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

Somatic cell hybrids between mouse mammary tumour cells (TA3B) and diploid rat embryo fibroblasts (REF) or between TA3B and Syrian hamster sarcoma cells (BI) were examined for the in vitro characteristics of transformed cells as soon as possible after cell fusion. Unlike the parental tumour cells as three of four TA3B X REF and five BI X TA3B independent hybrid lines had low colony-forming efficiencies in agar, exhibited density-dependent inhibition of growth and did not form colonies on confluent monolayers of 3T3 cells, demonstrating that the transformed phenotype was suppressed in these hybrids. In addition tests of some of the hybrid lines for tumour production in nude mice showed that this was also suppressed. Suppression was more stable in the TA3B X REF than in the BI X TA3B hybrids, variants of the BI X TA3B hybrids with the properties of transformed cells could be readily isolated by subculturing cells that had grown in agar. Tumour growth selected for hybrids with the characteristics of transformed cells, and derivatives of the hybrids selected to show the transformed phenotype readily produced tumours. These correlations suggest that the transformed phenotype and malignancy may be under the same control in these cells. The phenomenon of suppression may be explained by the hypothesis that neoplastic transformation results from recessive mutations in genes which control the normal phenotype. On this model the finding of suppression in hybrids between two different tumour lines is interpreted as complementation and indicates that the mutations are not the same in all cell lines.
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PMID:Suppression of the transformed phenotype in somatic cell hybrids. 72 2

A testable hypothesis on the role of hormones in carcinogenic processes is presented. The hypothesis has been based on the findings that (1) hormones regulate cell division in normal cells, (2) successful neoplastic transformation requires hormonal stimulation of cells receiving carcinogenic insult, (3) normal cells have finite divisional capabilities, whereas neoplastic cells possess infinite divisional capabilities, and (4) normal cells, when present in high ratio, inhibit the growth of neoplastic cells. According to the hypothesis, hormones are considered to be neither mutagenic nor carcinogenic. (Carcinogen is defined as an agent which initiates normal-to-neoplastic transformation). Instead, they play a dual role in carcinogenesis. First, hormones are considered necessary for the fixation of the cell genome neoplastically transformed by carcinogens. Second, hormones, by enhancing the rate of cell division, shorten the life span of normal cells, thus causing a reduction of the normal- to tumor-cell ratio in the population--a condition which facilitates growth of tumor cells.
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PMID:Hormonal carcinogenesis: a novel hypothesis for the role of hormones. 72 16

Adenocarcinoid is a form of appendiceal carcinoid possessing features of both carcinoid and adenocarcinoma. There are two histologic types. Thirty patients had the goblet cell type, characterized by nests of large mucin-distended cells. Nine patients had the tubular type, characterized by small glandular structures lined by uniform cells. Despite abundant mucin and a goblet cell or acinar-like arrangement, a closer relationship to carcinoid than to adenocarcinoma is suggested by a concentration of tumor elements below the crypts of Lieberkuhn, a lack of evidence of neoplastic transformation of the appendiceal mucosa, and the demonstration of argentaffin or argyrophil granules in 88% of the lesions. Six tumors, all of the goblet cell type, metastasized and resulted in the death of the patients. One of the tumours that metastasized had a prominent tubular component. Most adenocarcinoids can be adequately treated by appendectomy, but hemicolectomy is recommended for those tumors showing atypical foci, a high mitotic count, or spread beyond the appendix.
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PMID:Adenocarcinoid, a mucin-producing carcinoid tumor of the appendix: a study of 39 cases. 72 74

Integral membrane proteins are visualized as intramembrane particles (IMP) at the cleaved surfaces of freeze-fractured plasma membranes. Topographical distributions of the IMP of the urinary bladder epithelial cells membranes in normal Fischer rat bladder and noninvasive and invasive N-(4-(5-nitro-2-furyl)-2-thiazolyl)formamide (FANFT)-induced bladder tumors are shown to be significantly different. Using several statistical methods that test IMP topography vis-a-vis the Poisson (random) hypothesis, it is demonstrated that IMP are mathematically randomly distributed in the large majority of plasma membranes of cells in normal rat bladder epithelium and in invasive N-(4-(5-nitro-2-furyl)-2-thiazolyl)formamide tumors. In noninvasive rat bladder carcinomas, IMP are in a lattice-like arrangement in half of the tumor cells and randomly distributed in the remainder. IMP numerical densities are also altered in the course of neoplastic transformation. IMP are equally increased above control values in both noninvasive and invasive N-(4-(5-nitro-2-furyl)-2-thiazolyl)formamide tumors. Although transformation into noninvasive tumors is associated with increased numbers of IMP, there is no evidence that this parameter is specifically related to tumor biologic behavior in this model system.
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PMID:Topography and numerical densities of intramembrane particles in chemical carcinogen-induced urinary bladder carcinomas in Fischer rats. 73 60

A review of the literature and current biochemical studies is presented which provides significant evidence of alteration in the level of the enzyme ribonuclease activity in cancer. Current studies reveal that 80% of all cancer patients have alteration in ribonuclease activity and that individuals known to be at high risk for the development of cancer also demonstrate significant alteration of ribonuclease activity. It is noted that while elevation of serum ribonuclease exists within the cancer state and appears to be independent of clinical status (relapse, remission, or cured), diminished activity is found within the tumor itself. Animal models are reviewed which demonstrate that ribonuclease activity becomes elevated in the murine species subsequent to the transplantation of tumor and following the infection of the host with oncogenic virus. The occurrence of elevated ribonuclease activity in high tumor incidence strain mice long before the development of overt tumor is alos discussed. To date it is not possible to assign a specific function to the changes in the level of ribonuclease in connection with the cancer state. However, evidence indicating that tumor chemotherapy is generally associated with early elevation of ribonuclease activity within the tumor cell suggests that increased ribonuclease activity may play a role in the process by which the host restricts neoplastic transformation. The potential of this enzyme as a biochemical marker in cancer is discussed.
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PMID:Alteration of human serum ribonuclease activity in malignancy. 75 46

A study of 213 ovarian tumors was undertaken with respect to the published assumption that there may be a relationship between presence of crystals of silicate in the ovarian tissue and neoplastic transformation. The histological review gave the opportunity to classify these tumors according to the recommendations of the World Health Organization. The frequency of histological types, age distribution and the site of involvement were determined. These data were compared to those in the literature. Our findings confirm the high incidence of serous tumors and bilaterality reported by others as well as the high risk of ovarian cancer in women in their fifties. A comparative study of the age distribution of cytadenomas was made. It suggests that cystadenomas might be considered as a precursor to the cystadenocarcinomas because of their appearance at younger age. A deliberate search for silicate crystals in periovarian adhesions and in tumor tissue showed a minimal incidence of crystalline material. This does not support a direct relationship between silicate crystals and ovarian tumors. However, it is suggested that neoplastic changes may occur in the ovarian surface as a result of adhesions engendered by deposition of silicate crystals.
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PMID:A ten year study of ovarian tumors. 80 20

Chromosomal abnormalities are a frequent concomitant of neoplasia, and although it is tempting to relate these mutations and alterations in chromatin (DNA) function to cancer, their relationship to the initiation or progression of carcinogenesis is unknown. Mammalian cells in culture, after interacting with chemical carcinogens, often exhibit chromosome damage consisting of breaks and exchanges of chromatid material. The pattern of damage of banded metaphases indicates that negative bands are especially vulnerable to the action of chemical carcinogens, probably because of differential chromatin condensation. Damage to individual chromosomes may be random or nonrandom, depending on the species. Cell death can be correlated with chromatid alterations that occur shortly after treatment with chemical carcinogens. There is also a correlation between mutagenic and carcinogenic activity of some chemical carcinogens and the frequency of sister chromatid exchanges. The question of whether specific chromosome changes are absolutely required for neoplastic transformation cannot be answered because of conflicting data and diverse results from studies even with known carcinogens. Cell transformation may occur without any visible chromosome changes. A universal specific numerical or visible structural chromosomal alteration is not necessarily associated with chemical or viral transformation. Chromosome changes are independent of the etiologic agents: different carcinogens may produce transformation associated with the same abnormal chromosomes, but not all transformed lines invariably exhibit the same abnormality, even with the same chemical. In some species, chromosome having nucleolar organizer regions may be more frequently involved in numerical or structural deviations. Progressively growing tumors also may occur as a result of the proliferation of transformed cells without detectable chromosome changes, indicating that tumorigenicity need not be related to an imbalance of chromosome number or structure. Our studies indicate that chromosome changes are not essential for establishment of neoplasms but that karyotypic instability may result in response to selective growth pressures.
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PMID:Relationship of chromosome changes to neoplastic cell transformation. 82 68

The possibility that neoplastic transformation may characteristically alter cell surface morphology prompted a comparison by scanning electron microscopy of nonneoplastic and tumorigenic cell lines from a single clone of mouse embryo cells. Among those studied by scanning electron microscopy, six lines of this clone proved nonneoplastic, and nine others underwent neoplastic transformation in culture, as evidenced by tumor production in vivo. Combined cinephotomicrography and scanning electron microscopy allowed the determination of postmitotic time and topography of individual cells without perturbing the cells or detectably altering their surface morphology; no pattern of morphological change as a function of postmitotic time was evident in either nonneoplastic or neoplastic cell populations. Accordingly, these cell populations could be compared under their usual conditions of attached asynchronous growth despite differences in proliferation rates. Cells of the neoplastic lines were characteristically less spread, and some lines displayed greater morphological variability than was evident among cells of nonneoplastic lines. However, most cells in all nine neoplastic lines and all six nonneoplastic lines were smooth surfaced. Thus, the exaggerated incidence of microvilli, ruffles, or blebs reported for established tumor-derived lines and most morphologically transformed lines did not prove a reliable criterion of neoplastic state for these cell lines of common origin grown under the same culture conditions.
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PMID:Topography of nonneoplastic and neoplastic cells of common origin. 83 80

Weaning male and female C3HAvyfB mice were fed a low-fat (4.5%) diet until they were 60-70 days of age when they were fed high-fat (18.6%) diets containing either sunflower-seed oil (polyunsaturated fat diet) or tallow (saturated fat diet). After receiving either of the high-fat diets for 4 weeks, each mouse received an inoculum of approximately 1,700 single cells from a transplantable mammary adenocarcinoma. The cumulative incidence of tumor-bearing mice was significantly greater among both males and females fed the polyunsaturated fat diet than among males and females fed the saturated fat diet. The mean times elapsed before palpable tumors developed were less when mice were fed the polyunsaturated fat diet than when mice were fed the saturated fat diet, but these differences were not statistically significant. The cumulative incidence of tumor-bearing mice was also significantly greater among females than males. The results supported the suggestion from previous work in this laboratory that the polyunsaturated fat diet exerts its effect on the promotional stage of carcinogenesis rather than on the initial event of neoplastic transformation.
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PMID:Effect of dietary polyunsaturated fat on the growth of a transplantable adenocarcinoma in C3HAvyfB mice. 83 68

Adherent fibroblast-like cells from paired lines, one non-neoplastic and the other "spontaneously" transformed neoplastic, were compared in simultaneous in vivo and in vitro assays. The in vivo assay was the i.m. implantation of 10(6) or 10(7) cells in irradiated syngeneic animals, and the two in vitro assays were the evaluation of colony morphology on plastic and the enumeration of colony growth in semisolid agarose. The percentage of colonies diagnosed from their morphology as neoplastic correlated with tumorigenicity as follows: 100% always indicated a tumorigenic cell population with tumor latent periods from 6 to 230 days and tumor incidence from 40 to 100%; 0% always indicated a nontumorigenic cell population; 1 to 32% indicated either a tumorigenic cell line with long tumor latent period (218 days) with 70% tumor incidence or a nontumorigenic cell line. Growth in agarose, as measured by colony number and size, correlated with tumorigenicity as follows: nontumorigenic cell lines produced no colonies; tumorigenic cell lines produced colonies, but not always larger than 0.1 mm in diameter. The number of size or colonies did not correlate with the tumor latent period or tumor incidence. Therefore, both in vitro tests were reliable qualitative assays of spontaneous neoplastic transformation, but they did not correlate directly with the tumor incidence or mean tumor latent period. The relative success of the agarose assay emphasizes the importance of decreased anchorage dependence for progressive growth of injected cells as a malignant neoplasm in vivo.
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PMID:Colony morphology and growth in agarose as tests for spontaneous neoplastic transformation in vitro. 85 64


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