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Biomedical subjects

A M Yeager

Publications and source records attributed to A M Yeager.

78 records · Page 5Linked to original sources
PubMed1982

Effects of cyclophosphamide on murine bone marrow and splenic megakaryocyte-CFC, granulocyte-macrophage-CFC, and peripheral blood cell levels.

The effect of cyclophosphamide (CY) on megakaryocytopoiesis in mice was examined with assays of megakaryocyte colony-forming cells (Meg-CFC) in bone marrow and spleen and simultaneous determinations of peripheral blood counts, after a single intraperitoneal dose (200 mg/kg) of CY. Significant rebound thrombocytosis (170% of normal) occurred at day 11 after injection with CY, although only modest preceding thrombocytopenia (70% of normal) was observed. After an initial 3-5 day period of suppression, total megakaryocyte colony-forming cells (Meg-CFC) in both bone marrow and spleen of CY-treated mice demonstrated rebound increases at 5 and 7 days, respectively, after administration of the drug. Granulocyte-macrophage colony-forming cells (GM-CFC) exhibited alterations which were similar to those of Meg-CFC, suggesting similar sensitivities of Meg-CFC and GM-CFC to CY. The increase in Meg-CFC in both bone marrow and spleen preceded development of thrombocytosis by 4-6 days. This suggests that increased platelet counts in CY-treated mice are attributable, at least in part, to alterations in feedback mechanisms which control megakaryocytopoiesis, with resultant stimulation of the megakaryocyte progenitor compartment.

Animals↗
PubMed1980

Varicella-associated thrombocytopenia: clues to the etiology of childhood idiopathic thrombocytopenic purpura.

The temporal patterns of varicella-associated thrombocytopenia in five children seen at the Johns Hopkins Hospital suggest the existence of at least two pathogenetic mechanisms: one "infectious," with thrombocytopenia during the period of viremia; the other "post-infectious," with thrombocytopenia continuing for weeks or months afterward. Because of the subtleties of many viral illnesses, the frequency with which an active infection produces childhood idiopathic thrombocytopenic purpura may be underestimated. Studies to evaluate this hypothesis may enhance our knowledge of etiologic factors and enable more rational therapy.

Chickenpox↗
PubMedDate not supplied

Phenylbutyrate attenuates the expression of Bcl-X(L), DNA-PK, caveolin-1, and VEGF in prostate cancer cells.

Phenylbutyrate (PB) is a histone deacetylase inhibitor that has been shown to induce differentiation and apoptosis in various cancer cell lines. Although these effects are most likely due to modulation of gene expression, the specific genes and gene products responsible for the effects of PB are not well characterized. In this study, we used cDNA expression arrays and Western blot to assess the effect that PB has on the expression of various cancer and apoptosis-regulatory gene products. We show that PB attenuates the expression of the apoptosis antagonist Bcl-X(L), the double-strand break repair protein DNA-dependent protein kinase, the prostate progression marker caveolin-1, and the pro-angiogenic vascular endothelial growth factor. Furthermore, PB was found to act in synergy with ionizing radiation to induce apoptosis in prostate cancer cells. Taken together, our results point to the possibility that PB may be an effective anti-prostate cancer agent when used in combination with radiation or chemotherapy and for the inhibition of cancer progression.

Apoptosis↗
PubMedDate not supplied

Steroid-refractory cutaneous graft-versus-host disease after transplantation of haploidentical parental CD34+ cells in children with Down's syndrome and recurrent acute leukemia.

PURPOSE: This study evaluated the feasibility of performing haploidentical CD34+ selected transplants for children with Down's syndrome (DS) and recurrent leukemia. PATIENTS AND METHODS: Within a cohort of 15 children, two patients had DS. Transplantation of CD34+ cells from haploidentical parents was performed after the children were conditioned with fractionated total body irradiation, cyclophosphamide, and antithymocyte globulin (ATG). Graft-versus-host disease (GVHD) prophylaxis consisted of cyclosporine and a short course of methotrexate. RESULTS: The preparative regimen was well tolerated, and engraftment of polymorphonuclear cells and platelets took place promptly (by day 20) in both patients with DS. However, both patients with DS experienced severe grade IV GVHD that was limited to the skin and was refractory to salvage with high-dose methylprednisolone therapy. In one patient, GVHD responded to second-line salvage therapy with ATG, but the patient died on day 234 from leukemic relapse. The second patient had GVHD that did not respond to ATG and died of multisystem organ failure and refractory GVHD on day 44. Two of two DS patients had steroid refractory severe acute GVHD of the skin, while only one of 11 evaluated and identically treated non-DS patients had severe GVHD (p < 0.05). CONCLUSION: These observations in patients who underwent mismatched bone marrow transplantation suggests that patients with DS have an increased risk of severe acute GVHD of the skin in this context.

Antigens, CD34↗
PubMedDate not supplied

Incidence and clinical significance of CDKN2/MTS1/P16ink4A and MTS2/P15ink4B gene deletions in childhood acute lymphoblastic leukemia.

We have examined the incidence and clinical significance of deletions of two candidate tumor suppressor genes, CDKN2/MTS1/p16ink4A and MTS2/p15ink4B, in pediatric acute lymphoblastic leukemia (ALL). Gene deletion was evaluated in leukemic bone marrow (BM) cells obtained at diagnosis from 105 pediatric ALL patients: 83 with B-cell precursor (BCP-ALL) ALL and 22 with T-ALL. CDKN2/p16 deletion was seen in 23 of the 83 (28%) BCP-ALL and 15 of the 22 (68%) T-ALL cases. A virtually identical pattern of MTS2/p15 deletion was detected in these patients: p15 was deleted in 37 of 38 cases with p16 deletion, and p15 was not deleted in any p16-positive specimens. P16/p15 deletions were significantly related to poor prognosis factors including age under 1 year (P < 0.001), initial white cell counts greater than 50 x 10(9) per liter (P < .001), and T cell phenotype P < .005). Analysis of all 105 patients revealed that the 5-year disease-free survival rate was 68% for patients without p16/p15 deletions and 35% for those with p16/p15 deletions (P < .005). The association between gene deletion at initial diagnosis and unfavorable outcome suggests that loss of these genes is clinically significant and indicates a need for prospective studies of p16/p15 deletion in pediatric ALL patients.

Adolescent↗