Bruton’s Tyrosine Kinase Targeting in Multiple Myeloma
Multiple myeloma (MM), a clonal plasma cell disorder, disrupts the bones’ hematopoiesis and microenvironment homeostasis and ability to mediate an immune response against malignant clones. Despite prominent survival improvement with newer treatment modalities since the 2000s, MM is still considered...
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doaj-b26cc9bd38c74bec9e24eaac4808073d2021-06-01T01:18:13ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672021-05-01225707570710.3390/ijms22115707Bruton’s Tyrosine Kinase Targeting in Multiple MyelomaMax Von Suskil0Kazi Nasrin Sultana1Weam Othman Elbezanti2Omar S. Al-Odat3Robert Chitren4Amit K. Tiwari5Kishore B. Challagundla6Sandeep Kumar Srivastava7Subash C. Jonnalagadda8Tulin Budak-Alpdogan9Manoj K. Pandey10Department of Biomedical Sciences, Cooper Medical School of Rowan University, Camden, NJ 08103, USADepartment of Biosciences, Manipal University Jaipur, Jaipur 303007, IndiaDepartment of Biomedical Sciences, Cooper Medical School of Rowan University, Camden, NJ 08103, USADepartment of Biomedical Sciences, Cooper Medical School of Rowan University, Camden, NJ 08103, USADepartment of Biomedical Sciences, Cooper Medical School of Rowan University, Camden, NJ 08103, USADepartment of Pharmacology and Experimental Therapeutics, The University of Toledo, Toledo, OH 43606, USADepartment of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE 68198, USADepartment of Biosciences, Manipal University Jaipur, Jaipur 303007, IndiaDepartment of Chemistry and Biochemistry, College of Science and Mathematics, Rowan University, Glassboro, NJ 08028, USADepartment of Hematology, MD Anderson Cancer Center at Cooper, Cooper Health University, Camden, NJ 08103, USADepartment of Biomedical Sciences, Cooper Medical School of Rowan University, Camden, NJ 08103, USAMultiple myeloma (MM), a clonal plasma cell disorder, disrupts the bones’ hematopoiesis and microenvironment homeostasis and ability to mediate an immune response against malignant clones. Despite prominent survival improvement with newer treatment modalities since the 2000s, MM is still considered a non-curable disease. Patients experience disease recurrence episodes with clonal evolution, and with each relapse disease comes back with a more aggressive phenotype. Bruton’s Tyrosine Kinase (BTK) has been a major target for B cell clonal disorders and its role in clonal plasma cell disorders is under active investigation. BTK is a cytosolic kinase which plays a major role in the immune system and its related malignancies. The BTK pathway has been shown to provide survival for malignant clone and multiple myeloma stem cells (MMSCs). BTK also regulates the malignant clones’ interaction with the bone marrow microenvironment. Hence, BTK inhibition is a promising therapeutic strategy for MM patients. In this review, the role of BTK and its signal transduction pathways are outlined in the context of MM.https://www.mdpi.com/1422-0067/22/11/5707multiple myelomamicroenvironmentBruton’s Tyrosine Kinase (BTK) inhibitorsresistancedrug development |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Max Von Suskil Kazi Nasrin Sultana Weam Othman Elbezanti Omar S. Al-Odat Robert Chitren Amit K. Tiwari Kishore B. Challagundla Sandeep Kumar Srivastava Subash C. Jonnalagadda Tulin Budak-Alpdogan Manoj K. Pandey |
spellingShingle |
Max Von Suskil Kazi Nasrin Sultana Weam Othman Elbezanti Omar S. Al-Odat Robert Chitren Amit K. Tiwari Kishore B. Challagundla Sandeep Kumar Srivastava Subash C. Jonnalagadda Tulin Budak-Alpdogan Manoj K. Pandey Bruton’s Tyrosine Kinase Targeting in Multiple Myeloma International Journal of Molecular Sciences multiple myeloma microenvironment Bruton’s Tyrosine Kinase (BTK) inhibitors resistance drug development |
author_facet |
Max Von Suskil Kazi Nasrin Sultana Weam Othman Elbezanti Omar S. Al-Odat Robert Chitren Amit K. Tiwari Kishore B. Challagundla Sandeep Kumar Srivastava Subash C. Jonnalagadda Tulin Budak-Alpdogan Manoj K. Pandey |
author_sort |
Max Von Suskil |
title |
Bruton’s Tyrosine Kinase Targeting in Multiple Myeloma |
title_short |
Bruton’s Tyrosine Kinase Targeting in Multiple Myeloma |
title_full |
Bruton’s Tyrosine Kinase Targeting in Multiple Myeloma |
title_fullStr |
Bruton’s Tyrosine Kinase Targeting in Multiple Myeloma |
title_full_unstemmed |
Bruton’s Tyrosine Kinase Targeting in Multiple Myeloma |
title_sort |
bruton’s tyrosine kinase targeting in multiple myeloma |
publisher |
MDPI AG |
series |
International Journal of Molecular Sciences |
issn |
1661-6596 1422-0067 |
publishDate |
2021-05-01 |
description |
Multiple myeloma (MM), a clonal plasma cell disorder, disrupts the bones’ hematopoiesis and microenvironment homeostasis and ability to mediate an immune response against malignant clones. Despite prominent survival improvement with newer treatment modalities since the 2000s, MM is still considered a non-curable disease. Patients experience disease recurrence episodes with clonal evolution, and with each relapse disease comes back with a more aggressive phenotype. Bruton’s Tyrosine Kinase (BTK) has been a major target for B cell clonal disorders and its role in clonal plasma cell disorders is under active investigation. BTK is a cytosolic kinase which plays a major role in the immune system and its related malignancies. The BTK pathway has been shown to provide survival for malignant clone and multiple myeloma stem cells (MMSCs). BTK also regulates the malignant clones’ interaction with the bone marrow microenvironment. Hence, BTK inhibition is a promising therapeutic strategy for MM patients. In this review, the role of BTK and its signal transduction pathways are outlined in the context of MM. |
topic |
multiple myeloma microenvironment Bruton’s Tyrosine Kinase (BTK) inhibitors resistance drug development |
url |
https://www.mdpi.com/1422-0067/22/11/5707 |
work_keys_str_mv |
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