Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Addition of diluted blood serum from tumor-bearing rats stimulated significantly the synthesis of cholesteryl esters from labeled cholesterol and endogenous fatty acids in the cytosol derived from normal rat liver. With both Zajdela and Walker transplantable tumors this effect was found to be associated with the most intensive period of tumor growth. During chemical carcinogenesis induced by a single subcutaneous administration of benzo(a)pyrene the stimulating effect of sera was found to precede several weeks the appearance of palpable tumors and persisted during the period of progressive tumor growth. With all tumors used, sera in ultimate stages of tumor growth failed to show a stimulating effect. The stimulating effect was due to the presence of a yet unidentified lipid. Higher quantities of this substance may appear in the serum of tumor-bearing animals to meet higher requirements for cholesteryl esters during tumor growth. The stimulating effect of the blood serum on cholesteryl esters may be a useful marker of malignant tumors in humans.
 ...
PMID:Stimulating effect of blood serums from tumor-bearing rats on cholesteryl ester synthesis in normal rat liver cytosol in vitro. 223 14

Radiation induced (30 Gy) morphological changes of experimental malignant brain tumors, which were produced by chemical carcinogenesis, were investigated by microangiography and correlated with the histological findings in 62 BD-IX-rats. In randomized groups the investigations were performed 2, 3, 6 and 8 weeks after the radiation was finished. Morphologically different reactions could be differentiated: remissions or partial recovery of the tumors, rest or recurrent tumor and uninfluenced tumor growth. The characteristic findings, the reasons for different courses and possible conclusions concerning the radiotherapeutical effect are discussed.
 ...
PMID:[Neuroradiology of the normal and pathological anatomy of the rat brain.--III Morphology and growth behaviour of experimental brain tumours following radiation therapy (author's transl)]. 621 8

The hypothesis that immunodepression favors a carcinogenetic process and thus subsequent tumor development remains controversial in spite of numerous experimental studies. This is due, on one hand, to the difficulty in demonstrating the presence of tumor-associated antigens and, on the other, to the complex immunological mechanisms which lead to the destruction of tumors cells. With respect to immunosurveillance, the present situation can be summarized as follows: the development of virus-induced tumors is under the control of a T-cell dependent system; a T-cell depression (thymectomy, congenital absence of thymus, anti-lymphocytic serum) increases the number of these tumors; chemically induced tumors or spontaneous tumors are under the control of non-specific effectors such as macrophages and NK cells; NK cell deficiency (of congenital origin such as in beige mice) or acquired (chemically induced) increases tumor growth; carcinogens can induce general immunodepression (chemical carcinogenesis) or stimulate specific suppressive cells (U.V. radiation) thus allowing tumors development. The tumors being established, it may itself contribute to an immunodepressive state thus fostering its growth through the activity of: immune complexes; specific or non specific suppressive cells; an increase in the level of alpha 2-globulin immunosuppressive molecules which are present under normal conditions; a release of several factors acting at different levels such as prostaglandin E, anti-inflammatory factors acting on monocytes, etc. The apparition of an antigenic and immunogenic tumor heterogeneity due to development of new clones will also modify host-tumor relationships. The complexity of the immunological mechanisms which are involved in the control of tumor growth may explain the variable results of immune prevention and of the immunotherapy of cancer.
 ...
PMID:[Cancer and immunosuppression : experimental aspects]. 623 Jan 25

In spite of steep elevation of cancer mortality in the aged, it has been believed that ageing reduces susceptibility to carcinogens. Ebbesen, however, presented contradictory result recently. We examined influences of ageing on chemical carcinogenesis using 6 different age groups of rats given N-bis (2-hydroxypropyl) nitrosamine (DHPN). The results suggested (1) susceptibility to initiating process did not differ much, but promoting process might be prolonged in aged rats, and (2) susceptibility difference was enlarged in aged individuals. These data were supported by doubling time of lung tumors. Another evidence suggesting retarded tumor growth in the aged was observed in frequency of organ metastasis of gastric cancer. The conspicuous finding was shown in the number of cases of gastric cancer without any organ metastasis, i.e. 42.3% in the aged male and 9.3% in the younger male. Occurrence of lymphangitis carcinomatosa in the lung also showed distinct difference between the aged and the younger groups. This type of metastasis mostly derived from gastric cancer, especially signet ring cell cancer. Degree of differentiation of developed tumor may be another point of consideration to estimate the age dependency of tumor metastasis. We also have to pay some attention to the cancers increasing with age.
 ...
PMID:[Aging and development, growth and spreading of cancer]. 663

In chemical carcinogenesis induced by methylcholanthrene in mice C57BL the antitumor activity of sera ind lymphocytes are studied, which was assessed by their capacity to inhibit-stimulate spheroid formation by autologous tumor cells. The serum of animals being at the initial stage of the blastomatous process is found to inhibit the formation of spheroids but to reduce the functional activity of lymphocytes, while in the terminal stage of blastoma growth it contributes to the enhancement of tumor growth under direct interaction with cell-targets or indirectly through lymphocytes.
 ...
PMID:[Antitumor activity of the serum and lymphocytes of C57BL mice in chemical carcinogenesis]. 736 93

From clinical, chemical carcinogenesis and transgenic animal studies, it is evident that wounding has a tumor-promoting effect. We discuss the role of TGF-beta (with special emphasis on TGF-beta 1) in this process and suggest that stromal alterations during wound healing, induced by TGF-beta, can be an important determinant of tumor growth. A tumor and a wound both require similar stromal microenvironments. Thus, a chemically initiated or an oncogene-expressing cell could be complemented to grow into a tumor if it finds itself in a hospitable wound-healing stroma.
 ...
PMID:The tumor-promoting effect of wounding: a possible role for TGF-beta-induced stromal alterations. 784 89

By analysis of skin tumors from F1 hybrid mice we demonstrated that the genetic events that occur during tumor progression depend on the type of chemical carcinogenesis protocol used to induce tumor growth. More than 95% of tumors induced by initiation with 7,12-dimethylbenz[a]anthracene (DMBA) and promotion with 12-O-tetradecanoyl-phorbol-13-acetate (TPA) exhibited mutations in Ha-ras and trisomy of chromosome 7. Carcinomas induced with multiple DMBA treatments had a lower frequency of alterations on chromosome 7 (50%), but only in tumors with Ha-ras mutations, and had a much wider spectrum of alterations, including trisomy, mitotic recombination, deletion, and gene duplication. Carcinomas induced with multiple N-methyl-N'-nitro-N-nitrosoguanidine treatments only rarely exhibited alterations on chromosome 7 (8%), even if they contained mutant Ha-ras. More frequent numerical alterations of chromosome 11 were also seen in TPA-promoted tumors (23%) than in tumors induced by multiple carcinogen treatments (8%). These results show that postinitiation events are nonrandom and fit a model in which promoting agents induce numerical chromosomal alterations but in which mutagens cause more directed mutational events.
 ...
PMID:Induction of different genetic changes by different classes of chemical carcinogens during progression of mouse skin tumors. 791 97

The modulation of chemical carcinogenesis by three biological response modifiers was assessed in a mouse model. CBA mice given 20-methylcholanthrene s.c. were treated with peptidoglycan monomer, azure B and indomethacin for one month, either from day 0 or 75 after methylcholanthrene injection to assess their effects on tumor incidence (on days 150 and 300), time of tumor appearance, time of death, and duration and dynamics of tumor growth. All three agents significantly influenced some of the parameters of tumor growth, except tumor incidence on day 300. Highly significant sex differences in tumor appearance and growth were observed. Tumors with late appearance grew faster in comparison to tumors with early appearance. The data presented indicate that the effectiveness of anti-cancer body defense mechanisms can be best defined by the time of tumor appearance.
 ...
PMID:Effect of three biological response modifiers on chemical carcinogenesis in mice. 827 49

Mutations in the transforming growth factor beta type II receptor (TGF-betaRII) have been identified in human cancers, which suggests a causal role for the loss of TGF-betaRII in cancer development. To directly test this in vivo, we have generated transgenic mice expressing a dominant negative TGF-betaRII (delta betaRII) in the epidermis, using a truncated mouse loricrin promoter (ML). ML.delta betaRII transgenic mice exhibited a thickened skin due to epidermal hyperproliferation. When these mice were subjected to a standard two-stage chemical carcinogenesis protocol, they exhibited an increased sensitivity, with an earlier appearance and a 2-fold greater number of papillomas than control mice. In addition, papillomas in control mice regressed after termination of 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment; whereas ML.delta betaRII papillomas progressed to carcinomas. Furthermore, TPA promotion alone induced papilloma formation in ML.delta betaRII mice, which suggests an initiating role for delta betaRII in skin carcinogenesis. ML.delta betaRII tumors also exhibited increased neovascularization and progressed to metastases, although the primary tumors were still classified as carcinoma in situ or well-differentiated carcinomas. Increased expression of vascular endothelial growth factor, an angiogenesis factor, and decreased expression of thrombospondin-1, an angiogenesis inhibitor, were also observed in ML.delta betaRII tumors. The increased angiogenesis correlated with elevated endogenous TGF-beta1 in ML.delta betaRII tumors. These data provide in vivo evidence that inactivation of TGF-betaRII accelerates skin carcinogenesis at both earlier and later stages, and increased angiogenesis is one of the important mechanisms of accelerated tumor growth and metastasis.
 ...
PMID:Blocking transforming growth factor beta signaling in transgenic epidermis accelerates chemical carcinogenesis: a mechanism associated with increased angiogenesis. 1038 47

When imagining to monitor animal cells through a microscope with resolution at the molecular level, a salient attribute of their surfaces will be the abundance of glycan chains. They present galactosides at their termini widely extending like tentacles into the extracellular space. Their spatial accessibility and their potential for structural variability endow especially these glycan parts with capacity to act as docking points for molecular sensors (sugar receptors such as lectins). Binding and ligand clustering account for transmission of post-binding signals into the cell interior. The range of triggered activities has turned plant lectins into popular tools in cell biology and immunology. Potential for clinical application has been investigated rigorously only in recent years. As documented in vitro and in vivo for the galactoside-specific mistletoe lectin, its apparent immunomodulatory capacity reflected in upregulation of production of proinflammatory cytokines will not necessarily be clinically favorable but a double-edged sword. In fact, lectin application has been shown to stimulate tumor growth in cell lines, histocultures of human tumors and in two animal models using chemical carcinogenesis or tumor transplantation. When testing immunological effects of the endogenous lectin galectin-1, protection against disorders mediated by activated T cells came up for consideration. Elimination of these cells via CD7-dependent induction of apoptosis, and a shift to the Th2 response by the galectin, are factors to ameliorate disease states. This result encourages further efforts with other galectins. Functional redundancy, synergism, diversity or antagonism among galectins are being explored to understand the actual role of this class of endogenous lectins in inflammation. Regardless of the results of further preclinical testing for galectin-1, these two case studies break new ground in our understanding how glycans as ligands for lectins convey reactivity to immune cells, with impact on the course of a tumor or autoimmune disease.
 ...
PMID:Probing the cons and pros of lectin-induced immunomodulation: case studies for the mistletoe lectin and galectin-1. 1152 95


1 2 3 4 Next >>