the randomised controlled trial remains the gold standard for assessing efficacy and safety, there is increasing interest in the use of observational data to enable more rapid, informed and widespread availability and access to important anticancer medicines. Taking real-world evidence into account in regulatory and health technology assessment in a thoughtful and balanced fashion will enrich and justify sound decision-making.
Assuntos
Antineoplásicos/uso terapêutico , Desenvolvimento de Medicamentos/métodos , Neoplasias/tratamento farmacológico , Avaliação da Tecnologia Biomédica/métodos , Pesquisa Biomédica/economia , Pesquisa Biomédica/métodos , Pesquisa Biomédica/estatística & dados numéricos , Custos de Medicamentos , Desenvolvimento de Medicamentos/economia , Desenvolvimento de Medicamentos/estatística & dados numéricos , Humanos , Estudos Observacionais como Assunto/economia , Estudos Observacionais como Assunto/métodos , Estudos Observacionais como Assunto/estatística & dados numéricos , Avaliação de Resultados em Cuidados de Saúde/economia , Avaliação de Resultados em Cuidados de Saúde/métodos , Avaliação de Resultados em Cuidados de Saúde/estatística & dados numéricos , Ensaios Clínicos Controlados Aleatórios como Assunto/economia , Ensaios Clínicos Controlados Aleatórios como Assunto/métodos , Ensaios Clínicos Controlados Aleatórios como Assunto/estatística & dados numéricos , Avaliação da Tecnologia Biomédica/economia , Avaliação da Tecnologia Biomédica/estatística & dados numéricosRESUMO
Comprehensive Cancer Centres (CCCs) serve as critical drivers for improving cancer survival. In Europe, we have developed an Excellence Designation System (EDS) consisting of criteria to assess "excellence" of CCCs in translational research (bench to bedside and back), with the expectation that many European CCCs will aspire to this status.
Assuntos
Institutos de Câncer , Neoplasias/terapia , Qualidade da Assistência à Saúde , Pesquisa Translacional Biomédica , Institutos de Câncer/normas , Europa (Continente) , Humanos , Qualidade da Assistência à Saúde/normas , Pesquisa Translacional Biomédica/métodos , Pesquisa Translacional Biomédica/normasRESUMO
BACKGROUND: Little is known about the prevalence and associations of clinically relevant fatigue (CRF) in recurrence-free prostate cancer survivors. PATIENTS AND METHODS: Four hundred and sixteen recurrence-free prostate cancer survivors who were >1 year post-radiotherapy or radical prostatectomy were surveyed. The prevalence of CRF (defined as Brief Fatigue Inventory >3) was determined and compared with a noncancer control group. Other measures included the Hospital Anxiety and Depression Scale, International Prostate Symptom Score, European Organization for Research and Treatment of Cancer Quality of Life Questionnaire. Relationships between these factors and CRF were explored in univariate and multivariate analyses. RESULTS: Analyzable data were obtained from 91% (377/416) of patients. The prevalence of CRF was 29% (108/377) versus 16% (10/63) in the controls (P=0.031). CRF was more common in post-radiotherapy than in post-prostatectomy 33% (79/240) versus 22% (29/133), P=0.024. However, when other factors (current depression, anxiety, urinary symptoms, medical comorbidities, pain and insomnia) were controlled for, previous treatment did not predict CRF. Current depression [Hospital Anxiety and Depression Scale≥8 was by far the strongest association [odds ratio 9.9, 95% confidence interval 4.2-23.5)]. CONCLUSIONS: Almost one-third of recurrence-free prostate cancer survivors report CRF. Depression, anxiety, urinary symptoms, pain and insomnia measured at outcome are more strongly associated than type of cancer treatment previously received.
Assuntos
Fadiga/epidemiologia , Fadiga/etiologia , Neoplasias da Próstata/complicações , Sobreviventes/estatística & dados numéricos , Idoso , Ansiedade/epidemiologia , Comorbidade , Estudos Transversais , Depressão/epidemiologia , Fadiga/psicologia , Humanos , Masculino , Dor/epidemiologia , Prevalência , Qualidade de Vida , Inquéritos e QuestionáriosRESUMO
BACKGROUND: The purpose of the study was to determine the prevalence and associations of clinically relevant fatigue (CRF) in men with biochemically controlled prostate cancer on long-term androgen deprivation therapy (ADT). PATIENTS AND METHODS: One hundred and ninety-eight men were surveyed and the prevalence of CRF (Brief Fatigue Inventory score >3) determined. Associations with other measures (Hospital Anxiety and Depression Scale; International Prostate Symptom Score; European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire; Brief Pain Inventory worst pain; clinical and demographic information) were explored in univariate and multivariate analyses. RESULTS: Eight-one per cent (160 of 198) of questionnaires were analysable. CRF prevalence was 43% (68 of 160). CRF associations included moderate/severe urinary symptoms, anxiety and medical co-morbidities; the strongest associations were depression [odds ratio (OR) 9.8, 95% confidence interval (CI) 4.3-22.8] and pain (OR 9.2, 95% CI 4.0-21.5). After controlling for other factors, the independent associations were depression (OR 4.7, 95% CI 1.6-14.0) and pain (OR 3.1, 95% CI 1.0-8.9). There was no association with age, disease burden or treatment duration. CONCLUSIONS: Two-fifths of men with biochemically controlled prostate cancer on long-term ADT report CRF that interferes with function. Management aimed at improving CRF should address depression and pain.
Assuntos
Antineoplásicos Hormonais/efeitos adversos , Fadiga/induzido quimicamente , Hormônio Liberador de Gonadotropina/análogos & derivados , Hormônio Liberador de Gonadotropina/efeitos adversos , Neoplasias da Próstata/tratamento farmacológico , Idoso , Idoso de 80 Anos ou mais , Antineoplásicos Hormonais/uso terapêutico , Ansiedade/complicações , Estudos Transversais , Depressão/complicações , Fadiga/epidemiologia , Fadiga/etiologia , Hormônio Liberador de Gonadotropina/uso terapêutico , Humanos , Modelos Logísticos , Masculino , Pessoa de Meia-Idade , Análise Multivariada , Neoplasias Hormônio-Dependentes/tratamento farmacológico , Dor/complicações , Prevalência , Neoplasias da Próstata/complicações , Qualidade de Vida , AutorrelatoRESUMO
BACKGROUND: Tumour necrosis factor-alpha (TNF-alpha) is an important regulator of the chronic inflammation contributing to tumour progression. Infliximab, an anti-TNF-alpha monoclonal antibody was investigated in this trial of patients with advanced cancer. The primary objectives were to determine the safety profile and biological response of infliximab in a cancer population. Clinical response was a secondary objective. PATIENTS AND METHODS: Forty-one patients received infliximab at 5 mg/kg (n = 21) or 10 mg/kg (n = 20) i.v. at 0 and 2 weeks and then every 4 weeks. Post-treatment samples were measured for changes in plasma and serum TNF-alpha, CCL2, IL-6 and C-reactive protein (CRP). RESULTS: Infliximab was well tolerated with no dose-limiting toxic effects. At both doses of infliximab, neutralisation of serum TNF-alpha was observed after 1 h while plasma CCL2, IL-6 and serum CRP were decreased 24 and 48 h following infliximab administration. Seven patients experienced disease stablisation (range 10-50+ weeks). There was no evidence of disease acceleration in any patient. CONCLUSIONS: Infliximab treatment was safe and well tolerated in patients with advanced cancer. There was evidence of biological activity with baseline TNF-alpha and CCL2 being correlated with infliximab response.
Assuntos
Anticorpos Monoclonais/uso terapêutico , Hipersensibilidade a Drogas , Hipersensibilidade Tardia , Neoplasias/tratamento farmacológico , Fator de Necrose Tumoral alfa/antagonistas & inibidores , Adulto , Idoso , Anticorpos Monoclonais/administração & dosagem , Anticorpos Monoclonais/efeitos adversos , Proteína C-Reativa/análise , Quimiocina CCL2/sangue , Relação Dose-Resposta a Droga , Esquema de Medicação , Feminino , Humanos , Hipersensibilidade Tardia/induzido quimicamente , Infliximab , Infusões Intravenosas , Interleucina-6/sangue , Modelos Lineares , Masculino , Pessoa de Meia-Idade , Neoplasias/sangue , Neoplasias/patologia , Sensibilidade e Especificidade , Estomatite/induzido quimicamente , Resultado do Tratamento , Fator de Necrose Tumoral alfa/sangueRESUMO
Kahalalide F (KF) is a small natural peptide that showed activity in vitro and in vivo. The dose-limiting toxicity in clinical trials was transaminitis. We investigated the cytotoxicity of KF in cell lines from breast, ovary, prostate and colon cancers, but focused on hepatoma cell lines, performing mechanistic studies in HepG2 (IC50 = 0.3 microM) and PLC/PRF/5C (IC50 = 5 microM). Following KF exposure, HepG2 cells demonstrated profound ATP depletion, associated with cell swelling and cell blebbing, and increased permeability to propidium iodide (PI), annexin V (AV) and release of lactate dehydrogenase (LDH). PLC/PRF/5C cells retained their cell structure, but were permeable to PI and, following exposure to high concentrations of KF, to AV. The pattern of cell permeability is similar to maitotoxin, another small cytotoxic peptide, but the differential effects on the cell membrane induced by KF in HepG2 and PLC/PRF/5C suggest specific interactions with membranes or proteins. This could lead to better drug design aimed at exploiting the potential for cell selectivity.
Assuntos
Carcinoma Hepatocelular/metabolismo , Depsipeptídeos/farmacologia , Neoplasias Hepáticas/metabolismo , Trifosfato de Adenosina/deficiência , Linhagem Celular Tumoral , Membrana Celular/efeitos dos fármacos , Depsipeptídeos/farmacocinética , Humanos , Permeabilidade/efeitos dos fármacosRESUMO
WWOX is a candidate tumour suppressor gene that exhibits LOH or homozygous deletion in several tumour types. As well as the predominant full-length transcript (variant 1) there also exist alternatively spliced transcripts found previously only in malignant tissue. It has been suggested that proteins encoded by these variants may interfere with normal WWOX function in a dominant negative fashion. The most prevalent alternate transcript demonstrated in ovarian cancer is variant 4, which lacks exons 6-8. Here, we report the first comparison of the mRNA expression of WWOX variants 1 and 4 in human ovarian tumours and normal ovaries, and correlate expression with clinical data. We demonstrate significantly lower WWOX variant 1 expression in tumours than in normal ovaries. This reduction was not associated with any specific clinical subgroup. Variant 4 was expressed at low levels, and significantly associated with high grade and advanced stage ovarian cancer. Furthermore, tumours co-expressing variant 4 and relatively high levels of variant 1 showed significantly worse survival than tumours expressing variant 1 alone. However, variant 4 was also frequently identified in non-malignant ovarian tissue. These results support the role of WWOX variant 1 as a suppressor of ovarian tumourigenesis, but the role of variant 4 remains speculative.
Assuntos
Perfilação da Expressão Gênica , Genes Supressores de Tumor , Neoplasias Epiteliais e Glandulares/metabolismo , Neoplasias Ovarianas/metabolismo , Oxirredutases/genética , RNA Mensageiro/análise , Feminino , Humanos , Estadiamento de Neoplasias , Neoplasias Ovarianas/mortalidade , Neoplasias Ovarianas/patologia , Ovário/metabolismo , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Proteínas Supressoras de Tumor , Oxidorredutase com Domínios WWRESUMO
E7070 is a synthetic chloro-indolyl sulphonamide that is being developed as an anti cancer agent. In this phase II study, 28 patients with metastatic melanoma received 700 mg/m(2) of E7070 as a 60-min infusion repeated every 3 weeks. Although therapy was well tolerated, with one patient receiving 14 courses of treatment, there were only minor responses on independent radiological review. E7070 does not warrant further development as a single agent for the treatment of metastatic melanoma.
Assuntos
Melanoma/tratamento farmacológico , Neoplasias Cutâneas/tratamento farmacológico , Sulfonamidas/uso terapêutico , Adulto , Idoso , Progressão da Doença , Feminino , Humanos , Infusões Intravenosas , Masculino , Melanoma/patologia , Pessoa de Meia-Idade , Neoplasias Cutâneas/patologia , Sulfonamidas/administração & dosagem , Sulfonamidas/efeitos adversos , Resultado do TratamentoAssuntos
Antineoplásicos/farmacologia , Interferon gama/farmacologia , Neoplasias Ovarianas/tratamento farmacológico , Animais , Antineoplásicos/imunologia , Antineoplásicos/uso terapêutico , Divisão Celular/efeitos dos fármacos , Ensaios Clínicos como Assunto , Feminino , Humanos , Interferon gama/imunologia , Interferon gama/uso terapêutico , Neoplasias Ovarianas/imunologia , Neoplasias Ovarianas/patologia , Células Tumorais Cultivadas , Ensaios Antitumorais Modelo de XenoenxertoAssuntos
Inibidor p16 de Quinase Dependente de Ciclina/genética , Genes p53/genética , Linfoma de Células B/genética , Animais , Apoptose/genética , Dano ao DNA , Resistencia a Medicamentos Antineoplásicos/genética , Camundongos , Camundongos Transgênicos , Transplante de Neoplasias , Transfecção , Resultado do TratamentoRESUMO
Mixed mesodermal tumours (MMTs) are relatively rare gynaecological tumours that have been poorly studied in clinical and molecular terms. They are chemosensitive (at least initially), although ultimately they have a poor prognosis. The biology of the tumour is fascinating in view of its composition of both epithelial and mesenchymal entities. We review herein the literature on the clinical and biological aspects of this malignancy.
Assuntos
Neoplasias dos Genitais Femininos , Tumor Misto Maligno , Tumor Mesodérmico Misto , Antineoplásicos/uso terapêutico , Terapia Combinada/métodos , Feminino , Neoplasias dos Genitais Femininos/etiologia , Neoplasias dos Genitais Femininos/patologia , Neoplasias dos Genitais Femininos/terapia , Humanos , Tumor Misto Maligno/etiologia , Tumor Misto Maligno/patologia , Tumor Misto Maligno/terapia , Tumor Mesodérmico Misto/etiologia , Tumor Mesodérmico Misto/patologia , Tumor Mesodérmico Misto/terapia , PrognósticoRESUMO
The modulating effects of the orally active epidermal growth factor receptor-specific tyrosine kinase inhibitor ZD 1839 ("Iressa") on cell growth and signalling were evaluated in four ovarian cancer cell lines (PE01, PE04, SKOV-3, OVCAR-5) that express the epidermal growth factor receptor, and in A2780, which is epidermal growth factor receptor-negative. Transforming growth factor-alpha stimulated growth was completely inhibited by concentrations of ZD 1839 > or =0.3 microM in the epidermal growth factor receptor-expressing cell lines, as were transforming growth factor-alpha stimulated phosphorylation of the epidermal growth factor receptor and downstream components of the MAP kinase and PI-3 kinase signalling cascades. Growth inhibition in the absence of added transforming growth factor-alpha was also observed which could be consistent with suppression of action of autocrine epidermal growth factor receptor-activating ligands by ZD 1839. In support of this, transforming growth factor-alpha, EGF and amphiregulin mRNAs were detected by RT-PCR in the epidermal growth factor receptor-expressing cell lines. ZD 1839 inhibited growth of the PE04 ovarian cancer xenograft at 200 mg kg(-1)day(-1). These data lend further support to the view that targeting the epidermal growth factor receptor in ovarian cancer could have therapeutic benefit.
Assuntos
Receptores ErbB/fisiologia , Neoplasias Ovarianas/tratamento farmacológico , Proteínas Tirosina Quinases/antagonistas & inibidores , Quinazolinas/uso terapêutico , Animais , Divisão Celular/efeitos dos fármacos , Receptores ErbB/efeitos dos fármacos , Feminino , Gefitinibe , Humanos , Camundongos , Camundongos Nus , Neoplasias Ovarianas/patologia , Transdução de Sinais/efeitos dos fármacos , Transplante Heterólogo , Células Tumorais CultivadasRESUMO
c-Raf is an essential component of the extracellular related kinase (ERK) signal transduction pathway. Immunohistochemical staining indicated that c-Raf was present in 49/53 ovarian adenocarcinomas investigated and high c-Raf expression correlated significantly with poor survival (P = 0.002). c-Raf protein was detected in 15 ovarian cancer cell lines. Antisense oligodeoxynucleotides (ODNs) (ISIS 5132 and ISIS 13650) reduced c-Raf protein levels and inhibited cell proliferation in vitro. Selectivity was demonstrated by the lack of effect of ISIS 5132 on A-Raf or ERK, while a random ODN produced only minor effects on growth and did not influence c-Raf expression. ISIS 5132 produced enhanced apoptosis and cells accumulated in S and G(2)/M phases of the cell cycle. In vivo, ISIS 5132 inhibited growth of the s.c. SKOV-3 xenograft while a mismatch ODN had no effect. These data indicate that high levels of c-Raf expression may be important in ovarian cancer and use of antisense ODNs targeted to c-Raf could provide a strategy for the treatment of this disease.
Assuntos
DNA Antissenso/farmacologia , Neoplasias Ovarianas/tratamento farmacológico , Proteínas Proto-Oncogênicas c-raf/efeitos dos fármacos , Animais , Ciclo Celular/efeitos dos fármacos , Ciclo Celular/fisiologia , Divisão Celular/efeitos dos fármacos , DNA Antissenso/uso terapêutico , Relação Dose-Resposta a Droga , Feminino , Humanos , Imuno-Histoquímica , Camundongos , Camundongos Nus , Transplante de Neoplasias , Neoplasias Ovarianas/metabolismo , Neoplasias Ovarianas/patologia , Proteínas Proto-Oncogênicas c-raf/biossíntese , Proteínas Proto-Oncogênicas c-raf/genética , Análise de Sobrevida , Fatores de Tempo , Ensaios Antitumorais Modelo de XenoenxertoRESUMO
Two multicentre phase II trials were designed to determine if tumour responses can be achieved in progressive small-cell lung cancer (SCLC) or non-small cell lung cancer (NSCLC) patients treated with ISIS 5132, an inhibitor of C-raf kinase mRNA expression (CGP 69846A; ISIS Pharmaceuticals Inc, Carlsbad, CA), and to further characterise the safety of the compound. Between August 1998 and November 1999, 26 patients (18 NSCLC, 8 SCLC) were entered. Out of these, 23 were eligible, 22 (18 NSCLC, 4 SCLC) were treated with ISIS 5132 (2 mg/kg/day, 21 days continuous intravenous (i.v.) infusion every 4 weeks) and were evaluable for toxicity and 18 (15 NSCLC, 3 SCLC) were evaluable for efficacy. For the whole group haematological toxicity did not exceed grade 2. One patient experienced a grade 4 increased prothrombin time. Non-haematological toxicity was mild to moderate, with the observation of asthenia and nausea and vomiting. Progressive disease (PD) was diagnosed in 10 patients (8 NSCLC and 2 SCLC). 8 more patients (7 NSCLC, 1 SCLC) were considered as treatment failures. In conclusion, this study using ISIS 5132 with this dose and schedule of administration excludes a 20% response rate with 95% confidence intervals for NSCLC and cannot draw any conclusions for SCLC patients as only a few were involved in the study.
Assuntos
Antineoplásicos/uso terapêutico , Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico , Carcinoma de Células Pequenas/tratamento farmacológico , Neoplasias Pulmonares/tratamento farmacológico , Oligodesoxirribonucleotídeos Antissenso/uso terapêutico , Tionucleotídeos/uso terapêutico , Adulto , Idoso , Antineoplásicos/efeitos adversos , Progressão da Doença , Esquema de Medicação , Inibidores Enzimáticos/efeitos adversos , Inibidores Enzimáticos/uso terapêutico , Feminino , Doenças Hematológicas/induzido quimicamente , Humanos , Masculino , Pessoa de Meia-Idade , Oligodesoxirribonucleotídeos Antissenso/efeitos adversos , Proteínas Proto-Oncogênicas c-raf/antagonistas & inibidores , Tionucleotídeos/efeitos adversos , Resultado do TratamentoRESUMO
PURPOSE: Arg-D-Trp-NmePhe-D-Trp-Leu-Met-NH(2) (Antagonist G), a substance P (SP 6-11) analogue, inhibits mitogenesis stimulated by a broad spectrum of neuropeptides and has demonstrated antitumor activity in vitro and in vivo with IC(50) concentrations of 10-20 microM in small cell lung cancer and other cell lines. Because neuropeptides are part of complex neurohumoral pathways, we have sought to develop novel pharmacodynamic approaches as part of the early clinical development of this potential anticancer drug. EXPERIMENTAL DESIGN: A Phase I trial was performed in two stages. In stage 1, Antagonist G was administered at 3- week intervals using an accelerated dose-escalation strategy until the target maximum plasma concentration (C(max)) of 10 microM was achieved. In stage 2, dose intensity was increased to weekly, and the inhibitory effect of i.v. Antagonist G was assessed by forearm blood flow (FBF) using SP as a vasodilator, as measured by venous plethysmography. RESULTS: In stage 1, dose was escalated from 2 to 300 mg/m(2) in 12 dose levels using only 15 patients. In stage 2, nine patients were entered at three dose levels (300, 350, and 400 mg/m(2)) and a C(max) of 45 microM was achieved. Facial flushing was the only consistent toxicity but was not dose limiting. FBF studies demonstrated that Antagonist G consistently inhibited the vasodilatory effects of SP (mean, 62 +/- 2% inhibition). CONCLUSIONS: Antagonist G can be safely administered up to 400 mg/m(2), achieving C(max)s >20 microM by weekly 6-h i.v. infusion. FBF studies in patients demonstrated that Antagonist G inhibits SP vasodilatory effects in vivo at these doses in the absence of dose-limiting toxicity.
Assuntos
Antineoplásicos/uso terapêutico , Antebraço/irrigação sanguínea , Neoplasias/tratamento farmacológico , Oligopeptídeos/uso terapêutico , Vasodilatadores/farmacologia , Adulto , Idoso , Antineoplásicos/efeitos adversos , Antineoplásicos/farmacocinética , Artéria Braquial/efeitos dos fármacos , Bradicinina/farmacologia , Relação Dose-Resposta a Droga , Feminino , Rubor/induzido quimicamente , Humanos , Bombas de Infusão , Masculino , Taxa de Depuração Metabólica , Pessoa de Meia-Idade , Neoplasias/fisiopatologia , Neuropeptídeos/antagonistas & inibidores , Oligopeptídeos/sangue , Oligopeptídeos/farmacocinética , Fluxo Sanguíneo Regional/efeitos dos fármacos , Substância P/farmacologia , Resultado do TratamentoRESUMO
About 6000 women in the United Kingdom develop ovarian cancer each year and about two-thirds of the women will die from the disease. Establishing the prognosis of a woman with ovarian cancer is an important part of her evaluation and treatment. Prognostic models and indices in ovarian cancer should be developed using large databases and, ideally, with complete information on both prognostic indicators and long-term outcome. We developed a prognostic model using Cox regression and multiple imputation from 1189 primary cases of epithelial ovarian cancer (with median follow-up of 4.6 years). We found that the significant (P< or = 0.05) prognostic factors for overall survival were age at diagnosis, FIGO stage, grade of tumour, histology (mixed mesodermal, clear cell and endometrioid versus serous papillary), the presence or absence of ascites, albumin, alkaline phosphatase, performance status on the ZUBROD-ECOG-WHO scale, and debulking of the tumour. This model is consistent with other models in the ovarian cancer literature; it has better predictive ability and, after simplification and validation, could be used in clinical practice.
Assuntos
Modelos Teóricos , Estadiamento de Neoplasias , Neoplasias Ovarianas/patologia , Adolescente , Adulto , Idade de Início , Idoso , Idoso de 80 Anos ou mais , Fosfatase Alcalina/sangue , Ascite/patologia , Feminino , Nível de Saúde , Humanos , Pessoa de Meia-Idade , Neoplasias Ovarianas/terapia , Valor Preditivo dos Testes , Prognóstico , Análise de Regressão , Albumina SéricaRESUMO
The human homeobox BARX2 is located at 11q24-q25, within a minimal region associated with frequent loss of heterozygosity and adverse survival in epithelial ovarian cancer. BARX2 is a transcription factor that regulates transcription of specific cell adhesion molecules in the mouse. We show that BARX2 and cadherin 6 are expressed in normal human ovarian surface epithelium. BARX2 and cadherin 6 both have significantly lower expression in a clinical sample of endometrioid and clear cell ovarian cancers, as compared with serous or mixed mesodermal tumors. In a series of ovarian cancer cell lines, BARX2 expression showed a significant direct correlation with cadherin 6 expression. In OAW42, an ovarian cancer cell line that does not endogenously express BARX2, in vitro transfection of human BARX2 cDNA induced cadherin 6 expression. Transfection of BARX2 into OAW42 inhibited Matrigel invasion, haptotactic cellular migration to a collagen IV signal, and adhesion to collagen IV-coated plates. Our data demonstrate that BARX2 is expressed in the ovarian surface epithelium and has functional suppressor properties in ovarian cancer cells.