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Biomedical subjects

P Tripputi

Publications and source records attributed to P Tripputi.

At least 19 recordsLinked to original sources
PubMed2001

Chromosome 7 monosomy and deletions in myeloproliferative diseases.

We studied deletion and monosomy of chromosome 7 in 150 patients with myeloproliferative diseases. We found 8/150 patients with monosomy 7 by cytogenetics and 4/150 with deletions of the long arm of chromosome 7 by restriction fragment length polymorphism (RFLP) analysis performed with Southern and polymerase chain reaction. To overcome limitation of RFLP analysis, we restricted loss of heterozygosity study with microsatellites to 45 patients, observing deletion 7q31.1 in 7/45 patients. In all patients with molecular alterations the deletion was observed only in myeloid cells, while the monosomy was detected in both myeloid precursor and lymphocytes. This finding suggests a CD34-totipotent stem cell origin for the monosomy and a colony forming unit - granulocyte, erythrocyte, monocyte, megakaryocytes (CFU-GEMM) stem cell origin for the deletions.

Chromosomes, Human, Pair 7↗
PubMed2000

A common T/C polymorphism in the promoter region of the beta T-cell receptor gene.

Polymorphisms in the T-cell receptor genes can provide important information for the study of the immune response system, particularly for autoimmune diseases. This report characterizes a common T to C polymorphism in the promoter of the beta 2 constant chain of the T-cell receptor, which abolishes a recognition site for BglII restriction endonuclease.

Adult↗
PubMed1994

[Multiple myeloma. Role of prognostic factors and staging in a therapeutic program].

Patients affected with multiple myeloma constitute an heterogeneous population with very different clinical patterns, varying from asymptomatic to very compromised patients with severe and uncontrolled disease. Most common clinical and biological staging systems have been in use for many years. Recently new prognostic factors have been identified; among them, serum levels of beta-2 microglobulin, C-reactive protein and interleukin-6 employed with already known parameters have been useful in the new staging system, permitting a more focalized therapy. As today is not yet possible to define the best treatment schedule, as the most common treatments are incapable to eradicate myeloma neoplastic clone even in responsive patients. Nevertheless extensive use of biologic response modifiers in the last years, as alpha interferon, have added new powerful and hopeful therapeutic tools even if the results need to be confirmed in future trials. It is important to remind the primary role of bone marrow transplantation associated with high dose polychemotherapy even if just a minority of patients is eligible for this therapeutic chance.

Forecasting↗
PubMed1993

Susceptibility of human-mouse T cell hybrids to HIV-productive infection.

Interspecies human x mouse cell hybrids were used to investigate the genetic basis of human permissivity to HTLV-IIIB infection. T cell hybrids between the mouse BW 51.47 T lymphoma line and normal, PHA-IL-2 activated, human peripheral mononuclear cells (PBMCs) were generated. These hybrids preferentially segregated human chromosomes, as assessed by phenotype and karyotype analysis. Viral integration occurred only in those hybrids expressing CD4+ at the cell surface. However, infectious progeny production was demonstrated only in two of the three CD4+ hybrids tested. By segregation analysis, we could correlate the absence of human chromosomes 1, 3, and 9 with the lack of infectious viral progeny.

Animals↗
PubMed1993

Detection of human chromosomes in somatic cell hybrids by PCR analysis.

The detection of human chromosomes in somatic cell hybrids is usually made by chromosomal analysis, Southern blot analysis with human probes, and starch-gel electrophoresis of isoenzymes. We describe here a new, quick, and very efficient method to detect human chromosomes in somatic cell hybrids between human and rodent (rat and mouse) cells. The method is based on the polymerase chain reaction to promote amplification of human DNA, using primers derived from localized genes or DNA fragments from each human chromosome.

Animals↗
PubMed1992

Assignment of the urokinase-type plasminogen activator receptor gene (PLAUR) to chromosome 19q13.1-q13.2.

The urokinase-type plasminogen activator receptor (uPAR) is a key molecule in the regulation of cell-surface plasminogen activation and, as such, plays an important role in many normal as well as pathological processes. We applied a cDNA probe from the corresponding gene (PLAUR) in a location analysis using a panel of human/rodent cell hybrids and in a multipoint linkage analysis of 40 CEPH families. These two independent studies both found PLAUR to be located on chromosome 19. The cell hybrid study suggested that PLAUR is located at chromosome 19q13-qter, and the multipoint analysis indicated that PLAUR is located at chromosome 19q13.1-q13.2 and surrounded by DNA markers in the following way (with distances given in recombination fractions): D19S27-.11-CYP2A-.06-PLAUR-.03-D19S8-.04-APOC 2-.24-PRKCG. Further, a ligand-binding study performed on cell hybrids verified the species specificity of the uPAR and confirmed the chromosome assignment.

Animals↗
PubMed1990

A rapid method for monitoring DNA labelling reactions with haptens.

A rapid and simple method for evaluating the efficiency of DNA labelling reactions with haptens is described. The method, called the Flow-Through Hapten-DNA Assay (FT-HDA), relies on binding of anti-hapten antibodies/alkaline phosphatase conjugates to hapten-DNA, immobilized on disposable capillary absorbent filters, and visual detection of blue-grey coloured spots appearing on the filter after chromogenic reaction with enzyme substrates. FT-HDA of hapten-DNA is markedly faster and simpler than conventional diffusion assays on membranes.

Alkaline Phosphatase↗
PubMed1990

Increased amplification of abl oncogene in K562 cells after passage in nude mice.

Human chronic myelogenous leukemic cells K562, carrying the Ph+ chromosome and an amplified abl oncogene, were injected subcutaneously in nude mice and gave rise to myeloid solid tumors after 4-5 weeks. DNA from the cells of the solid tumors was analyzed by Southern blotting using v-abl and actin probes. Increased amplification of human abl oncogene, but not of the actin gene was found. This suggests a clonal selection of a cell population with more copies of the abl oncogene. This in vivo selection appears to increase the tumorigenicity of K562 cells since, in a second transplantation in nude mice, we observed a shorter period of latency before tumor appearance (3 weeks) when compared to the initial transplantation.

Actins↗
PubMed1988

Two mechanisms for the extinction of gene expression in hybrid cells.

When two different mammalian cell types are fused to generate a stable hybrid cell line, genes that are active in only one of the parents are frequently shut off, a phenomenon called extinction. In this study two distinct, complementary mechanisms for such extinction of growth hormone gene expression were identified. In hybrids formed by fusing fibroblasts to pituitary cells, pituitary-specific proteins that bind to the growth hormone promoter were absent. In addition, a negative regulatory element located near the rat growth hormone promoter was specifically activated.

Acetyltransferases↗
PubMed1986

Human histone genes map to multiple chromosomes.

Histone genes were mapped to at least three human chromosomes by Southern blot analysis of DNAs from a series of mouse-human somatic cell hybrids (using 32P-labeled cloned human histone DNA as probes). Chromosome assignment was confirmed by in situ hybridization of radiolabeled histone gene probes (3H-labeled) to metaphase chromosomes. One human histone gene cluster (lambda HHG41) containing an H3 and H4 gene resides only on chromosome 1, whereas other clusters containing core (H3, H4, H2A, and H2B) alone (lambda HHG17) or core together with H1 histone genes (lambda HHG415) have been assigned to chromosomes 1, 6, and 12. These results suggest that the multigene family of histone coding sequences that reside in a series of clusters may be derived from a single cluster containing one each of the genes for the five principal classes of histone proteins. During the course of evolution, a set of events, probably involving reduplication, sequence modification, and recombination, resulted in the present pattern of human histone gene distribution among several chromosomes.

Biological Evolution↗
PubMed1986

Tissue-type plasminogen activator gene is on chromosome 8.

Tissue plasminogen activator is one of the two plasminogen activators, both serine proteases, that catalyze the conversion of inactive plasminogen to plasmin, which then degrades the fibrin network of blood clots. By combining somatic cell genetics, in situ hybridization, and Southern blot hybridization, we localized the human tissue plasminogen activator gene to the pericentromeric region of chromosome 8.

Animals↗
PubMed1985

Specific immunoglobulin production and enhanced tumorigenicity following ascites growth of human hybridomas.

Human X human hybridomas constructed with the B6 lymphoblastoid clone, which produces antitetanus toxoid (TT) antibody, and the lymphoblastoid cell line KR-4 or human hybrid myeloma KR-12, were adapted to growth as ascites in pristane-treated BALB/c nude mice by a single prior passage as a solid subcutaneous (s.c.) tumor in irradiated nude mice followed by in vitro culture. Both B6 X KR-4 and B6 X KR-12 hybrids produced anti-TT antibody and phenotypically resembled the lymphoblastoid KR-4, or the hybrid myeloma KR-12 parent, respectively. Growth as ascites increased the tumorigenicity of both hybrids in nude mice as measured by tumor incidence and rate of tumor growth. The observed increase in tumorigenicity of these hybrid cells after ascites growth was associated with a substantial loss of chromosomes. Passage of the B6 X KR-4 lymphoblastoid hybrid resulted in several reversible morphological changes characteristic of myeloma cells. These changes correlated with increased human Ig production. These observations provide a system for greatly amplifying human monoclonal antibody production.

Animals↗
PubMed1985

Human urokinase gene is located on the long arm of chromosome 10.

Urokinase is one of the two plasminogen activators that catalyze the conversion of inactive plasminogen to plasmin. By combining somatic cell genetics, in situ hybridization, and Southern hybridization, we localized the human urokinase gene on the distal third of the long arm (q24-qter) of chromosome 10.

Chromosome Mapping↗
PubMed1984

A major human histone gene cluster on the long arm of chromosome 1.

A human histone gene cluster was assigned to chromosome 1 by Southern blot analysis of DNA's from a series of mouse-human somatic cell hybrids with 32P-labeled cloned human H4 and H3 histone DNA as probes. Localization of this histone gene cluster on the long arm of chromosome 1 was confirmed by in situ hybridization of this DNA probe to metaphase chromosomes.

Animals↗
PubMed1984

A human c-erbA oncogene homologue is closely proximal to the chromosome 17 breakpoint in acute promyelocytic leukemia.

A human cDNA library was screened for sequences homologous to the erbA gene of avian erythroblastosis virus (AEV). One such clone, cHerbA-1, was used to map the chromosomal location of highly homologous human sequences that were found to be present on chromosome 17 as judged by Southern blot screening of a panel of mouse-human hybrid cell lines segregating human chromosomes. cHerbA-1 was hybridized in situ to metaphase chromosomes from a normal male subject and from a female patient with an acute promyelocytic leukemia (APL) having the typical t(15;17) translocation. The results localized the cellular c-erbA sequences on chromosome 17 to the q21-q24 region of normal chromosomes and indicated that the c-erbA sequences remained on the 17q- chromosome in the APL cells, suggesting that they could be assigned to the 17(q21-q22) region. For additional data, we hybridized human neoplastic cells derived from a poorly differentiated acute leukemia carrying a t(17;21) translocation with thymidine kinase (TK)-deficient LMTK- mouse cells. A resulting hybrid, containing only the 21q+ chromosome, did not have human c-erbA sequences. Since the breakpoint on 17q in this translocation was similar to that in the APL t(15;17) translocation, this supported the assignment of c-erbA to the q21-q22 region of chromosome 17. The apparent close proximity of the c-erbA sequences to the chromosomal breakpoints in these two leukemias suggests a possible role for this oncogene homologue in the development of these neoplasms.

Animals↗
PubMed1984

A human hybrid myeloma for production of human monoclonal antibodies.

We produced somatic cell hybrids between human myeloma cells and a lymphoblastoid cell line that is hypoxanthine phosphoribosyl transferase-deficient and ouabain-resistant. These hybrids were phenotypically similar to the human myeloma parental cells and grew as well as the human lymphoblastoid parental cells. After counterselection in 6-thioguanine, mutants that were 6-thioguanine-and ouabain-resistant were obtained, one of which was used as a fusion partner with lymphoblastoid B cells that produce anti-tetanus toxoid (TT) antibodies. These hybrids secreted human anti-TT monoclonal antibodies in much larger amounts than the parental lymphoblastoid cells, and were stable for a period of over 10 mo until the present time. Thus, by hybridizing plasmacytomas with lymphoblastoid cells, we constructed a fusion partner that secretes large amounts of immunoglobulin (Ig), grows at a fast rate, has a high fusion frequency, and supports the production of monoclonal antibodies over long periods of time. Moreover, anti-TT antibody-producing hybrids have been grown as solid tumors in irradiated BALB/c nude mice and then adopted to ascites growth, producing 1 to 8 mg of human immunoglobulin per 1 ml of ascites fluid.

Animals↗