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F Gilbert

Publications and source records attributed to F Gilbert.

At least 109 records · Page 6Linked to original sources
PubMed1986

Enhanced expression of the N-myc gene in Wilms' tumors.

Activation of myc-family oncogenes has been implicated in the genesis of a variety of neoplasms. In addition, these genes exhibit specific patterns of expression during murine development. We now report that N- and c-myc are differentially expressed in normal developing human renal tissues and in Wilms' tumor, a neoplasm which derives from primitive kidney cells. Twelve of 13 Wilms' tumors tested exhibited greatly enhanced levels of expression which occurred in the absence of gene amplification. We also detected N-myc expression in other primitive neoplasms including medulloblastoma and hepatoblastoma. Our observations suggest that N-myc expression is not limited to neuroectodermal tumors as was previously thought, but is a marker for several neoplasms that derive from primitive cell precursors. Finally, high level expression of N-myc was associated with markedly diminished levels of c-myc, suggesting that enhanced expression of N-myc gene might lead to down-regulation of c-myc.

Fetus↗
PubMed1985

A cytogenetic study of embryonal rhabdomyosarcoma.

In the cytogenetic analysis of an embryonal rhabdomyosarcoma after short-term culture, individual cells were found to contain multiple copies of chromosomes #2, #6, #8, #12, #13, #18, #20 and #21, and del(1)(:p21----qter). The tumor was hypotriploid (mode, 56 chromosomes). The relationship between these findings and published reports of karyotypes from rhabdomyosarcoma is discussed.

Aneuploidy↗
PubMed1985

Familial hypocalciuric hypercalcemia: description of a new kindred with emphasis on its difference from primary hyperparathyroidism.

In order to better understand the difference between familial hypocalciuric hypercalcemia (FHH) and primary hyperparathyroidism (PHP), 4 adults with this disease (FHH(+], from the same kindred, and spanning 2 generations, were compared with 6 patients with PHP, 10 normal controls (N) and 3 unaffected members of the same kindred (FHH(-]. Clinically speaking, the FHH(+) patients were asymptomatic while those with PHP had recurring renal stones. Various phosphocalcic balance elements were measured in blood and urine, in a fasting state, following oral loading of 1 g calcium, as well as in 24-hour urine specimens. Serum calcium levels were slightly higher (11.90 +/- .14 vs 11.37 +/- .24 mg/dl; p less than .05), in patients with FHH(+), but serum phosphorus (2.47 +/- .38 vs 2.88 +/- .40 mg/dl), serum parathyroid hormone (301 +/- 147 vs 291 +/- 224 pg/ml) and serum 1,25(OH)2D (52.8 +/- 6.7 vs 55.0 +/- 12.0 pg/ml) values were similar to those observed in patients with PHP. Urinary calcium present in FHH(+), while fasting (.064 +/- .043 mg/100 ml G.F.), after the calcium loading (.150 +/- .071) and in the 24-hour specimen (.089 +/- .016), was below the 95% confidence limit of values obtained in patients with PHP (.225 +/- .026, p less than .001; .413 +/- .066, p less than .001; 314 +/- .080, p less than .001), but similar to those obtained in N and FHH(-).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMed1984

Solid tumors of children: chromosome abnormalities and the development of cancer.

Chromosome abnormalities in five solid tumors which occur predominantly in children and young adults are described. Four of the tumors are associated with rearrangements involving particular chromosome segments: deletion 13q14 in retinoblastoma, deletion 11p13 in Wilms' tumor, deletions/rearrangements of 1p (distal to band 1p31) in neuroblastoma, and translocation 22/autosome in Ewing sarcoma. Though aneuploidy for a number of chromosomes may occur in the fifth tumor, rhabdomyosarcoma, it has yet to be associated with a consistent marker arrangement. A general classification of chromosome abnormalities in cancer is presented. Possible roles for the gene changes produced by each class of chromosome abnormality in the development of cancer are discussed.

Child↗
PubMed1984

The 13p HSR in a human neuroblastoma cell line does not contain rRNA genes.

We have studied a human neuroblastoma cell line containing a homogeneously staining region (HSR) on the short (p) arm of chromosome #13. The HSRs are believed to represent sites of gene amplification, containing multiple copies of one or a small number of genes. The 18S and 28S ribosomal RNA genes are the only structural genes so far assigned to the p arms of the human acrocentric chromosomes, which include number #13. Using two recombinant DNA probes specific for sequences in the 18S/28S ribosomal RNA (rRNA) gene complex for in situ hybridization, we have been able to establish that the 13pHSR in this line does not contain rRNA genes.

Cell Line↗
PubMed1984

Human neuroblastomas and abnormalities of chromosomes 1 and 17.

Structural rearrangements of chromosome 1p have been reported previously as a frequent finding in human neuroblastomas. In a review of karyotypes from 35 neuroblastomas (including 29 published cases and 6 unpublished tumors and cell lines), it was found that, in addition to the abnormalities of chromosome 1p (found in approximately 70% of cases), abnormalities involving only 2 other chromosome segments occurred with significant frequency (in 20% or more of cases) in this cancer. These abnormalities involved trisomies for the long arms of chromosomes 1 and 17. In addition, two novel cytogenetic aberrations, homogeneously staining regions and double minutes, were identified in two-thirds of the cases. It is postulated that the gene change(s) produced by the abnormalities of chromosome 1p in neuroblastoma play a primary role in the development of this cancer. The gene changes produced by the abnormalities of chromosomes 1q and 17q and by the homogeneously staining regions and double minutes are presumed to contribute to tumor progression.

Cell Line↗
PubMed1984

Change in glycosylation of membrane glycoproteins after transfection of NIH 3T3 with human tumor DNA.

Altered glycosylation of membrane glycoproteins was demonstrated in NIH 3T3 cells transformed by transfection with DNA from human neuroblastoma and bladder carcinoma cell lines. The oncogenes of these two cell lines have been identified as N-ras and c-H-ras-1, respectively. The fucose-labeled membrane glycopeptides of transfection-induced transformants had decreased binding to concanavalin A-Sepharose when compared in dual-isotope experiments to those from NIH 3T3 cells, whereas binding to lentil lectin-Sepharose and leukoagglutinating phytohemagglutinin-agarose was increased. Binding affinities to these immobilized lectins lead to the interpretation of the results as a decrease in biantennary glycopeptides with a simultaneous increase in tri- or tetraantennary glycopeptides. Sephadex G-50 profiles also indicated a size increase of the glycopeptides of the transformants. None of these changes was growth related. This altered glycosylation, representing a heretofore unreported effect of the onc genes, may be necessary for the transformed phenotype.

Animals↗
PubMed1983

Homogeneously staining regions and tumorigenicity.

A homogeneously staining region (HSR), a chromosome abnormality associated with gene amplification, was found to increase in length coincident with an enhancement in tumorigenicity when cells from a human retinoblastoma cell line were serially passaged in athymic (nu/nu) mice.

Animals↗
PubMed1983

Transposition and amplification of oncogene-related sequences in human neuroblastomas.

We have cloned a 2.0-kb EcoRI fragment of human genomic DNA (NB-19-21) which has homology to the v-myc oncogene but is distinct from the classical c-myc gene. This sequence is amplified from 25- to 700-fold in eight of nine tested human neuroblastoma cell lines which contain either homogeneously staining regions or double minutes (HSRs or DMs), the caryological manifestations of amplified genes. In the remaining line, the c-myc proto-oncogene is amplified approximately 30-fold. NB-19-21 hybridizes to a 3.2-kb cytoplasmic, poly(A)+ RNA species that is abundant only in lines in which the sequence is amplified. We propose that the gene encoding the NB-19-21-related RNA species may represent a new oncogene, which we call N-myc. NB-19-21 derives from chromosome 2; but in the five HSR-containing lines that have amplified this sequence, none has HSRs on chromosome 2. NB-19-21 is associated with DMs in a DM-containing line. A second, randomly cloned, amplified DNA segment from the HSR of one of the neuroblastoma lines is amplified in a subset of the lines in which NB-19-21 is amplified. In addition, this probe identifies a novel joint in the amplification unit of one line relative to that of the others. We suggest that, in the eight lines which have amplified NB-19-21, the amplification units are overlapping, but not identical, and that transposition of the common sequences may occur prior to amplification.

Base Sequence↗
PubMed1983

Clonal evolution in a human neuroblastoma.

Tumor samples, obtained from a single patient at two points in his illness, have enabled us to study clonal evolution in a neuroblastoma. Cells from the primary tumor demonstrated considerable heterogeneity in terms of chromosome number; cells from 4 subsequent metastases were all nearly diploid; and cells from a tumor produced in a mouse by the injection of cells from the primary tumor were hypotriploid in modal number. All of the tumor samples contained the same marker chromosome rearrangements, indicating their origin from a common precursor. Each of the cell lines analyzed (including those from the patient's metastases, those from the tumor in a mouse, and those from the primary tumor after 11 months in continuous culture) also contained different and distinguishing chromosome abnormalities. The differences in karyotype among these tumor samples and cell lines presumably reflect the different selection pressures at work in each instance.

Abdominal Neoplasms↗
PubMed1983

Homogeneously staining regions and double minutes in a human cell line: chromatin organization and DNA content.

Homogeneously staining regions (HSR) and double minutes, two novel chromosome abnormalities, are believed to represent sites of gene amplification. The basic organization of chromatin in an HSR in a human neuroblastoma cell line was shown, by electron microscopy, to be similar to that in a normal chromosome. Double minutes from another human neuroblastoma cell line were found, by dry mass determination, to contain an average of 1.41 X 10(-14) g DNA. This quantity corresponds to 6.38 X 10(3) kilobase DNA per double minute.

Cell Line↗