Responses of Blood System to Doxorubicin/Docetaxel Chemotherapy in Patients with Breast Cancer.

We studied the effects of combined chemotherapy with doxorubicin/docetaxel on erythroid and granulocytic hematopoietic lineages with particular attention focused on their recovery in patients with stages III-IV breast cancer. Intensification of differentiation of erythroid and granulocytic CFU (even under conditions of their suppressed proliferation) provided the increase in the content of mature and morphologically differentiated elements in the bone marrow and peripheral blood. High proliferative activity of erythroid and granulomonocytic precursors resulted from enhanced production of hematopoiesis-stimulating activities by microenvironment elements.

Mechanisms of Granulocytopoiesis Recovery Stimulation with Filgrastim in Breast Cancer Patients Receiving Chemotherapy.

We studied myelotoxicity of modern schemes of chemotherapy for breast cancer (docetaxel/doxorubicin and cyclophosphamide/doxorubicin/5-fluorouracil) towards granulocytopoiesis, the mechanisms determining the differences of hematological effects of these schemes, and the efficiency of correction of the observed changes with granulocyte CSF (filgrastim). Granulocytopoiesis stimulation with filgrastim during the treatment with docetaxel/doxorubicin combination was more pronounced than during cyclophosphamide/doxorubicin/5-fluorouracil therapy. The observed differences were found at all levels of granulocyte lineage organization (central and peripheral), which is related to different effects of the cytostatic substances used in the proposed protocols on the structures controlling hemopoiesis.

Assessment of Erythroid and Granulocytic Hematopoietic Lineages in Patients with Non-Small-Cell Lung Carcinoma.

The toxic effects of combined cisplatin/docetaxel therapy cycles on erythroid and granulocytic hematopoietic lineages as well as their intercycle recovery were examined in patients with stage III-IV non-small-cell lung carcinoma. Responsiveness of the blood system to this therapy remained at a high level. Combined therapy pronouncedly activated the key elements of the erythroid and granulocytic hematopoietic lineages leading to accumulation of immature and mature myelokaryocytes in the bone marrow, enlargement of the medullary pool of mature neutrophils, and increase in the count of medullary erythroid and granulocytic precursor cells under conditions of their accelerated maturation.

[Hemostimulating properties of cropanol during cytostatics-induced myelosuppression]. / Gemostimuliruiushchie svoistva kropanola pri tsitostaticheskoi mielosupressii.

The granulocyte lineage reaction and its mechanism were studied in the bone marrow of patients with breast cancer in stage III-IV treated according to a specific CAF scheme including cropanol, an antitumor drug of the animal origin. It was found that the bone marrow cytopoiesis suppressed by the cytostatics is stimulated by cropanol on the level of committed precursors, morphologically differentiated bone marrow elements, and peripheral blood.

Mechanisms of stimulation of granulocytopoiesis with neupogen in patients with breast cancer during chemotherapy.

The mechanisms of granulocytopoiesis stimulation with granulocytic CSF (neupogen), added to chemotherapy protocol (adriablastine+taxotere) in patients with stages III-IV breast cancer, were studied. The hemostimulatory effect of granulocytic CSF preparation is based on stimulation of proliferation and differentiation of granulomonocytopoisis precursor cell in the hemopoietic tissue, due to neupogen effects on hemopoietic elements and on the hemopoiesis-inducing microenvironment cells.

Compensatory reactions during impairment of granulocytic stem in patients with lung cancer receiving antitumor chemotherapy.

We compared changes in the granulocytic hemopoietic stem in patients with stage III-IV lung cancer receiving cytostatic therapy by the original CVC and standard CAM schemes. In patients treated with the CVC regimen, the granulocytic hemopoietic stem possessed more potent compensatory capacities.