RESUMO
The cell line PTC-1113A was established from a metastasizing recurrent papillary thyroid cancer. The cell line was growing as monolayer and showed a complex karyotype with chromosome numbers ranging from 30 to 140/metaphase. A proportion of metaphases contained double minutes and/or pulverized chromosomes. Extrachromosomal DNA seemed to originate from a B-group chromosome. A chromosome 4 painting probe hybridized to extrachromosomal material, representing double minutes (dmin) and possibly minutes. In addition, fluorescence in situ hybridization (FISH) with the chromosome 4 library detected a translocation chromosome and a pulverized chromosome originating from chromosome 4. PTC-1113A is, to our knowledge, the single papillary thyroid cancer cell line demonstrating evidence of gene amplification.
Assuntos
Carcinoma Papilar/patologia , Amplificação de Genes , Neoplasias da Glândula Tireoide/patologia , Idoso , Carcinoma Papilar/genética , Cromossomos Humanos/ultraestrutura , Humanos , Hibridização in Situ Fluorescente , Masculino , Metástase Neoplásica , Neoplasias da Glândula Tireoide/genética , Células Tumorais CultivadasRESUMO
Adrenocortical tumors are detected with increasing frequency, but symptomatic cases with excessive hormone production are rare. We investigated cytogenetically one benign aldosterone-producing tumor (Conn Syndrome)(case 1) and one malignant cortisol-producing tumor (Cushing Syndrome)(case 2). Radioimmunoassay of cell culture supernatant of case 2 detected cortisol secretion during 2 months in culture. Flow cytometry of spill-out cells from case 2 showed a bimodal pattern (DNA Index 1.0, 1.4). Case 1 revealed a marker chromosome in 4/25 cells analyzed; the marker was a long acrocentric partially derived from chromosome 2,der(2q). In case 2, a cytogenetic harvest was achieved after prolonged culture time (6 weeks) and a marker chromosome, add(11)(p15), was detected in 16/22 cells. A breakpoint of 11p13, as well as loss of heterozygosity of alleles on 11p15, has been reported in the literature for other malignant adrenocortical cancers.
Assuntos
Neoplasias do Córtex Suprarrenal/genética , Aberrações Cromossômicas , Cromossomos Humanos Par 11 , Síndrome de Cushing/genética , Hiperaldosteronismo/genética , Síndromes Endócrinas Paraneoplásicas/genética , Neoplasias do Córtex Suprarrenal/metabolismo , Neoplasias do Córtex Suprarrenal/patologia , Idoso , Feminino , Humanos , Cariotipagem , Pessoa de Meia-IdadeRESUMO
Results of cell culture and cytogenetic analysis (standard and fluorescent in situ hybridization, FISH) of two sporadic gastrinomas are reported. Maintenance of hormonal activity was assessed by detection of gastrin levels during the first 3 months in culture. Case 1 showed clonal aberrations consisting of two marker chromosomes: marker 1 is a large metacentric chromosome and marker 2 is a small acrocentric chromosome. Case 2 showed a constitutional polymorphism with chromosome 15p+ and a clone in the tumor cell culture with trisomy for chromosome 3. To our knowledge, this is the first cytogenetic report of sporadic gastrinomas (Zollinger-Ellison syndrome).
Assuntos
Aberrações Cromossômicas/genética , Neoplasias Duodenais/genética , Gastrinoma/genética , Idoso , Neoplasias Duodenais/metabolismo , Neoplasias Duodenais/patologia , Feminino , Gastrinoma/metabolismo , Gastrinoma/patologia , Gastrinas/metabolismo , Humanos , Hibridização in Situ Fluorescente , Cariotipagem , Masculino , Pessoa de Meia-IdadeAssuntos
Obstrução das Vias Respiratórias/etiologia , Bócio Nodular/complicações , Doença Aguda , Idoso , Idoso de 80 Anos ou mais , Obstrução das Vias Respiratórias/diagnóstico por imagem , Obstrução das Vias Respiratórias/cirurgia , Feminino , Bócio Nodular/diagnóstico por imagem , Bócio Nodular/cirurgia , Hemorragia/complicações , Hemorragia/diagnóstico por imagem , Hemorragia/cirurgia , Humanos , RadiografiaRESUMO
To assess the contribution of the renin-angiotensin-aldosterone system and renal hemodynamics to acute renal sodium handling in essential hypertension we studied 21 subjects who had essential hypertension (16 with normal renin, 5 with low renin) and 9 normal subjects. All were in balance on a 10 mEq sodium intake before receiving a small sodium load, 60 mEq intravenously over 1 hour. Hypertensive subjects with low renin showed the anticipated exaggerated natriuresis, which was transient and occurred without a rise in blood pressure. Natriuresis in hypertensive subjects with normal renin was either normal or blunted; delayed sodium excretion occurred in a subset, along with delayed suppression of the renin-angiotensin-aldosterone system by the saline load. Neither renal plasma flow nor glomerular filtration rate changed during the saline load. After 72 hours of converting enzyme inhibition with enalapril, renal plasma flow increased substantially more in the subjects with a blunted renin response and their natriuretic response to the sodium load returned to normal. These results indicate that when prior sodium intake is controlled, large sodium loads are avoided, and low renin hypertension is removed as a confounding variable, blunted rather than exaggerated natriuresis is the common feature of essential hypertension. This abnormality is reversed by angiotensin converting enzyme inhibition, perhaps because of converting enzyme inhibition-induced renal vasodilatation.
