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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

All known tumor types have been reported in the neonate. A numerical listing and discussion are beyond the scope of this review. Wells and Fraumeni give some insight into common congenital malignant neoplasms. Table 2 lists the percentage of neonatal deaths caused by type-specific cancers. Retinoblastoma is probably the most common malignant tumor in the neonate. About seven per cent of these tumors have been apparent at birth. This tumor is not discussed in either article because it is not lethal until muypes in neonatal and pediatric patients. Some congenital malformations in the in the neonate are recognized as being frankly benign (cysts), potentially malignant (teratomas), and frankly malignant (neuroblastoma). A high percentage of teratomas are benign in the newborn period. Leukemia in the newborn appears to be more aggressive yet neuroblastoma has a better prognosis. More studies are needed to help us define why the neonate does better with some tumors and worse with others. Surface cell markers on neonatal leukemia, B and T cell function studies, and other immunologic surveillance studies are needed. Study of neonatal oncology may add to our knowledge of carcinogenesis and oncogenesis in the future.
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PMID:Neonatal oncology. 19 75

Oat-cell carcinoma and bronchial carcinoid share histologic features with the Kultschitzky cell, and this argues for a common origin from the Kultschitzky cell for these tumors. In this view, the carcinoid represents the less malignant form and the oat-cell carcinoma the highly malignant adenocarcinoma of the colon, the epidemiologies of the benign and malignant forms of tumor arising from the same precursor are similar. However, the epidemiology of carcinoid tumor and that of oat-cell carcinoma are different. Although the ectopic production of hormones links the two kinds of tumor, it is also seen in other histologic types of lung carcinoma. Lung carcinoids occur in the genetic disorder of multiple endocrine adenomatosis, suggesting a genetic etiology for at least some carcinoids. This contrasts with the exogenous etiologic agents of cigarette smoking, occupational exposure, and urban domicile for oat-cell carcinoma. All these strong differences between lung carcinoid and oat-cell carcinoma indicate a markedly different process of carcinogenesis, which casts doubt on the hypothesis of a common cell precursor.
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PMID:Comparative epidemiology of carcinoid and oat-cell tumors of the lung. 19 2

The concentrations of putrescine, spermidine, and spermine in liver of rats fed on 4-dimethylaminoazobenzene and in the resultant hepatomas were found to be significantly higher than were those observed in normal liver from rats of the same strain, sex, and age. These modifications were due to the carcinogen and not to the special low-riboflavin diet used to obtain the carcinogenic effect of 4-dimethylaminoazobenzene. The first change observed during liver carcinogenesis was the early increase in the putrescine level, followed by an increase of spermidine and spermine, which reached maximum levels in growing hepatomas. A significant increase of urinary polyamines was also observed in tumor-bearing rats. Experiments on leucine incorporation into proteins of tissue slices, which were obtained from the same tissues on which polyamine determinations were carried out, showed that in rat liver carcinogenesis the rate of protein synthesis was well correlated with the polyamine levels. These results suggest that polyamines may play a role in the process of carcinogenesis and in tumor protein synthesis in vivo.
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PMID:Changes in polyamine levels and protein synthesis rate during rat liver carcinogenesis induced by 4-dimethylaminoazobenzene. 20 66

Bilateral electrolytic lesions were placed in the median eminence area of the hypothalamus in 12-week-old male Wistar rats. Sham-operated and untreated control rats were also included. Two weeks later, one-half of them were given 0.03% N-2-fluorenylacetamide incorporated into the diet for 16 weeks with adequate resting periods in between. The animals were killed 34 weeks after the last carcinogen feeding. The results show that lesions in the hypothalamus effectively inhibited liver tumor formation (0 of 16, 0%). In contrast, the incidence of hepatocellular carcinomas in sham-operated rats was 38.5% (5 of 13), and that of untreated controls was 42.9% (6 oactive thyroid glands, and shorter nasoanal lengths were observed in rats with lesions in the hypothalamus irrespective of carcinogen treatment. It is apparent from these data that lesions in the median eminence area of the hypothalamus inhibit the induction of liver carcinogenesis with N-2-fluorenylacetamide in male rats.
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PMID:Inhibitory effect of hypothalamic lesions on liver tumor induction by N-2-fluorenylacetamide in male rats. 20 76

Previous studies on the natural history of neoplasia, utilizing mouse skin as a model, have demonstrated that the process of epidermal carcinogenesis may be separated into at least two different phases. The first of these, termed "initiation," is essentially irreversible; the second phase, that of promotion, may be modulated or reversed by a variety of environmental conditions. More recently, similar stages have been demonstrated for other organ systems during carcinogenesis, in particular that of murine liver. At the same time, investigations of a variety of systems including those in plants, amphibians, and, most recently, in mammals have demonstrated that the initiation process of neoplasia may not be as irreversible as previously considered, but in several of these systems, including those in plants and in the mouse teratoma, the neoplastic process appears to be reversible from its initial stages under appropriate conditions. A proposed scheme is presented which takes into account the reversibility of the process of initiation in the natural history of neoplasia.
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PMID:The stability of events in the natural history of neoplasia. 20 65

Using the modified technique of transplantation test, ITR serum activity was found in most (14 out of 21) individual hamster sera obtained during the latent period of primary SV40 carcinogenesis (60 days after virus infection when newborn). On the other hand, as a rule, no ITR activity was observed in the sera of the same hamsters after tumor appearance and during their growth. ITR activity rapidly disappeared from sera of hamsters neonatally infected with SV40 after their successful immunization with the same virus during the latent period. There appears to be a correlation between the presence of ITR serum factor during the latent period and the subsequent primary SV40 tumor appearance in hamsters.
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PMID:Serum activity inhibiting specific simian virus 40-induced transplantation resistance and its correlation with primary SV40 tumors appearance in hamsters. 20 79

Spontaneous hepatomas and hepatic preneoplastic changes were observed in sand rats (Psammomys obesus) from two colonies. Both colonies originated from 10 sand rats captured in the Judean desert in 1969. At the age of 6 months, and increasing in multiplicity with advancing age, histologic examination revealed nodules containing hepatocytes characterized by hyperbasophilia, accumulation of glycogen, eosinophilic cytoplasm, or a mixture of these cells. In animals over 25 months old hepatocellular carcinoma was diagnosed. The histologic changes described here were reported to be characteristic of chemical hepatomagenesis in rats. No external chemical carcinogen could be demonstrated in our animal colonies, and a hereditary predisposition to tumor formation is presumed. Identity of hepatic carcinogenesis, irrespective of etiology in distantly related rodents, ie, the laboratory rat and the sand rat, which in reality is a gerbil, supports the assumption of the existence of a general law governing hepatic carcinogenesis.
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PMID:The histogenesis of hepatoma occurring spontaneously in a strain of sand rats (Psammomys obesus). 20 93

Four-week-old rainbow trout (Salmo gairdneri) were fed diets containing 0, 3, 50, 200, 400, and 800 ppm dimethylnitrosamine (DMN) for 52 weeks. At the end of 52 weeks, the fish were fed a control diet without DMN for an additional 26 weeks. Samples were taken at 26, 52, and 78 weeks to determine tumor incidence. A dose-related carcinogenic response was established from these results, and an equation was derived to relate the level of the carcinogen to the hepatocellular carcinoma incidence. From a published dose-response study that used outbred Porton rats, a second equation was derived for comparison. Rats and trout were approximately equal in their sensitivity to DMN carcinogenesis. The median lethal dose after ip injection of DMN was 1,770 mg/kg body weight in rainbow trout. Relative to the range of 15-50 mg/kg body weight reported for several mammalian species, trout were resistant to the acute toxicity of DMN.
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PMID:Carcinogenicity and acute toxicity of dimethylnitrosamine in rainbow trout (Salmo gairdneri). 20 62

Mitochondria were isolated from a slow-growing (9618A) and two intermediate-to-fast-growing (5123C, 5123tc) Morris hepatomas and host livers. The mitochondrial proteins were solubilized and fractionated on sodium dodecyl sulfate:polyacrylamide slab gels. One Coomassie blue-stained band was absent or reduced in amount in all tumors relative to host livers. In addition, a major mitochondrial enzyme present in normal liver, carbamyl phosphate synthetase, was missing or greatly reduced in the slow-growing, highly differentiated hepatoma 9618A, a tumor that is considered to be similar to normal liver in many biochemical and morphological respects. Incubation of mitochondria with [35S]methionine and a suitable amino acid incorporation system resulted in labeling of specific mitochondrial proteins. Autoradiography of the slab gels disclosed four prominently labeled fractions and a number of minor fractions. Preparations from hepatoma 5123tc demonstrated two labeled bands that were absent or greatly reduced in host liver. Host liver preparations displayed a minor band that was absent or greatly reduced in hepatoma 5123C. However, no single change in labeling pattern was common to all three tumors, suggesting the absence of a causal relationship between carcinogenesis and mutations in mitochondrial DNA.
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PMID:Differences in total mitochondrial proteins and proteins synthesized by mitochondria from rat liver and Morris hepatomas 9618A, 5123C, and 5123tc. 20 52

The effect of reovirus type 3 infection on the pulmonary adenoma response to urethan in strain A mice was examined. Urethan carcinogenesis in this system was suppressed from 30 to 60% when mice were exposed to reovirus either 6 days before, on the same day as, or 14 days after urethan administration. These findings suggested that reovirus infection interfered with the progression of urethan-induced pulmonary adenoma rather than the induction of lung tumors by urethan. When mice received multiple exposures to reovirus, the lung tumor response was enhanced. These findings indicated that reovirus infection in particular and virus infection in general may play an important role in the carcinogenic response to environmental chemicals.
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PMID:Effect of reovirus infection on pulmonary tumor response to urethan in strain A mice. 20 99


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