Literature DB >> 33509437

Epigenetic modifier directed therapeutics to unleash healthy genes in unhealthy cells.

Babal K Jha1, Yogen Saunthararajah2.   

Abstract

A common thread through malignant and nonmalignant diseases alerts us to a therapeutic opportunity to seize: disease may originate from genetic mutations, but resulting maladaptive/unhealthy cell fates and functions are mediated by epigenetic enzymes, that are druggable. Epigenetic enzymes modify DNA, and/or the histones around which DNA is organized, to regulate access to genes by the basal transcription factor machinery that transcribes genes. Epigenetic enzymes can be divided usefully into those that facilitate gene transcription ("on" enzymes or coactivators) and those that favor gene repression ("off" enzymes or corepressors). DNA-binding master transcription factors cooperate to recruit coactivators, and repulse corepressors, from thousands of genes, to thereby activate the gene expression programs that define cell fates and functions. In malignancy, this usual exchange of corepressors for coactivators fails, because of mutations to master transcription factors or the coactivators they recruit. Inhibiting corepressor enzymes using small molecules uses pharmacology to redress this coactivator/corepressor imbalance that originates from genetics, to in this way release cancer cells to the terminal lineage-fates intended by their master transcription factor content. Similarly, in nonmalignant β-hemoglobinopathies, inhibiting corepressors exploits transcription factor and lineage-context to activate unmutated fetal over mutated adult globin genes, to thereby treat these nonmalignant genetic diseases. Master transcription factors then are the "natural forces" in the Hippocratic dictum "Natural forces within us are the true healers of disease," and drugging epigenetic enzymes (corepressors) a way to harness these forces to heal.
Copyright © 2020 Elsevier Inc. All rights reserved.

Entities:  

Keywords:  Cancer; Epigenetics; Hemoglobinopathy; Leukemia; Therapy

Mesh:

Substances:

Year:  2020        PMID: 33509437      PMCID: PMC8832995          DOI: 10.1053/j.seminhematol.2020.11.009

Source DB:  PubMed          Journal:  Semin Hematol        ISSN: 0037-1963            Impact factor:   3.851


  13 in total

1.  RUNX1 regulates corepressor interactions of PU.1.

Authors:  Zhenbo Hu; Xiaorong Gu; Kristine Baraoidan; Vinzon Ibanez; Arun Sharma; ShriHari Kadkol; Reinhold Munker; Steven Ackerman; Giuseppina Nucifora; Yogen Saunthararajah
Journal:  Blood       Date:  2011-04-25       Impact factor: 22.113

Review 2.  Ultimate Precision: Targeting Cancer but Not Normal Self-replication.

Authors:  Vamsidhar Velcheti; David Schrump; Yogen Saunthararajah
Journal:  Am Soc Clin Oncol Educ Book       Date:  2018-05-23

3.  Evaluation of noncytotoxic DNMT1-depleting therapy in patients with myelodysplastic syndromes.

Authors:  Yogen Saunthararajah; Mikkael Sekeres; Anjali Advani; Reda Mahfouz; Lisa Durkin; Tomas Radivoyevitch; Ricki Englehaupt; Joy Juersivich; Kathleen Cooper; Holleh Husseinzadeh; Bartlomiej Przychodzen; Matthew Rump; Sean Hobson; Marc Earl; Ronald Sobecks; Robert Dean; Frederic Reu; Ramon Tiu; Betty Hamilton; Edward Copelan; Alan Lichtin; Eric Hsi; Matt Kalaycio; Jaroslaw Maciejewski
Journal:  J Clin Invest       Date:  2015-01-26       Impact factor: 14.808

4.  A pilot study of subcutaneous decitabine in β-thalassemia intermedia.

Authors:  Nancy F Olivieri; Yogen Saunthararajah; Vivek Thayalasuthan; Janet Kwiatkowski; Russell E Ware; Frans A Kuypers; Hae-Young Kim; Felicia L Trachtenberg; Elliott P Vichinsky
Journal:  Blood       Date:  2011-06-23       Impact factor: 22.113

5.  Leukemogenic nucleophosmin mutation disrupts the transcription factor hub that regulates granulomonocytic fates.

Authors:  Xiaorong Gu; Quteba Ebrahem; Reda Z Mahfouz; Metis Hasipek; Francis Enane; Tomas Radivoyevitch; Nicolas Rapin; Bartlomiej Przychodzen; Zhenbo Hu; Ramesh Balusu; Claudiu V Cotta; David Wald; Christian Argueta; Yosef Landesman; Maria Paola Martelli; Brunangelo Falini; Hetty Carraway; Bo T Porse; Jaroslaw Maciejewski; Babal K Jha; Yogen Saunthararajah
Journal:  J Clin Invest       Date:  2018-07-17       Impact factor: 14.808

6.  Runx1 regulation of Pu.1 corepressor/coactivator exchange identifies specific molecular targets for leukemia differentiation therapy.

Authors:  Xiaorong Gu; Zhenbo Hu; Quteba Ebrahem; John S Crabb; Reda Z Mahfouz; Tomas Radivoyevitch; John W Crabb; Yogen Saunthararajah
Journal:  J Biol Chem       Date:  2014-04-02       Impact factor: 5.157

7.  Severe pyoderma gangrenosum caused by myelodysplastic syndrome successfully treated with decitabine administered by a noncytotoxic regimen.

Authors:  Mostafa F M Saleh; Yogen Saunthararajah
Journal:  Clin Case Rep       Date:  2017-10-31

Review 8.  Targeting sickle cell disease root-cause pathophysiology with small molecules.

Authors:  Yogen Saunthararajah
Journal:  Haematologica       Date:  2019-08-08       Impact factor: 9.941

9.  Extended experience with a non-cytotoxic DNMT1-targeting regimen of decitabine to treat myeloid malignancies.

Authors:  Hassan Awada; Reda Z Mahfouz; Ashwin Kishtagari; Teodora Kuzmanovic; Jibran Durrani; Cassandra M Kerr; Bhumika J Patel; Valeria Visconte; Tomas Radivoyevitch; Alan Lichtin; Hetty E Carraway; Jaroslaw P Maciejewski; Yogen Saunthararajah
Journal:  Br J Haematol       Date:  2019-11-17       Impact factor: 6.998

10.  Runx1 deficiency permits granulocyte lineage commitment but impairs subsequent maturation.

Authors:  K P Ng; Z Hu; Q Ebrahem; S Negrotto; J Lausen; Y Saunthararajah
Journal:  Oncogenesis       Date:  2013-11-04       Impact factor: 7.485

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