RÉSUMÉ
<p><b>OBJECTIVE</b>To establish a novel Myc gene transgenic mouse model for spontaneously forming B-lymphoma and assessing its tumorigenesis potential.</p><p><b>METHODS</b>Freshly isolated hematopoietic progenitor cells served as the target for Myc gene transfer mediated by a retrovirus vector. These cells were engrafted into C57BL/6 mice with (60)Co-gamma ray radiation in advance. Tumor latency was measured and the tumor loaded mice were followed for survival time. Tumor was identified with histology and immunostaining. The exogenous Myc gene was detected by Western blot (in liver, spleen, tumor tissue) and flow cytometry (FCM) \[in bone marrow (BM)\].</p><p><b>RESULTS</b>Mice BM-infected with mutant Myc gene more readily gave rise to B-cell lymphomas than those infected with wild type Myc gene did Myc gene was expressed highly in BM and tumor tissues but not in liver and spleen.</p><p><b>CONCLUSION</b>Our model will be a tool in assessing the transforming potential of Myc mutants and in studying cooperation between Myc and other oncogenes. Mutant Myc is more effective than wild-type Myc in promoting B cell lymphomagenesis in mice.</p>
Sujet(s)
Animaux , Souris , Lymphocytes B , Transformation cellulaire néoplasique , Cytométrie en flux , Lymphomes , Lymphome B , Souris de lignée C57BL , Souris transgéniques , Infections à RetroviridaeRÉSUMÉ
<p><b>OBJECTIVE</b>To explore the risk factors for hepatoblastoma.</p><p><b>METHODS</b>A case-cohort study using Logistic regression multiple variables analysis of medical record data sets was conducted to examine infant and perinatal risk factors for hepatoblastoma.</p><p><b>RESULTS</b>Birth weight less than 1,000 g was associated with a strongly increased risk of hepatoblastoma (odds risk, OR = 26.0, 95% confidence interval, CI: 14.0 to 65.7). After adjustment of birth weight, a moderately increased risk of hepatoblastoma was found for older maternal age ( > 35 years vs. 20 to 34 years: OR = 2.6, 95% CI: 0.9 to 5.9), maternal smoking (OR = 2.9, 95% CI: 1.1 to 4.2) and higher maternal pregnancy body mass index (OR = 3.2, 95% CI: 1.0 to 6.7).</p><p><b>CONCLUSION</b>Very low birth weight and maternal characteristics including overweight, smoking are associated with hepatoblastoma risk.</p>
Sujet(s)
Enfant , Enfant d'âge préscolaire , Femelle , Humains , Nourrisson , Nouveau-né , Mâle , Grossesse , Études cas-témoins , Intervalles de confiance , Études de suivi , Hépatoblastome , Épidémiologie , Nourrisson très faible poids naissance , Tumeurs du foie , Épidémiologie , Surpoids , Études rétrospectives , Facteurs de risque , FumerRÉSUMÉ
<p><b>OBJECTIVE</b>To review the outcomes of living-related liver transplantation (LRLT) in treating 3 cases of cavernous transformation of portal vein (CTPV) with severe portal hypertension.</p><p><b>METHODS</b>Three children (two boys and one girl) were presented to our hospital with recurring esophageal variceal bleeding, decompensating ascites, splenomegaly and refractory anemia. CTPV was confirmed by intravenous computed tomographic portography using a helical computed tomography scanner and 3-dimensional image reconstruction. LRLT were performed in these 3 patients from July 2006 to January 2007. The evaluation of the outcomes was made by referring to their clinical features and laboratory and imaging examination findings.</p><p><b>RESULTS</b>Although one patient died from early graft thrombosis, the other two patients showed excellent prognoses. They lived and stayed well during a follow-up period of 12-14 months. Following the transplantations, there had been no esophageal variceal hemorrhage, the ascites disappeared and the portal hypertension vanished. Their hemoglobin, blood platelets count, and serum albumin reached normal values.</p><p><b>CONCLUSION</b>LRLT is an effective procedure in treating CTPV with severe portal hypertension. The reconstruction of the portal vein is the difficult part of the LRLT procedure.</p>
Sujet(s)
Enfant , Femelle , Humains , Mâle , Hypertension portale , Anatomopathologie , Chirurgie générale , Transplantation hépatique , Donneur vivant , Parents , Veine porte , Anatomopathologie , Résultat thérapeutiqueRÉSUMÉ
<p><b>OBJECTIVE</b>To observe the effect of Fn-TPO gene modification on human bone marrow mesenchymal stem cells (MSCs).</p><p><b>METHODS</b>Retroviral vector containing Fn-TPO gene was constructed and bone marrow MSCs was modified by this vector. The transcription of Fn-TPO gene in MSCs was observed. The proliferation capacities, hematopoietic cells adhering capacities and TPO secretion capacities of gene modified MSCs were assayed respectively. Cord blood CD34 cells were seeded on the gene modified MSCs layers and several essential growth factors were added. After co-culturing in vitro for 7 days, the number of CD34 cells and their colony forming capacities were assayed by flow cytometry and semisolid culture assay.</p><p><b>RESULTS</b>Retroviral vector containing Fn-TPO gene was successfully constructed and bone marrow MSCs were modified by this vector. Fn-TPO gene was expressed by bone marrow MSCs after gene modification. The viability of MSCs had no significant difference between pre- and post-gene-modification [(7.18 +/- 0.89) 10(4)/ml vs. (6.92 +/- 0.77) 10(4)/ml, P > 0.05]. The hematopoietic cells adhering ability of gene modified bone marrow MSCs was reinforced(0. 188 +/- 0.018 vs. 0.167 +/- 0.017, P < 0.01). The concentration of TPO in the MSCs culture supernatant raised from (5.58 +/- 0.37) ng/ml to (7.46 +/- 0.59) ng/ml (P < 0.01) and did not significantly decline in a short-time period, but influenced by the growth status of MSCs. After co-culturing with gene modified MSCs for 7 days, the absolute number of nucleated cells, the percentage of CD34+ cells and the colony numbers of BFU-E, CFU-GM, CFU-GEMM were (29.9 +/- 2.7) x 10(4), (33.3 +/- 2.8)% , 109.3 +/- 4.1, 163.7 +/- 7.1, 13.3 +/- 1.5, respectively, being significantly higher than that co-cultured with non-modified MSCs.</p><p><b>CONCLUSIONS</b>Fn-TPO gene modification can improve the capacity of human bone marrow MSCs for hematopoietic cells adhering, TPO secretion and cord blood CD34 cells amplification.</p>
Sujet(s)
Humains , Cellules de la moelle osseuse , Biologie cellulaire , Métabolisme , Adhérence cellulaire , Prolifération cellulaire , Cellules cultivées , Fibronectines , Génétique , Fusion de gènes , Vecteurs génétiques , Cellules souches mésenchymateuses , Biologie cellulaire , Métabolisme , Retroviridae , Génétique , Thrombopoïétine , Génétique , Métabolisme , TransfectionRÉSUMÉ
<p><b>OBJECTIVE</b>To explore the myelo-protection effect of mdr1 transfected cord blood cells (CBMNCs) graft against high-dose homoharringtonine leukemia-bearing severe combined immunodeficient (SCID) mice model.</p><p><b>METHODS</b>Multidrug resistant (mdr1)gene was transferred into CBMNCs by a retrovirus vector, containing full-length cDNA of human mdr1 gene. CBMNCs and high-titer retrovirus supernatant were cocultured with cytokine combinations for 5 - 6 days. The SCID mouse models bearing human HL-60 cell leukemia were divided into three groups. Group A received tail vein injection of 2 x 10(6) mdr1 gene transduced CBMNCs at day 1 and 3, groups B and C 2 x 10(6) un-transduced CBMNCs and same volume of normal saline, respectively. The 3 groups of the mouse model were treated with weekly escalated doses of homoharringtonine. The peripheral white blood cell (WBC) counts, the human leukemia cells percentage in peripheral blood, the histological findings of main organs were assayed. The CD33 positive HL-60 cells in bone marrow were determined by flow cytometry. The function and expression of mdr1 gene were examined by PCR, immunochemistry (IC) and DNR extrusion test in vivo.</p><p><b>RESULTS</b>(1) mdr1 gene was transferred into CBMNCs successfully and the transfection frequency was 30%. (2) Leukemia SCID mice were xenotransplanted with mdr1-transfected BMMNCs by a programmed procedure and could be used as a valuable model for in vivo evaluating myelo-protection effects. (3) The transfected mice could tolerate homoharringtonine 5 approximately 6 folds higher than conventional dose and kept peripheral WBC count at a mean of 3 x 10(9)/L, with the peripheral human myeloid leukemia cells percentage decreasing to less than 5%. Histological examination showed that there was no leukemia infiltration in the main organs, the CD33 positive HL-60 cells in bone marrow were less than 5%. (4) The repopulation frequency of the transfected CBMNs in marrow were 9.13%. DNR extrusion test confirmed that the P-gp product maintained its biological function in the marrow.</p><p><b>CONCLUSION</b>mdr1 transferred-human CBMNC can xenotransplanted and repopulated in leukemia-bearing SCID mouse and are protected from chemotherapy-induced myelosuppression.</p>
Sujet(s)
Animaux , Femelle , Humains , Mâle , Souris , Glycoprotéine P , Génétique , Métabolisme , Antinéoplasiques d'origine végétale , Utilisations thérapeutiques , Transplantation de cellules souches de sang du cordon , Méthodes , Sang foetal , Biologie cellulaire , Vecteurs génétiques , Cellules HL-60 , Harringtonines , Utilisations thérapeutiques , Leucémie aiguë promyélocytaire , Traitement médicamenteux , Anatomopathologie , Chirurgie générale , Agranulocytes , Biologie cellulaire , Métabolisme , Transplantation , Souris SCID , Répartition aléatoire , Retroviridae , Génétique , Transfection , Résultat thérapeutique , Tests d'activité antitumorale sur modèle de xénogreffeRÉSUMÉ
<p><b>OBJECTIVE</b>To investigate the collagen constitution of hyperplastic scar (HS) in different ages and the change of relative factors.</p><p><b>METHODS</b>Thirty cases with HS were divided into two groups according to patients' age: group 1 (1 - 19 years, A) and group 2 (20 - 50 years, B). The normal skin (NS) from corresponding age of volunteers was employed as control group. The changes in TGFbeta1, collagenase (MMP-1) and tissue inhibitor of metalloproteinase (TIMP-1beta) and the collagen ratio were observed by means of in situ hybridization technique and SABC (Strept-Avidin-Biotin complex) immunohistochemistry and image analysis.</p><p><b>RESULTS</b>The ratio of type I to type III collagen in A group was 6.48 in average and 3.76 in B group, but there was no evident difference in the ratio during the disease process in both groups. The expression of TGFbeta1 in A group was much higher than that in B group (P < 0.01). The TIMP-1 mRNA expression showed no difference among all age groups in HS patients, but it was much higher than that in NS group. The MMP-1 expression was evidently lower than TIMP-1 expression, and there was no difference in MMP-1 expression compared with NS group.</p><p><b>CONCLUSION</b>(1) The TGFbeta1 expression in HS patients was negatively correlated with age, and the increased expression of TGFbeta1 produced an increase ratio of type I to type III collagen. (2) High level expression of TIMP-1 led to the formation of HS by inhibiting MMP-1 expression, and the expression was not related to age.</p>