Multipotent Mesenchymal Stromal Cells in Patients with Chronic Myeloid Leukemia before Discontinuation of Tyrosine Kinase Inhibitors
We analyzed changes in multipotent mesenchymal stromal cells of patients with chronic myeloid leukemia before discontinuation of tyrosine kinase inhibitors. Withdrawal syndrome was significantly more common in patients who have been taking tyrosine kinase inhibitors for a longer time and in patients...
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| Veröffentlicht in: | Bulletin of experimental biology and medicine 2019-08, Vol.167 (4), p.580-583 |
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| creator | Petinati, N. A. Petrova, A. N. Chelysheva, E. Yu Shukhov, O. A. Bykova, A. V. Nemchenko, I. S. Sats, N. V. Turkina, A. G. Drize, N. I. |
| description | We analyzed changes in multipotent mesenchymal stromal cells of patients with chronic myeloid leukemia before discontinuation of tyrosine kinase inhibitors. Withdrawal syndrome was significantly more common in patients who have been taking tyrosine kinase inhibitors for a longer time and in patients of older age and with lower body weight. In patients with withdrawal syndrome, the total production of mesenchymal stromal cells and expression of
FGFR2
and
MMP2
genes were significantly lower; loss of deep molecular response was also less frequent in this group of patients. At the same time, the expression of genes important for the maintenance of stem cells (
SOX9
,
PDGFRa
, and
LIF
) was significantly lower in the mesenchymal stromal cells of patients with withdrawal syndrome and loss of deep molecular response. We observed a clear-cut relationship between the development of withdrawal syndrome and the loss of deep molecular response. The decrease in the expression of
FGFR2
and
MMP2
genes in the mesenchymal stromal cells of patients with chronic myeloid leukemia before discontinuation of treatment can be a predictor of withdrawal syndrome, while simultaneous decrease in the expression of
SOX9
,
PDGFRa
, and
LIF
in these cells attests to undesirability of therapy discontinuation at the moment. |
| doi_str_mv | 10.1007/s10517-019-04575-0 |
| format | Article |
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FGFR2
and
MMP2
genes were significantly lower; loss of deep molecular response was also less frequent in this group of patients. At the same time, the expression of genes important for the maintenance of stem cells (
SOX9
,
PDGFRa
, and
LIF
) was significantly lower in the mesenchymal stromal cells of patients with withdrawal syndrome and loss of deep molecular response. We observed a clear-cut relationship between the development of withdrawal syndrome and the loss of deep molecular response. The decrease in the expression of
FGFR2
and
MMP2
genes in the mesenchymal stromal cells of patients with chronic myeloid leukemia before discontinuation of treatment can be a predictor of withdrawal syndrome, while simultaneous decrease in the expression of
SOX9
,
PDGFRa
, and
LIF
in these cells attests to undesirability of therapy discontinuation at the moment.</description><identifier>ISSN: 0007-4888</identifier><identifier>EISSN: 1573-8221</identifier><identifier>DOI: 10.1007/s10517-019-04575-0</identifier><identifier>PMID: 31502137</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Biomedical and Life Sciences ; Biomedicine ; Body weight ; Care and treatment ; Cell Biology ; Chronic myeloid leukemia ; Female ; Fibroblast growth factor receptor 2 ; Gelatinase A ; Gene expression ; Genes ; Humans ; Internal Medicine ; Laboratory Medicine ; Leukemia ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology ; Male ; Mesenchymal stem cells ; Mesenchymal Stem Cells - pathology ; Mesenchyme ; Middle Aged ; Myeloid leukemia ; Pathology ; Phenols ; Platelet-derived growth factor ; Protein Kinase Inhibitors - therapeutic use ; Sox9 protein ; Stem cells ; Stromal cells ; Substance Withdrawal Syndrome - pathology ; Tyrosine ; Tyrosine kinase inhibitors ; Young Adult</subject><ispartof>Bulletin of experimental biology and medicine, 2019-08, Vol.167 (4), p.580-583</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2019</rights><rights>COPYRIGHT 2019 Springer</rights><rights>COPYRIGHT 2020 Springer</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature 2019.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c571t-93fd7e4aaef0c6e627576e87e62842db1442f42e49a59b6bde9f6c44e34acbd43</citedby><cites>FETCH-LOGICAL-c571t-93fd7e4aaef0c6e627576e87e62842db1442f42e49a59b6bde9f6c44e34acbd43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10517-019-04575-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10517-019-04575-0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31502137$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Petinati, N. A.</creatorcontrib><creatorcontrib>Petrova, A. N.</creatorcontrib><creatorcontrib>Chelysheva, E. Yu</creatorcontrib><creatorcontrib>Shukhov, O. A.</creatorcontrib><creatorcontrib>Bykova, A. V.</creatorcontrib><creatorcontrib>Nemchenko, I. S.</creatorcontrib><creatorcontrib>Sats, N. V.</creatorcontrib><creatorcontrib>Turkina, A. G.</creatorcontrib><creatorcontrib>Drize, N. I.</creatorcontrib><title>Multipotent Mesenchymal Stromal Cells in Patients with Chronic Myeloid Leukemia before Discontinuation of Tyrosine Kinase Inhibitors</title><title>Bulletin of experimental biology and medicine</title><addtitle>Bull Exp Biol Med</addtitle><addtitle>Bull Exp Biol Med</addtitle><description>We analyzed changes in multipotent mesenchymal stromal cells of patients with chronic myeloid leukemia before discontinuation of tyrosine kinase inhibitors. Withdrawal syndrome was significantly more common in patients who have been taking tyrosine kinase inhibitors for a longer time and in patients of older age and with lower body weight. In patients with withdrawal syndrome, the total production of mesenchymal stromal cells and expression of
FGFR2
and
MMP2
genes were significantly lower; loss of deep molecular response was also less frequent in this group of patients. At the same time, the expression of genes important for the maintenance of stem cells (
SOX9
,
PDGFRa
, and
LIF
) was significantly lower in the mesenchymal stromal cells of patients with withdrawal syndrome and loss of deep molecular response. We observed a clear-cut relationship between the development of withdrawal syndrome and the loss of deep molecular response. The decrease in the expression of
FGFR2
and
MMP2
genes in the mesenchymal stromal cells of patients with chronic myeloid leukemia before discontinuation of treatment can be a predictor of withdrawal syndrome, while simultaneous decrease in the expression of
SOX9
,
PDGFRa
, and
LIF
in these cells attests to undesirability of therapy discontinuation at the moment.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Body weight</subject><subject>Care and treatment</subject><subject>Cell Biology</subject><subject>Chronic myeloid leukemia</subject><subject>Female</subject><subject>Fibroblast growth factor receptor 2</subject><subject>Gelatinase A</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Laboratory Medicine</subject><subject>Leukemia</subject><subject>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy</subject><subject>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology</subject><subject>Male</subject><subject>Mesenchymal stem cells</subject><subject>Mesenchymal Stem Cells - pathology</subject><subject>Mesenchyme</subject><subject>Middle Aged</subject><subject>Myeloid leukemia</subject><subject>Pathology</subject><subject>Phenols</subject><subject>Platelet-derived growth factor</subject><subject>Protein Kinase Inhibitors - therapeutic use</subject><subject>Sox9 protein</subject><subject>Stem cells</subject><subject>Stromal cells</subject><subject>Substance Withdrawal Syndrome - pathology</subject><subject>Tyrosine</subject><subject>Tyrosine kinase inhibitors</subject><subject>Young Adult</subject><issn>0007-4888</issn><issn>1573-8221</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNks-P1CAcxRujccfVf8CDITExXroCpUCPm_HXxplo4nomtP2yZe3ACDRm7v7hUmd1Z42ZmB4o9PMe9PGK4inBZwRj8SoSXBNRYtKUmNWiLvG9YkFqUZWSUnK_WOBMlUxKeVI8ivF6nmJOHhYnFakxJZVYFD_W05js1idwCa0hguuG3UaP6HMKfh6XMI4RWYc-6WQzFNF3mwa0HIJ3tkPrHYze9mgF01fYWI1aMD4Aem1j512ybsoy75A36HIXfLQO0AfrdAR04Qbb2uRDfFw8MHqM8ORmPC2-vH1zuXxfrj6-u1ier8quFiSVTWV6AUxrMLjjwKmoBQcp8ptktG8JY9QwCqzRddPytofG8I4xqJju2p5Vp8XLve82-G8TxKQ2-Zj5B7UDP0VFqZQYc06rjD7_C732U3D5dDMlcngcN7fUlR5BWWd8CrqbTdU5l4TlkHl1nMKSyKoRIlNn_6Dy0-dcc5ZgbF6_Y_t_goMdXhwIBtBjGqIfp_mC4l3n4-CBI92DXb7aGMCobbAbHXaKYDV3VO07qnJH1a-OKpxFz26indoN9H8kv0uZgWoPxPzJXUG4zf6I7U9UmO7J</recordid><startdate>20190801</startdate><enddate>20190801</enddate><creator>Petinati, N. 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A. ; Petrova, A. N. ; Chelysheva, E. Yu ; Shukhov, O. A. ; Bykova, A. V. ; Nemchenko, I. S. ; Sats, N. V. ; Turkina, A. G. ; Drize, N. 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A.</creatorcontrib><creatorcontrib>Petrova, A. N.</creatorcontrib><creatorcontrib>Chelysheva, E. Yu</creatorcontrib><creatorcontrib>Shukhov, O. A.</creatorcontrib><creatorcontrib>Bykova, A. V.</creatorcontrib><creatorcontrib>Nemchenko, I. S.</creatorcontrib><creatorcontrib>Sats, N. V.</creatorcontrib><creatorcontrib>Turkina, A. G.</creatorcontrib><creatorcontrib>Drize, N. I.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Applied & Life Sciences</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Bulletin of experimental biology and medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Petinati, N. A.</au><au>Petrova, A. N.</au><au>Chelysheva, E. Yu</au><au>Shukhov, O. A.</au><au>Bykova, A. V.</au><au>Nemchenko, I. S.</au><au>Sats, N. V.</au><au>Turkina, A. G.</au><au>Drize, N. I.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Multipotent Mesenchymal Stromal Cells in Patients with Chronic Myeloid Leukemia before Discontinuation of Tyrosine Kinase Inhibitors</atitle><jtitle>Bulletin of experimental biology and medicine</jtitle><stitle>Bull Exp Biol Med</stitle><addtitle>Bull Exp Biol Med</addtitle><date>2019-08-01</date><risdate>2019</risdate><volume>167</volume><issue>4</issue><spage>580</spage><epage>583</epage><pages>580-583</pages><issn>0007-4888</issn><eissn>1573-8221</eissn><abstract>We analyzed changes in multipotent mesenchymal stromal cells of patients with chronic myeloid leukemia before discontinuation of tyrosine kinase inhibitors. Withdrawal syndrome was significantly more common in patients who have been taking tyrosine kinase inhibitors for a longer time and in patients of older age and with lower body weight. In patients with withdrawal syndrome, the total production of mesenchymal stromal cells and expression of
FGFR2
and
MMP2
genes were significantly lower; loss of deep molecular response was also less frequent in this group of patients. At the same time, the expression of genes important for the maintenance of stem cells (
SOX9
,
PDGFRa
, and
LIF
) was significantly lower in the mesenchymal stromal cells of patients with withdrawal syndrome and loss of deep molecular response. We observed a clear-cut relationship between the development of withdrawal syndrome and the loss of deep molecular response. The decrease in the expression of
FGFR2
and
MMP2
genes in the mesenchymal stromal cells of patients with chronic myeloid leukemia before discontinuation of treatment can be a predictor of withdrawal syndrome, while simultaneous decrease in the expression of
SOX9
,
PDGFRa
, and
LIF
in these cells attests to undesirability of therapy discontinuation at the moment.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>31502137</pmid><doi>10.1007/s10517-019-04575-0</doi><tpages>4</tpages></addata></record> |
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| ispartof | Bulletin of experimental biology and medicine, 2019-08, Vol.167 (4), p.580-583 |
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| subjects | Adult Aged Aged, 80 and over Biomedical and Life Sciences Biomedicine Body weight Care and treatment Cell Biology Chronic myeloid leukemia Female Fibroblast growth factor receptor 2 Gelatinase A Gene expression Genes Humans Internal Medicine Laboratory Medicine Leukemia Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology Male Mesenchymal stem cells Mesenchymal Stem Cells - pathology Mesenchyme Middle Aged Myeloid leukemia Pathology Phenols Platelet-derived growth factor Protein Kinase Inhibitors - therapeutic use Sox9 protein Stem cells Stromal cells Substance Withdrawal Syndrome - pathology Tyrosine Tyrosine kinase inhibitors Young Adult |
| title | Multipotent Mesenchymal Stromal Cells in Patients with Chronic Myeloid Leukemia before Discontinuation of Tyrosine Kinase Inhibitors |
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