Targeting epigenetic mechanisms to overcome venetoclax resistance
The BH-3 mimetic venetoclax overcomes apoptosis and therapy resistance caused by high expression of BCL2 or loss of BH3-only protein function. Although a promising therapy for hematologic malignancies, increased expression of anti-apoptotic MCL-1 or BCL-XL, as well as other resistance mechanisms pre...
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| Published in | Biochimica et biophysica acta. Molecular cell research Vol. 1868; no. 8; p. 119047 |
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| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
Netherlands
Elsevier B.V
01.07.2021
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| Subjects | |
| Online Access | Get full text |
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| Abstract | The BH-3 mimetic venetoclax overcomes apoptosis and therapy resistance caused by high expression of BCL2 or loss of BH3-only protein function. Although a promising therapy for hematologic malignancies, increased expression of anti-apoptotic MCL-1 or BCL-XL, as well as other resistance mechanisms prevent a durable response to venetoclax. Recent studies demonstrate that agents targeting epigenetic mechanisms such as DNA methyltransferase inhibitors, histone deacetylase (HDAC) inhibitors, histone methyltransferase EZH2 inhibitors, or bromodomain reader protein inhibitors may disable oncogenic gene expression signatures responsible for venetoclax resistance. Combination therapies including venetoclax and epigenetic therapies are effective in preclinical models and the subject of many current clinical trials. Here we review epigenetic strategies to overcome venetoclax resistance mechanisms in hematologic malignancies.
•Mutations affecting epigenetic regulation of gene expression are frequent in cancer and impact apoptosis mechanisms.•Venetoclax is a promising therapy for malignancies, but altered expression of BCL2 family members can cause resistance.•Combinations of venetoclax with epigenetic therapies have been approved and demonstrated effective in clinical trials. |
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| AbstractList | The BH-3 mimetic venetoclax overcomes apoptosis and therapy resistance caused by high expression of BCL2 or loss of BH3-only protein function. Although a promising therapy for hematologic malignancies, increased expression of anti-apoptotic MCL-1 or BCL-XL, as well as other resistance mechanisms prevent a durable response to venetoclax. Recent studies demonstrate that agents targeting epigenetic mechanisms such as DNA methyltransferase inhibitors, histone deacetylase (HDAC) inhibitors, histone methyltransferase EZH2 inhibitors, or bromodomain reader protein inhibitors may disable oncogenic gene expression signatures responsible for venetoclax resistance. Combination therapies including venetoclax and epigenetic therapies are effective in preclinical models and the subject of many current clinical trials. Here we review epigenetic strategies to overcome venetoclax resistance mechanisms in hematologic malignancies. The BH-3 mimetic venetoclax overcomes apoptosis and therapy resistance caused by high expression of BCL2 or loss of BH3-only protein function. Although a promising therapy for hematologic malignancies, increased expression of anti-apoptotic MCL-1 or BCL-XL, as well as other resistance mechanisms prevent a durable response to venetoclax. Recent studies demonstrate that agents targeting epigenetic mechanisms such as DNA methyltransferase inhibitors, histone deacetylase (HDAC) inhibitors, histone methyltransferase EZH2 inhibitors, or bromodomain reader protein inhibitors may disable oncogenic gene expression signatures responsible for venetoclax resistance. Combination therapies including venetoclax and epigenetic therapies are effective in preclinical models and the subject of many current clinical trials. Here we review epigenetic strategies to overcome venetoclax resistance mechanisms in hematologic malignancies.The BH-3 mimetic venetoclax overcomes apoptosis and therapy resistance caused by high expression of BCL2 or loss of BH3-only protein function. Although a promising therapy for hematologic malignancies, increased expression of anti-apoptotic MCL-1 or BCL-XL, as well as other resistance mechanisms prevent a durable response to venetoclax. Recent studies demonstrate that agents targeting epigenetic mechanisms such as DNA methyltransferase inhibitors, histone deacetylase (HDAC) inhibitors, histone methyltransferase EZH2 inhibitors, or bromodomain reader protein inhibitors may disable oncogenic gene expression signatures responsible for venetoclax resistance. Combination therapies including venetoclax and epigenetic therapies are effective in preclinical models and the subject of many current clinical trials. Here we review epigenetic strategies to overcome venetoclax resistance mechanisms in hematologic malignancies. The BH-3 mimetic venetoclax overcomes apoptosis and therapy resistance caused by high expression of BCL2 or loss of BH3-only protein function. Although a promising therapy for hematologic malignancies, increased expression of anti-apoptotic MCL-1 or BCL-XL, as well as other resistance mechanisms prevent a durable response to venetoclax. Recent studies demonstrate that agents targeting epigenetic mechanisms such as DNA methyltransferase inhibitors, histone deacetylase (HDAC) inhibitors, histone methyltransferase EZH2 inhibitors, or bromodomain reader protein inhibitors may disable oncogenic gene expression signatures responsible for venetoclax resistance. Combination therapies including venetoclax and epigenetic therapies are effective in preclinical models and the subject of many current clinical trials. Here we review epigenetic strategies to overcome venetoclax resistance mechanisms in hematologic malignancies. •Mutations affecting epigenetic regulation of gene expression are frequent in cancer and impact apoptosis mechanisms.•Venetoclax is a promising therapy for malignancies, but altered expression of BCL2 family members can cause resistance.•Combinations of venetoclax with epigenetic therapies have been approved and demonstrated effective in clinical trials. |
| ArticleNumber | 119047 |
| Author | Prado, Gabriel Licht, Jonathan D. Bennett, Richard L. Kaestner, Charlotte L. |
| Author_xml | – sequence: 1 givenname: Gabriel surname: Prado fullname: Prado, Gabriel – sequence: 2 givenname: Charlotte L. surname: Kaestner fullname: Kaestner, Charlotte L. – sequence: 3 givenname: Jonathan D. surname: Licht fullname: Licht, Jonathan D. – sequence: 4 givenname: Richard L. surname: Bennett fullname: Bennett, Richard L. email: bennettr@ufl.edu |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33945824$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_3389_fphar_2023_1291920 crossref_primary_10_1158_2159_8290_CD_21_1334 crossref_primary_10_1177_20406207241306553 crossref_primary_10_1038_s41698_022_00315_2 crossref_primary_10_3390_cancers15143650 crossref_primary_10_1186_s13148_025_01823_1 crossref_primary_10_4062_biomolther_2023_149 crossref_primary_10_3390_ijms241210374 crossref_primary_10_1016_j_bbamcr_2022_119213 crossref_primary_10_1038_s41392_025_02176_0 |
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| Keywords | Azacytidine Decitabine JQ1 Venetoclax EZH2 |
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| SubjectTerms | Antineoplastic Agents - chemistry Antineoplastic Agents - pharmacology Azacytidine Bridged Bicyclo Compounds, Heterocyclic - chemistry Bridged Bicyclo Compounds, Heterocyclic - pharmacology Decitabine Drug Resistance, Neoplasm - drug effects Drug Resistance, Neoplasm - genetics Enzyme Inhibitors - chemistry Enzyme Inhibitors - pharmacology Epigenesis, Genetic - drug effects Epigenesis, Genetic - genetics EZH2 Humans JQ1 Neoplasms - drug therapy Neoplasms - metabolism Neoplasms - pathology Sulfonamides - chemistry Sulfonamides - pharmacology Venetoclax |
| Title | Targeting epigenetic mechanisms to overcome venetoclax resistance |
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