Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001418 (adenocarcinoma)
 68,496 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study was undertaken to investigate the antitumor activity of DA-125, a promising new analogue of adriamycin (ADM) containing fluorine, against human gastric and pulmonary adenocarcinoma cell lines and their sublines resistant to ADM and cisplatin (CDDP) by MTT assay. The cells used were MKN-45, human gastric adenocarcinoma, PC-14, human pulmonary adenocarcinoma, and their sublines resistant to ADM, MKN/ADM and PC/ADM, and CDDP, MKN/DDP and PC/DDP. MKN/ADM and PC/ADM were 12.6- and 13.9-fold resistant to ADM, respectively, compared to the respective parental cell lines in terms of IC50. The survival was less in cells treated with DA-125 than that treated with ADM in all lines tested. The antitumor activity of DA-125 was compared with that of ADM using IC50 values and relative resistance (RR). RR was defined as the ratio of the IC50 value of the resistant subline to that of the parent line. In all lines tested, the mean IC50 values for both DA-125 and ADM were lowest in the parent cells, followed by CDDP-resistant cells and ADM-resistant cells. The IC50 values for DA-125 were lower than those for ADM in all six lines tested, although statistical significance was observed in four lines. ADM-resistant sublines were highly resistant to DA-125 (RRs for ADM and DA-125; 12.6 and 7.6 MKN/ADM and 13.9 and 10.3 in PC/ADM, respectively). On the other hand, CDDP-resistant sublines were also resistant to ADM and DA-125 when compared with the respective parent cell lines (RRs for ADM and DA-125; 2.3 and 2.0 in MKN/DDP and 4.8 and 6.0 in PC/DDP, respectively). Although DA-125 showed cross-resistance to ADM and CDDP, we recommended DA-125 to be a good candidate for further development because DA-125 exhibited remarkable antitumor activity against the parent cell lines.
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PMID:Antitumor activity of DA-125, a novel anthracycline, in human gastric and pulmonary adenocarcinoma cells resistant to adriamycin and cisplatin. 941 12

A cell line derived from human endometrial clear cell adenocarcinoma was newly established and named TEN. The tumor cells were obtained from uterine body of a 74-year-old who had been undergone an abdominal simple hysterectomy. The histologic features of the tumor cells showed abundant clear cytoplasm with diastase digested glycogen granule growing in solid nest and tubular pattern. The TEN cells were continuously propagated in vitro during the past 45 months and they were at 75th passage. They grew in a monolayered sheet with a doubling time of about 53 hours. The TEN cells resembled the structure of the original tumor and had abundant glycogen granules, lipid droplets in the cytoplasm. The histopathology of the transplanted tumor in SCID mice resembled that of the original tumors. The TEN cells secreted a high content of CA125. Immunohistochemically, the TEN cells had c-erbB-2 and Cathepsin D immunoreactivity in some parts of the cell population. But they did not have estrogen, progesterone and EGF receptor. Sensitivities of the TEN cells to a variety of anti-cancer drugs were examined. In in-vitro tests, MTT assays employed. The results suggested that the TEN cells were not sensitive to any of 13 agents. On the other hand, in-vivo sensitivity test of transplanted tumor in SCID mice, the tumors were sensitive to CPT-11 and paclitaxel. We conclude that the TEN cell line will be effective material for chemosensitivities against the endometrial clear cell adenocarcinoma.
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PMID:Characterization of a newly established human tumor cell line (TEN) from a patient with clear cell carcinoma of the uterine body and its sensitivity to anti-cancer agents. 943 40

The effects of lipoxygenase inhibitors were investigated using human lung cancer cell lines and A/J mice. By RT-PCR, 5-, 12-, and 15-lipoxygenase mRNA was detected in NSCLC cells. NDGA inhibited 5-LO activity in adenocarcinoma cell line NCI-H1264. Using an MTT assay, NDGA, MK591 and AA861 inhibited the growth of NSCLC cell lines tested with IC50 values of 3, 2, and 7 microM, respectively. Using a clonogenic assay, 10 microM NDGA significantly reduced NSCLC colony number. NDGA significantly slowed NSCLC xenograft growth in nude mice. When the tumors were excised and analyzed, nude mice treated with NDGA had significantly more apoptotic figures than did untreated tumors. A/J mice treated with urethane developed adenomas after 4 months and NDGA administration significantly reduced lung adenoma number. These data indicate that lipoxygenase inhibitors inhibit lung cancer growth and prevent lung carcinogenesis.
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PMID:Lipoxygenase inhibitors prevent lung carcinogenesis and inhibit non-small cell lung cancer growth. 965 87

The aim of this study was to assess the role of in vitro chemosensitivity testing in ovarian cancer using the MTT assay. Cells were separated from solid biopsy or ascitic fluid samples from 73 patients with ovarian adenocarcinoma, FIGO stage III to IV, on presentation. A 48 h drug exposure was followed by the MTT assay to determine sensitivity. Patients were treated by conventional regimens containing platinum. There was a marked variation in sensitivity to the platinum drugs between individual patients. Clinical data were available for 37 patients. Eleven out of seventeen (65%) patients in the sensitive group had a complete response to therapy, compared with 3 out of 20 (15%) in the resistant group (p = 0.005). The overall survival rates were 36% for the sensitive group compared with 18% for the resistant group (p = 0.37). This study suggests that chemosensitivity testing in ovarian cancer may be effective in improving initial clinical response.
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PMID:The clinical relevance of chemosensitivity testing in ovarian cancer. 967 73

Series of 2-methyl-4,9-dihydro-1H-imidazo[4,5-g]quinoxaline-4, 9-diones and 5,10-pyrazino[2,3-g]quinoxalinediones have been synthesized from 6,7-dichloro-5,8-quinoxalinedione for developing new anticancer drugs. Intercalation complex of 2-methyl-4, 9-dihydro-1-methyl-1H-imidazo[4,5-g]quinoxaline-4,9-dione with GC/GC base pairs by a computer graphics-aided method was parallel to the axis of the helix. The interaction energies of synthetic compounds were low. 2-Methyl-4,9-dihydro-1-(4-bromophenyl)-1H-imidazo[4, 5-g]quinoxaline-4,9-dione, which has the lowest interaction energy of the test compounds, was identified as being more cytotoxic against human gastric adenocarcinoma cells (MKN 45) than adriamycin and cis-platin in vitro using the MTT assay. The IC50 value of this compound was 1.30 microM, whereas those of adriamycin and cis-platin were 3.13 and 86.5 microM, respectively. The cytotoxicity of 2, 3-diethyl-5,10-pyrazino[2,3-g]quinoxalinedione was comparable to that of adriamycin in the in vitro assay. However these compounds showed loss of activity on human lung adenocarcinoma cells (PC 14) and human colon adenocarcinoma cells (colon 205). These results suggest that 2-methyl-4,9-dihydro-1-(4-bromophenyl)-1H-imidazo[4, 5-g]quinoxaline-4,9-dione, with the lowest interaction energy, might be an excellent and selective antitumor agent against MKN 45.
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PMID:Synthesis and cytotoxicity of 2-methyl-4, 9-dihydro-1-substituted-1H-imidazo[4,5-g]quinoxaline-4,9-diones and 2,3-disubstituted-5,10-pyrazino[2,3-g]quinoxalinediones. 982 42

The cytotoxicities of 6,7-modified-5,8-quinoxalinedione derivatives and heterocyclic quinoxaline derivatives containing nitrogen, sulfur, and oxygen on human lung adenocarcinoma cell (PC 14), human gastric adenocarcinoma cell (MKN 45), and human colon adenocarcinoma cell (colon 205) were examined in vitro using MTT assay. Pyrido[1,2-a]imidazo[4,5-g]quinoxaline-6,11-dione (10) was markedly cytotoxic against MKN 45 compared with adriamycin and cis-platin used as anticancer drugs. The IC50 value of compound 10 was 0.073 microM while those of adriamycin and cis-platin were 0.12 microM and 2.67 microM, respectively.
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PMID:Cytotoxic effects of quinoxaline derivatives on human cancer cell lines. 984 81

The therapeutic antitumor effect of clarithromycin (CAM) was examined with the 13762NF mammary adenocarcinoma and F-344 rat system. When CAM treatment at a dosage of 2 mg/kg of body weight orally for 21 days was commenced after inoculation of the tumor, no significant decrease in death rate was observed, although the loss in body weight was less than that in the untreated group. When tumor-bearing (TB) rats were treated with CAM in combination with carboplatin or cyclophosphamide, a significant decrease in the death rate was obtained, although neither treatment alone proved to be effective. A beneficial effect was also observed when CAM treatment was combined with surgical treatment. CAM showed no direct cytotoxicity to this tumor in vitro according to the MTT (3-[4, 5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) assay. Spleen cells obtained from TB rats receiving CAM treatment showed a stronger tumor-neutralizing activity than those from rats which had not received CAM treatment (Winn assay). Enhanced induction of cytotoxic cells to allogeneic tumor was also observed in rats immunized with allogeneic tumor cells together with CAM treatment (51Cr release assay). The 13762NF tumor produces transforming growth factor-beta (TGF-beta), tumor necrosis factor alpha, and matrix metalloproteinase-9, and treatment of tumor cells with CAM in vitro for 24 h significantly inhibited the expression of the genes coding for these proteins (reverse transcription-PCR). Levels of expression of the TGF-beta and interleukin-6 genes of spleen cells obtained from CAM-treated TB rats were both significantly lower than those of spleen cells from CAM-untreated TB rats. This study suggests that CAM has biological response modifier activities resulting in a beneficial therapeutic antitumor effect and might be useful for the treatment of human cancers.
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PMID:Therapeutic effect of clarithromycin on a transplanted tumor in rats. 986 67

In our previous paper we have described the isolation and characterization of a doxorubicin (DOX) resistant subline of breast adenocarcinoma SC6 cells. These cells were obtained after the treatment with low, clinically relevant doses of doxorubicin. They became cross-resistant to different wide used cytostatics. The expression of several genes involved in mitotic signal transduction, as well as cathepsins D and L, was similar in both parental and doxorubicin treated cells. The aim of this study was to examine the molecular mechanisms involved in resistance of these cells to doxorubicin. Activity of plasma membrane Pgp was examined in parental and resistant cells due to rhodamine-accumulation assay. The involvement of glutathione (GSH) and glutathione S-transferase (GST) in resistance to doxorubicin was determined in MTT modified assay due to the addition of specific inhibitors: buthionine sulfoximine (for GSH) or ethacrynic acid (for GST). The kinetic of apoptosis was followed after the treatment with DOX in control and SC6 cells by fluorescent microscope. The occurrence of apoptosis was confirmed by analysing DNA fragmentation in agarose gel. Our results indicate that P-glycoprotein, glutathione or glutathione transferases were not involved in resistance of SC6 cells to doxorubicin. However, the apoptosis was inhibited in doxorubicin-resistant cells. Therefore, even low doses of doxorubicin can induce the resistance to this drug due to inhibition of apoptosis.
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PMID:Inhibition of apoptosis is the cause of resistance to doxorubicin in human breast adenocarcinoma cells. 989 Jun 65

In order to improve the therapeutic efficacy of adoptive immunotherapy of cancer using IL-2-activated NK (A-NK) cells, we developed a bi-specific monoclonal antibody (BimAb) 3.2.3xCC52. One specificity of the BimAb (mAb 3.2.3) was directed against rat CD161A (NKR-P1A) which has been shown to be an activation structure on rat NK cells involved in lysis of target cells and cytokine secretion. The other specificity (mAb CC52) was directed against a tumor associated antigen on the rat colon adenocarcinoma cell line CC531. The hybridomas producing 3.2.3 and CC52 were fused, resulting in a quadroma producing the desired 3.2.3xCC52 BimAb. The hybridomas produced antibodies of different isotypes (IgG2b and IgG1 respectively) which enabled us to pre-select quadromas with a high likelihood for production of BimAb, through testing for the production of bi-isotypic antibodies. Production of functional BimAb by the selected quadromas was demonstrated in an assay showing enhanced conjugate formation between CD161A+ cells and CC531 tumor cells. We also tested the 3.2.3xCC52 BimAb for its capacity to enhance NK cell-mediated lysis of CC531 tumor cells in 4 h and 19 h 51Cr release assays; in a prolonged (2 day) tumor neutralization assay using a tetrazolium salt (MTT)-based assay; and in tests for apoptosis using Annexin V-FITC. Although this BimAb was not demonstrated to cause enhanced lysis of CC531 cells by CD161A+ effector cells in vitro, it might be a useful tool to enhance the number of NK cells at the tumor site and/or prolong contact between tumor cells and NK cells in vivo, thereby probably enhancing the therapeutic efficacy of NK cells.
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PMID:The development of a bi-specific anti-CD161A x anti-tumor antibody for rat NK cell targeting. 1008 94

Adriamycin and daunomycin anticancer drugs are detectable in leukemias and solid tumors by cell fluorescence. We observed initial cytoplasmic fluorescence followed by slow nuclear localization of adriamycin and daunomycin after incubation with cultured human squamous cell (P3, FADU) and adenocarcinoma (HT29, SW620) lines by digital video imaging microscopy. Tumor cells incubated with 10 mug/ml of these drugs exhibited increased uptake for more than 3 h with intracellular levels in the range 0.5-2.5 mug/10 6 cells measured by dimethyl sulfoxide (DMSO) extraction and fluorescence spectrophotometry. Daunomycin had 10- to 100-fold higher toxicity for these carcinoma cells than for normal human epithelial keratinocytes measured by in vitro MTT tetrazolium assays. The viability of daunomycin-sensitized carcinoma cells was decreased 2- to 10-fold further by argon laser illumination at 488 nm (5W, T max = 8 degrees C) for 2-3 minutes. The results suggest that adriamycin derivatives may be useful targeting agents for adjuvant treatment and chemophototherapy of human solid tumors by MR-guided laser fiberoptic endoscopy.
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PMID:Laser and daunomycin chemophototherapy of human carcinoma cells. 1014 65


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