Immunosuppressive Properties of Mesenchymal Stem Cells

Abumaree, Mohamed; Jumah, Mohammed Al; Pace, Rishika A.; Kalionis, Bill

doi:10.1007/s12015-011-9312-0

Cited by 224 publications

(178 citation statements)

References 188 publications

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“…90 MSC-DEs have low immunogenicity capacity rather than MSCs 66, 91 and have no infection risks. In addition, there is the risk of ectopic differentiation of MSCs after systemic infusion; 92 hence, exosome-based therapy can be a good replacement for mesenchymal stem cell-based therapy soon.…”

Section: Discussionmentioning

confidence: 99%

Mesenchymal Stem Cell-Derived Exosomes: New Opportunity in Cell-Free Therapy

2016

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Section: Discussionmentioning

confidence: 99%

Mesenchymal Stem Cell-Derived Exosomes: New Opportunity in Cell-Free Therapy

2016

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“…3 The inability to find a primary tumor may not merely depend on its small size but may involve newly described cell biological processes related to stem cell characteristics, microenvironment, immunoediting and senescence-apoptosis which may halt tumor growth and induce phenotypic changes. [3][4][5] In essence, an increased understanding of the interplay of host and tumor during the protracted process of carcinogenesis has made CUP less of a conundrum and more as a learning opportunity, in a 21st century parallel to the cancer biology gains provided by unravelling of several hereditary cancer syndromes in the previous century. Our recent studies support these data and suggest that the lung is a more common primary tissue than what the earlier data show.…”

Section: Dear Sirmentioning

confidence: 99%

Smoking and body mass index as risk factors for subtypes of cancer of unknown primary

et al. 2014

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Cancer of unknown primary site (CUP) accounts for 3-5% of all cancer but because it is a fatal disease it ranks high among causes of cancer deaths. It has been called "an orphan disease" because it is diagnosed through metastatic tissue and the primary tumor often remains undetected. Based on autopsy data, the most common primaries were lung (27%), pancreas (24%), liver/bile (8%) and kidney/adrenals (8%). 1 CUP can be called "orphan disease" also because, as a metastatic disease, it is disregarded as a cancer entity when only primary cancers are considered. Thus, hardly anything is known about the underlying causes or risk factors. A recent European study published in this Journal showed that heavy smoking causes a risk of 3.66 for CUP patients of diverse and unspecified histologies; alcohol drinking and wide waist circumference were borderline risk factors. 2 The pathophysiology of CUP has remained an enigma, exemplified by the question presented in a review on CUP: "unknown primary or unknown biology?" 3 The inability to find a primary tumor may not merely depend on its small size but may involve newly described cell biological processes related to stem cell characteristics, microenvironment, immunoediting and senescence-apoptosis which may halt tumor growth and induce phenotypic changes. [3][4][5] In essence, an increased understanding of the interplay of host and tumor during the protracted process of carcinogenesis has made CUP less of a conundrum and more as a learning opportunity, in a 21st century parallel to the cancer biology gains provided by unravelling of several hereditary cancer syndromes in the previous century. Our recent studies support these data and suggest that the lung is a more common primary tissue than what the earlier data show. [6][7][8] In the present letter, we extend the study of Kaaks et al. addressing the question of tobacco smoking and body mass index (BMI) as risk factors of site-specific CUP, that is, by location of the diagnosed metastasis. 2 We hypothesize that smoking would have an effect on sites where smoking risks are highest among primary cancers, that is, lung. Patients and cancer-free controls were recruited from three Swedish prospective biobanks, the Umea Medical Biobank with 203 CUP patients and 1015 controls and the Malmo Diet and Cancer Study and the Prevention Study, jointly with 272 CUP patients and 1360 controls; 9 the controls were frequency matched on sex and age at interview. In Umea, the mean age at sampling was 57 years and at diagnosis it was 66 years; in Malm€ o, the respective ages were 51 and 71 years. Cancers were identified up to year 2012 through the regional Oncology Centers. Diagnoses were based on International Classification of Diseases (ICD) codes 7, 9 and 10, the latter two were particularly useful because they included the anatomic site where metastases were found. These included "unspecified CUP" (ICD-9 code 1990-1991, CUP often spread to multiple organs), "liver CUP" with liver metastasis, "lung CUP" with lung involvement (including thorax ...

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“…6 Preclinical studies suggest that MSCs do not replace lost neurons after stroke but instead provide benefit through multiple parallel processes that modulate the tissue microenvironment, including paracrine delivery of growth factors, local and distant immunomodulation, reduced apoptosis, reduced perilesional glial scar formation, promotion of axonal outgrowth and synaptic remodeling, astrocytic and oligodendrocyte precursor cell proliferation, neurogenesis, and angiogenesis. 4,[7][8][9][10][11] This is a potential advantage over pharmacologic therapies that act via a single treatment mechanism. 7,8,11 In addition, MSCs have an excellent safety record in clinical trials of humans with many different diseases.…”

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confidence: 99%

Meta-analysis of preclinical studies of mesenchymal stromal cells for ischemic stroke

et al. 2014

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Objectives:To evaluate the quality of preclinical evidence for mesenchymal stromal cell (MSC) treatment of ischemic stroke, determine effect size of MSC therapy, and identify clinical measures that correlate with differences in MSC effects.Methods: A literature search identified studies of MSCs in animal models of cerebral ischemia. For each, a Quality Score was derived, and effect size of MSCs was determined for the most common behavioral and histologic endpoints.Results: Of 46 studies, 44 reported that MSCs significantly improved outcome. The median Quality Score was 5.5 (of 10). The median effect size was 1.78 for modified Neurological Severity Score, 1.73 for the adhesive removal test, 1.02 for the rotarod test, and 0.93 for infarct volume reduction. Quality Score correlated significantly and positively with effect size for the modified Neurological Severity Score. Effect sizes varied significantly with clinical measures such as administration route (intracerebral . intra-arterial . IV, although effect size for IV was nonetheless very large at 1.55) and species receiving MSCs (primate . rat . mouse). Because many MSC mechanisms are restorative, analyses were repeated examining only the 36 preclinical studies administering MSCs $24 hours poststroke; results were overall very similar. Conclusions:In preclinical studies, MSCs have consistently improved multiple outcome measures, with very large effect sizes. Results were robust across species studied, administration route, species of MSC origin, timing, degree of immunogenicity, and dose, and in the presence of comorbidities. In contrast to meta-analyses of preclinical data for other stroke therapies, higher-quality MSC preclinical studies were associated with larger behavioral gains. These findings support the utility of further studies to translate MSCs in the treatment of ischemic stroke in humans.

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Immunosuppressive Properties of Mesenchymal Stem Cells

Cited by 224 publications

References 188 publications

Mesenchymal Stem Cell-Derived Exosomes: New Opportunity in Cell-Free Therapy

Mesenchymal Stem Cell-Derived Exosomes: New Opportunity in Cell-Free Therapy

Smoking and body mass index as risk factors for subtypes of cancer of unknown primary

Meta-analysis of preclinical studies of mesenchymal stromal cells for ischemic stroke

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