gossypol-acetic-acid and Leukemia--Myeloid--Acute

gossypol-acetic-acid has been researched along with Leukemia--Myeloid--Acute* in 2 studies

Other Studies

2 other study(ies) available for gossypol-acetic-acid and Leukemia--Myeloid--Acute

Article	Year
Synthetic lethality of combined AT-101 with idarubicin in acute myeloid leukemia via blockade of DNA repair and activation of intrinsic apoptotic pathway. Cancer letters, 2019, Oct-01, Volume: 461 Leukemia stem cells (LSCs) are deemed to the mainspring for treatment failure in acute myeloid leukemia (AML). Conventional chemotherapeutic drugs fail to eradicate leukemia stem cells, which becomes the root of drug resistance and disease recurrence. Hence, new therapeutic strategies targeting LSCs are supposed to be critical for patients with AML. Here we report that combination of Bcl-2 inhibitor AT-101 and chemotherapeutic drug idarubicin (IDA) results in synergistic lethality in CD34 Topics: Adolescent; Adult; Aged; Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Biomarkers, Tumor; Case-Control Studies; Cell Proliferation; DNA Repair; Drug Synergism; Female; fms-Like Tyrosine Kinase 3; Follow-Up Studies; Gene Expression Regulation, Neoplastic; Gossypol; Humans; Idarubicin; Leukemia, Myeloid, Acute; Male; Mice; Mice, Inbred NOD; Mice, SCID; Middle Aged; Prognosis; RUNX1 Translocation Partner 1 Protein; Survival Rate; Synthetic Lethal Mutations; Tumor Cells, Cultured; Xenograft Model Antitumor Assays; Young Adult	2019
The pan-Bcl2 Inhibitor AT101 Activates the Intrinsic Apoptotic Pathway and Causes DNA Damage in Acute Myeloid Leukemia Stem-Like Cells. Targeted oncology, 2017, Volume: 12, Issue:5 Leukemia stem cells (LSCs) are considered to be the cause of treatment failure and relapse in acute myeloid leukemia (AML). Overexpression of the Bcl-2 family of anti-apoptotic proteins such as Bcl-2, Bcl-xl, and Mcl-1 accounts for survival and self-renewal of LSCs. AT101 binds to the BH3 motif of all Bcl-2 family anti-apoptotic proteins and demonstrates anti-tumor activity in multiple types of tumor. Thus, we hypothesized that this agent might have the potential to deplete LSCs.. The present study aims to investigate if and by what mechanism AT101 is able to target AML stem-like cells.. AT101 inhibited proliferation and induced apoptosis in CD34. AT101 effectively eliminates LSCs in vitro through the induction of DNA damage and activation of the intrinsic apoptotic pathway. AT101 is effective towards leukemic cells from patients with adverse prognostic factors, suggesting that AT101 could have the potential as an alternative salvage therapy for the treatment of relapsed and refractory AML. Topics: Antineoplastic Agents, Phytogenic; Apoptosis; Cell Proliferation; DNA Damage; Gossypol; Humans; Leukemia, Myeloid, Acute; Neoplastic Stem Cells; Proto-Oncogene Proteins c-bcl-2	2017

Article

Year

Synthetic lethality of combined AT-101 with idarubicin in acute myeloid leukemia via blockade of DNA repair and activation of intrinsic apoptotic pathway.

Cancer letters, 2019, Oct-01, Volume: 461

Leukemia stem cells (LSCs) are deemed to the mainspring for treatment failure in acute myeloid leukemia (AML). Conventional chemotherapeutic drugs fail to eradicate leukemia stem cells, which becomes the root of drug resistance and disease recurrence. Hence, new therapeutic strategies targeting LSCs are supposed to be critical for patients with AML. Here we report that combination of Bcl-2 inhibitor AT-101 and chemotherapeutic drug idarubicin (IDA) results in synergistic lethality in CD34

Topics: Adolescent; Adult; Aged; Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Biomarkers, Tumor; Case-Control Studies; Cell Proliferation; DNA Repair; Drug Synergism; Female; fms-Like Tyrosine Kinase 3; Follow-Up Studies; Gene Expression Regulation, Neoplastic; Gossypol; Humans; Idarubicin; Leukemia, Myeloid, Acute; Male; Mice; Mice, Inbred NOD; Mice, SCID; Middle Aged; Prognosis; RUNX1 Translocation Partner 1 Protein; Survival Rate; Synthetic Lethal Mutations; Tumor Cells, Cultured; Xenograft Model Antitumor Assays; Young Adult

2019

The pan-Bcl2 Inhibitor AT101 Activates the Intrinsic Apoptotic Pathway and Causes DNA Damage in Acute Myeloid Leukemia Stem-Like Cells.

Targeted oncology, 2017, Volume: 12, Issue:5

Leukemia stem cells (LSCs) are considered to be the cause of treatment failure and relapse in acute myeloid leukemia (AML). Overexpression of the Bcl-2 family of anti-apoptotic proteins such as Bcl-2, Bcl-xl, and Mcl-1 accounts for survival and self-renewal of LSCs. AT101 binds to the BH3 motif of all Bcl-2 family anti-apoptotic proteins and demonstrates anti-tumor activity in multiple types of tumor. Thus, we hypothesized that this agent might have the potential to deplete LSCs.. The present study aims to investigate if and by what mechanism AT101 is able to target AML stem-like cells.. AT101 inhibited proliferation and induced apoptosis in CD34. AT101 effectively eliminates LSCs in vitro through the induction of DNA damage and activation of the intrinsic apoptotic pathway. AT101 is effective towards leukemic cells from patients with adverse prognostic factors, suggesting that AT101 could have the potential as an alternative salvage therapy for the treatment of relapsed and refractory AML.

Topics: Antineoplastic Agents, Phytogenic; Apoptosis; Cell Proliferation; DNA Damage; Gossypol; Humans; Leukemia, Myeloid, Acute; Neoplastic Stem Cells; Proto-Oncogene Proteins c-bcl-2

2017