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New Insights into Blood Disorders in Basic Research

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: closed (20 May 2023) | Viewed by 2481

Special Issue Editors


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Guest Editor
Department of Clinical and Biological Sciences, University of Turin, 10043 Orbassano, Italy
Interests: leukemia and cancer; molecular mechanisms; TKI resistance; Dictyostelium discoideum model organism
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Guest Editor
Department of Oncology, University of Turin, 10043 Turin, Italy
Interests: signal transduction; G-protein; GPCR; ubiquitin; peroxisome; lipid; Dictyostelium
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Department of Oncology, University of Turin, 10043 Turin, Italy
Interests: ubiquitination system; chemotaxis and aerotaxis; omics science; simple model; leukemia and cancer
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Dipartimento di Chirurgia e Specialità Medico-Chirurgiche, Sezione di Ematologia, Università degli Studi di Catania, 95126 Catania, Italy
Interests: signal transduction; G-protein; ubiquitin; Dictyostelium; developmental biology; proteomic mass spectrometry; chemotaxis

Special Issue Information

Dear Colleagues, 

Hematopoietic malignancies are heterogeneous disorders, usually characterized by genetic mutations in the hematopoietic stem cells (HSCs). The identification of novel markers has completely transformed the diagnosis, the prognosis, and the follow-up, thus becoming critical for monitoring the minimal residual disease and relapse. We would like to focus our attention on the no genetic alteration-driven processes that may be involved in leukemogenesis. In this regard, post-translational modifications, including phosphorylation, ubiquitination, and acetylation are fascinating mechanisms by which cells monitor essential pathways including cell cycle, apoptosis, and differentiation, and play a key role, when deregulated, in several pathologies, including blood disorders. Shedding light on this topic will help to figure out several unsolved issues.

Thus, in this special issue, we invite researchers to submit original research articles or reviews describing innovative functions of the non-genomic altered mechanisms and the processes regulating them (hypoxia, ubiquitin-proteasome system (UPS), autophagy, oxidative stress) in the leukemia field. Furthermore, research studies ranging from simple model organisms to human hematological diseases will be highly considered.

Dr. Cristina Panuzzo
Dr. Enrico Bracco
Dr. Barbara Pergolizzi
Dr. Alessandra Romano
Guest Editors

Manuscript Submission Information

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Keywords

  • myeloproliferative neoplasms
  • acute myeloid leukemia
  • myelodisplastic sindrome
  • post-translational modifications
  • phosphorylation
  • autophagy
  • oxidative stress
  • model organisms
  • translational research
  • oncosuppressors
  • oncogenes
  • drug therapies

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Published Papers (1 paper)

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Research

17 pages, 4200 KiB  
Article
mTORC2 Is Activated under Hypoxia and Could Support Chronic Myeloid Leukemia Stem Cells
by Cristina Panuzzo, Lucrezia Pironi, Alessandro Maglione, Simone Rocco, Serena Stanga, Chiara Riganti, Joanna Kopecka, Muhammad Shahzad Ali, Barbara Pergolizzi, Enrico Bracco and Daniela Cilloni
Int. J. Mol. Sci. 2023, 24(2), 1234; https://doi.org/10.3390/ijms24021234 - 8 Jan 2023
Cited by 2 | Viewed by 2201
Abstract
Hypoxia is a critical condition that governs survival, self-renewal, quiescence, metabolic shift and refractoriness to leukemic stem cell (LSC) therapy. The present study aims to investigate the hypoxia-driven regulation of the mammalian Target of the Rapamycin-2 (mTORC2) complex to unravel it as a [...] Read more.
Hypoxia is a critical condition that governs survival, self-renewal, quiescence, metabolic shift and refractoriness to leukemic stem cell (LSC) therapy. The present study aims to investigate the hypoxia-driven regulation of the mammalian Target of the Rapamycin-2 (mTORC2) complex to unravel it as a novel potential target in chronic myeloid leukemia (CML) therapeutic strategies. After inducing hypoxia in a CML cell line model, we investigated the activities of mTORC1 and mTORC2. Surprisingly, we detected a significant activation of mTORC2 at the expense of mTORC1, accompanied by the nuclear localization of the main substrate phospho-Akt (Ser473). Moreover, the Gene Ontology analysis of CML patients’ CD34+ cells showed enrichment in the mTORC2 signature, further strengthening our data. The deregulation of mTOR complexes highlights how hypoxia could be crucial in CML development. In conclusion, we propose a mechanism by which CML cells residing under a low-oxygen tension, i.e., in the leukemia quiescent LSCs, singularly regulate the mTORC2 and its downstream effectors. Full article
(This article belongs to the Special Issue New Insights into Blood Disorders in Basic Research)
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