ijms-logo

Journal Browser

Journal Browser

Special Issue "Deciphering the Therapeutic Resistance of Hematologic Malignancies"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 31 December 2021.

Special Issue Editor

Prof. Dr. Tomáš Stopka
E-Mail Website
Guest Editor
Department of Haematology, First Faculty of Medicine, Charles University and General Hospital, 12808 Prague, Czech Republic
Interests: RNA; cancer

Special Issue Information

Dear Colleagues,

Tumor biology has decades of history in deciphering therapies to fight the hyperproliferative nature of many tumors, especially in hematology. Recent discoveries in stem cell biology have led to the development of the concept of leukemia-initiating cells. Despite many attempts to identify novel drugs with antitumor function, a large proportion of patients relapse or progress onto other therapies. The mechanisms that remain behind therapeutic resistance in leukemias and lymphomas are the subject to this Special Issue of IJMS. We are open to publications that focus on delineating genetic or epigenetic mechanisms of resistance as well as biomarker studies that associate biological parameters with adverse clinical outcome.

Prof. Dr. Tomáš Stopka
Guest Editor

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.

Keywords

  • Myelodysplasia
  • leukemogenesis
  • Epigenetic regulation
  • Azacitidine

Published Papers (3 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Jump to: Review

Article
Melittin Increases Cisplatin Sensitivity and Kills KM-H2 and L-428 Hodgkin Lymphoma Cells
Int. J. Mol. Sci. 2021, 22(1), 343; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22010343 - 31 Dec 2020
Viewed by 833
Abstract
Hodgkin lymphoma (HL) is neoplasia with high cure rates. However, not all patients can be cured with the current treatment. Chemo-resistance of tumor cells is one factor involved in treatment failure. In addition to its pore-forming activity on lipid bilayer membranes, the toxin [...] Read more.
Hodgkin lymphoma (HL) is neoplasia with high cure rates. However, not all patients can be cured with the current treatment. Chemo-resistance of tumor cells is one factor involved in treatment failure. In addition to its pore-forming activity on lipid bilayer membranes, the toxin melittin from bee venom is an inhibitor of several cancer-related signaling pathways. Moreover, melittin analogs have been shown to inhibit the activity of ATP binding cassette (ABC) transporters which are known to play important roles in the chemo-resistance of tumor cells. Therefore, we tested the toxicity of melittin for HL cell lines KM-H2 and L-428 and whether melittin can increase the chemo-sensitivity of cisplatin-resistant HL cells. We found high toxicity of melittin for KM-H2 and L-428 cells. In co-cultures with normal blood cells, melittin preferentially killed KM-H2 and L-428 cells. In addition, we observed increased cisplatin sensitivity of chemo-resistant L-428 cells after treatment with melittin. ABC transporter activity was not reduced after treatment with melittin. Our data suggest that melittin or melittin analogs might be promising agents for the future development of treatment strategies for HL patients with resistant disease. Full article
(This article belongs to the Special Issue Deciphering the Therapeutic Resistance of Hematologic Malignancies)
Show Figures

Figure 1

Communication
Identification of Lenalidomide Sensitivity and Resistance Mechanisms in Non-Del(5q) Myelodysplastic Syndromes
Int. J. Mol. Sci. 2020, 21(9), 3323; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21093323 - 08 May 2020
Cited by 2 | Viewed by 818
Abstract
Whereas lenalidomide is an effective therapy for del(5q) MDS patients, a minority of non-del(5q) MDS patients achieve hematologic improvement with lenalidomide. We used computational biology modeling and digital drug simulation to examine genomic data from 56 non-del(5q) MDS patients treated with lenalidomide, and [...] Read more.
Whereas lenalidomide is an effective therapy for del(5q) MDS patients, a minority of non-del(5q) MDS patients achieve hematologic improvement with lenalidomide. We used computational biology modeling and digital drug simulation to examine genomic data from 56 non-del(5q) MDS patients treated with lenalidomide, and then matched treatment response with molecular pathways. The computer inferred genomic abnormalities associating with lenalidomide treatment response in non-del(5q) MDS to include trisomy 8, del(20q), or RUNX1 loss of function mutations. Genomic abnormalities associating with lenalidomide resistance in non-del(5q) MDS patients included mutations in SF3B1, TET2, WNT3A amplification, MCL1 amplification, and/or PSEN2 amplification. These results may inform protocols for determining appropriateness of lenalidomide in non-del(5q) MDS. Full article
(This article belongs to the Special Issue Deciphering the Therapeutic Resistance of Hematologic Malignancies)
Show Figures

Figure 1

Review

Jump to: Research

Review
Deciphering the Therapeutic Resistance in Acute Myeloid Leukemia
Int. J. Mol. Sci. 2020, 21(22), 8505; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21228505 - 12 Nov 2020
Cited by 2 | Viewed by 896
Abstract
Acute myeloid leukemia (AML) is a clonal hematopoietic disorder characterized by abnormal proliferation, lack of cellular differentiation, and infiltration of bone marrow, peripheral blood, or other organs. Induction failure and in general resistance to chemotherapeutic agents represent a hindrance for improving survival outcomes [...] Read more.
Acute myeloid leukemia (AML) is a clonal hematopoietic disorder characterized by abnormal proliferation, lack of cellular differentiation, and infiltration of bone marrow, peripheral blood, or other organs. Induction failure and in general resistance to chemotherapeutic agents represent a hindrance for improving survival outcomes in AML. Here, we review the latest insights in AML biology concerning refractoriness to therapies with a specific focus on cytarabine and daunorubicin which still represent milestones agents for inducing therapeutic response and disease eradication. However, failure to achieve complete remission in AML is still high especially in elderly patients (40–60% in patients >65 years old). Several lines of basic and clinical research have been employed to improve the achievement of complete remission. These lines of research include molecular targeted therapy and more recently immunotherapy. In terms of molecular targeted therapies, specific attention is given to DNMT3A and TP53 mutant AML by reviewing the mechanisms underlying epigenetic therapies’ (e.g., hypomethylating agents) resistance and providing critical points and hints for possible future therapies overcoming AML refractoriness. Full article
(This article belongs to the Special Issue Deciphering the Therapeutic Resistance of Hematologic Malignancies)
Show Figures

Figure 1

Back to TopTop