Nour Alhuda Hammoud
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Nour Alhuda Hammoud has a total of 4 co-authors. Here are the top co-authors by number of shared publications:
- Alexandra V. Bruter
Institute of Gene Biology, Russian Academy of Sciences, Vavilov St., 34/5, Moscow 119334, Russia
1 shared publication - Alvina I. Khamidullina
Laboratory of Molecular Oncobiology, Institute of Gene Biology, Russian Academy of Sciences, Moscow 119334, Russia
1 shared publication - Ekaterina A. Varlamova
Institute of Gene Biology, Russian Academy of Sciences, Moscow, Russia
1 shared publication - Margarita A. Yastrebova
Institute of Gene Biology, Russian Academy of Sciences, 34/5 Vavilov Street, 119334 Moscow, Russia
1 shared publication
Latest Publications
- Open Access
- 8 July 2021
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 22 (14) , 7340
Gene Transcription as a Therapeutic Target in Leukemia
Blood malignancies often arise from undifferentiated hematopoietic stem cells or partially differentiated stem-like cells. A tight balance of multipotency and differentiation, cell division, and quiescence underlying normal hematopoiesis requires a special program governed by the transcriptional machinery. Acquisition of drug resistance by tumor cells also involves reprogramming of their transcriptional landscape. Limiting tumor cell plasticity by disabling reprogramming of the gene transcription is a promising strategy for improvement of treatment outcomes. Herein, we review the molecular mechanisms of action of transcription-targeted drugs in hematological malignancies (largely in leukemia) with particular respect to the results of clinical trials.
- 8 July 2021
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 22 (14) , 7340
Open AccessGene Transcription as a Therapeutic Target in Leukemia
Blood malignancies often arise from undifferentiated hematopoietic stem cells or partially differentiated stem-like cells. A tight balance of multipotency and differentiation, cell division, and quiescence underlying normal hematopoiesis requires a special program governed by the transcriptional machinery. Acquisition of drug resistance by tumor cells also involves reprogramming of their transcriptional landscape. Limiting tumor cell plasticity by disabling reprogramming of the gene transcription is a promising strategy for improvement of treatment outcomes. Herein, we review the molecular mechanisms of action of transcription-targeted drugs in hematological malignancies (largely in leukemia) with particular respect to the results of clinical trials.