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Cancers
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Chronic Lymphocytic Leukemia: Insights into Biology and Therapy
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Chronic Lymphocytic Leukemia: Insights into Biology and Therapy

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Pathophysiology".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 9306

Special Issue Editor

Prof. Dr. Tatjana Stankovic

E-Mail Website
Guest Editor
Institute of Cancer and Genomic Sciences, College of Medical and Dental Sciences, Birmingham B15 2TT, UK
Interests: pathophysiology and targeting of hematological malignancies

Special Issue Information

Dear Colleagues,

Chronic lymphocytic leukemia (CLL) is an incurable B-cell malignancy with a variable clinical course. During their lifespans, leukemic cells recirculate between different tissue compartments, including peripheral blood, bone marrow and lymph nodes, and adjust to different microenvironments in order to survive. Consequently, CLL remains a model disease with which to study the prognostic impact of both tumor and microenvironment features. Recent advances in these areas have highlighted a number of prognostic factors including the status of the p53 pathway, NOTCH and BCR signaling, the levels of APRIL and BAFF cytokines, and the extent of the proliferation of different T-cell subsets.

The last decade has also brought to light a range of novel therapeutic options for CLL, from inhibitors of BCR signaling, pro-apoptotic BH3 mimetics, and immunomodulatory agents to cell therapies. These strategies have counteracted some but not all of the features of poor CLL prognosis. In addition, the considerable plasticity of CLL tumor cells has created novel forms of tumor resistance. Therefore, it is important to continuously re-evaluate CLL prognostic markers and devise novel therapeutic strategies based on an enhanced understanding of CLL biology.

This Special Issue will emphasize the current state of the art in CLL biology, the remaining challenges in the management of CLL and emerging therapeutic strategies.

Prof. Dr. Tatjana Stankovic
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 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.

Keywords

  • CLL genetics
  • CLL epigenetics
  • CLL metabolism
  • CLL microenvironment
  • CLL animal models
  • targeted therapy
  • minimal residual disease (MRD)

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Published Papers (3 papers)

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Review

15 pages, 2326 KiB  
Review
To β or Not to β: How Important Is β-Catenin Dependent and Independent WNT Signaling in CLL?
by Karol D. Urbanek, Stephan Stilgenbauer and Daniel Mertens
Cancers 2023, 15(1), 194; https://doi.org/10.3390/cancers15010194 - 28 Dec 2022
Viewed by 2120
Abstract
WNT pathways play an important role in cancer development and progression, but WNT pathways can also inhibit growth in melanoma, prostate, and ovarian cancers. Chronic lymphocytic leukemia (CLL) is known for its overexpression of several WNT ligands and receptors. Canonical WNT signaling is [...] Read more.
WNT pathways play an important role in cancer development and progression, but WNT pathways can also inhibit growth in melanoma, prostate, and ovarian cancers. Chronic lymphocytic leukemia (CLL) is known for its overexpression of several WNT ligands and receptors. Canonical WNT signaling is β-catenin-dependent, whereas non-canonical WNT signaling is β-catenin-independent. Research on WNT in CLL focuses mainly on non-canonical signaling due to the high expression of the WNT-5a receptor ROR1. However, it was also shown that mutations in canonical WNT pathway genes can lead to WNT activation in CLL. The focus of this review is β-catenin-independent signaling and β-catenin-dependent signaling within CLL cells and the role of WNT in the leukemic microenvironment. The major role of WNT pathways in CLL pathogenesis also makes WNT a possible therapeutic target, directly or in combination with other drugs. Full article
(This article belongs to the Special Issue Chronic Lymphocytic Leukemia: Insights into Biology and Therapy)
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21 pages, 1700 KiB  
Review
In Vitro and In Vivo Models of CLL–T Cell Interactions: Implications for Drug Testing
by Eva Hoferkova, Sona Kadakova and Marek Mraz
Cancers 2022, 14(13), 3087; https://doi.org/10.3390/cancers14133087 - 23 Jun 2022
Cited by 5 | Viewed by 4125
Abstract
T cells are key components in environments that support chronic lymphocytic leukemia (CLL), activating CLL-cell proliferation and survival. Here, we review in vitro and in vivo model systems that mimic CLL–T-cell interactions, since these are critical for CLL-cell division and resistance to some [...] Read more.
T cells are key components in environments that support chronic lymphocytic leukemia (CLL), activating CLL-cell proliferation and survival. Here, we review in vitro and in vivo model systems that mimic CLL–T-cell interactions, since these are critical for CLL-cell division and resistance to some types of therapy (such as DNA-damaging drugs or BH3-mimetic venetoclax). We discuss approaches for direct CLL-cell co-culture with autologous T cells, models utilizing supportive cell lines engineered to express T-cell factors (such as CD40L) or stimulating CLL cells with combinations of recombinant factors (CD40L, interleukins IL4 or IL21, INFγ) and additional B-cell receptor (BCR) activation with anti-IgM antibody. We also summarize strategies for CLL co-transplantation with autologous T cells into immunodeficient mice (NOD/SCID, NSG, NOG) to generate patient-derived xenografts (PDX) and the role of T cells in transgenic CLL mouse models based on TCL1 overexpression (Eµ-TCL1). We further discuss how these in vitro and in vivo models could be used to test drugs to uncover the effects of targeted therapies (such as inhibitors of BTK, PI3K, SYK, AKT, MEK, CDKs, BCL2, and proteasome) or chemotherapy (fludarabine and bendamustine) on CLL–T-cell interactions and CLL proliferation. Full article
(This article belongs to the Special Issue Chronic Lymphocytic Leukemia: Insights into Biology and Therapy)
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Graphical abstract

15 pages, 2748 KiB  
Review
Immunoglobulin Gene Sequence as an Inherited and Acquired Risk Factor for Chronic Lymphocytic Leukemia
by Moumita Datta and Hassan Jumaa
Cancers 2022, 14(13), 3045; https://doi.org/10.3390/cancers14133045 - 21 Jun 2022
Cited by 4 | Viewed by 2397
Abstract
Chronic lymphocytic leukemia (CLL) is a lymphoproliferative disease characterized by the accumulation of CD5+ CD19+ malignant B cells. Autonomous ligand-independent B-cell signaling is a key process involved in the development of CLL pathogenesis. Together with other cytogenetic alterations, mutations in the [...] Read more.
Chronic lymphocytic leukemia (CLL) is a lymphoproliferative disease characterized by the accumulation of CD5+ CD19+ malignant B cells. Autonomous ligand-independent B-cell signaling is a key process involved in the development of CLL pathogenesis. Together with other cytogenetic alterations, mutations in the immunoglobulin heavy chain variable (IGHV) gene act as a prognostic marker for CLL, with mutated CLL (M-CLL) being far more indolent than unmutated CLL (U-CLL). Recent studies highlight the role of a specific light chain mutation, namely, IGLV3-21R110G, in the development and prognosis of CLL. Such a mutation increases the propensity of homotypic BCR–BCR interaction, leading to cell autonomous signaling. In this article, we review the current findings on immunoglobulin gene sequence mutations as a potential risk factor for developing CLL. Full article
(This article belongs to the Special Issue Chronic Lymphocytic Leukemia: Insights into Biology and Therapy)
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