Leukemia: Cellular Mechanism and Therapeutic Potential

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (31 January 2024) | Viewed by 1830

Special Issue Editor


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Guest Editor
VA Boston/Brigham & Women's Hospital, Harvard Medical School, Boston, MA 02132, USA
Interests: clinical and translational research on MDS; MPN; leukemia; lymphoma; hematopoietic stem cell transplant/cellular therapy outcome research; bone marrow clonal malignant disease progression and leukemia transformation biomarkers and mechanisms
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Special Issue Information

Dear Colleagues,

Leukemia is a term for cancers of the blood cells, usually beginning in the bone marrow and resulting in great numbers of abnormal blood cells. There are four main types of leukemia, including acute lymphoblastic leukemia (ALL), acute myeloid leukemia (AML), chronic lymphocytic leukemia (CLL), and chronic myeloid leukemia (CML). Leukemia happens when there are changes in the genetic material (DNA) in bone marrow cells. The cause of these genetic changes is unknown.

Currently, common leukemia treatment methods include chemotherapy, radiation therapy, stem cell transplantation, CAR T-cell therapy, targeted therapy, etc. Although we have made progress in understanding the biology and therapy of leukemia, the outcomes remain unsatisfactory.

The purpose of this Special Issue is to highlight recent findings regarding mechanisms, diagnostics, and therapies for leukemia. We are pleased to invite you to contribute original articles, reviews, communications, etc. We are looking forward to your contributions to this Special Issue.

Dr. Jeffrey Pu
Guest Editor

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Keywords

  • leukemia
  • cellular mechanism
  • molecular mechanism
  • diagnosis
  • biomarkers
  • tumor microenvironment
  • targeted therapy
  • chemotherapy

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Published Papers (1 paper)

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Research

20 pages, 3382 KiB  
Article
Unveiling IL6R and MYC as Targeting Biomarkers in Imatinib-Resistant Chronic Myeloid Leukemia through Advanced Non-Invasive Apoptosis Detection Sensor Version 2 Detection
by Chia-Hwa Lee, Kai-Wen Hsu, Yao-Yu Hsieh, Wei-Ting Li, Yuqing Long, Chun-Yu Lin and Shu-Huey Chen
Cells 2024, 13(7), 616; https://doi.org/10.3390/cells13070616 - 2 Apr 2024
Viewed by 1582
Abstract
The management of chronic myelogenous leukemia (CML) has seen significant progress with the introduction of tyrosine kinase inhibitors (TKIs), particularly Imatinib. However, a notable proportion of CML patients develop resistance to Imatinib, often due to the persistence of leukemia stem cells and resistance [...] Read more.
The management of chronic myelogenous leukemia (CML) has seen significant progress with the introduction of tyrosine kinase inhibitors (TKIs), particularly Imatinib. However, a notable proportion of CML patients develop resistance to Imatinib, often due to the persistence of leukemia stem cells and resistance mechanisms independent of BCR::ABL1 This study investigates the roles of IL6R, IL7R, and MYC in Imatinib resistance by employing CRISPR/Cas9 for gene editing and the Non-Invasive Apoptosis Detection Sensor version 2 (NIADS v2) for apoptosis assessment. The results indicate that Imatinib-resistant K562 cells (K562-IR) predominantly express IL6R, IL7R, and MYC, with IL6R and MYC playing crucial roles in cell survival and sensitivity to Imatinib. Conversely, IL7R does not significantly impact cytotoxicity, either alone or in combination with Imatinib. Further genetic editing experiments confirm the protective functions of IL6R and MYC in K562-IR cells, suggesting their potential as therapeutic targets for overcoming Imatinib resistance in CML. This study contributes to understanding the mechanisms of Imatinib resistance in CML, proposing IL6R and MYC as pivotal targets for therapeutic strategies. Moreover, the utilization of NIADS v2 enhances our capability to analyze apoptosis and drug responses, contributing to a deeper understanding of CML pathogenesis and treatment options. Full article
(This article belongs to the Special Issue Leukemia: Cellular Mechanism and Therapeutic Potential)
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