Achieving clinical success with BET inhibitors as anti-cancer agents

The transcriptional upregulation of oncogenes is a driving force behind the progression of many tumours. However, until a decade ago, the concept of ‘switching off’ these oncogenic pathways represented a formidable challenge. Research has revealed that members of the bromo- and extra-terminal domain...

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Published inBritish journal of cancer Vol. 124; no. 9; pp. 1478 - 1490
Main Authors Shorstova, Tatiana, Foulkes, William D., Witcher, Michael
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 27.04.2021
Nature Publishing Group
Subjects
631/67/1059/602
692/53/2423
Antineoplastic Agents - therapeutic use
Antitumor agents
Biomarkers
Biomedical and Life Sciences
Biomedicine
Cancer Research
Chromatin
Drug Resistance
Epidemiology
Humans
Molecular Medicine
Neoplasms - drug therapy
Neoplasms - metabolism
Neoplasms - pathology
Oncology
Prognosis
Proteins - antagonists & inhibitors
Review
Review Article
Transcription
Transcription Factors - antagonists & inhibitors
Tumors
Online AccessGet full text

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Abstract The transcriptional upregulation of oncogenes is a driving force behind the progression of many tumours. However, until a decade ago, the concept of ‘switching off’ these oncogenic pathways represented a formidable challenge. Research has revealed that members of the bromo- and extra-terminal domain (BET) motif family are key activators of oncogenic networks in a spectrum of cancers; their function depends on their recruitment to chromatin through two bromodomains (BD1 and BD2). The advent of potent inhibitors of BET proteins (BETi), which target either one or both bromodomains, represents an important step towards the goal of suppressing oncogenic networks within tumours. Here, we discuss the biology of BET proteins, advances in BETi design and highlight potential biomarkers predicting their activity. We also outline the logic of incorporating BETi into combination therapies to enhance its efficacy. We suggest that understanding mechanisms of activity, defining predictive biomarkers and identifying potent synergies represents a roadmap for clinical success using BETi.
AbstractList The transcriptional upregulation of oncogenes is a driving force behind the progression of many tumours. However, until a decade ago, the concept of 'switching off' these oncogenic pathways represented a formidable challenge. Research has revealed that members of the bromo- and extra-terminal domain (BET) motif family are key activators of oncogenic networks in a spectrum of cancers; their function depends on their recruitment to chromatin through two bromodomains (BD1 and BD2). The advent of potent inhibitors of BET proteins (BETi), which target either one or both bromodomains, represents an important step towards the goal of suppressing oncogenic networks within tumours. Here, we discuss the biology of BET proteins, advances in BETi design and highlight potential biomarkers predicting their activity. We also outline the logic of incorporating BETi into combination therapies to enhance its efficacy. We suggest that understanding mechanisms of activity, defining predictive biomarkers and identifying potent synergies represents a roadmap for clinical success using BETi.
The transcriptional upregulation of oncogenes is a driving force behind the progression of many tumours. However, until a decade ago, the concept of 'switching off' these oncogenic pathways represented a formidable challenge. Research has revealed that members of the bromo- and extra-terminal domain (BET) motif family are key activators of oncogenic networks in a spectrum of cancers; their function depends on their recruitment to chromatin through two bromodomains (BD1 and BD2). The advent of potent inhibitors of BET proteins (BETi), which target either one or both bromodomains, represents an important step towards the goal of suppressing oncogenic networks within tumours. Here, we discuss the biology of BET proteins, advances in BETi design and highlight potential biomarkers predicting their activity. We also outline the logic of incorporating BETi into combination therapies to enhance its efficacy. We suggest that understanding mechanisms of activity, defining predictive biomarkers and identifying potent synergies represents a roadmap for clinical success using BETi.The transcriptional upregulation of oncogenes is a driving force behind the progression of many tumours. However, until a decade ago, the concept of 'switching off' these oncogenic pathways represented a formidable challenge. Research has revealed that members of the bromo- and extra-terminal domain (BET) motif family are key activators of oncogenic networks in a spectrum of cancers; their function depends on their recruitment to chromatin through two bromodomains (BD1 and BD2). The advent of potent inhibitors of BET proteins (BETi), which target either one or both bromodomains, represents an important step towards the goal of suppressing oncogenic networks within tumours. Here, we discuss the biology of BET proteins, advances in BETi design and highlight potential biomarkers predicting their activity. We also outline the logic of incorporating BETi into combination therapies to enhance its efficacy. We suggest that understanding mechanisms of activity, defining predictive biomarkers and identifying potent synergies represents a roadmap for clinical success using BETi.
Author Witcher, Michael
Foulkes, William D.
Shorstova, Tatiana
Author_xml – sequence: 1
  givenname: Tatiana
  surname: Shorstova
  fullname: Shorstova, Tatiana
  organization: Departments of Oncology and Experimental Medicine, McGill University, Lady Davis Institute and Segal Cancer Centre, Jewish General Hospital
– sequence: 2
  givenname: William D.
  surname: Foulkes
  fullname: Foulkes, William D.
  organization: Departments of Oncology and Human Genetics, McGill University, Lady Davis Institute and Segal Cancer Centre, Jewish General Hospital
– sequence: 3
  givenname: Michael
  orcidid: 0000-0002-4466-9166
  surname: Witcher
  fullname: Witcher, Michael
  email: michael.witcher@mcgill.ca
  organization: Departments of Oncology and Experimental Medicine, McGill University, Lady Davis Institute and Segal Cancer Centre, Jewish General Hospital
BackLink https://www.ncbi.nlm.nih.gov/pubmed/33723398$$D View this record in MEDLINE/PubMed
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Snippet The transcriptional upregulation of oncogenes is a driving force behind the progression of many tumours. However, until a decade ago, the concept of ‘switching...
The transcriptional upregulation of oncogenes is a driving force behind the progression of many tumours. However, until a decade ago, the concept of 'switching...
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SubjectTerms 631/67/1059/602
692/53/2423
Antineoplastic Agents - therapeutic use
Antitumor agents
Biomarkers
Biomedical and Life Sciences
Biomedicine
Cancer Research
Chromatin
Drug Resistance
Epidemiology
Humans
Molecular Medicine
Neoplasms - drug therapy
Neoplasms - metabolism
Neoplasms - pathology
Oncology
Prognosis
Proteins - antagonists & inhibitors
Review
Review Article
Transcription
Transcription Factors - antagonists & inhibitors
Tumors
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Title Achieving clinical success with BET inhibitors as anti-cancer agents
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