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Cancers
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Novel Targeted Therapies for Blood Cancer
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Novel Targeted Therapies for Blood Cancer

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Methods and Technologies Development".

Deadline for manuscript submissions: closed (17 November 2023) | Viewed by 3558

Special Issue Editor

Dr. Mohammad Hojjat-Farsangi

E-Mail Website
Guest Editor
Department of Oncology-Pathology, Karolinska Institute and Karolinska University Hospital Solna, 17164 Stockholm, Sweden
Interests: targeted cancer therapy; tyrosine kinase inhibitors; small molecule inhibitors; apoptosis; monoclonal antibodies; immunomodulators; leukemia; lymphoma; acquired drug resistance; intracellular signaling
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer is one of the leading causes of death worldwide. Blood-related cancers are types of cancers that affect blood cells. The most frequent types of blood cancers are leukemia, lymphoma, and myeloma. Various factors can induce DNA changes, leading to the uncontrolled proliferation of mostly undifferentiated blood cells. Genetic, mutagenesis factors in foods and environment, radiations, and defects in the immune system are the most important factors that lead to abnormal behaviors of normal blood cells leading to cancer.

Chemotherapy, radiation, and surgery are usually the first choices for cancer treatment and are widely used in the treatment of cancer. Despite the improvements in patient health quality, the effectiveness of conventional treatments is compromised by several disadvantages. Therefore, new effective treatments focusing on removing malignant cells and minimizing side effects are of great importance. Targeted therapies or personalized medicine are new types of emerging treatments. Several reagents and methods have been improved during recent decades. Chemically synthesized or natural small molecule inhibitors (SMIs), monoclonal antibodies, immunomodulatory reagents, siRNAs, and synthetic peptides are among the reagents that specifically target tumor cells with fewer side effects on normal cells. Currently, several targeted therapy drugs have been approved by FDA for cancer treatment. However, cancer remains an incurable disease and needs special attention from authorities and scientists to recognize the obstacles in front of cancer treatment that remain to be solved.

The current Special Issue of Cancers therefore encompasses new research articles and timely reviews on new targeted therapy reagents and methods for targeting various types of blood cancers.

You may choose our Joint Special Issue in Current Oncology.

Dr. Mohammad Hojjat-Farsangi
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 submissions that pass pre-check are 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. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). 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.

Published Papers (3 papers)

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Research

16 pages, 2688 KiB  
Article
PI3Kδ Inhibition Potentiates Glucocorticoids in B-lymphoblastic Leukemia by Decreasing Receptor Phosphorylation and Enhancing Gene Regulation
by Jessica A. O. Zimmerman, Mimi Fang and Miles A. Pufall
Cancers 2024, 16(1), 143; https://doi.org/10.3390/cancers16010143 - 27 Dec 2023
Viewed by 869
Abstract
Glucocorticoids are the cornerstone of B-lymphoblastic leukemia (B-ALL) therapy. Because response to glucocorticoids alone predicts overall outcomes for B-ALL, enhancing glucocorticoid potency should improve treatment. We previously showed that inhibition of the lymphoid-restricted PI3Kδ with idelalisib enhances glucocorticoid activity in B-ALL cells. Here, [...] Read more.
Glucocorticoids are the cornerstone of B-lymphoblastic leukemia (B-ALL) therapy. Because response to glucocorticoids alone predicts overall outcomes for B-ALL, enhancing glucocorticoid potency should improve treatment. We previously showed that inhibition of the lymphoid-restricted PI3Kδ with idelalisib enhances glucocorticoid activity in B-ALL cells. Here, we show that idelalisib enhances glucocorticoid potency in 90% of primary B-ALL specimens and is most pronounced at sub-saturating doses of glucocorticoids near the EC50. Potentiation is associated with enhanced regulation of all glucocorticoid-regulated genes, including genes that drive B-ALL cell death. Idelalisib reduces phosphorylation of the glucocorticoid receptor (GR) at PI3Kδ/MAPK1 (ERK2) targets S203 and S226. Ablation of these phospho-acceptor sites enhances sensitivity to glucocorticoids with ablation of S226 in particular reducing synergy. We also show that phosphorylation of S226 reduces the affinity of GR for DNA in vitro. We propose that PI3Kδ inhibition improves glucocorticoid efficacy in B-ALL in part by decreasing GR phosphorylation, increasing DNA binding affinity, and enhancing downstream gene regulation. This mechanism and the response of patient specimens suggest that idelalisib will benefit most patients with B-ALL, but particularly patients with less responsive, including high-risk, disease. This combination is also promising for the development of less toxic glucocorticoid-sparing therapies. Full article
(This article belongs to the Special Issue Novel Targeted Therapies for Blood Cancer)
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14 pages, 1274 KiB  
Article
Understanding the Role of Activation Loop Mutants in Drug Efficacy for FLT3-ITD
by Julhash U. Kazi, Lina Al Ashiri, Rituraj Purohit and Lars Rönnstrand
Cancers 2023, 15(22), 5426; https://doi.org/10.3390/cancers15225426 - 15 Nov 2023
Cited by 1 | Viewed by 975
Abstract
The type III receptor tyrosine kinase FLT3 is a pivotal kinase for hematopoietic progenitor cell regulation, with significant implications in acute myeloid leukemia (AML) through mutations like internal tandem duplication (ITD). This study delves into the structural intricacies of FLT3, the roles of [...] Read more.
The type III receptor tyrosine kinase FLT3 is a pivotal kinase for hematopoietic progenitor cell regulation, with significant implications in acute myeloid leukemia (AML) through mutations like internal tandem duplication (ITD). This study delves into the structural intricacies of FLT3, the roles of activation loop mutants, and their interaction with tyrosine kinase inhibitors. Coupled with this, the research leverages molecular contrastive learning and protein language modeling to examine interactions between small molecule inhibitors and FLT3 activation loop mutants. Utilizing the ConPLex platform, over 5.7 million unique FLT3 activation loop mutants—small molecule pairs were analyzed. The binding free energies of three inhibitors were assessed, and cellular apoptotic responses were evaluated under drug treatments. Notably, the introduction of the Xepto50 scoring system provides a nuanced metric for drug efficacy. The findings underscore the modulation of molecular interactions and cellular responses by Y842 mutations in FLT3-KD, highlighting the need for tailored therapeutic approaches in FLT3-ITD-related malignancies. Full article
(This article belongs to the Special Issue Novel Targeted Therapies for Blood Cancer)
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12 pages, 1100 KiB  
Article
Predictive Risk Score for Acute Kidney Injury in Hematopoietic Stem Cell Transplant
by Natacha Rodrigues, Mariana Fragão-Marques, Cláudia Costa, Carolina Branco, Filipe Marques, Pedro Vasconcelos, Carlos Martins, Adelino Leite-Moreira and José António Lopes
Cancers 2023, 15(14), 3720; https://doi.org/10.3390/cancers15143720 - 22 Jul 2023
Viewed by 1297
Abstract
Hematopoietic stem cell transplant (HSCT) is an important treatment option for hematologic malignancies. Acute kidney injury (AKI) is a common complication in HSCTs and is related to worse outcomes. We aimed to create a predictive risk score for AKI in HSCT considering variables [...] Read more.
Hematopoietic stem cell transplant (HSCT) is an important treatment option for hematologic malignancies. Acute kidney injury (AKI) is a common complication in HSCTs and is related to worse outcomes. We aimed to create a predictive risk score for AKI in HSCT considering variables available at the time of the transplant. We performed a retrospective cohort study. AKI was defined by the KDIGO classification using creatinine and urinary output criteria. We used survival analysis with competing events. Continuous variables were dichotomized according to the Liu index. A multivariable analysis was performed with a backward stepwise regression. Harrel’s C-Statistic was used to evaluate the performance of the model. Points were attributed considering the nearest integer of two times each covariate’s hazard ratio. The Liu index was used to establish the optimal cut-off. We included 422 patients undergoing autologous (61.1%) or allogeneic (38.9%) HSCTs for multiple myeloma (33.9%), lymphoma (27.3%), and leukemia (38.8%). AKI cumulative incidence was 59.1%. Variables eligible for the final score were: hematopoietic cell transplant comorbidity index ≥2 (HR: 1.47, 95% CI: 1.08–2.006; p = 0.013), chronic kidney disease (HR: 2.10, 95% CI: 1.31–3.36; p = 0.002), lymphoma or leukemia (HR: 1.69, 95% CI: 1.26–2.25; p < 0.001) and platelet-to-lymphocyte ratio > 171.9 (HR: 1.43, 95% CI: 1.10–1.86; p = 0.008). This is the first predictive risk score for AKI in patients undergoing HSCTs and the first study where the platelet-to-lymphocyte ratio is independently associated with AKI. Full article
(This article belongs to the Special Issue Novel Targeted Therapies for Blood Cancer)
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