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Special Issue "Transcription in Cancer Initiation and Progression"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 June 2022.

Special Issue Editors

Dr. Agnieszka Zdzislawa Robaszkiewicz
E-Mail Website
Guest Editor
Department of General Biophysics, Faculty of Biology and Environmental Protection, University of Lodz, 90-236 Lodz, Poland
Interests: transcription; epigenetics; PARP1; SWI/SNF; EP300; differentiation; cancerogenesis; chromatin; transcription factors; transcription co-factors
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Andre Tremblay
E-Mail Website1 Website2
Guest Editor
Department of Biochemistry and Molecular Medicine, and Department of Obstetrics & Gynecology, Faculty of Medicine, University of Montreal, Montréal, QC H3T 1J4, Canada
Interests: nuclear receptor; transcription factor; cellular kinase pathway; estrogen receptor; upstream cellular signals; PPARs
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The transformation of normal, healthy cells into cancer cells is a complex multistep process associated in most cases with the de-differentiation of specialized cells, re-entrance of G0/G1 arrested cells to mitotic divisions, ability to spread and invade tissues, as well as with immortality. Although the initiation of carcinogenesis is linked with mutations and loss of genomic stability, the following promotion and progression steps require alteration also in other “-omics”. Transcriptional reprogramming adapts the proteome of the transforming cell to new phenotypes by facilitating the gradual decrease in expression of cell type or highly specific tissue genes, and enhancing expression of factors that promote proliferation, migration, and metastases.

Our issue is dedicated to the elucidation of the essential transcription-relevant events that contribute to carcinogenesis, and to the identification of emerging hubs where gene transcription and malignancy interact with each other. Therefore, we invite submissions that cover genome-wide as well as gene-specific chromatin remodeling that accompanies all stages of tumor development. We aim to identify transcription factors, co-factors, nucleosome readers, writers, and erasers that drive cell transformation. Our Specials Issue also aims to publish papers dealing with the molecular basis of oncogene expression, repression of tumor suppressors, role of cell cycle progression, and E2F-dependent gene transcription in gaining the cancer phenotype. Likewise, we are particularly interested in all aspects dealing with transcription of factors, which make malignant cells resistant to anti-cancer approaches.

Dr. Agnieszka Zdzislawa Robaszkiewicz
Prof. Dr. Andre Tremblay
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.


  • Cancer
  • Transcription
  • Transcription factors and co-factors
  • Chromatin remodeling
  • Epigenetic modification
  • Oncogenes
  • Suppressors
  • Cell cycle
  • E2F-dependent gene transcription
  • Tumor resistance
  • Signaling

Published Papers (1 paper)

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BET Proteins as Attractive Targets for Cancer Therapeutics
Int. J. Mol. Sci. 2021, 22(20), 11102; https://doi.org/10.3390/ijms222011102 - 14 Oct 2021
Cited by 1 | Viewed by 664
Transcriptional dysregulation is a hallmark of cancer and can be an essential driver of cancer initiation and progression. Loss of transcriptional control can cause cancer cells to become dependent on certain regulators of gene expression. Bromodomain and extraterminal domain (BET) proteins are epigenetic [...] Read more.
Transcriptional dysregulation is a hallmark of cancer and can be an essential driver of cancer initiation and progression. Loss of transcriptional control can cause cancer cells to become dependent on certain regulators of gene expression. Bromodomain and extraterminal domain (BET) proteins are epigenetic readers that regulate the expression of multiple genes involved in carcinogenesis. BET inhibitors (BETis) disrupt BET protein binding to acetylated lysine residues of chromatin and suppress the transcription of various genes, including oncogenic transcription factors. Phase I and II clinical trials demonstrated BETis’ potential as anticancer drugs against solid tumours and haematological malignancies; however, their clinical success was limited as monotherapies. Emerging treatment-associated toxicities, drug resistance and a lack of predictive biomarkers limited BETis’ clinical progress. The preclinical evaluation demonstrated that BETis synergised with different classes of compounds, including DNA repair inhibitors, thus supporting further clinical development of BETis. The combination of BET and PARP inhibitors triggered synthetic lethality in cells with proficient homologous recombination. Mechanistic studies revealed that BETis targeted multiple essential homologous recombination pathway proteins, including RAD51, BRCA1 and CtIP. The exact mechanism of BETis’ anticancer action remains poorly understood; nevertheless, these agents provide a novel approach to epigenome and transcriptome anticancer therapy. Full article
(This article belongs to the Special Issue Transcription in Cancer Initiation and Progression)
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