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Carcinoma, colon

Gastrin receptors Gastrin carcinomas, colonic carcinomas... [Pg.267]

Acoustic neurofibroma Acute myeloid leukemia (AML) Astrocytoma, high grade Bladder carcinoma Breast carcinoma Colon carcinoma Lung carcinoma, small cell Lung carcinoma, other Melanoma (standard and uveal) Meningioma... [Pg.141]

Familial adenomatous polyposis Malignant lymphoma Stomach carcinoma Colon adenocarcinoma... [Pg.457]

Carcinomas that are almost invariably negative but may occasionally show rare CK7-positive cells include hepatocellular carcinomas, duodenal ampullary carcinomas, colon carcinomas, renal (clear cell type), prostate, and adrenal cortical tumors. [Pg.214]

A Phase I/II clinical trial was conducted in 10 patients with metastatic tumors (renal cell carcinoma, colon carcinoma, melanoma). Tumor material from each patient was isolated, and the cells were ex vivo double-transfected using MIDGE vectors encoding GM-GSF and IL-7. Thereafter, the cells were irradiated and dSLIM added. This autologous therapeutic agent was injected into the patients four times at intervals of 14 days. At the injection site, the APCs were in contact with TAAs and immunomodulating molecules, and this led to a tumor-specific immune response. In total, 50% of the patients responded clinically to the therapy, exhibiting complete or partial response, or stable disease (Fig. 7.14) [60]. [Pg.218]

P53 Parp-1 mice Carcinomas (colon breast) t Tong et al 2001... [Pg.204]

Glioblastoma, melanoma, lymphoma, renal cell carcinoma, colon carcinoma... [Pg.109]

Uracil is used more effectively, in nucleic acid synthesis within a rat hepatoma than in normal liver. This observation appears to have stimulated the synthesis of 5-fluorouracil (1027) as an antimetabolite mainly because the introduction of a fluorine atom involves a minimal increase in size. In the event, 5-fluorouracil did prove to have antineoplastic activity and it is now a valuable drug for treatment of tumors of the breast, colon or rectum, and to a lesser extent, gastric, hepatic, pancreatic, uterine, ovarian and bladder carcinomas. As with other drugs which interfere with DNA synthesis, the therapeutic index is quite low and great care is required during treatment (69MI21301). [Pg.152]

Ralitrexed is a folate analog with greater selectivity. It easily crosses the cell membrane and undergoes polyglutamation. Within tissues, ralitrexed may be stored up to 29 days. It directly inhibits thymidylate synthase, the key enzyme for synthesizing thymidine triphosphate (TTP). The drug has been described to induce apoptosis in tumor cells. Ralitrexed is used for the treatment of colon carcinomas. [Pg.148]

The proton NMR spectrum shows chem shifts of 6.93 5.957- (Ref 1). Photolysis with a Hg arc lamp gives N, nitrous oxide, methane, and ethane (Ref 2). It was found to produce colon and rectal carcinomas in rats after oral administration at 12mg/kg weekly, induction period 235 days (Ref 3)... [Pg.86]

KIRLIN w G, CAi J, DELONG M J, PATTEN E J and JONES D P (1999) Dietary compoimds that induce cancer preventive phase 2 enzymes activate apoptosis at comparable doses in HT29 colon carcinoma cells , JNutr, 129 1827-35. [Pg.64]

OITATE M, NAKAKI R, KOYABU N, TAKANAGA H, MATSUO H, OHTANI H, SAWADA Y (2001) TranSCellular transport of genistein, a soybean-derived isoflavone, across human colon carcinoma cell line (Caco-2). Biopharm Drug Dispos. 22 23-9. [Pg.182]

In culture, the human colon carcinoma cell hne Caco-2 spontaneously differentiates at confluency into polarized cells with enterocyte-like characteristics. The principle of this approach consists of following the passage of the compound of interest from the apical or lumen-like sides to the basolateral or lymph-hke sides of Caco-2 cells, thus following the absorption of the compound per se. One obhgate step for fat-soluble nutrients such as carotenoids to cross the intestinal barrier is their incorporation into CMs assembled in the enterocytes. Under normal cell culture conditions, Caco-2 cells are unable to form CMs. When supplemented with taurocholate and oleic acid, Caco-2 cells were reported to assemble and secrete CMs. ... [Pg.153]

The physiological role of the ICOR is not clear and may be heterogeneous in the various tissues. In the thick ascending limb of the loop of Henle this channel appears to serve as the exit for CP at the basal cell pole [16,65,66], This conductive mechanism, therefore, is required for the reabsorption of Na and CP by this segment of the nephron [16]. In the rectal gland of Squalus acanthias a very similar channel is utilized for Na" and CP secretion. In these latter cells the CP-channel is present in the luminal membrane and is controlled by cytosolic cAMP [15,56,71]. It has been claimed that this kind of channel is also responsible for the secretion of CP in the colonic crypt cell, in colonic carcinoma cells and in respiratory epithelial cells [17,19,20,22]. Recent data have cast some doubt on this concept ... [Pg.280]

CP-channels with smaller conductance have first been noted in the rectal gland of Squalus acanthias by ourselves and in the colonic carcinoma cell line HT29 [61,73]. Later these types of 5-15 pS CP-channels were also found in pancreatic ducts, A6-cells and many other cells [74,75]. It is now claimed that this kind of channel is much more relevant than the ICOR for the pathophysiology of cystic fibrosis [12]. [Pg.280]

CP-channels with even smaller conductance have been described for the lacrimal and other exocrine glands [76,77]. These channels have a conductance of 1-2 pS. Unlike the ICOR-channel they appear to be blocked by millimolar concentrations of furosemide [77]. Most recent and only partially published data from my own laboratory obtained with the above modified nystatin technique [50,133,134] indicate that the respiratory epithelial cells and colonic carcinoma cells possess these types of small CP channels, and that these channels are involved in hormonal regulation of CP-conductance (cf. section 5). These CP-channels are regulated by cytosolic Ca. Hormonally induced increases in cytosolic Ca lead to an abrupt increase in the probability of these small CP-channels being open, yet they have no effect on the ICOR-channel. Data of this kind reinforce that the physiological importance of these small CP-channels may have been grossly underestimated. [Pg.280]

Fig. 3. Cellular model for NaCl secretion ([16] e.g., in a colonic carcinoma cell). The symbols have the following meaning = (Na" + K )-ATPase (J = Na 2Cl K -cotransporter - = ion... Fig. 3. Cellular model for NaCl secretion ([16] e.g., in a colonic carcinoma cell). The symbols have the following meaning = (Na" + K )-ATPase (J = Na 2Cl K -cotransporter - = ion...
Meanwhile we have shown that the excision activation of ICOR channels is due to disinhibition [72]. The respective inhibitor, operationally named cytosolic inhibitor (Cl), is present in the cytosol of placenta trophoblast cells HT29- and Tg4-colonic carcinoma cells and RE cells of normal and CF patients. The molecule has an apparent molecular weight of 700-1 500 Da it is amphiphilic heat stable and not digested by trypsin, proteases, nucleotidases, lipases or amylase [72]. Burc-khardt, Fromter and their collaborators [114] have confirmed our results and extracted a similar or identical Cl from kidney cortex. [Pg.289]

It has been known for some time that the Cl -conductance of epithelial cells can, in addition to its regulation via cAMP, be enhanced by increases in cytosolic Ca " (cf. Fig. 3). This has been shown with Ca -ionophores [120,121] or with hormones increasing cytosolic Ca such as carbachol, neurotensin, ATP, etc. [50,103,104]. Usually these agonists have dual effects. They increase the Cl - as well as the K" -conductance [104]. Stubs et al. [122] have shown that CF cells still increase their Cl -conductance in response to ATP. Another mechanism of Cl -channel activation has been described in whole-cell patches of colonic carcinoma and RE cells [123,124] when the cells are exposed to hypotonic media they swell and increase their Cl -conductance. This is a rather general phenomenon which is present in a lot of cells [11]. In their effort to reduce cell volume in hypotonic media (regulatory... [Pg.290]

Inhibition of DNA topo I activity in HCT 116 (human colon carcinoma) cells by CPT, CPT-11, SN-38, TPT, and EGCG (Table 8) ... [Pg.59]

The above three equations (Eqs. 10-12) for the different cell lines are very similar to each other, which suggests that the inhibition against DNA topo I is probably one of the most important antitumor mechanisms for these compounds (CPT, CPT-11, SN-38, TPT, and EGCG) against the three human colon carcinoma (HCT 116, VACO 241, and SW 480) cell lines. In these equations, the number of data points (four or five) is small, but the correlations are statistically significant. [Pg.60]

McKeever, J., Qureshi, A., Gorey, T., Kay, E., Byrne, P. and Hennessey, T.P.J. (1992). Azoxymethane induced free radical activity in rat colon carcinoma. Gastroenterology 102, A378. [Pg.167]


See other pages where Carcinoma, colon is mentioned: [Pg.294]    [Pg.559]    [Pg.114]    [Pg.460]    [Pg.12]    [Pg.981]    [Pg.294]    [Pg.559]    [Pg.114]    [Pg.460]    [Pg.12]    [Pg.981]    [Pg.434]    [Pg.85]    [Pg.430]    [Pg.743]    [Pg.1320]    [Pg.585]    [Pg.589]    [Pg.291]    [Pg.403]    [Pg.100]    [Pg.202]    [Pg.49]    [Pg.174]    [Pg.362]    [Pg.175]    [Pg.291]    [Pg.46]    [Pg.58]    [Pg.281]   
See also in sourсe #XX -- [ Pg.79 , Pg.87 ]

See also in sourсe #XX -- [ Pg.79 , Pg.87 ]

See also in sourсe #XX -- [ Pg.79 , Pg.87 ]




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Cancer Colon carcinoma

Cancer cell lines colon carcinoma

Cell line colon carcinoma caco

Colon 26-L5 carcinoma

Colon carcinoma cells

Colonic carcinoma

Cytotoxicity in COLO-205 (colon carcinoma

HT-29 (human colon carcinoma

Human colon carcinoma

Human colon carcinoma HCT

Human colon carcinoma cell line model

Human colon carcinoma cells

Lipid for C38 colon carcinoma

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