Thymodepressin inhibits migration of CD34+ cells from bone marrow in normal and granulocyte CSF-stimulated hemopoiesis

Semina, O. V.; Semenets, T. N.; Замулаева, И. А.; Selivanova, E. I.; Il’ina, T. P.; Malyutina, Ya. V.; Semin, D. Yu.; Дейгин, В. И.; Саенко, А.С.

doi:10.1007/s10517-007-0442-y

Cited by 2 publications

(2 citation statements)

References 14 publications

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“…Each preceding relapse-free period, during which the stem cells are outside a tumor, is favorable for the imitation of an optimistic prognosis. [136]. However, a lag time between pics of both parameters (horizontal arrows in Figure 4) are reducing along with shortening life span.…”

Section: Cd34 Cells In Tissues and Death Ratementioning

confidence: 94%

Time for a New Paradigm in Oncology? Viewpoint of the Radiobiologist

Shoutko

2024

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The current immunooncology artificially ignores the connection with lymphopoiesis, though is only its derivative. Hematopoietic stem cells (HSC) provide physiological regeneration of biomass of the host, fetus, and malignant tumors, as well, as the cells' reparation after sub-lethally injuring in any tissues and their renewal. HSC, especially of lymphoid lineage, are the most vulnerable of those, which are responsible for viability of organism. Natural and artificial deficits of HSC determine aging, multi-organs syndromes and death of the host, because their current proliferative resource (CPR) is individually limited at birth, and is spending irreversibly during wounds' healing, pregnancy, tumor growth, and on. CPR, being an integral value of the number of stem cells along the length of their telomeres, is a "shagreen skin", for which the tumor competes with normal tissues as a quasi-embryonic favorite and winner, especially in the final period of a shortening the life. The primary approach to cancer treatment must prioritize the preservation of CPR remnants, rather than their destruction, in order to temporarily halt the malignant process. The re-targeting of HSC from tumors in favor of normal tissues is the immediate objective of competitive therapy, which allows for preserving the rest of the CPR host's resources, especially in patients with advanced cancer. However, the contradictory and insignificant practically, the dogma of antitumor cellular immunity continues to dominate and hinder progress in oncology.

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Section: Cd34 Cells In Tissues and Death Ratementioning

confidence: 94%

Time for a New Paradigm in Oncology? Viewpoint of the Radiobiologist

Shoutko

2024

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“…O. V. Semina Synthetic dipeptide γ-d-Glu-d-Trp (thymodepressin) consisting of artificial d-amino acid residues suppresses proliferation and differentiation of hemopoietic stem cells and reduces their migration from the bone marrow into the peripheral blood in healthy mice and in animals treated with granulocytic CSF. These properties are most likely determined by the effect of the peptide on receptor expression on hemopoietic precursors and accessory cells responsible for mobilization and homing, essential components of normal hemopoiesis [1][2][3][4]. Extremely unfavorable effects of increased migration of CD34 + early hemopoietic precursors from the bone marrow into the peripheral blood on the growth and metastasizing of solid tumors were demonstrated: CD34 + cells settled in the tumor tissue suppress cell immunity [9], promote tumor growth by activating angiogenesis [10], and initiate the formation of metastatic niches, which leads to enlargement of metastases [5].…”

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Dipeptide γ-d-Glu-d-Trp (thymodepressin) inhibits migration of Cd34+ cells from the bone marrow into peripheral blood during tumor growth

et al. 2008

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We studied the effect of dipeptide gamma-d-Glu-d-Trp (thymodepressin) on migration of CD34+ hemopoietic precursors and their direct adhesion to fibronectin in tumor-bearing mice on days 8, 11, 15, and 17 of tumor growth and on expression of CXCR-4 (CD184+) to SDF-1 and integrin beta1 (CD29+) by bone marrow cells. In tumor-bearing mice treated with gamma-d-Glu-d-Trp, the percent of CD34+ hemopoietic precursors in the peripheral blood considerably decreased throughout the observation period; the content of CD34+ hemopoietic precursors in the tumor tissue was 2-3-fold below the control against the background of increased content of CD34+ cells in the bone marrow. In animals treated with the peptide, the content of cells expressing CXCR-4 in the peripheral blood, bone marrow, and tumor tissue significantly decreased, while the percent of cells expressing integrin beta1 receptor (CD29+) in the bone marrow increased 2-fold, which was paralleled by an almost 2-fold increase in the percent of cells binding to fibronectin. We hypothesized that dipeptide gamma-d-Glu-d-Trp suppressed mobilization/migration of CD34+ hemopoietic precursor cells from the bone marrow to the peripheral blood of tumor-bearing mice.

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Thymodepressin inhibits migration of CD34+ cells from bone marrow in normal and granulocyte CSF-stimulated hemopoiesis

Cited by 2 publications

References 14 publications

Time for a New Paradigm in Oncology? Viewpoint of the Radiobiologist

Time for a New Paradigm in Oncology? Viewpoint of the Radiobiologist

Dipeptide γ-d-Glu-d-Trp (thymodepressin) inhibits migration of Cd34+ cells from the bone marrow into peripheral blood during tumor growth

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