Dual Targeting of Multiple Myeloma Stem Cells and Myeloid-Derived Suppressor Cells for Treatment of Chemotherapy-Resistant Multiple Myeloma
Here we review the insights and lessons learned from early clinical trials of T-cell engaging bispecific antibodies (BsABs) as a new class of biotherapeutic drug candidates with clinical impact potential for the treatment of multiple myeloma (MM). BsABs are capable of redirecting host T-cell cytotox...
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Frontiers Media S.A.
2021
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oai:doaj.org-article:11695cf4ab3a40e68a0db44dd99e9bf02021-11-10T08:07:33ZDual Targeting of Multiple Myeloma Stem Cells and Myeloid-Derived Suppressor Cells for Treatment of Chemotherapy-Resistant Multiple Myeloma2234-943X10.3389/fonc.2021.760382https://doaj.org/article/11695cf4ab3a40e68a0db44dd99e9bf02021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fonc.2021.760382/fullhttps://doaj.org/toc/2234-943XHere we review the insights and lessons learned from early clinical trials of T-cell engaging bispecific antibodies (BsABs) as a new class of biotherapeutic drug candidates with clinical impact potential for the treatment of multiple myeloma (MM). BsABs are capable of redirecting host T-cell cytotoxicity in an MHC-independent manner to malignant MM clones as well as immunosuppressive myeloid-derived suppressor cells (MDSC). T-cell engaging BsAB targeting the BCMA antigen may help delay disease progression in MM by destroying the MM cells. T-cell engaging BsAB targeting the CD38 antigen may help delay disease progression in MM by depleting both the malignant MM clones and the MDSC in the bone marrow microenvironment (BMME). BsABs may facilitate the development of a new therapeutic paradigm for achieving improved survival in MM by altering the immunosuppressive BMME. T-cell engaging BsiABs targeting the CD123 antigen may help delay disease progression in MM by depleting the MDSC in the BMME and destroying the MM stem cells that also carry the CD123 antigen on their surface.Fatih M. UckunFatih M. UckunFatih M. UckunFrontiers Media S.A.articletumor microenvironment (TME)multiple myeloma (MM)bispecific T-cell engagers (BiTEs)bispecific antibodies (BsABs)bone marrow microenvironment (BMME)myeloid-derived suppressor cells (MDSC)Neoplasms. Tumors. Oncology. Including cancer and carcinogensRC254-282ENFrontiers in Oncology, Vol 11 (2021) |
institution |
DOAJ |
collection |
DOAJ |
language |
EN |
topic |
tumor microenvironment (TME) multiple myeloma (MM) bispecific T-cell engagers (BiTEs) bispecific antibodies (BsABs) bone marrow microenvironment (BMME) myeloid-derived suppressor cells (MDSC) Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282 |
spellingShingle |
tumor microenvironment (TME) multiple myeloma (MM) bispecific T-cell engagers (BiTEs) bispecific antibodies (BsABs) bone marrow microenvironment (BMME) myeloid-derived suppressor cells (MDSC) Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282 Fatih M. Uckun Fatih M. Uckun Fatih M. Uckun Dual Targeting of Multiple Myeloma Stem Cells and Myeloid-Derived Suppressor Cells for Treatment of Chemotherapy-Resistant Multiple Myeloma |
description |
Here we review the insights and lessons learned from early clinical trials of T-cell engaging bispecific antibodies (BsABs) as a new class of biotherapeutic drug candidates with clinical impact potential for the treatment of multiple myeloma (MM). BsABs are capable of redirecting host T-cell cytotoxicity in an MHC-independent manner to malignant MM clones as well as immunosuppressive myeloid-derived suppressor cells (MDSC). T-cell engaging BsAB targeting the BCMA antigen may help delay disease progression in MM by destroying the MM cells. T-cell engaging BsAB targeting the CD38 antigen may help delay disease progression in MM by depleting both the malignant MM clones and the MDSC in the bone marrow microenvironment (BMME). BsABs may facilitate the development of a new therapeutic paradigm for achieving improved survival in MM by altering the immunosuppressive BMME. T-cell engaging BsiABs targeting the CD123 antigen may help delay disease progression in MM by depleting the MDSC in the BMME and destroying the MM stem cells that also carry the CD123 antigen on their surface. |
format |
article |
author |
Fatih M. Uckun Fatih M. Uckun Fatih M. Uckun |
author_facet |
Fatih M. Uckun Fatih M. Uckun Fatih M. Uckun |
author_sort |
Fatih M. Uckun |
title |
Dual Targeting of Multiple Myeloma Stem Cells and Myeloid-Derived Suppressor Cells for Treatment of Chemotherapy-Resistant Multiple Myeloma |
title_short |
Dual Targeting of Multiple Myeloma Stem Cells and Myeloid-Derived Suppressor Cells for Treatment of Chemotherapy-Resistant Multiple Myeloma |
title_full |
Dual Targeting of Multiple Myeloma Stem Cells and Myeloid-Derived Suppressor Cells for Treatment of Chemotherapy-Resistant Multiple Myeloma |
title_fullStr |
Dual Targeting of Multiple Myeloma Stem Cells and Myeloid-Derived Suppressor Cells for Treatment of Chemotherapy-Resistant Multiple Myeloma |
title_full_unstemmed |
Dual Targeting of Multiple Myeloma Stem Cells and Myeloid-Derived Suppressor Cells for Treatment of Chemotherapy-Resistant Multiple Myeloma |
title_sort |
dual targeting of multiple myeloma stem cells and myeloid-derived suppressor cells for treatment of chemotherapy-resistant multiple myeloma |
publisher |
Frontiers Media S.A. |
publishDate |
2021 |
url |
https://doaj.org/article/11695cf4ab3a40e68a0db44dd99e9bf0 |
work_keys_str_mv |
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_version_ |
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