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At least 163 records · Page 9Linked to original sources
PubMed1992

Tumour suppressor gene products, proliferation, and differentiation markers in lung neuroendocrine neoplasms.

Typical carcinoid, atypical carcinoid, and small cell lung cancer (SCLC) fall within the spectrum of neuroendocrine lung neoplasms. This paper investigates the immunohistochemical expression of the products of tumour suppressor genes p53 and retinoblastoma (RB), together with proliferation (PCNA and Ki67) and neuroendocrine differentiation markers, in 14 typical carcinoids, ten atypical carcinoids, four borderline atypical carcinoid/SCLC, and 11 SCLC. We demonstrated that the phosphoprotein p53 and RB product can be immunolocalized on routine histological material. p53 protein was absent in all typical and atypical carcinoids, while it was abnormally expressed in eight SCLC and one borderline case. RB product was detected in all typical carcinoids and in two atypical carcinoids, while it was consistently absent in the other cases. PCNA-labelled cells were less than 4 per cent in typical carcinoids, about 40 per cent in atypical carcinoids, and over 70 per cent in SCLC. PCNA labelling index discriminates between typical and atypical carcinoids. Neuroendocrine differentiation was evaluated by a semi-quantitative method: a mean score value was obtained, which was high in typical carcinoids, intermediate in atypical carcinoids, and low in SCLC. Our data was obtained, which was high in typical carcinoids, intermediate in atypical carcinoids, and low in SCLC. Our data show that the decrease in neuroendocrine features from typical carcinoid to SCLC is paralleled by an increase in proliferative activity and by an altered expression of tumour suppressor gene products. The above findings have diagnostic relevance.

Antigens, Neoplasm↗
PubMed1994

Synthesis of insulin and its effects in Y79 human retinoblastoma cells.

This paper demonstrates that Y79 human retinoblastoma cells contain immunoreactive insulin (IRI) and release it in the medium. Cells cultured either in suspension or in monolayer showed a similar content of IRI. Moreover, in both conditions, IRI concentration was higher in cells cultured in serum-supplemented medium rather than in serum-free medium. Retinoblastoma cells are capable of synthesizing insulin. This was demonstrated by incubating Y79 cells with [3H]leucine. The synthesized radioactive insulin was separated and assayed by means of a HPLC procedure described in this paper. Both cell growth and [3H]thymidine and [3H]uridine incorporation into acid-insoluble fraction was reduced (-75%) in Y79 cells cultured without serum with respect to those cultured in the presence of serum. The addition of insulin to the serum-free medium stimulated both cell division and DNA and RNA labeling, with values approaching those obtained with serum supplemented cultures. Insulin-like growth factor I exerted similar effects, but at a much lower concentration than insulin. We suggest that both insulin and IGF-I may represent mitogenic signals for these cells which might be mediated through insulin-like growth factor I receptors.

Cell Division↗
PubMed1993

An association of the RB gene with osteosarcoma: molecular genetic evaluation of a case of hereditary retinoblastoma.

A 24-year-old male patient with hereditary retinoblastoma and a poorly differentiated osteoblastic osteogenic sarcoma was found to carry a mutant RB1 allele in all cells. This findings was most likely a point mutation or microdeletion because Southern blot analysis of peripheral blood DNA failed to disclose any structural aberration of the RB1 gene. A somatic mutation (deletion) affecting the other allele was found in the osteosarcoma cells. Management of tumor by external radiotherapy in early age is questioned because the effect of irradiation is to significantly increase the total incidence of second tumors above the already high incidence in non-irradiated patients.

Adult↗
PubMed1989

Epigenetic changes may contribute to the formation and spontaneous regression of retinoblastoma.

Epigenetic models for tumor formation assume that oncogenic transformation results from changes in the activity of otherwise normal genes. Since gene activity can be inhibited by DNA methylation, and inactivation of tumor suppressor genes is a fundamental process in oncogenesis, we investigated the methylation status of the retinoblastoma suppressor gene (RB gene) on chromosome 13, in blood and tumor cells from 21 retinoblastoma patients. Using methylation-sensitive restriction enzymes and a cloned DNA probe for the unmethylated CpG island at the 5' end of RB gene, we obtained evidence of hypermethylation of this gene in a sporadic unilateral retinoblastoma tumor. The closely linked esterase D gene and a CpG-rich island on chromosome 15 were not affected. We suggest that changes in the methylation pattern of the RB gene play a role in the development and spontaneous regression of some retinoblastoma tumors.

DNA Restriction Enzymes↗
PubMed1984

Chromosome 13 restriction fragment length polymorphisms.

The gene locus for hereditary retinoblastoma is on human chromosome 13, band q14. With this gene localization in mind, we cloned DNA fragments from this chromosome. Three of the fragments identify restriction fragment length polymorphisms. These three fragments are from the region 13q12-13q22, the chromosome region which contains the retinoblastoma locus. We expect that these restriction fragment length polymorphisms will be linked to the retinoblastoma locus, and that they will serve in certain retinoblastoma families as predictors of retinoblastoma gene carriers. They will also be useful in studies of other gene loci thought to be on chromosome 13.

Alleles↗
PubMed1996

Imaging in the trilateral retinoblastoma syndrome.

The medical records, CT, and MRI of ten children with trilateral retinoblastoma were reviewed. The intracranial pathology consisted of eight pineal neoplasms and two parasellar lesions, at least seven of the which were calcified. Two lesions demonstrated calcification only (no soft tissue mass) at initial presentation. Hydrocephalus was seen in eight cases, and concurrent or subsequent subarachnoid dissemination was documented in seven. Only one patient is known to be alive at the present time. The imaging features of the midline intracranial tumors mirror those of the ocular neoplasm. As calcification may be the only clue to the presence of the intracranial malignancy, close surveillance of high-risk patients with retinoblastoma with initial CT and follow-up MRI is suggested.

Brain↗
PubMed1997

Diagnosis of intraocular lymphoma by polymerase chain reaction.

BACKGROUND: Cytopathological examinations have been used in the diagnosis of intraocular lymphoma. However, sometimes it is not easy to detect malignant cells in the biopsy specimens. We applied a method that identified monoclonal proliferation of B lymphocytes by using polymerase chain reaction (PCR) in the diagnosis of patients suspected to have intraocular B-cell lymphoma. METHODS: Three specimens of the diagnostic vitrectomy were studied by cytological examination and by PCR to amplify the complementary determining region (CDR3) of immunoglobulin heavy chain (IgH) gene. As a positive control, a biopsy specimen of an orbital lymphoma was examined; four vitrectomy specimens from patients with diabetic retinopathy, proliferative vitreo-retinopathy, acute retinal necrosis (ARN) and macular hole were negative controls. RESULTS: On cytologic examination, no malignant cells were found in three specimens: suspected intraocular lymphoma and one ARN. In contrast, a discrete band that reflected monoclonal proliferation of B lymphocytes was detected by PCR in specimens from two patients and the positive control. Vitrectomy specimens from the negative controls, including ARN, did not show a discrete band on PCR. CONCLUSIONS: Two cases of ocular malignant lymphoma were diagnosed by PCR identification of monoclonal proliferation of B lymphocytes. This method may be an additional diagnostic tool in the diagnosis of intraocular B-cell lymphoma.

Aged↗
PubMed1993

Calcification of scleral-wrapped orbital implant in patients with retinoblastoma.

Calcification detected by CT is a valuable technique to confirm a clinical impression of retinoblastoma. However, when calcification is detected following enucleation with placement of a scleral-wrapped orbital implant, the presence of calcium may be dystrophic, instead of indicating recurrent tumor growth. Cautious follow-up is warranted, and this report suggests that such calcification, probably associated with the scleral wrapping, can remain stable over many years.

Calcinosis↗
PubMed1982

Histological and scanning electron microscopic study of tissue invasion of Bangerter nylon implant after enucleation.

An incidentally extirpated Bangerter-type nylon implant was examined by light microscopy and scanning electron microscopy. Three months after implantation, the implant was densely filled with tissues, which were shown by light microscopy to be muscle cells in the margin of the implant; the muscle cells were fixed there at the time of implantation, and fibrocytic cells were inside the implant. Scanning electron microscopy showed interlacing fibrous cells with erythrocytes and leukocytes among the nylon fibers, lamellar accumulation of fibrous cells around nylon fibers, and a smooth surface of the margin of the nylon implant. This invasion of fibrous cells into the nylon implant is one reason why the Bangerter type of nylon implant rarely falls out of the orbital socket.

Connective Tissue↗