الفهرس 
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Abstract
Since the identification of mesenchymal stem cells (MSCs) from adult bone marrow (BM), numerous studies have been performed globally to understand their characteristics and functions. Therefore, it is widely known that MSCs have multi-lineage potential, differentiating into various types of cells, such as adipocytes, chondroblasts, osteoblasts, and tissue macrophage-like cells. The multi-potent properties of MSCs make them promising therapeutic targets and one of the most indispensable sources of new clinical therapies. In fact, MSCs have been widely used in regenerative medicine for bone and cardiovascular repair. Moreover, they can migrate to damaged tissue, can self-renew, and exert immunomodulatory and antitumor effects.
Among a variety of therapeutic modalities, mesenchymal stem cells (MSCs) are of special interest due to their potential clinical use. Therapies involving MSCs are showing increasing promise in cancer treatment and anti-cancer drug screening applications; however, results have been inconclusive, possibly due to the heterogeneity of MSC populations.
There is less known about the function of MSCs in hematologic malignancies, such as leukemia, lymphoma, and multiple myeloma, than for solid malignancies. However, the dual function of MSCs may be applicable to hematologic cancers. According to several studies, it is evident that MSCs possess the ability to inhibit or promote tumor growth by suppressing proliferation or apoptosis of tumor cells, respectively, in hematologic malignancies. Although minor reports have shown that MSCs can directly promote proliferation of hematologic malignant cells or promote apoptosis, the primary hypothesis is that MSCs suppress both proliferation and apoptosis. Thus, the use of MSCs for the treatment of hematologic malignancies is currently unclear, because inhibitory and promoting effects of MSCs on malignancies are known, both in vitro and in vivo.
Thus, MSCs have been the focus of a regime of emerging therapeutics to regenerate damaged tissue and treat inflammation resulting from cardiovascular disease and myocardial infarction (MI), brain and spinal cord injury, cartilage and bone injury, Crohn’s disease, and graft-versus-host disease (GVHD) during bone marrow transplantation.
The aim of this work was to review and clarify mesenchymal stem cell properties, function, immunomodulation effect, and the therapeutic implication of MSC transplantation in blood diseases.
from the previous studies we can be Concluded that:
MSC-based clinical outcomes have shown a wide range of variation likely due to non-standardized experimental methods, lack of specific cell surface markers to identify subsets of MSCs, and heterogeneous characteristics of MSCs that are easily affected by the surrounding environment. Several studies have been conducted to investigate the effects of MSCs in carcinogenesis or tumor microenvironments, but a single principle cannot explain both the antitumorigenic and protumor genic functions of MSCs.
The antitumor effects of MSCs are mainly a result of suppressed proliferation of malignant cells. More specific mechanisms or molecules involved remain unclear, but arrest at the G0/G1 phase of the cell cycle is an acknowledged mechanism. To utilize this antitumorigenic activity for clinical use in the future, other factors must be considered. MSCs possess certain beneficial characteristics, such as the potential to be used as delivery vehicles and the ability to inhibit vascular growth and arrest the cell cycle. However, unfavorable characteristics such as favoring tumor growth by suppressing apoptosis, supporting tumor vasculature, involvement in immunomodulation of cancer cells, activation of metastasis/recurrence, and protection of cancer cells from drug-induced apoptosis leading to chemo-resistance are a hindrance to their use as a therapeutic agent. Tumor-associated MSCs, essential components of the tumor microenvironment, are also associated with a protumor genic effect because they tend to enhance tumor cell stemness.
Specifically, the development of molecules that can either increase antitumorigenic effects or decrease protumor genic effects would be promising for advanced therapies.