Malignant colo-jejunal fistula.
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Adenocarcinoma↗
Biomedical subjects
Y Ziv
Publications and source records attributed to Y Ziv.
The effect of tamoxifen and fenretinimide on human colorectal cancer cell lines in vitro.
BACKGROUND: The natural history of colorectal neoplasia may be influenced by steroid hormones and nutritional compounds. We evaluated the effect of the anti-estrogenic tamoxifen (Tx), and the synthetic retinoid fenretinimide (4-HPR) on the growth of human colorectal cancer cells. METHODS: DLD-1, CACO-2, SW-620, and COLO-205 colon cancer cells, and SW-1463 and SW-837 rectal cancer cells were cultured under serum-free conditions. Quadruplicates wells (4 x 10(4) cells/well) were created for each treated, and untreated groups in each cell line. Cells were treated with 1 microM Tx, 5 microM Tx, 1 microM 4-HPR, 1 microM Tx with 1 microM 4-HPR, and 5 microM Tx with microM 4-HPR. Cell growth was measured colorimetrically with the hexosaminidase assay (405 nm), and was compared among the different groups. Cells were analyzed for estrogen receptors using an enzyme immunoassay. RESULTS: Tamoxifen, 4-HPR, or both, inhibited the growth in DLD-1 (P = .001), COLO-205 (P = .02), SW-620 (P = .001), and CACO-2 (P = .02) cell lines. Tamoxifen with 4-HPR inhibited cell growth more (P = .03) than did either Tx or 4-HPR in DLD-1, COLO-205, and SW620 cancer cells. Tamoxifen, 4-HPR, or both, had no effect on the growth of SW-837 (P = .14) cancer cells. Tamoxifen with 4-HPR promoted (P = .02) growth in SW-1463 cells, but not when added separately. Estrogen receptors were not found in any of the cells. CONCLUSIONS: Under serum-free conditions, Tx, 4-HPR, or both, inhibit the growth of human colon cancer cells but not of rectal cancer cells. Combined treatment with Tx and 4-HPR is more effective than treatment with either of the agents alone in inhibiting of cell growth. The mechanism of inhibition is not clear yet, and further studies are warranted.
Adenocarcinoma↗
The effect of tamoxifen on established human colorectal cancer cell lines in vitro.
UNLABELLED: The purpose of this study was to evaluate the effect of the anti-estrogenic tamoxifen (Tx) on the growth of human colorectal cancer cells. METHODS: Serial concentrations (0.005 microM, 0.05 microM, 0.5 microM, 5 microM, and 50 microM) of the anti-estrogenic tamoxifen (Tx) were added and analyzed for their effect on the growth of established human colorectal cancer cells. HT-29 and SW-620 colon cancer cells and SW-1463 rectal cancer cells were tested in both serum-free media and serum-containing media (10% fetal calf serum). COLO-205 colon cancer and SW-837 rectal cancer cells were only tested in 10% fetal calf serum-containing media. Cell growth was measured with the hexosaminidase assay and was compared among the different groups. Cells were analyzed for estrogen receptors using enzyme immunoassay. RESULTS: In serum-free media, Tx inhibited the growth of HT-29 (P = .05) and SW-620 (P = .01) colon cancer cells at all concentrations tested. RESULTS: In serum-containing media, Tx inhibited (P = .04) the growth of the SW-837 rectal cancer cells at all concentrations and SW-1463 (P = .05) rectal cancer cells at the concentrations of 0.05 microM and 0.5 microM Tx. The inhibition of cell growth in HT-29, SW-620 and SW-1463 line was greater (P < .001) under serum-free media conditions. Estrogen receptors were not detected in any of the cell lines tested. CONCLUSIONS: Hormonal manipulation with colo-rectal cancers is possible, but the effect of Tx on the growth of colon cancer cells differs from the effect on rectal cancer cells under various conditions. The mechanism of inhibition is not clear yet, and further studies are warranted before any clinical implications can be postulated.
Antineoplastic Agents, Hormonal↗
Effect of tamoxifen on 1,2-dimethylhydrazine-HCl-induced colon carcinogenesis in rats.
BACKGROUND: Evidence suggests that steroid hormones may affect the natural history of colon cancer. METHODS: Baseline levels of estrogen receptors, polyamines, and ornithine decarboxylase in colonic mucosa, and blood estradiol were measured in 10 normal Sprague-Dawley outbread female rats. Therefore, 151 rats were fed a 15% fat diet and divided into three groups. Rats in the control group (n = 20) received weekly s.c injections of the 1,2-Dimethylhydrazine-HCl (DMH) vehicle. To induce colon cancer, 131 rats received weekly subcutaneous injections of DMH (20 mg/kg). Of these 131 rats, 65 also ingested 0.5 microgram/g tamoxifen, daily. Half of the rats in each group were sacrificed at 14 weeks, the remainder at 28 weeks. All measurements were repeated at these times and tumor incidence was calculated. RESULTS: The number of rats with tumors was 41% higher (P = .07) in rats treated with DMH vs those treated with tamoxifen and DMH (72.7% vs 51.5%). Tumor cells in both groups had higher levels of polyamines and ornithine decarboxylase activities (P = .03 to P < .001) and lower levels of estrogen receptors (P = .005) to P < .001) compared to adjacent normal colonic mucosa. Estrogen receptors were not detected in the colons of the rats in the control group. No correlations were found between estradiol and estrogen receptors in normal (r = .01, P = .95) or tumor (r = .03, P = .86) cells, or between polyamines or ornithine decarboxylase and estrogen receptors in normal (r = .01 to .14, P = .63 to .95) or tumor (r = .07 to .26, P = .16 to .86) cells. CONCLUSIONS: Tamoxifen reduced the incidence of DMH-induced colon cancer in rats and may thus have chemopreventive effects. Although it was not statistically significant, further studies are justified to continue this line of research.
1,2-Dimethylhydrazine↗