mebendazole has been researched along with Melanoma in 7 studies
Mebendazole: A benzimidazole that acts by interfering with CARBOHYDRATE METABOLISM and inhibiting polymerization of MICROTUBULES.
mebendazole : A carbamate ester that is methyl 1H-benzimidazol-2-ylcarbamate substituted by a benzoyl group at position 5.
Melanoma: A malignant neoplasm derived from cells that are capable of forming melanin, which may occur in the skin of any part of the body, in the eye, or, rarely, in the mucous membranes of the genitalia, anus, oral cavity, or other sites. It occurs mostly in adults and may originate de novo or from a pigmented nevus or malignant lentigo. Melanomas frequently metastasize widely, and the regional lymph nodes, liver, lungs, and brain are likely to be involved. The incidence of malignant skin melanomas is rising rapidly in all parts of the world. (Stedman, 25th ed; from Rook et al., Textbook of Dermatology, 4th ed, p2445)
Excerpt | Relevance | Reference |
---|---|---|
" the apoptosis as well as autophagy and their related signaling in several stabilized cell lines as well as human explant melanoma cells treated with flubendazole (FLU)." | 7.96 | An analysis of mitotic catastrophe induced cell responses in melanoma cells exposed to flubendazole. ( Rudolf, E; Rudolf, K, 2020) |
" We find that MBZ synergizes with the MEK inhibitor trametinib to inhibit growth of BRAFWT-NRASQ61K melanoma cells in culture and in xenografts, and markedly decreased MEK and ERK phosphorylation." | 7.85 | The repurposed anthelmintic mebendazole in combination with trametinib suppresses refractory NRASQ61K melanoma. ( Abdussamad, M; Atkins, MB; Byers, SW; Calvert, V; Chen, YS; Dakshanamurthy, S; Fang, HB; Gaur, A; Petricoin, EF; Rosenthal, DS; Simbulan-Rosenthal, CM; Zapas, J; Zhou, H, 2017) |
"Mebendazole (MBZ) was identified as a promising therapeutic on the basis of its ability to induce apoptosis in melanoma cell lines through a B-cell lymphoma 2 (BCL2)-dependent mechanism." | 7.79 | XIAP downregulation accompanies mebendazole growth inhibition in melanoma xenografts. ( Byron, SA; Doudican, NA; Orlow, SJ; Pollock, PM, 2013) |
"In recent years, treatment of melanoma and a range of other deadly cancers has involved immunotherapy with programmed cell death protein-1 (PD-1)/PD-1 ligand (PD-L1) checkpoint blockade which has improved survival." | 5.51 | The anthelmintic flubendazole blocks human melanoma growth and metastasis and suppresses programmed cell death protein-1 and myeloid-derived suppressor cell accumulation. ( Acharya, G; Elahy, M; Khachigian, LM; Li, Y; Xin, H, 2019) |
"Flubendazole (FLU) is a widely used anthelmintic drug belonging to benzimidazole group." | 5.48 | Flubendazole induces mitotic catastrophe and apoptosis in melanoma cells. ( Čáňová, K; Rozkydalová, L; Rudolf, E; Vokurková, D, 2018) |
"Mebendazole was prioritized to further characterize its mechanism of melanoma growth inhibition based on its favorable pharmacokinetic profile." | 5.35 | Mebendazole induces apoptosis via Bcl-2 inactivation in chemoresistant melanoma cells. ( Doudican, N; Orlow, SJ; Osman, I; Rodriguez, A, 2008) |
" the apoptosis as well as autophagy and their related signaling in several stabilized cell lines as well as human explant melanoma cells treated with flubendazole (FLU)." | 3.96 | An analysis of mitotic catastrophe induced cell responses in melanoma cells exposed to flubendazole. ( Rudolf, E; Rudolf, K, 2020) |
" We find that MBZ synergizes with the MEK inhibitor trametinib to inhibit growth of BRAFWT-NRASQ61K melanoma cells in culture and in xenografts, and markedly decreased MEK and ERK phosphorylation." | 3.85 | The repurposed anthelmintic mebendazole in combination with trametinib suppresses refractory NRASQ61K melanoma. ( Abdussamad, M; Atkins, MB; Byers, SW; Calvert, V; Chen, YS; Dakshanamurthy, S; Fang, HB; Gaur, A; Petricoin, EF; Rosenthal, DS; Simbulan-Rosenthal, CM; Zapas, J; Zhou, H, 2017) |
"Mebendazole (MBZ) was identified as a promising therapeutic on the basis of its ability to induce apoptosis in melanoma cell lines through a B-cell lymphoma 2 (BCL2)-dependent mechanism." | 3.79 | XIAP downregulation accompanies mebendazole growth inhibition in melanoma xenografts. ( Byron, SA; Doudican, NA; Orlow, SJ; Pollock, PM, 2013) |
"In recent years, treatment of melanoma and a range of other deadly cancers has involved immunotherapy with programmed cell death protein-1 (PD-1)/PD-1 ligand (PD-L1) checkpoint blockade which has improved survival." | 1.51 | The anthelmintic flubendazole blocks human melanoma growth and metastasis and suppresses programmed cell death protein-1 and myeloid-derived suppressor cell accumulation. ( Acharya, G; Elahy, M; Khachigian, LM; Li, Y; Xin, H, 2019) |
"Flubendazole (FLU) is a widely used anthelmintic drug belonging to benzimidazole group." | 1.48 | Flubendazole induces mitotic catastrophe and apoptosis in melanoma cells. ( Čáňová, K; Rozkydalová, L; Rudolf, E; Vokurková, D, 2018) |
"Mebendazole was prioritized to further characterize its mechanism of melanoma growth inhibition based on its favorable pharmacokinetic profile." | 1.35 | Mebendazole induces apoptosis via Bcl-2 inactivation in chemoresistant melanoma cells. ( Doudican, N; Orlow, SJ; Osman, I; Rodriguez, A, 2008) |
Timeframe | Studies, this research(%) | All Research% |
---|---|---|
pre-1990 | 0 (0.00) | 18.7374 |
1990's | 0 (0.00) | 18.2507 |
2000's | 1 (14.29) | 29.6817 |
2010's | 5 (71.43) | 24.3611 |
2020's | 1 (14.29) | 2.80 |
Authors | Studies |
---|---|
Rudolf, K | 1 |
Rudolf, E | 2 |
Čáňová, K | 1 |
Rozkydalová, L | 1 |
Vokurková, D | 1 |
Li, Y | 1 |
Acharya, G | 1 |
Elahy, M | 1 |
Xin, H | 1 |
Khachigian, LM | 1 |
Barrett, JE | 1 |
Kim, FJ | 1 |
Simbulan-Rosenthal, CM | 1 |
Dakshanamurthy, S | 1 |
Gaur, A | 1 |
Chen, YS | 1 |
Fang, HB | 1 |
Abdussamad, M | 1 |
Zhou, H | 1 |
Zapas, J | 1 |
Calvert, V | 1 |
Petricoin, EF | 1 |
Atkins, MB | 1 |
Byers, SW | 1 |
Rosenthal, DS | 1 |
Doudican, N | 1 |
Rodriguez, A | 1 |
Osman, I | 1 |
Orlow, SJ | 2 |
Doudican, NA | 1 |
Byron, SA | 1 |
Pollock, PM | 1 |
Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
---|---|---|---|---|---|---|---|
A Phase I Study of Mebendazole for the Treatment of Pediatric Gliomas[NCT01837862] | Phase 1/Phase 2 | 36 participants (Anticipated) | Interventional | 2013-10-22 | Recruiting | ||
[information is prepared from clinicaltrials.gov, extracted Sep-2024] |
7 other studies available for mebendazole and Melanoma
Article | Year |
---|---|
An analysis of mitotic catastrophe induced cell responses in melanoma cells exposed to flubendazole.
Topics: Aged; Antineoplastic Agents; Apoptosis; Autophagy; Cell Cycle; Cell Line, Tumor; Cytochromes c; Huma | 2020 |
Flubendazole induces mitotic catastrophe and apoptosis in melanoma cells.
Topics: Antinematodal Agents; Apoptosis; Cell Line, Tumor; Cell Proliferation; Humans; Mebendazole; Melanoma | 2018 |
The anthelmintic flubendazole blocks human melanoma growth and metastasis and suppresses programmed cell death protein-1 and myeloid-derived suppressor cell accumulation.
Topics: Animals; Antinematodal Agents; Antineoplastic Agents; Cell Growth Processes; Cell Line, Tumor; Femal | 2019 |
The purpose of repurposing.
Topics: Anthelmintics; Humans; Mebendazole; Melanoma; Pyridones; Pyrimidinones | 2017 |
The repurposed anthelmintic mebendazole in combination with trametinib suppresses refractory NRASQ61K melanoma.
Topics: Animals; Antinematodal Agents; Antineoplastic Combined Chemotherapy Protocols; Cell Line, Tumor; Cel | 2017 |
Mebendazole induces apoptosis via Bcl-2 inactivation in chemoresistant melanoma cells.
Topics: Animals; Apoptosis; bcl-2-Associated X Protein; Benzimidazoles; Cell Line, Tumor; Cell Proliferation | 2008 |
XIAP downregulation accompanies mebendazole growth inhibition in melanoma xenografts.
Topics: Animals; Apoptosis; Cell Line, Tumor; Dacarbazine; Down-Regulation; Drug Resistance, Neoplasm; Femal | 2013 |