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)

The effects of a single application of various dose levels of acetic acid or the weak tumor promoter, phorbol-12,13-ditetradecanoate, on the incorporation of tritiated thymidine (3H-TDR), 3H-cytidine, and 3H-leucine into DNA, RNA, and protein of mouse epidermis, respectively, were determined and compared with histologic changes in the skin. Treatment with either 500 or 833 mumoles acetic acid induced a sequential and sustained stimulation of RNA, protein, and DNA synthesis, which was followed by extensive epidermal hyperplasia similar to that reported for the strong promoter and irritant, 12-O-tetradecanoyl-phorbol-13-acetate. A dose-response relationship between the amount of acetic acid and the rate of DNA synthesis was found between the dose levels of 33 to 833 mumoles of acetic acid per application. The latter dose induced the maximum activation of 3H-TDR into DNA at 723% of control at 2 days, whereas 33 mumoles stimulated DNA synthesis earlier and peaked at 210% of control at 3 hours. Phorbol-12,13-ditetradecanoate also stimulated macromolecular synthesis in a similar sequence, though to a lesser degree. No observable inflammation and only a slight hyperplastic response were noted with phorbol-12,13-ditetradecanoate. Weekly applications of 667 mumoles of acetic acid produced a maximal tumor response of 0.73 papilloma/mouse after 32 weeks of promotion. However, a weekly dose of 677 mumoles of acetic acid was essentially inactive when given in two divided doses. When croton oil was administered twice weekly at a 0.25%-dose level, 10.2 papillomas/mouse were induced after 32 weeks of promotion. The results showed that the previously considered nonpromoting inflammatory agent, acetic acid, must be a weak promoter. However, there was no correlation between stimulated macromolecular synthesis or hyperplasia and tumor promotion when phorbol esters were compared with acetic acid.
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PMID:Acetic acid, a potent stimulator of mouse epidermal macromolecular synthesis and hyperplasia but with weak tumor-promoting ability. 118 13

Spleen cells from BALB/c mice bearing syngeneic sarcomas and from BALB/c mice whose sarcomas had been excised were cultivated in vitro. The culture supernatants were tested for two activities: their ability (1) to supress ("block") specific lymph-node cell-mediated cytotoxic reactions directed against the respective neoplasms; and (2) to induce antibody-dependent cellular cytotoxicity (ADC) specific for the antigens of the respective tumors. Both specific activities, blocking and induction of ADC, were detected in culture supernatants from spleens of tumor-bearing mice, even when repeatedly harvested at intervals over a 7-day period. Supernatants of cultured spleen cells from mice whose sarcomas had been excised 3-4 weeks previously also had ADC but no blocking activity. Supernatnats of cultures treated with inhibitors of protein synthesis lacked both blocking and ADC activities; the inhibitory effect of cycloheximide on these activities, as well as on protein synthesis, was reversible. Factors in the culture supernatants responsible for blocking and for ADC were labelled when the culture were incubated with 14C-leucine. The labelled material was retained by, and could be eluted from, immunoadsorbents for mouse immunoglobulins. In addition, the labelled material bound preferentially to those tumor cells for which specific blocking or ADC activities were observed. The findings indicate that factors responsible for the blocking and ADC phenomena were indeed synthesized by the spleen cells in vitro.
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PMID:In vitro synthesis of tumor-specific factors with blocking and antibody-dependent cellular cytotoxicity (ADC) activities. 120 73

Increased ferritin synthesis by Hodgkin's disease splenic tumor tissue was demonstrated by incorporation of 14C-leucine and radioautography. This suggests that elevated tumor and serum ferritin concentrations found in patients with Hodgkin's disease is derived from tumor tissue per se.
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PMID:Ferritin synthesis by splenic tumor tissue of Hodgkin's disease. 120 96

Following short-term suspension culture, cells from the Balb/C sarcoma Meth A were allowed to incorporate both [14C] leucine and 2-deoxy-D-glucose-1-[3H] (2DG). The 2DG is trapped as a small anionic marker of the cytosol. Deviation from the kinetics of spontaneous efflux of the markers is interpreted as reflecting perturbation of the target cell membrane. In the presence of guinea pig complement and a rabbit antiserum to Meth A, enhanced 2DG efflux was effected in a titer comparable to that detected with a 51Cr-release assay. With a number of alloantisera and syngeneic immune sera, 2DG efflux was enhanced while 51Cr-release was unaffected. Only in the presence of syngeneic immune sera from mice bearing a low tumor mass, syngeneic splenic leukocytes effect a retardation in the spontaneous 2DG efflux. Sera from animals with a large tumor mass were ineffective. Effux of proteins labeled with [14C] leucine was not altered. The phenomenon was not dependent on the presence of a heat-inactivatable syngeneic complement source. The method described provides a sensitive probe of target cell membrane permeability in the tumor model studied. The phenomenon detected is the capacity of serum, sampled relatively early in syngeneic oncogenesis, to direct syngeneic splenic leukocytes to interact with the target cell membrane differentially altering its permeability to the small cytosol marker.
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PMID:The use of 2-deoxy-D-glucose to assess changes in tumor target cell membranes in vitro. 120 22

Discontinuation of recommencement of estrone-progesterone treatment causes regression and regrowth, respectively, of transplantable hormone-dependent GR mouse mammary tumors. This tumor model was found convenient for the demonstration of hormonal responses in hormone-dependent mouse mammary tumor cells. Tumor regression was palpable 2 days after discontinuation of hormonal treatment and tumors reached half their size within 3-6 days. At this point, hormones were readministered and 2-4 days later the tumors had grown to their preregression size. In the growing and regressing tumor we have investigated: (1) the content of RNA, DNA and protein per g wet weight, (2) in vivo incorporation for 45 min of 32P-orthophosphate into RNA and DNA and the 35S-methionine incorporation into protine; (3) SDS polyacrylamide gel electrophoresis of soluble proteins after in vivo incorporation of 14C- and 3H-leucine. The RNA content per g wet weight was found to decrease during regression and to increase during regrowth. DNA and protein content showed no variation. RNA/DNA ratio thus varied in parallel to the RNA content. The precuursor incorporation into all three macromolecular species decreased during regression. The incorporation into DNA showed the most pronounced decrease. After readministration of hormones, regrowth was accompanied by a rapid increase in precursor incorporation into RNA, while the incorporation into DNA showed a lag of 1 to 2 days. SDS polyacrylamide gel electrophoresis was carried out with soluble proteins labelled in vivo with 14C- and 3H-leucine during regression and regrowth, respectively. No differences in 14C/3H ratios could be demonstrated for the major fractions detectable in the electropherogram.
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PMID:Biochemical changes during regression and regrowth of hormone-dependent GR mouse mammary tumors. 124 97

Using the double thymidine block technique. Ehrlich ascites tumor cells (ELD) carried in continuous spinner culture have been synchronized. Simultaneous monitoring of 3H-thymidine incorporation, cell number and mitotic index yielded a cell cycle time of approximately 13.5 hours. This is composed of an S period of 3-4 hours. G2 of 6-8 hours and M of 1-2 hours. No appreciable G1 is present. Ehrlich cells synchronized in this manner were used to investigate the characteristics of two neutral amino acid transport systems during progression through the cell cycle. Unidirectional influx via the Na-dependent system A was studied using C14-alpha-aminoisobutyrate (AIB) as substrate. The Na-independent system L was monitored using 3H-leucine and 14C-cycloleucine as substrates. Transport by the A system was minimal in M and early S. It underwent a three-fold increase during late S and early G2. In mid G2 the transport via this system rapidly dropped and remained low again through M and early S. The intracellular/extracellular ratios of AIB indicate that the system is actively transporting AIB thoughout the cell cycle. The minimum ratios of approximately 3 were achieved during early M and the maximum ratios of approximately 9 were achieved in late S, early G2. The uptake of leucine and cycloleucine by the L system was quite different during the cell cycle. Maximal unidirectional influx by this system occurred during early and mid S period. Upon progression into G2 the transport rate dropped and remained reduced throughout M. Intracellular/extracellular ratios of leucine or cycloleucine were near unity at the peak of the transport activity (early S) and dropped to values of 0.5 to 0.6 throughout the remainder of the cycle. This result indicates that inward transport by the L system is, for the most part, non-active in growing cells.
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PMID:Membrane transport in synchronized Ehrlich ascites tumor cells: uptake of amino acids by the A and L system during the cell cycle. 126 7

Synthesis and release of radiolabeled macromolecules and tumor-associated antigens (MAA) by murine B16 melanoma was studied by pulse labeling cells in culture with 3H-leucine. Approximately 36% of newly synthesized macromolecules and 44% of newly synthesized MAA were released in 48 hr. MAA release was slightly, but consistently, more rapid than the average release of other macromolecules. Release of MAA did not result solely from cell death since it was greater than that of 51Cr-labeled molecules and cell viability was over 98%. The rate of release of newly synthesized MAA was not significantly influenced by cell replication. However, synthesis of MAA was much greater during the logarithmic than the stationary phase of cell growth, suggesting a concomitant increase in the amount of MAA available for release. These findings indicate that antigens and other macromolecules can be rapidly released by viable tumor cells.
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PMID:Release of tumor-associated antigens by murine melanoma cells. 127 Jul 97

Point mutations in ras genes resulting in substitutions of amino acid Gly in positions 12 and 13, and Gln in position 61 of the ras gene product p21, are commonly found in human tumors. Peptides derived from aberrant p21 may elicit a tumor specific T cell response, provided that these peptides can bind to HLA molecules of the tumor and the patient has T cells able to recognize the corresponding peptide-HLA complex. Here we report that CD4+ T cells of memory type (CD45RO+) from a patient with a follicular thyroid carcinoma respond against a synthetic peptide derived from aberrant p21 ras having a Gln-->Leu substitution at position 61. Such responses were not observed when T cells from healthy volunteers or cancer patients where this mutation does not usually occur were stimulated with this peptide. The responding T cells did not cross-react with the corresponding peptide derived from native p21 ras nor did they recognize peptides carrying other substitutions in position 61. T cells clones were generated which recognized this Leu61 peptide when presented by HLA-DQ8 molecules. These T cell clones also recognized the corresponding intact p21 ras protein. By using several different synthetic peptides, a peptide with optimal stimulatory capacity was defined. Performing polymerase chain reaction and oligonucleotide probing we were, however, not able to detect the p21 ras gene encoding the Gln-->Leu substitution in DNA from tumor biopsies from the patient. This may indicate that tumor cells harboring the mutation leading to the Gln-->Leu substitution had been eliminated and that tumor progression was due to cells that had deleted the mutated ras gene. The finding that ras derived peptides and recombinant mutated p21 ras are immunogenic in man may form the basis for the development of cancer immunotherapy based on synthetic oncogene derived peptides.
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PMID:Memory T cells of a patient with follicular thyroid carcinoma recognize peptides derived from mutated p21 ras (Gln-->Leu61). 128 32

A case of rare extra-adrenal tumor composed of pheochromocytoma-ganglioneuroma which developed in a 48-year-old Japanese male is reported. Histologically, the tumor contained equal proportion of two distinct patterns, pheochromocytoma and ganglioneuroma. Immunohistochemical examination revealed that pheochromocytoma cells were positive for Leu-7 and ganglion cells in ganglioneuroma were positive for vasoactive intestinal peptide (VIP), respectively. Neuron specific enolase (NSE) was positive in the neoplastic cells of both components, and S-100 protein was also positive in fibers around ganglion cells. Ultrastructural examination revealed that neurosecretory granules were present in the neoplastic cells.
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PMID:Extra-adrenal pheochromocytoma-ganglioneuroma. A case report. 130 Jun 5

By means of nuclide precursor incorporation, the effects of 211At labelled monoclonal antibody against gastric cancer (211At-3H11McAb) on DNA, RNA and protein synthesis in gastric cancer cell were studied. The results show that 211At-3H11McAb and Na211At-3 inhibit 3H-TdR, 3H-UR and 3H-Leu incorporation, especially 3H-UR incorporation, into gastric cancer cell at 3.7 x 10(4)Bq and 1.85 x 10(5)Bq; the inhibiting rates depend on concentration. The DNA biosynthesis in gastric cancer cell gradually recover after the drug is removed, suggesting that the drug should exert an inhibiting action on DNA biosynthesis in tumor cell through interference of DNA metabolism.
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PMID:[The effect of 211At labelled monoclonal antibody against gastric cancer on DNA, RNA and protein synthesis in gastric cancer cell]. 130 36


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