Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eighty newborn C3H/BifB/Ki strain mice received a single intraocular inoculation of 0.002--0.003 ml of 10(8.0) TCID 50/0.1 ml human adenovirus 12 (AD 12), within 24 h after birth. Forty mice survived and in seven of these (17.5%) a solid retinoblastomalike neoplasm developed between 64 and 236 days. The tumors have been successfully cultured and also transplanted subcutaneously into syngeneic hosts. Morphologically, all tumors revealed characteristic features of retinoblastoma associated with the Homer Wright type of rosettes. Bizarre giant cells were commonly detectable. Ad 12-specific T-antigens were demonstrated in both the primary and cultured tumor cells using immunofluorescent techniques. Some giant cells also showed numerous T-positive filaments. Electron microscopy disclosed poorly differentiated unipolar cells possessing a large ovoid nucleus. Many tumor cells appeared to contain a well organized solitary cilium consisting of a typical ring of nine doublets with no axial (9 + 0) in close association with a pair of centrioles. Some multinucleated giant tumor cells also contained multiple cilia-centriole complexes within their broad syncytial cytoplasm. Occasional endogenous C particle-like virions unique to murine neuroblastomas were observed for the first time in virus-induced retinal tumors. This unprecedented tumor model in a pure strain mouse adds to the range of known animals sensitive to Ad 12 oncogenesis.
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PMID:Retinoblastoma-like neoplasm induced in C3H/BifB/Ki strain mice by human adenovirus serotype 12. 33 42

Retinoblastoma is a radiosensitive malignancy of neuroblastic origin that primarily affects young children. Its relatively low incidence belies its potential importance in the understanding of tumor biology in general. A case is made for referral of all retinoblastoma patients to centers with retinoblastoma protocols.
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PMID:Retinoblastoma. 37 7

The genetic basis of retinoblastoma is reviewed and the following conclusions are drawn: 1) The mode of inheritance of the hereditary variety of retinoblastoma (R) is autosomal dominant with about 90% penetrance. 2) About 68% of inherited cases are bilateral, and about 32%, unilateral. There is an intrafamilial correlation between penetrance as measured by segregation ratio and expressivity as measured by the fraction of bilaterally affected patients. 3) The vast majority of all R patients are sporadic cases, i.e., they are the only affected members of otherwise unaffected families. The porportion of bilateral cases is much lower among sporadic than among hereditary cases. 4) All bilaterally affected patients with sporadic R and patients with unilateral sporadic R with more than one primary tumor have to be regarded as germ cell mutants; they will transmit the gene to 50% of their offspring. Only 10%-12% of unilateral sporadic cases are germ cell mutants; 88%-90% are nonhereditary; in these cases the tumor is probably caused by a somatic mutation. 5) In a minority of cases, deletion of the chromosome segment 13q14(=intersitital deletion of the long arm of chromosome 13) has been observed. In addition to R, the patients show a variable degree of general or mental retardation; often there are few external indications of a chromosome aberration. Other chromosome studies suggest anomalies of chromosome 13 in tumor tissue even in cases not showing an anomaly of this chromosome in blood cultures, and possibly a slightly increased chromosome instability. 6) Patients with bilateral, and possibly in general with hereditary, R run an increased risk of becoming affected with other tumor diseases, such as osseous sarcomas, in later life. 7) Knudson's hypothesis of two mutational steps leading to both the hereditary and the nonhereditary variants of R is discussed critically, and the alternative possibility is suggested that in the nonhereditary variant a single mutational step--possibly a small chromosome aberration--could be enough to produce a tumor. 8) Evidence indicating a possible viral origin of R is cited, and animal experiments are mentioned in which R-like tumors have successfully been produced by local DNA virus inoculation. 9) As a consequence of improved survival and reproduction of R patients, an increased in the incidence of R and in the proportion of bilateral cases among all R patients must be anticipated. 10) Detailed rules for genetic counseling in families affected by R are given.
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PMID:Genetics of retinoblastoma. 39 14

Based on the Third National Cancer Survey (1969 to 1971), the incidence of malignant neoplasms in the United States was 183.4 per million live births per year in infants younger than 1 year and 36.5 in newborns younger than 29 days. In both age groups, neuroblastoma was the most commonly diagnosed neoplasm. Overall, cancer incidence in infants younger than 1 year was almost 3.5 times greater than mortality determined from US death certificates from 1960 to 1969. For individual tumor types, the ratio between incidence and mortality varied between 159 for retinoblastoma and 1.5 for leukemia largely reflecting relative differences in survival due to treatment.
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PMID:US cancer incidence and mortality in the first year of life. 42 Jan 85

Annulate lamellae have been found in a primitive neuroectodermal tumor, a metastatic cerebellar tumor, a testicular seminoma, a retinoblastoma and three melanomas. These annulate lamellae are arranged in stacked parallel arrays in the cytoplasm of tumor cells. The number of annulate lamellae observed to comprise a single stack varies from 2--4 in the seminoma tumor to 5--18 in the cerebellar tumor. Although the functional significance of annulate lamallae is still unknown, in many instances they have been found to be continuous with rough-surfaced cisternae of the endoplasmic reticulum and ribosomes have been demonstrated on the surface of annulate lamellae. This may suggest that annulate lamellae participate in protein synthesis.
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PMID:Annulate lamellae in human tumor cells. 45 90

Sequential histopathological observations were made of the rabbit corneas after an implantation of viable and nonviable tumor cells in the corneal stroma. They showed a nonspecific localized interstitial keratitis accompanied by inflammatory cells and new capillaries. We could not observe any significant clinical or histopathological differences between the corneas containing live or dead tumor implants, or between those with different tumor types (i.e., retinoblastoma and melanoma). Some variation in the severity of the inflammatory response was observed in different animals with the same tumor. In all cases, the extent of the corneal neovascularization correlated with the degree of inflammation. However, in rabbits made immune-deficient by radiation, there was negligible inflammation and vascularization when tumor was implanted.
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PMID:Evaluation of tumor angiogenesis factor with the rabbit cornea model. 45 56

A 41-year-old man had a 6 x 6 x 5-disk diameter amelanotic tumor in the posterior fundus. The clinical and fluorescein angiographic appearance suggested a benign retinal vascular tumor, although amelanotic choroidal melanoma and retinoblastoma were diagnostic possibilities. An incisional 48-hour radioactive phosphorus (32P) uptake test was performed and the result showed an increased uptake over the tumor mass of 100% as compared to the control quadrants. The globe was enucleated and the pathologic diagnosis was isolated astrocytic glioma of the retina with minimal, if any, malignant potential. The highly developed vascular system of the tumor probably contributed to the false-positive test result.
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PMID:Retinal astrocytoma. 46 11

This study includes all cases of retinoblastoma reported in Sweden between 1958 and 1971. The incidence of the disease was 1 per 18 000 live births. Only in six cases was there a familial history and five of these cases were bilateral. The tumour was bilateral in 37.5% of all cases. All cases with unilateral tumour had been treated with enucleation. In the bilateral cases one eye had also been enucleated and the other eye treated by local irradiation therapy. Tumour invasion into choroid was found in 29% and into the optic nerve on 11% of the cases. The mortality was only 4.5%.
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PMID:Retinoblastoma in Sweden 1958--1971. A clinical and histopathological study. 47 80

The lactic dehydrogenase (LDH) activity of the aqueous humour has been estimated in both eyes of 7 patients having uniocular retinoblastoma. In 1 patient the aqueous humour LDH activity in the healthy eye was above normal, but there was no clinical evidence of malignancy. Tumour tissue was detected in this eye 9 months later, and the aqueous humour showed a rise in LDH activity. A high LDH activity persisted even after irradiation, though no tumour tissue was visible ophthalmoscopically. It is suggested that the estimation of the LDH activity in the aqueous humour of the healthy eye in cases of uniocular retinoblastoma might be of value in the early detection of a bilateral retinoblastoma.
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PMID:Prognostic significance of aqueous humour lactic dehydrogenase activity. 47 33

Age-specific incidence data from 244 bilateral and 31 familial unlateral cases of retinoblastoma were analyzed. In the bilateral cases, a high intraclass correlation between ages of the patients at diagnosis in the right and left eyes was noted, even after removal of the bias due to the fact that the diagnosis for each eye is never independent. This finding indicated strongly that the age at onset was largely determined by host factors common to both eyes. The mean ages of the patients at diagnosis of the inherited cases among the bilateral or unilateral group varied consistently with parental phenotype. This finding implied that inherited host resistance played an important role in the latency period for the gene carriers. The fraction of cases not yet diagnosed fit well to a negative exponential distribution, and in the less susceptible group with hereditary unilateral cases, tumor formation may have been suppressed about twice that in the most susceptible group with bilateral cases. It was argued that the presumed second hit initiating tumor formation in the gene carriers was not a mutational process, but probably an error in the process of differentiation that could be suppressed completely in the most resistant group who could remain unaffected, but that could not be suppressed completely in the less resistant group.
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PMID:Hereditary retinoblastoma: host resistance and age at onset. 48 Mar 85


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