ISSN:0163-5581    

DOI:10.1080/01635589009514072

出版商:Taylor&Francis Group    

年代:1990

数据来源: Taylor

摘要:

AbstractColorectal cancer is the second most common cancer in the United States. Various dietary, colonic, and fecal components have been implicated as causative factors. Although numerous studies have been conducted to test them, so far no one factor has stood out as the most likely cause of colorectal cancer. This review presents the evidence for and against the major factors and concludes that bile acids are the most strongly implicated factors in the etiology of colorectal cancer.

ISSN:0163-5581    

DOI:10.1080/01635589009514073

出版商:Taylor&Francis Group    

年代:1990

数据来源: Taylor

摘要:

AbstractThe effects of dietary vitamin B‐6 supplementation on the development of human malignant melanoma (M21‐HPB) xenografts and on in vitro responses of leukocytes were examined. Male athymic nude mice, five weeks old, were divided into two groups of 48 each and fed 20% casein diets containing pyridoxine (PN) at 4.1 (control diet) and 61.6 mg/kg diet for 10 weeks. After four weeks of dietary treatment, 20 animals from each dietary group were injected subcutaneously with 3×107melanoma cells. After 4, 8, and 10 weeks of dietary regimen, animals from each group were killed and blood, liver, and spleen samples were obtained. Food consumption and mouse body weights were similar between groups, and no difference was noted in tumor incidence or volume. Noninjected and tumor‐bearing mice given the PN 61.6 diet generally exhibited greater oxygen radical production by phagocytic cells from blood and spleen than did animals fed the PN 4.1 diet. Spleen and blood B lymphocyte proliferation in response to lipopolysaccharide (LPS) was enhanced (10 and 30%) in the noninjected animals given the PN 61.6 diet. In addition, tumor‐bearing mice fed the PN 61.6 diet had significantly greater LPS‐induced spleen cell proliferation at eight weeks when compared with mice consuming the PN 4.1 diet. Despite immune enhancement, tumor incidence and progression was not modified by a high level of dietary vitamin B‐6. Therefore, it is tempting to speculate that tumor inhibition by high dietary vitamin B‐6 may be mediated by T lymphocyte‐dependent mechanisms that are lacking in these genetically immuno‐deficient mice.

ISSN:0163-5581    

DOI:10.1080/01635589009514074

出版商:Taylor&Francis Group    

年代:1990

数据来源: Taylor

摘要:

AbstractVitamin E succinate inhibited proliferation of C4#I celts, an established avian retrovirus freticuloendotheliosis virus (REV)]‐transformed immature lymphoid tumor cell line, in a dose‐dependent manner. The cytostatic effects of vitamin E succinate were reversible in that treated cells regained their ability to divide after vitamin E succinate removal. Possible mechanism(s) for the antiproliferative actions of vitamin E succinate were investigated. Analyses of C4#1 cell surface membrane antigen profiles and morphology indicated that vitamin E succinate was not inducing differentiation of the tumor cells to a more mature, differentiated, nonproliferative state. Five antioxidants, including a synthetic analogue of vitamin E, Trolox, as well as the active vitamin form, DL‐α‐tocopherol, were incapable of inhibiting C4#1 tumor cell growth, indicating that a mechanism of action other than or in addition to functions as an antioxidant may be operating. Cell cycle analyses suggested that C4#1 tumor cells treated with vitamin E succinate were blocked in the G0G1/early S phases of the cell cycle. Tumor growth arrested by vitamin E succinate did not affect the expression of the REV‐encoded oncogene, v‐rel, at either the RNA or protein level. These studies demonstrated that vitamin E, in the form of vitamin E succinate, inhibited the growth of retrovirus‐transformed tumor cells in vitro and suggested that the antiproliferative effects of vitamin E succinate did not involve antioxidant properties but rather, as yet, unidentified mechanisms leading to cell cycle blockage.

ISSN:0163-5581    

DOI:10.1080/01635589009514075

出版商:Taylor&Francis Group    

年代:1990

数据来源: Taylor

摘要:

AbstractThe anchorage‐dependent and anchorage‐independent growth of the human mammary carcinoma cell line MDA‐MB‐231 is inhibited by vitamin A (retinol). Clones resistant to growth inhibition by retinol were isolated from this cell line in soft agar without the use of mutagens. This paper describes the isolation and characterization of the resistant lines. The clones were selectively resistant to retinol. There was significant growth inhibition after treatment with retinoic acid and 13‐cis‐retinoic acid. The resistant clones maintain their resistance to retinol through multiple passages. Resistance is specific for inhibition of growth, because treatment of the resistant clones results in stimulation of plasminogen activator activity without alteration of proliferation. Sodium dodecyl sulfate‐polyacrylamide gel electrophoresis shows no significant qualitative or quantitative difference in the clones when compared with the MDA‐MB‐231 parent line. Although the clones do not regrow in soft agar, they are tumorigenic in athymic mice. Tumors are produced at a rate similar to the parent line. The advantage of this isolation method is that sensitive and resistant malignant cells derived from the same parent cell line are now available to study the molecular events involved in the inhibition of cellular proliferation after treatment with retinol.

ISSN:0163-5581    

DOI:10.1080/01635589009514076

出版商:Taylor&Francis Group    

年代:1990

数据来源: Taylor

摘要:

AbstractBecause long‐term oral administration of the adrenal steroid dehydroepiandrosterone (DHEA) has previously been shown to inhibit the development of spontaneous breast cancer and chemically induced lung, colon, skin, and liver tumors in various mouse and rat strains, the effect of DHEA on the development of rat kidney tumors by a single dose of 30 mg/kg dimethylnitrosamine (DMN) was tested. DHEA was administered in the diet for a 26‐week period commencing 2 weeks after DMN treatment. DHEA administration caused a reduction in body weight gain in accordance with its known antiobesity activity. However, it did not exert any inhibitory effect on either renal mesenchymal or cortical epithelial tumor induction by DMN, nor did it alter the average survival time. There was a statistically significant increase in the incidence of renal adenocarcinomas in the DHEA‐treated group but not of renal adenomas. The results were discussed in relation to the mesodermal origin of kidney and the potency of single‐dose systems of experimental cancer induction.

ISSN:0163-5581    

DOI:10.1080/01635589009514077

出版商:Taylor&Francis Group    

年代:1990

数据来源: Taylor

摘要:

AbstractThe relationship between body size (adult height and weight) and cancer incidence was investigated in an international ecological study of 24 populations. Site‐specific and total cancer incidence rates (age standardized) from 1973 to 1977 were correlated with body size data generally obtained between 1954 and 1974. All‐sites cancer incidence was highly correlated with height among both men (r = 0.50; p≤0.01) and women (r = 0.70; p≤0.001). Among men, there were significant correlations between height and cancers of the central nervous system (r = 0.72), prostate (r = 0.66), bladder (r = 0.65), pancreas (r = 0.59), lung (r = 0.47), and colon (r = 0.46). Significant correlations were observed for cancers of the rectum (r = 0.76), pancreas (r = 0.75), ovary (r = 0.73), central nervous system (r = 0.68), breast (r = 0.65), uterine corpus (r = 0.50), and bladder (r = 0.48) in women. Adjustment for weight altered these correlations only minimally. Weight was significantly correlated to all‐sites cancer only among women (r = 0.44; p<0.05), and site‐specific correlations were significant for the same sites as for height, but the magnitude of the correlation coefficients was somewhat diminished. In addition, adjustment for height greatly reduced the correlations with weight. These findings support previously observed associations between height and specific cancers (e.g., breast and colon) and identify several additional cancer sites that may be similarly related.

ISSN:0163-5581    

DOI:10.1080/01635589009514078

出版商:Taylor&Francis Group    

年代:1990

数据来源: Taylor

ISSN:0163-5581    

DOI:10.1080/01635589009514071

出版商:Taylor&Francis Group    

年代:1990

数据来源: Taylor