The Experts below are selected from a list of 3528 Experts worldwide ranked by ideXlab platform
Cristina Grange - One of the best experts on this subject based on the ideXlab platform.
-
Combining doxorubicin-nanobubbles and shockwaves for Anaplastic Thyroid Cancer treatment: preclinical study in a xenograft mouse model
Endocrine-related Cancer, 2017Co-Authors: Francesca Marano, Cristina Grange, Roberto Frairia, Letizia Rinella, Monica Argenziano, Benedetta Bussolati, Raffaella Mastrocola, Isabella Castellano, Laura Berta, Roberta CavalliAbstract:Anaplastic Thyroid Cancer is one of the most lethal diseases, and a curative therapy does not exist. Doxorubicin, the only drug approved for Anaplastic Thyroid Cancer treatment, has a very low response rate and causes numerous side effects among which cardiotoxicity is the most prominent. Thus, doxorubicin delivery to the tumor site could be an import goal aimed to improve the drug efficacy and to reduce its systemic side effects. We recently reported that, in human Anaplastic Thyroid Cancer cell lines, combining doxorubicin-loaded nanobubbles with extracorporeal shock waves, acoustic waves used in lithotripsy and orthopedics without side effects, increased the intracellular drug content and in vitro cytotoxicity. In the present study, we tested the efficacy of this treatment on a human Anaplastic Thyroid Cancer xenograft mouse model. After 21 days, the combined treatment determined the greatest drug accumulation in tumors with consequent reduction of tumor volume and weight, and an extension of the tumor doubling time. Mechanistically, the treatment induced tumor apoptosis and decreased cell proliferation. Finally, although doxorubicin caused the increase of fibrosis markers and oxidative stress in animal hearts, loading doxorubicin into nanobubbles avoided these effects preventing heart damage. The improvement of doxorubicin anti-tumor effects together with the prevention of heart damage suggests that the combination of doxorubicin-loaded nanobubbles with extracorporeal shock waves might be a promising drug delivery system for Anaplastic Thyroid Cancer treatment.
-
histone deacetylase inhibition modulates e cadherin expression and suppresses migration and invasion of Anaplastic Thyroid Cancer cells
The Journal of Clinical Endocrinology and Metabolism, 2012Co-Authors: Maria Graziella Catalano, Nicoletta Fortunati, Mariateresa Pugliese, Francesca Marano, Loredana Ortoleva, Roberta Poli, Sofia Asioli, Andrea Bandino, Nicola Palestini, Cristina GrangeAbstract:Context: Anaplastic Thyroid Cancer cells are characterized by a mesenchymal phenotype, as revealed by spindle-shaped cells and absent or reduced levels of E-cadherin. Epigenetic silencing is considered one of the leading mechanisms of E-cadherin impairment, which causes the acquisition of the invasive and metastatic phenotype of Anaplastic Thyroid Cancer. Objectives: In this study we investigated the effects of histone deacetylase inhibition on E-cadherin expression, cell motility, and invasion in Anaplastic Thyroid Cancer cell cultures. Design: Three stabilized cell lines and primary cultures of Anaplastic Thyroid Cancer were treated with various histone deacetylase inhibitors. After treatment, we evaluated histone acetylation by Western blotting and E-cadherin expression by RT-real time PCR. The proper localization of E-cadherin/β-catenin complex was assessed by immunofluorescence and Western blot. Transcription activity of β-catenin was measured by luciferase reporter gene and cyclin D1 expression. The...
-
Histone deacetylase inhibition modulates E-cadherin expression and suppresses migration and invasion of Anaplastic Thyroid Cancer cells.
The Journal of clinical endocrinology and metabolism, 2012Co-Authors: Maria Graziella Catalano, Nicoletta Fortunati, Mariateresa Pugliese, Francesca Marano, Loredana Ortoleva, Roberta Poli, Sofia Asioli, Andrea Bandino, Nicola Palestini, Cristina GrangeAbstract:Anaplastic Thyroid Cancer cells are characterized by a mesenchymal phenotype, as revealed by spindle-shaped cells and absent or reduced levels of E-cadherin. Epigenetic silencing is considered one of the leading mechanisms of E-cadherin impairment, which causes the acquisition of the invasive and metastatic phenotype of Anaplastic Thyroid Cancer. In this study we investigated the effects of histone deacetylase inhibition on E-cadherin expression, cell motility, and invasion in Anaplastic Thyroid Cancer cell cultures. Three stabilized cell lines and primary cultures of Anaplastic Thyroid Cancer were treated with various histone deacetylase inhibitors. After treatment, we evaluated histone acetylation by Western blotting and E-cadherin expression by RT-real time PCR. The proper localization of E-cadherin/β-catenin complex was assessed by immunofluorescence and Western blot. Transcription activity of β-catenin was measured by luciferase reporter gene and cyclin D1 expression. The effect on cell motility and invasion was studied both in vitro using scratch-wound and transwell invasion assays and in Anaplastic Thyroid carcinomas tumor xenografts in mice in vivo. Histone deacetylase inhibition induced the E-cadherin expression and the proper membrane localization of the E-cadherin/β-catenin complex, leading to reduced Cancer cell migration and invasion. We here demonstrate an additional molecular mechanism for the antiCancer effect of histone deacetylase inhibition. The antiinvasive effect in addition to the cytotoxic activity of histone deacetylase inhibitors opens up therapeutic perspectives for the Anaplastic Thyroid tumor that does not respond to conventional therapy.
Andrei Iagaru - One of the best experts on this subject based on the ideXlab platform.
-
F-18 FDG PET/CT demonstration of an adrenal metastasis in a patient with Anaplastic Thyroid Cancer.
Clinical Nuclear Medicine, 2020Co-Authors: Andrei Iagaru, Iain Ross McdougallAbstract:Abstract:An adrenal metastasis was identified on an F-18 FDG PET/CT scan in a patient with Anaplastic Thyroid Cancer. There are very few reports of Thyroid Cancer, even Anaplastic Thyroid Cancer, metastasizing to the adrenal.
-
Anaplastic Thyroid Cancer with extensive skeletal muscle metastases on 18f fdg pet ct
Clinical Nuclear Medicine, 2018Co-Authors: Ilana R Yurkiewicz, Kristen N Ganjoo, Andrei IagaruAbstract:: A 61-year-old woman with newly diagnosed Anaplastic Thyroid Cancer and known metastases to the brain, lungs, and adrenal glands complained of groin muscle pain. F-FDG PET/CT was performed to assess for extent of disease and showed extensive hypermetabolic lesions throughout the skeletal musculature concerning for metastatic disease. As this would be a very rare presentation for Anaplastic Thyroid carcinoma, a biopsy of the left gluteal muscle was conducted. Pathology demonstrated Anaplastic Thyroid carcinoma, metastatic to skeletal muscle.
Jan H M Schellens - One of the best experts on this subject based on the ideXlab platform.
-
dabrafenib and trametinib treatment in patients with locally advanced or metastatic braf v600 mutant Anaplastic Thyroid Cancer
Journal of Clinical Oncology, 2018Co-Authors: Vivek Subbiah, Maria E. Cabanillas, Robert J Kreitman, Zev A Wainberg, Jan H M Schellens, Jeancharles Soria, Christoph C Zielinski, Gladys Urbanowitz, Bijoyesh MookerjeeAbstract:PurposeWe report the efficacy and safety of dabrafenib (BRAF inhibitor) and trametinib (MEK inhibitor) combination therapy in BRAF V600E–mutated Anaplastic Thyroid Cancer, a rare, aggressive, and highly lethal malignancy with poor patient outcomes and no systemic therapies with clinical benefit.MethodsIn this phase II, open-label trial, patients with predefined BRAF V600E–mutated malignancies received dabrafenib 150 mg twice daily and trametinib 2 mg once daily until unacceptable toxicity, disease progression, or death. The primary end point was investigator-assessed overall response rate. Secondary end points included duration of response, progression-free survival, overall survival, and safety.ResultsSixteen patients with BRAF V600E–mutated Anaplastic Thyroid Cancer were evaluable (median follow-up, 47 weeks; range, 4 to 120 weeks). All patients had received prior radiation treatment and/or surgery, and six had received prior systemic therapy. The confirmed overall response rate was 69% (11 of 16; 95% C...
-
Dabrafenib and trametinib treatment in patients with locally advanced or metastatic BRAF V600–mutant Anaplastic Thyroid Cancer
Journal of Clinical Oncology, 2017Co-Authors: Vivek Subbiah, Maria E. Cabanillas, Robert J Kreitman, Zev A Wainberg, Jan H M Schellens, Jeancharles Soria, Christoph C Zielinski, Gladys UrbanowitzAbstract:PurposeWe report the efficacy and safety of dabrafenib (BRAF inhibitor) and trametinib (MEK inhibitor) combination therapy in BRAF V600E–mutated Anaplastic Thyroid Cancer, a rare, aggressive, and highly lethal malignancy with poor patient outcomes and no systemic therapies with clinical benefit.MethodsIn this phase II, open-label trial, patients with predefined BRAF V600E–mutated malignancies received dabrafenib 150 mg twice daily and trametinib 2 mg once daily until unacceptable toxicity, disease progression, or death. The primary end point was investigator-assessed overall response rate. Secondary end points included duration of response, progression-free survival, overall survival, and safety.ResultsSixteen patients with BRAF V600E–mutated Anaplastic Thyroid Cancer were evaluable (median follow-up, 47 weeks; range, 4 to 120 weeks). All patients had received prior radiation treatment and/or surgery, and six had received prior systemic therapy. The confirmed overall response rate was 69% (11 of 16; 95% C...
Bijoyesh Mookerjee - One of the best experts on this subject based on the ideXlab platform.
-
dabrafenib and trametinib treatment in patients with locally advanced or metastatic braf v600 mutant Anaplastic Thyroid Cancer
Journal of Clinical Oncology, 2018Co-Authors: Vivek Subbiah, Maria E. Cabanillas, Robert J Kreitman, Zev A Wainberg, Jan H M Schellens, Jeancharles Soria, Christoph C Zielinski, Gladys Urbanowitz, Bijoyesh MookerjeeAbstract:PurposeWe report the efficacy and safety of dabrafenib (BRAF inhibitor) and trametinib (MEK inhibitor) combination therapy in BRAF V600E–mutated Anaplastic Thyroid Cancer, a rare, aggressive, and highly lethal malignancy with poor patient outcomes and no systemic therapies with clinical benefit.MethodsIn this phase II, open-label trial, patients with predefined BRAF V600E–mutated malignancies received dabrafenib 150 mg twice daily and trametinib 2 mg once daily until unacceptable toxicity, disease progression, or death. The primary end point was investigator-assessed overall response rate. Secondary end points included duration of response, progression-free survival, overall survival, and safety.ResultsSixteen patients with BRAF V600E–mutated Anaplastic Thyroid Cancer were evaluable (median follow-up, 47 weeks; range, 4 to 120 weeks). All patients had received prior radiation treatment and/or surgery, and six had received prior systemic therapy. The confirmed overall response rate was 69% (11 of 16; 95% C...
Maria Graziella Catalano - One of the best experts on this subject based on the ideXlab platform.
-
histone deacetylase inhibition modulates e cadherin expression and suppresses migration and invasion of Anaplastic Thyroid Cancer cells
The Journal of Clinical Endocrinology and Metabolism, 2012Co-Authors: Maria Graziella Catalano, Nicoletta Fortunati, Mariateresa Pugliese, Francesca Marano, Loredana Ortoleva, Roberta Poli, Sofia Asioli, Andrea Bandino, Nicola Palestini, Cristina GrangeAbstract:Context: Anaplastic Thyroid Cancer cells are characterized by a mesenchymal phenotype, as revealed by spindle-shaped cells and absent or reduced levels of E-cadherin. Epigenetic silencing is considered one of the leading mechanisms of E-cadherin impairment, which causes the acquisition of the invasive and metastatic phenotype of Anaplastic Thyroid Cancer. Objectives: In this study we investigated the effects of histone deacetylase inhibition on E-cadherin expression, cell motility, and invasion in Anaplastic Thyroid Cancer cell cultures. Design: Three stabilized cell lines and primary cultures of Anaplastic Thyroid Cancer were treated with various histone deacetylase inhibitors. After treatment, we evaluated histone acetylation by Western blotting and E-cadherin expression by RT-real time PCR. The proper localization of E-cadherin/β-catenin complex was assessed by immunofluorescence and Western blot. Transcription activity of β-catenin was measured by luciferase reporter gene and cyclin D1 expression. The...
-
Histone deacetylase inhibition modulates E-cadherin expression and suppresses migration and invasion of Anaplastic Thyroid Cancer cells.
The Journal of clinical endocrinology and metabolism, 2012Co-Authors: Maria Graziella Catalano, Nicoletta Fortunati, Mariateresa Pugliese, Francesca Marano, Loredana Ortoleva, Roberta Poli, Sofia Asioli, Andrea Bandino, Nicola Palestini, Cristina GrangeAbstract:Anaplastic Thyroid Cancer cells are characterized by a mesenchymal phenotype, as revealed by spindle-shaped cells and absent or reduced levels of E-cadherin. Epigenetic silencing is considered one of the leading mechanisms of E-cadherin impairment, which causes the acquisition of the invasive and metastatic phenotype of Anaplastic Thyroid Cancer. In this study we investigated the effects of histone deacetylase inhibition on E-cadherin expression, cell motility, and invasion in Anaplastic Thyroid Cancer cell cultures. Three stabilized cell lines and primary cultures of Anaplastic Thyroid Cancer were treated with various histone deacetylase inhibitors. After treatment, we evaluated histone acetylation by Western blotting and E-cadherin expression by RT-real time PCR. The proper localization of E-cadherin/β-catenin complex was assessed by immunofluorescence and Western blot. Transcription activity of β-catenin was measured by luciferase reporter gene and cyclin D1 expression. The effect on cell motility and invasion was studied both in vitro using scratch-wound and transwell invasion assays and in Anaplastic Thyroid carcinomas tumor xenografts in mice in vivo. Histone deacetylase inhibition induced the E-cadherin expression and the proper membrane localization of the E-cadherin/β-catenin complex, leading to reduced Cancer cell migration and invasion. We here demonstrate an additional molecular mechanism for the antiCancer effect of histone deacetylase inhibition. The antiinvasive effect in addition to the cytotoxic activity of histone deacetylase inhibitors opens up therapeutic perspectives for the Anaplastic Thyroid tumor that does not respond to conventional therapy.
-
Effects of the histone deacetylase inhibitor valproic acid on the sensitivity of Anaplastic Thyroid Cancer cell lines to imatinib
Oncology Reports, 2009Co-Authors: Maria Graziella Catalano, Nicoletta Fortunati, Mariateresa Pugliese, Roberta Poli, Ornella Bosco, Raffaello Bertieri, Giuseppe BoccuzziAbstract:New therapeutic approaches are mandatory for Anaplastic Thyroid Cancer. We investigated the ability of a new combined treatment using valproic acid (VPA), the only clinically available histone deacetylase inhibitor, and the tyrosine-kinase inhibitor imatinib mesylate to control the cell growth of Anaplastic Thyroid Cancer cell lines. We showed that treatment with imatinib alone is unable to affect the cell growth of Anaplastic Thyroid Cancer cells, whereas in ARO cells, the combined treatment resulted in a cytostatic effect, with clinically achievable doses of imatinib and VPA. The effect is mediated by G1 growth arrest, acting through p21 expression and the impairment of AKT phosphorylation.
