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Biomedical subjects

L Trakhtenbrot

Publications and source records attributed to L Trakhtenbrot.

26 records · Page 2Linked to original sources
PubMed1995

Demonstration of thymopoietin transcripts in different hematopoietic cell lines.

We have cloned and characterized the human thymopoietin (TP) coding region and studied the mRNA expression of this gene in different hematopoietic cell lines. The 150-bp PCR fragment that encodes the 49-amino-acid human TP peptide was isolated from genomic placental DNA. Its colinearity with the cDNA sequence suggests lack of introns within the coding region. TP mRNA expression was demonstrated in lymphocytes from all the differentiation stages investigated, as well as in a myeloid cell line (K-562). These findings suggest a further expansion of the proposed TP functions.

Amino Acid Sequence↗
PubMed1993

Neural expression and chromosomal mapping of Neu differentiation factor to 8p12-p21.

Neu differentiation factor (NDF/heregulin) is a 44-kDa glycoprotein that interacts with the Neu/ErbB-2 receptor tyrosine kinase to increase its phosphorylation on tyrosine residues. In vitro NDF promotes differentiation of certain mammary tumor cell lines to milk-producing cells. As a first step toward understanding the physiological role of NDF, we performed in situ hybridization analyses to determine mRNA distribution in the mouse embryo and to map the gene to human karyotypes. In 14.5-day-postcoitum mouse embryos, NDF expression is confined predominantly to the central and peripheral nervous system, including the neuroepithelium that lines the lateral ventricles of the brain, the ventral horn of the spinal cord, and the intestinal as well as dorsal root ganglia. Other tissues that contain NDF transcripts are the adrenal gland, liver, and distinct cell layers of the dermis and germinal ridge. In situ hybridization of a 3H-labeled probe to human metaphase spreads localized the NDF gene to the short arm of chromosome 8 at bands p12-p21.

Animals↗
PubMed1992

Absence of negative growth regulation in three new murine radiation-induced myeloid leukemia cell lines with deletion of chromosome 2.

Murine radiation-induced acute myeloid leukemia (RI-AML) may be considered as the experimental counterpart of human secondary leukemia. Three new myelomonocytic cell lines derived from RI-AML and carrying a partially deleted chromosome 2 are described. The RI-AML cells responded with increased proliferation after being incubated with the hemopoietic growth factors rG-CSF, rGM-CSF and IL-3. Increased proliferation of the same extent without any effect in differentiation, was also demonstrated in the RI-AML cells after incubation with IL-6 and with mouse lung conditioned medium (CM) and Krebs ascites tumor cells CM which induce differentiation in normal and most leukemic myeloid cells. Down-regulation of the c-myc gene and induction of (2'-5') oligo-adenylate synthetase (reflecting autocrine interferon secretion), two essential mechanisms operating during arrest of growth and concomitant differentiation, were demonstrated to be absent in RI-AML cells. In contrast, the M1 cells responded to the above differentiating factors with growth arrest and differentiation and with appropriate c-myc down-regulation and synthetase induction. The genetic basis for the distinct RI-AML cells' behavior may be connected with the loss or structural and/or functional abnormalities of DNA sequences located in the deleted part of chromosome 2 or in the respective allele. The presently described new RI-AML cell lines may be used for studies concerning myeloid leukemogenesis in general and secondary leukemia in particular.

2',5'-Oligoadenylate Synthetase↗
PubMed1990

Chromosomal mapping of the murine c-abl proto-oncogene by in situ hybridization.

Deletion and rearrangement of chromosome 2 were shown to be major cytogenetic characteristics of radiation-induced murine myeloid leukemias. Analysis of the localization of the murine protooncogene c-abl, previously assigned by Goff et al. to chromosome 2, was done using the in situ hybridization method. The c-abl was located close to the centromere, within bands 2A-2B. This site does not correspond to the common characteristic deleted segments (2C-2D) predominantly observed in radiation induced murine myeloid leukemias.

Animals↗
PubMed1989

Cellular and molecular characteristics of an immortalized ataxia-telangiectasia (group AB) cell line.

Ataxia-telangiectasia (A-T) is a multisystem hereditary disease featuring neurodegeneration, immunodeficiency, extreme cancer proneness, chromosomal instability, and radiosensitivity. A-T is found in many ethnic groups, and is genetically heterogeneous: four complementation groups have been identified in A-T so far. Attempts to isolate the A-T gene are based in part on gene transfer experiments, using permanent A-T fibroblast lines, obtained by transformation with SV40. "Immortalization" of A-T primary diploid fibroblasts using SV40 is difficult, possibly because of the chromosomal instability of these cells. The number of currently available permanent A-T fibroblast lines is small, and not all of them have been assigned to specific complementation groups. Using the assay of X-ray induced inhibition of DNA synthesis, we have assigned the A-T strain AT22IJE to complementation group AB. Origin-defective SV40 was used to transfect these cells, and one transformant (AT22IJE-T), which survived crisis, was found to have the typical characteristics of permanent cell lines obtained in this way. "In-gel renaturation" analysis did not show any DNA amplification of high degree in AT22IJE-T. Cytogenetic analysis showed considerable chromosomal instability in the new cell line, and medium conditioned by these cells contained the clastogenic activity which is characteristic of the parental strain as well. Other parameters of the "cellular A-T phenotype" have also been retained in the immortalized cells: hypersensitivity to the lethal effects of X-rays and neocarzinostatin, as well as "radioresistant" DNA synthesis. However, the sensitivity of AT22IJE-T to both DNA-damaging agents is less pronounced than that of the parental cells. The capacity of the cells for uptake of foreign DNA was tested by introducing into them the plasmid pRSVneo, using three different transfection methods. Satisfactory frequency of G418-resistant transfectants (0.66%) was achieved using a protocol recently published by Chen and Okayama (Mol. Cell Biol., 7: 2745-2752, 1987), which was found to be superior to the traditional calcium phosphate transfection method and to the polybrene-based method.

Ataxia Telangiectasia↗
PubMed1988

Deletion of chromosome 2 is an early event in the development of radiation-induced myeloid leukemia in SJL/J mice.

In this study we have analyzed the chromosomal changes in the preleukemic phase in SJL/J mice treated with radiation and acute myeloid leukemias (AMLs) induced by radiation alone or with additional corticosteroid treatment. SJL/J mice exposed to 300 rad whole body irradiation developed a low incidence of AML (20-25%) that could be markedly increased (to 50-70%) by additional coleukemogenic treatment with corticosteroids. Partial deletion in one chromosome 2 was found in 100% of bone marrow and spleen cells of leukemic animals in both treatment modalities, whereas the age-matched controls exhibited a normal karyotype. Five types of deletion were observed according to site and size, but region D through G was the common missing part in all five types of chromosome 2 deletion. The occurrence of chromosome 2 deletion was also tested among bone marrow cells removed from 17 mice, 4 months after exposure to 300 rad whole body irradiation, long before the time when AML development is expected. About 80% of the mice tested had different levels of deleted chromosome 2 among their bone marrow population. Cytological and histological examination of bone marrow and spleen of most tested animals showed a normal hematologic picture. These results suggest that the marker chromosome is related to the process of radiation-induced initiation of AML in SJL/J mice.

Animals↗
PubMed1987

Cytogenetic studies on B-cell leukemias of AKR origin.

The karyotype of B-cell leukemias of AKR origin was studied by G-banding. In contrast to previous observations indicating trisomy of chromosome 15 in spontaneous and chemically-induced B-cell leukemias, 11 out of 15 tumors analyzed had normal diploid karyotypes. Four tumors with the modal number 39-41 had different chromosome markers specific for each tumor. The possible correlation between non-random chromosomal changes and the target cell involved in the initial transformation in AKR leukemogenesis is discussed.

Animals↗