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G Piaggio

Publications and source records attributed to G Piaggio.

At least 91 records · Page 5Linked to original sources
PubMed1993

In vitro effect of stem cell factor on colony growth from acquired severe aplastic anemia.

In this study we review our present understanding of the effect of stem cell factor (SCF) on the in vitro growth of hemopoietic progenitors from patients with acquired severe aplastic anemia (SAA). We have run three separate sets of experiments. First, we have tested the expression of receptor mRNAs for granulocyte-macrophage colony stimulating factor/interleukin 3 (GM-CSF/IL-3) and for c-kit protein on bone marrow (BM) cells from SAA patients. Molecular analysis revealed the presence of normal transcripts for alpha and beta chains of GM-CSF/IL-3 receptor and for c-kit protein by Northern blot analysis. Second, we have tested the in vitro response to SCF of BM cells derived from 11 SAA patients: SCF induced a significant enhancement of erythroid burst forming unit (BFU-E) growth (8 to 29, p = 0.01) and allowed the formation of granulocyte/erythroid/macrophage/megakaryocyte (GEMM) colonies which were not scored in baseline culture conditions (0 to 8, p = 0.01). Granulocyte-macrophage colony forming unit (CFU-GM) growth was also enhanced (4 to 20, p = 0.3). This was true for patients both at diagnosis and after antilymphocyte globulin (ALG) treatment. We concluded that SCF can promote the in vitro growth of hemopoietic progenitors in patients with acquired SAA. Third, we have tested the response to SCF of peripheral blood (PB) hemopoietic progenitors collected from patients receiving in vivo long-term treatment with granulocyte CSF (G-CSF). When PB cells were plated directly in the presence of GM-CSF there was no colony formation.(ABSTRACT TRUNCATED AT 250 WORDS)

Anemia, Aplastic↗
PubMed1993

Analysis of complications in a chronic peritoneal dialysis pediatric patient population. The Italian Registry of Pediatric Chronic Peritoneal Dialysis.

During the period 1986-1991, the Italian Registry of Pediatric Chronic Peritoneal Dialysis collected data from 140 patients younger than 15 years at the start of chronic peritoneal dialysis (CPD). In this study we review the Registry's complications and patient hospitalization data. A total of 395 complications directly related to CPD were registered during 2722 dialysis-months. There were 176 episodes of peritonitis (44.5%), 161 catheter-related complications (40.7%) (103 exit-site infections, 17 leakages, 15 obstructions, 15 cuff extrusions, 5 hemoperitoneum, and 6 other complications), and 58 technique-related complications (14.8%) (39 abdominal hernias, 10 hydroceles, 5 with abdominal pain, 4 hydrothorax complications). The patient hospitalization rate during the period 1989-1991 was evaluated; the analysis referred to 106 patients who underwent treatment for a total of 1520.5 dialysis-months. Patients starting CPD in the year and patients already on CAPD spent 5.8 and 2.1 days per patient-month in the hospital, respectively; the difference was not statistically significant. The evaluation of complications (both technical and systemic) causing patient hospitalization showed that peritonitis was responsible for 43.2% of patient admissions and 36.3% of days hospitalized, catheter-related complications for 22% and 19.8%, technique-related complications for 8.3% and 5.1%, and other clinical complications for 26.5% and 38.8%, respectively.

Catheters, Indwelling↗
PubMed1993

Cardiovascular function in a chronic peritoneal dialysis pediatric population on recombinant human erythropoietin treatment.

Anemia, through a hyperkinetic state, is an important contributor to myocardial function impairment. To determine the cardiovascular effects of recombinant human erythropoietin (rHuEPO) therapy, 10 chronic peritoneal dialysis (CPD)-treated anemic children were studied before and during 18 months of treatment. The following parameters were recorded: hemoglobin (Hb) [percent of target level (TL) = x-2 standard deviations of normal Hb values for age and sex], heart rate (HR, beats/minute), mean arterial pressure (MAP, mmHg), end-diastolic left ventricular diameter (EDLVD, mm/sm BSA), shortening fraction (SF, percent), and interventricular septal thickness (IVS, mm/sm BSA). Student's t-test for paired data showed (vs time before treatment, T0) a progressive increase in Hb, a progressive decrease in HR, and a progressive increase in MAP. EDLVD progressively decreased, while SF and IVS remained unchanged throughout the study. Regression analysis showed a close correlation between anemia correction and decrease of HR (p < 0.01), while no correlation was found between Hb and EDLVD or SF, IVS, or MAP. Our data indicate that anemia correction in these patients is mainly associated with a decrease in hyperkinetic state (HR reduction with SF unvaried), while left ventricular function and dimensions remain normal, despite an increase in MAP.

Anemia↗
PubMed1992

Effect of stem cell factor on colony growth from acquired and constitutional (Fanconi) aplastic anemia.

The aim of this study was to evaluate the effect of stem cell factor (SCF) on the in vitro growth of bone marrow hematopoietic progenitors from patients with acquired severe aplastic anemia (AA) or Fanconi's anemia (FA). For this purpose, we studied 11 patients with acquired AA (5 at diagnosis, 6 after ALG treatment), 12 patients with FA, and nine normal controls. Bone marrow cells were plated in vitro for colony-forming unit granulocyte-macrophage (CFU-GM) (in the presence of granulocyte-macrophage colony-stimulating factor [GM-CSF]), and for burst-forming unit-erythroid (BFU-E) and CFU-granulocyte, erythroid, monocyte, megakaryocyte (CFU-GEMM) colonies (in the presence of erythropoietin and interleukin-3 [IL-3]), with or without 20 ng/mL of SCF. In normal controls, SCF enhanced the growth of CFU-GM colonies from 103 to 263 (median), of BFU-E from 168 to 352, and of GEMM colonies from 6 to 38/10(5) cells plated. In patients with acquired AA, SCF induced a significant enhancement of BFU-E growth (8 to 29; P = .01) and allowed the formation of GEMM colonies that were not scored in baseline culture conditions (0 to 8; P = .01). CFU-GM growth was enhanced (4 to 20), but not significantly (P = .3). This was true both for patients at diagnosis and after antilymphocyte globulin treatment. By contrast, 10 of 12 FA patients grew no CFU-GM, BFU-E, or CFU-GEMM colonies, with or without SCF. In two FA patients (one transfusion-dependent and one transfusion-independent), an enhancement of CFU-GM and/or BFU-E was observed. The lack of response of hematopoietic progenitor cells from FA patients to GM-CSF+SCF or IL-3+SCF was not dependent on a defective expression of cytokine receptor messenger RNAs. Northern blot analysis showed in marrow cells from acquired AA and FA patients the presence of normal transcripts for alpha- and beta-chains of GM-CSF/IL-3 receptor and for c-kit protein. In conclusion, SCF promotes the in vitro growth of hematopoietic progenitors in patients with acquired AA, but not in patients with FA, pointing out the intrinsic nature of the defect in the latter disorder.

Adolescent↗
PubMed1992

Delayed puberty in uremia: pituitary-gonadal function during short-term pulsatile luteinizing hormone-releasing hormone administration.

Pubertal development is frequently delayed or disordered in children with chronic renal failure. Both neuroendocrine and peripheral alterations due to uremia have been hypothesized to explain the impairment in the pituitary gonadal axis. The aim of the present study was to evaluate quantitative (immunological) and qualitative (biological) LH secretion, as well as FSH and sex steroids, before and during 7 days of sc LHRH administration (136-150 ng/kg bw every 120 min) in 5 uremic children (13.1-14.8 yr) with delayed puberty. Six nonuremic children (13.2-17.8 yr) with delayed puberty underwent the same schedule and served as control group. On day 0 mean immunoreactive LH (I-LH) levels were higher in uremic (4.5 +/- 0.9 mIU/ml) than in nonuremic (1.9 +/- 03 mIU/ml; p < 0.05) subjects while no differences were observed in bioactive LH (B-LH) levels (2.9 +/- 0.7 mIU/ml vs 2.4 +/- 0.3 mIU/ml). In both groups of subjects testosterone was at prepubertal levels. Spontaneous I-LH and B-LH pulses were observed sporadically in both uremic and nonuremic subjects. Short-term pulsatile LHRH administration induced significant increases in B-LH, I-LH, FSH and testosterone. The B/I LH ratio increased from day 0 (0.7 +/- 0.2) to day 7 (1.3 +/- 0.4; p < 0.05) in uremics while it showed wide fluctuations in nonuremic subjects. On day 7, 4 uremic and 5 nonuremic subjects showed a pulsatile release of B-LH after exogenous LHRH pulses. Our data document that in uremia there are qualitative as well as quantitative abnormalities in pituitary gonadal secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Five years' experience of the Italian Registry of Pediatric Chronic Peritoneal Dialysis.

The results of the first 5 years' experience of the Italian Registry of Pediatric Chronic Peritoneal Dialysis (CPD) (1986-1990) are presented. Patients of less than 15 years of age at start of dialysis were enrolled and clinical data collected until the age of 19. The number of the dialysis centres participating in the Registry increased from 7 in 1986 to 15 in 1990. The total number of patients on CPD was 119, the number of new patients per year ranged from 15 to 28 and the percentage of all dialysed children treated with CPD increased from 40% in 1986 to 49% in 1990. The age of patients at start of CPD was 8.5 +/- 4.9 years and 16% of them were under 2 years. Only CAPD was utilized in 1986, while CCPD/NPD accounted for 53% and 65% of the treated patients in 1989 and 1990, respectively. At 4 years, patient survival was 91.3% and technique survival 79.3%. A comparison between data of 48 patients on CPD and 34 on hemodialysis, who started dialysis in the period 1989-1990, showed that CPD was the most frequent form of initial therapy (56%) and was the treatment of choice for children younger than 4 years.

Age Factors↗
PubMed1992

[Role of echo-Doppler in the screening of renal artery stenosis in children with kidney transplants].

Renal artery stenosis (RAS) in renal transplanted pediatric patients is a long-term complication. The clinical suspicion must be considered when patients exhibit signs of impaired renal function or refractory hypertension, not associated with other complications of renal transplantation -i.e., acute or chronic rejection, glomerulonephritis, cyclosporine toxicity. The intermediate step between clinical suspicion and angiography is represented by Doppler US. The authors report their experience with Doppler US in the screening of RAS in a pediatric series of transplanted patients. The incidence of RAS in our series (54 transplanted kidneys, 46 of them included in the study) was 4.3%. A severe stenosis was demonstrated by both Doppler US and angiography in 2 patients, with 100% Doppler sensitivity. In both stenoses, Doppler US showed high systolic peaks (blood flow velocity > or = 2.5 m/s) and post-stenotic turbulence. Thanks to its high sensitivity, Doppler US is considered to be very useful in the screening of vascular complications in renal transplanted children.

Adolescent↗
PubMed1992

Long-term marrow culture in patients with aplastic anemia compared with marrow transplant recipients and normal controls.

UNLABELLED: Patients with severe aplastic anemia (SAA; n = 46) were studied in long-term bone marrow culture (LTBMC) systems and compared with allogeneic marrow transplant (BMT) recipients (n = 16) (within 30 days following BMT) and normal control patients (n = 12). SAA patients were divided in two groups: transfusion-dependent (Tx-D) SAA patients (group A; n = 15) and transfusion-independent (Tx-I) patients after treatment with antilymphocyte globulin (group B; n = 31). Cultures were analyzed at three levels: stromal layer (SL) formation (score: 0, no SL; 1, half confluent SL; and 2, confluent SL), number of nucleated cells in suspension, and growth of CFU-GM colonies. SL formation was rapid and complete in SAA patients, groups A and B (mean score on day 14: 1.3 and 1.4), similar to controls (mean score on day 14: 1.3), whereas an impairment of SL formation was seen in BMT recipients (mean score on day 14: 1.0). The number of nucleated cells in suspension increased significantly on day 7 of culture in controls (7.6-fold), significantly more than in BMT and SAA patients, and declined thereafter. Colony formation was also significantly increased on day 7 in Tx-I SAA patients, BMT recipients, and normal controls (4-, 5-, and 16-fold, respectively), lasting respectively 2, 3, and 4 weeks. Increments of colony formation were also obtained in Tx-D SAA patients, but in the first week of culture only. IN CONCLUSION: 1) a significant impairment of SL formation was seen in BMT recipients, but not in SAA patients; 2) a significant increment of granulocyte-macrophage colony-forming units (CFU-GM) growth can be obtained in patients with marrow failure early after starting long-term culture; 3) the number of CFU-GM grown in these culture conditions from Tx-I SAA patients parallels the number of progenitors from early post-BMT recipients; and 4) progenitor cells from Tx-D SAA patients are not only reduced in numbers, but also exhibit a poor ability to survive in LTBMC.

Anemia, Aplastic↗
PubMed1992

Bone marrow harvest for marrow transplantation: effect of multiple small (2 ml) or large (20 ml) aspirates.

The aim of this study was to evaluate the yield of nucleated cells and CFU-GM and the T cell composition in bone marrow harvested by means of multiple small (2 ml) or large (20 ml) aspirations. Eleven marrow donors were studied: each donated 1000 ml of bone marrow in two aliquots of 500 ml for an HLA identical sibling transplant. In six cases the first 500 ml were harvested by means of multiple 2 ml aspirations (A) and the second 500 ml by means of 20 ml aspirations (B). In five cases the opposite was done: 20 ml aspirates first (C) and 2 ml afterwards (D). From each 500 ml aliquot a sample was taken for enumeration of nucleated cells and CD3+ lymphocytes and for CFU-GM growth. Small volume aspirations (groups A and D) yielded more nucleated cells (p = 0.02), more CFU-GM (p = 0.03) and fewer CD3+ cells (p = 0.1) when compared with large volume aspirations (groups B and C). This study shows that marrow harvesting by means of multiple small volume aspirations minimizes the dilution with peripheral blood and results in greater numbers of cells and hemopoietic progenitors.

Adult↗
PubMed1991

Biological activity of luteinizing hormone in uraemic children: spontaneous nocturnal secretion and changes after administration of exogenous pulsatile luteinizing hormone-releasing hormone--preliminary observations.

Normal pubertal progression is associated with quantitative and qualitative changes in gonadotrophin release. Uraemic children show a delayed or disturbed puberty. We have therefore examined nocturnal gonadotrophin and sex steroid secretion in seven males and three females [age 11-15 years, pubertal stage (PS) 1-3] with chronic renal failure on conservative treatment. In addition to immunoreactive luteinizing hormone (i-LH) we have measured the biological activity of LH (b-LH). Nine children aged 12-17 years with PS 1-3 and normal renal function served as a control group. In two uraemic children, i-LH, b-LH, follicle stimulating hormone and sex steroids were evaluated before and 7 days after pulsatile LH-releasing hormone (LHRH) administration (150 ng/kg body weight subcutaneously every 120 min). Mean i-LH levels were higher in uraemic children than in controls. An increase in i-LH during sleep was found in all controls and in eight of ten uraemic subjects. Mean b-LH levels were lower during sleep and the b/i LH ratio was reduced in uraemic children with PS 2-3 whether asleep or awake compared with controls. Pulsatile administration of LHRH provoked a rise of i-LH and b-LH levels with an increased b/i LH ratio, suggesting an intact pituitary responsiveness. These preliminary data indicate that the gonadotrophin control of LH is abnormal in uraemic children, and that biopotency of LH secretion might be improved after short-term pulsatile LHRH administration.

Adolescent↗
PubMed1991

Severe aplastic anemia (SAA): response to cyclosporin A (CyA) in vivo and in vitro.

The aim of the present study was to test the effect of cyclosporin A (CyA) in vitro on CFU-GM growth from patients with severe aplastic anemia (SAA). For this purpose, bone marrow (BM) cells from 9 SAA patients and 5 healthy individuals were incubated with or without CyA and then cultured for CFU-GM growth in the presence of exogenous recombinant human GM-CSF (30 ng/ml). SAA patients were tested before or after treatment with CyA, or after treatment with antilymphocyte globulin (ALG). In 3 patients responding to CyA, the addition of CyA in vitro enhanced colony growth from 13 +/- 10 to 40 +/- 20/10(5) BM cells (p = 0.01) - the median increment of colony formation was 2.4-fold. In 5 ALG responders, CyA produced no increment of CFU-GM growth (from 14 +/- 26 to 15 +/- 16/10(5) BM cells, p = 0.1). CyA did not enhance significantly CFU-GM growth in normal controls (from 57 +/- 45 to 58 +/- 81/10(5) BM cells, p = 0.9). In conclusion, it would appear that some patients with SAA can respond to CyA in vivo and in vitro, and ALG responders are not necessarily among these. This is in keeping with different mechanisms of action of CyA and ALG and possibly with the existence of distinct pathogenetic pathways in SAA.

Adolescent↗
PubMed1991

Response of CFU-GM to increasing doses of rhGM-CSF in patients with aplastic anemia.

The aim of this study was to test whether large amounts of recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) are capable of promoting the growth of hemopoietic progenitors from patients with marrow failure. For this purpose 0.1, 100, 1000, 10,000 and 20,000 ng/ml of rhGM-CSF were added to 10(5) light-density (adherent cell-depleted) bone marrow cells from 9 normal controls and from 52 patients with aplastic anemia, 25 cases of which were transfusion-dependent (Tx-D) aplastic anemia (AA) and 27 of which were transfusion-independent (Tx-I) aplastic anemia (AA). A dose-dependent increase of granulocyte-macrophage colony-forming units (CFU-GM) was observed in healthy donors, from 81 to 247 colonies at 0.1 and 1000 ng/ml of rhGM-CSF, with a plateau thereafter. Tx-I AA patients showed the best increase of CFU-GM in response to colony-stimulating factor, from 0.1 to 32.7 mean colonies at 0.1 and 20,000 ng/ml of rhGM-CSF, and the increment was greater when compared to controls. The ratio of CFU-GM grown from these patients and controls was 1:810 at 0.1 ng/ml of rhGM-CSF and 1:7.9 at 20,000 ng/ml. Eleven patients were studied at diagnosis; there was no in vitro response to rhGM-CSF (0 and 1.8 mean colonies/10(5) cells at 0.1 and 10,000 ng/ml). Overall, Tx-D AA patients showed minimal increments of CFU-GM growth at very high doses of rhGM-CSF. Two suggestions come from this study: 1) maturation of CFU-GM from recovering AA patients appears to require larger doses of GM-CSF than normal controls, and 2) very high doses of rhGM-CSF have little or no effect on CFU-GM growth in AA patients. This may be relevant for clinical studies designed to improve hemopoiesis in patients with marrow failure.

Adult↗
PubMed1991

In vitro response of T cells from aplastic anemia patients to antilymphocyte globulin and phytohemagglutinin: colony-stimulating activity and lymphokine production.

The aim of the present study was to compare the response of bone marrow (BM) lymphocytes from patients with aplastic anemia (AA) or normal controls to increasing doses of antilymphocyte globulin (ALG) or phytohemagglutinin (PHA). For this purpose BM T-enriched cells from 11 AA patients and 9 normal individuals were incubated with ALG (0-1000 micrograms/ml) or PHA (0%-10%) for 1 day, and the supernatants were tested for suppression/enhancement of granulocyte-macrophage colony-forming unit (CFU-GM) growth and for release of granulocyte-macrophage colony-stimulating factor (GM-CSF), tumor necrosis factor-alpha (TNF-alpha), and interferon-gamma (IFN-gamma) assayed with the enzyme-amplified sensitivity immunoassay (EASI). The production of colony-stimulating activity (CSA) by T cells primed with ALG and tested in the absence of exogenous GM-CSF correlated with the dose of ALG in priming cultures up to 14% EG (100% EG = CFU-GM growth with 30 ng/ml of GM-CSF). The amount of GM-CSF in the supernatants paralleled their capacity to sustain CFU-GM growth (up to 3.5 ng/ml of GM-CSF). Production of CSA or GM-CSF from T cells primed with PHA was significantly lower. Supernatants of PHA-primed T cells, when added to normal BM cells in the presence of exogenous GM-CSF, produced a dose-dependent inhibition of CFU-GM growth (down to 13% +/- 10% EG). The same supernatants contained detectable amounts of IFN-gamma and TNF-alpha (21 +/- 6.7 IU/ml and 4.6 +/- 2.9 ng/ml, respectively). IFN-gamma production from severe AA (SAA) T cells in response to PHA was significantly superior to the IFN-gamma production from normal T cells (21 +/- 6.7 IU/ml vs 9.5 +/- 7.1 IU/ml, p = 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Mapping of the gene TCF2 coding for the transcription factor LFB3 to human chromosome 17 by polymerase chain reaction.

A human clone corresponding to the gene for the DNA-binding factor LFB3, a protein highly homologous to the liver-specific transcription factor LFB1, has been isolated and partially sequenced. This gene is designated TCF2. Oligonucleotide primers have been designed for LFB3 and used to amplify specifically the human gene in human/rodent somatic cell hybrids using the polymerase chain reaction. By this means, the human LFB3 gene has been mapped to the long arm of chromosome 17, between the centromere and the APL breakpoint.

Animals↗
PubMed1990

Transcription of the promoter of the rat NF-1 gene depends on the integrity of an Sp1 recognition site.

The transcription start site and promoter of the rat gene coding for the transcription factor NF-1 have been identified. The NF-1 promoter was fused to the chloramphenicol acetyltransferase-coding sequence, and the resulting plasmid was transcriptionally active in the HepG2 cell line. Footprinting and gel retardation analysis indicated that the transcription factor Sp1 binds to the NF-1 promoter. Mutants in the Sp1-binding site displayed a strong reduction in transcriptional activity.

Animals↗
PubMed1990

Mixed chimerism after allogeneic marrow transplantation for leukaemia: correlation with dose of total body irradiation and graft-versus-host disease.

Fifty-four patients allografted for leukaemia were evaluated at various intervals after bone marrow transplantation for the presence of host haemopoiesis using red blood cell and cytogenetic markers. Out of 40 patients in remission, 10 showed functional host and donor haemopoiesis (mixed chimerism), whereas in the other 30 (complete chimerism) host haemopoiesis was never detected. Seven of the 14 evaluable patients who relapsed showed the reappearance of host haemopoiesis at the time of relapse. Analysis of the dose of total body irradiation (TBI) indicated that patients who achieved mixed chimerism, whether or not they relapsed, had received significantly lower doses than those with complete chimerism. However, some patients with complete chimerism had received a TBI dose equivalent to the dose received by those with mixed chimerism, suggesting that the TBI dose is not the only factor determining the reappearance of host haemopoiesis. The data on chimerism and relapse suggest that there is heterogeneity in radiosensitivity between normal marrow cells and leukaemic cells, and also within the different types of leukaemia. The incidence/severity of acute and chronic graft-versus-host-disease (GVHD) was significantly higher in patients with complete chimerism than in mixed chimeras, suggesting that mixed chimerism may play a role in the development of tolerance. Alternatively the absence of GVHD (i.e. tolerance) may be responsible for the persistence of host haemopoietic cells.

Bone Marrow Transplantation↗
PubMed1989

Ligand-induced phosphorylation of a murine tumor surface protein (TSP-180) associated with metastatic phenotype.

A tumor surface protein (TSP-180) has been identified on murine lung carcinomas using two monoclonal antibodies (MoAbs) (135-13C and 346-11A). Quantitative analysis of TSP-180 on 3LL variants maintained either in vitro or in vivo indicates that TSP-180 is highly expressed in highly malignant metastatic cells. In reducing conditions, sodium dodecyl sulfate-polyacrylamide gel electrophoresis banding patterns of TSP-180 obtained with MoAb 135-13C from cell lysates of 3LL metastatic cells show three proteins migrating to Mr 204,000, 134,000, and 116,000. In the same experimental conditions MoAb 135-13C precipitates from low metastasizing ones only one band, corresponding to the lower molecular weight (Mr 116,000). All bands of TSP-180 observed in 3LL variants are labeled by lactoperoxidase-catalyzed radioiodination of viable cells, incorporate 32PO4, and contain carbohydrates, as judged by binding to wheat germ agglutinin. These results indicate that all proteins have external exposure on the cell surface and that at least some of TSP-180 proteins could be differentially regulated in different tumor cells (highly metastatic versus low metastatic). Sodium dodecyl sulfate-polyacrylamide gel electrophoresis banding patterns and immunoblots obtained from cell lysates of 3LL variants by using a monoclonal antibody to phosphotyrosine (IG-2) indicate that this MoAb recognizes proteins migrating with molecular weights identical to those reported for TSP-180. Moreover, the immunoblots of solubilized immunocomplex, obtained from cell lysates of 3LL variants by using MoAb 135-13C, demonstrate that MoAb IG-2 specifically reacts with TSP-180 proteins. Experiments undertaken in order to assess if some or all of TSP-180 proteins have tyrosine kinase activity demonstrate that MoAb 135-13C binding to the cell surface induces specific phosphorylation of the Mr 204,000 protein of TSP-180. Phosphoaminoacid analysis of the ligand-induced phosphorylated protein (pp204) demonstrates that this protein is phosphorylated at serine and tyrosine. Results reported lead us to hypothesize that TSP-180 is involved in growth-regulation mechanisms and that its high expression on cells with more malignant phenotype could be responsible for a proliferative advantage of such tumor clones.

Amino Acids↗