|
Cervical intraepithelial neoplasia grade 2
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
To be eligible for this procedure superficial cervical PAP smears as well as colposcopic biopsies performed before therapy had to show CIN II with the lesion involving at least 15% of the cervix and being colposcopically visible.
|
12820459 |
2003 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Among the various genes identified in the 3p21.3 region, we tested the antitumor activity of the FUS1 gene in two human non-small-cell lung cancer (NSCLC) xenografts in vivo.
|
15486560 |
2004 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Our results show that myristoylation is required for Fus1-mediated tumor-suppressing activity and suggest a novel mechanism for the inactivation of tumor suppressors in lung cancer and a role for deficient posttranslational modification in tumor suppressor-gene-mediated carcinogenesis.
|
15126327 |
2004 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
This result demonstrates the potent tumor suppressive activity of the FUS1 gene and is a promising therapeutic agent for treatment of primary and disseminated human lung cancer.
|
15486560 |
2004 |
|
Malignant neoplasm of lung
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Our results show that myristoylation is required for Fus1-mediated tumor-suppressing activity and suggest a novel mechanism for the inactivation of tumor suppressors in lung cancer and a role for deficient posttranslational modification in tumor suppressor-gene-mediated carcinogenesis.
|
15126327 |
2004 |
|
Malignant neoplasm of lung
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
This result demonstrates the potent tumor suppressive activity of the FUS1 gene and is a promising therapeutic agent for treatment of primary and disseminated human lung cancer.
|
15486560 |
2004 |
|
Carcinoma of lung
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Our results show that myristoylation is required for Fus1-mediated tumor-suppressing activity and suggest a novel mechanism for the inactivation of tumor suppressors in lung cancer and a role for deficient posttranslational modification in tumor suppressor-gene-mediated carcinogenesis.
|
15126327 |
2004 |
|
Carcinoma of lung
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
This result demonstrates the potent tumor suppressive activity of the FUS1 gene and is a promising therapeutic agent for treatment of primary and disseminated human lung cancer.
|
15486560 |
2004 |
|
Primary malignant neoplasm of lung
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Our results show that myristoylation is required for Fus1-mediated tumor-suppressing activity and suggest a novel mechanism for the inactivation of tumor suppressors in lung cancer and a role for deficient posttranslational modification in tumor suppressor-gene-mediated carcinogenesis.
|
15126327 |
2004 |
|
Primary malignant neoplasm of lung
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
This result demonstrates the potent tumor suppressive activity of the FUS1 gene and is a promising therapeutic agent for treatment of primary and disseminated human lung cancer.
|
15486560 |
2004 |
|
Malignant Neoplasms
|
0.080 |
Biomarker
|
group |
BEFREE |
Loss of expression or a defect of myristoylation of the Fus1 protein was observed in human primary lung cancer and cancer cell lines.
|
15126327 |
2004 |
|
Primary malignant neoplasm
|
0.070 |
Biomarker
|
group |
BEFREE |
Loss of expression or a defect of myristoylation of the Fus1 protein was observed in human primary lung cancer and cancer cell lines.
|
15126327 |
2004 |
|
Secondary malignant neoplasm of lung
|
0.060 |
Biomarker
|
disease |
BEFREE |
A myristoylation-deficient mutant of the Fus1 protein abrogated its ability to inhibit tumor cell-induced clonogenicity in vitro, to induce apoptosis in lung tumor cells, and to suppress the growth of tumor xenografts and lung metastases in vivo and rendered it susceptible to rapid proteasome-dependent degradation.
|
15126327 |
2004 |
|
Secondary malignant neoplasm of lung
|
0.060 |
Biomarker
|
disease |
BEFREE |
Furthermore, intravenous injections of DOTAP:Chol-FUS1 complex into mice bearing experimental A549 lung metastasis demonstrated significant (P = .001) decrease in the number of metastatic tumor nodules.
|
15486560 |
2004 |
|
Carcinogenesis
|
0.050 |
AlteredExpression
|
phenotype |
BEFREE |
Our results show that myristoylation is required for Fus1-mediated tumor-suppressing activity and suggest a novel mechanism for the inactivation of tumor suppressors in lung cancer and a role for deficient posttranslational modification in tumor suppressor-gene-mediated carcinogenesis.
|
15126327 |
2004 |
|
Lung Neoplasms
|
0.040 |
Biomarker
|
group |
BEFREE |
Intratumoral administration of FUS1 gene complexed to DOTAP:cholesterol (DOTAP:Chol) liposome into subcutaneous H1299 and A549 lung tumor xenograft resulted in significant (P = .02) inhibition of tumor growth.
|
15486560 |
2004 |
|
Lung Neoplasms
|
0.040 |
AlteredExpression
|
group |
LHGDN |
A myristoylation-deficient mutant of the Fus1 protein abrogated its ability to inhibit tumor cell-induced clonogenicity in vitro, to induce apoptosis in lung tumor cells, and to suppress the growth of tumor xenografts and lung metastases in vivo and rendered it susceptible to rapid proteasome-dependent degradation.
|
15126327 |
2004 |
|
Cervical Intraepithelial Neoplasia
|
0.030 |
Biomarker
|
disease |
BEFREE |
Performance of the Roche AMPLICOR human papillomavirus (HPV) test in prediction of cervical intraepithelial neoplasia (CIN) in women with abnormal PAP smear.
|
16023184 |
2005 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
These findings provide strong evidence that c-Abl is a possible target in NSCLC patients that have reduced expression of Fus1 in their tumor cells.
|
17486070 |
2007 |
|
Non-Small Cell Lung Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In this study, we evaluated the combined effects of FUS1 and tumor suppressor p53 on antitumor activity and explored the molecular mechanisms of their mutual actions in human non-small cell lung cancer (NSCLC) cells.
|
17234782 |
2007 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Furthermore, we showed that the observed synergistic tumor suppression by FUS1 and p53 concurred with the FUS1-mediated down-regulation of murine double minute-2 (MDM2) expression, the accumulation and stabilization of p53 protein, as well as the activation of the apoptotic protease-activating factor 1 (Apaf-1)-dependent apoptotic pathway in human NSCLC cells.
|
17234782 |
2007 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Oncogenic activation of c-Abl in non-small cell lung cancer cells lacking FUS1 expression: inhibition of c-Abl by the tumor suppressor gene product Fus1.
|
17486070 |
2007 |
|
Malignant neoplasm of lung
|
0.100 |
Biomarker
|
disease |
BEFREE |
We also found that a systemic treatment with a combination of FUS1 and p53 nanoparticles synergistically suppressed the development and growth of tumors in a human H322 lung cancer orthotopic mouse model.
|
17234782 |
2007 |
|
Malignant neoplasm of lung
|
0.100 |
Biomarker
|
disease |
BEFREE |
The inhibitory Fus1 sequence was derived from a region that was deleted in a mutant FUS1 gene (FUS1 (1-80)) detected in some lung cancer cell lines.
|
17486070 |
2007 |
|
Carcinoma of lung
|
0.100 |
Biomarker
|
disease |
BEFREE |
The inhibitory Fus1 sequence was derived from a region that was deleted in a mutant FUS1 gene (FUS1 (1-80)) detected in some lung cancer cell lines.
|
17486070 |
2007 |