ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Books
  • Articles  (14)
  • Data
  • chemoprevention  (14)
  • Wiley-Blackwell  (14)
  • American Institute of Physics (AIP)
  • 2010-2014
  • 1995-1999  (14)
  • 1980-1984
  • 1975-1979
  • 1935-1939
  • 1925-1929
  • 2013
  • 1997  (14)
  • 1984
  • 1983
  • 1978
  • 1938
  • 1937
  • 1925
  • Medicine  (14)
  • Natural Sciences in General
Collection
  • Books
  • Articles  (14)
  • Data
Source
Keywords
Publisher
  • Wiley-Blackwell  (14)
  • American Institute of Physics (AIP)
Years
  • 2010-2014
  • 1995-1999  (14)
  • 1980-1984
  • 1975-1979
  • 1935-1939
    • +
Year
Topic
  • 1
    Electronic Resource
    Electronic Resource
    Tea antioxidants in cancer chemoprevention (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 59-67 
    Details
    ISSN: 0730-2312
    Keywords: antioxidants ; black tea ; chemoprevention ; epigallocatechin-3-gallate ; green tea ; tea polyphenols ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: In recent years, the concept of cancer chemoprevention has matured greatly. Significant reversal or suppression of premalignancy in several sites by chemopreventive agents appears achievable. This article summarizes experimental data on chemopreventive effects of tea polyphenols in different tumor bioassay systems. Tea (Camellia sinensis) is cultivated in about 30 countries, and is the most widely consumed beverage in the world. Three main commercial tea varieties - green, black, and oolong - are usually consumed, but most experimental studies demonstrating the antimutagenic and anticarcinogenic effects of tea have been conducted with water extract of green tea, or a polyphenolic fraction isolated from green tea (GTP). The majority of these studies have been conducted in a mouse skin tumor model system where tea is fed either as water extract through drinking water, or as purified GTP. GTP has been shown to exhibit antimutagenic activity in vitro, and inhibit carcinogen- as well as UV-induced skin carcinogenesis in vivo. Tea consumption has also been shown to afford protection against chemical carcinogen-induced stomach, lung, esophagus, duodenum, pancreas, liver, breast, and colon carcinogenesis in specific bioassay models. Several epicatechin derivatives (polyphenols) present in green tea have been shown to possess anticarcinogenic activity; the most active is (-)-epigallocatechin-3-gallate, which is also the major constituent of GTP. The mechanisms of tea's broad cancer chemopreventive effects are not completely understood. Several theories have been put forward, including inhibition of UV- and tumor promoter-induced ornithine decarboxylase, cyclo-oxygenase, and lipoxygenase activities, antioxidant and free radical scavenging activity; enhancement of antioxidant (glutathione peroxidase, catalase, and quinone reductase) and phase II (glutathione-S-transferase) enzyme activities; inhibition of lipid peroxidation, and anti-inflammatory activity. These properties of tea polyphenols make them effective chemopreventive agents against the initiation, promotion, and progression stages of multistage carcinogenesis. J. Cell. Biochem. Suppl. 27:59-67. Published 1998 Wiley-Liss, Inc.
    Additional Material: 1 Ill.
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
  • 2
    Electronic Resource
    Electronic Resource
    Breast cytology and biomarkers obtained by random fine needle aspiration: Use in risk assessment and early chemoprevention trials (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 101-110 
    Details
    ISSN: 0730-2312
    Keywords: biomarker ; breast ; breast cancer development ; chemoprevention ; clinical trials ; cytology ; ER ; EGFR ; fine needle aspiration ; FNA ; HER-2/neu ; high risk ; p53 ; ploidy ; risk assessment ; surrogate endpoint ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: In a prospective pilot study, we performed breast fine needle aspirations (FNAs) on 224 high-risk and 30 low-risk women and analyzed these aspirates for cytologic changes and biomarker abnormalities of aneuploidy and overexpressed estrogen receptor (ER), epidermal growth factor receptor (EGFR), p53 and HER-2/neu. High-risk women had a first-degree relative with breast cancer (74%), prior biopsy indicating premalignant breast disease (25%), a history of breast cancer (13%), or some multiple of these risk factors (12%). Median ages of the high- and low-risk groups were 44 and 42, respectively. Seventy percent of high-risk and 17% of low-risk women had cytologic evidence of hyperplasia with or without atypia (P〈. 0001). Aneuploidy and overexpression of EGFR and p53 occurred in 27, 37, and 29% of high-risk subjects but only 0, 3, and 3% of low-risk subjects (P〈. 0023). Overexpression of ER and HER-2/neu occurred in 7 and 20% of high-risk women but in none of the low-risk subjects. Biomarker abnormalities were more frequent with increasing cytologic abnormality. Restricting the analysis to those 3 biomarkers most frequently overexpressed in the high-risk group (ploidy, EGFR, p53), 13% of high-risk women with normal cytology, 19% of high-risk women with epithelial hyperplasia, and 49% of high-risk women with hyperplasia with atypia had abnormalities of 2 or more of these 3 biomarkers (P =. 00004). At a median follow-up of 32 months, four women have been diagnosed with invasive cancer and two with ductal carcinomain situ (DCIS). Later detection of these neoplastic conditions was associated (P ≤. 016) by univariate analysis with prior FNA evidence of hyperplasia with atypia; overexpression of p53 and EGFR; the modified Gail risk of breast cancer development at 10 years; and multiple biomarker abnormalities. By multivariate analysis, later detection of cancer was primarily predicted by the number of biomarker abnormalities in the 3-test battery (P=. 0005) and secondarily by the Gail risk at 10 years (P =. 0049). In turn, hyperplasia with atypia was associated with multiple biomarker abnormalities, particularly p53 and EGFR overexpression. Thus, hyperplasia with atypia and cytologic markers in breast FNAs have promise as risk predictors and as surrogate endpoint biomarkers for breast cancer chemoprevention trials. J. Cell. Biochem. Suppls. 28/29:101-110. Published 1998 Wiley-Liss, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
  • 3
    Electronic Resource
    Electronic Resource
    Polyamine measurements in the uterine cervix (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 125-132 
    Details
    ISSN: 0730-2312
    Keywords: chemoprevention ; cervical intraepithelial neoplasia (CIN) ; surrogate endpoint biomarker (SEB) ; α-difluoromethylornithine (DFMO) ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Cervical cancer remains a significant health problem. New strategies based on the molecular aspects of cervical carcinogenesis are needed. Chemoprevention represents a novel strategy for cervical cancer prevention. Our group plans phase I and II trials using α-difluoromethylornithine, a suicide inhibitor of ornithine decarboxylase and potent antiproliferative chemopreventive agent. We conducted a study to identify which polyamines in tissue could best serve as surrogate endpoint biomarkers for future trials. Thirty patients with biopsy-proven cervical intraepithelial neoplasia grade 3 underwent colposcopically directed biopsies of normal and abnormal areas of the uterine cervix for analysis of polyamine synthesis biomarkers. Statistically significant differences were found in the ornithine decarboxylase value and the spermidine:spermine ratio between normal and abnormal areas of the cervix. In general, the ranges in measurements varied widely. Differences in polyamine synthesis biomarkers between colposcopically normal and abnormal areas can be demonstrated. However, studies using polyamine synthesis biomarkers in the cervix would require large numbers of patients to achieve significance. J. Cell. Biochem. Suppls. 28/29:125-132. Published 1998 Wiley-Liss, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America.
    Additional Material: 1 Ill.
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
  • 4
    Electronic Resource
    Electronic Resource
    Protocol design considerations that relate to demonstrating the safety and effectiveness of chemopreventive agents (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 1-6 
    Details
    ISSN: 0730-2312
    Keywords: cancer ; chemoprevention ; clinical trial ; surrogate endpoint biomarker ; protocol design ; safety ; efficacy ; FDA ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: As with other drugs, applications for marketing approval of new chemopreventive agents in the United States must include data from adequate and well-controlled clinical trials that demonstrate effectiveness and safety for the intended use. Knowledge of a drug's pharmacologic actions and metabolism may benefit protocol design, by identifying the patient populations and dosing schedules associated with a favorable risk/benefit profile. With availability of appropriate preclinical data, including standard assessments of an agent's toxicology, effects on reproductive performance, and genotoxicity, initial Phase I studies of 1-3 months may be performed in normal volunteers or an appropriate higher-risk population. For chronic dosing studies of longer duration, preclinical toxicology studies of longer duration are relevant. Enrollment in chemoprevention studies should be directed toward individuals at sufficient risk of developing cancer so that potential benefit may counterbalance the unpredictable and possibly serious adverse effects that may be observed with prolonged administration of a study drug. Phase I and II studies with clinical dosing lasting up to 12 months often afford opportunities to assess drug effect on surrogate endpoint biomarkers that may correlate with endpoints of clinical effectiveness. Phase III and late phase II chemopreventive investigations should routinely utilize a prospective, randomized study design (double-masked and placebo-controlled, when possible). To support marketing approval, there must be evidence that a chemopreventive agent significantly delays or prevents the occurrence of malignancy, with acceptable safety. In some circumstances, modulation of a surrogate marker may provide a basis for marketing approval, before more definitive endpoint data become available. However, the acceptability of a surrogate depends on the nature and quality of the data supporting its predictive value. Given the considerations of large study size, long duration, and high cost that may hamper development of potential agents, studies designed to examine the predictive value of surrogate endpoint biomarkers are of great importance to the future development of chemoprevention research. J. Cell. Biochem. Suppl. 27:1-6. Published 1998 Wiley-Liss, Inc.
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
  • 5
    Electronic Resource
    Electronic Resource
    Chemopreventive properties of Indole-3-Carbinol (I3C): Inhibition of DNA adduct formation of the dietary carcinogen, 2-Amino-1-Methyl-6-Phenylimidazo [4,5-b]Pyridine (PhIP), in female F344 rats (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 42-51 
    Details
    ISSN: 0730-2312
    Keywords: food mutagens ; indole-3-carbinol ; chemoprevention ; DNA adducts ; PhIP ; heterocyclic amines ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Indole-3-carbinol (I3C), a naturally occurring inhibitor of experimental carcinogenesis, was evaluated for its possible inhibitory effect on DNA-adduct formation of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), a dietary mutagen, in female F344 rats. PhIP is a mammary carcinogen in female F344 rats and a colon carcinogen in male F344 rats. Four-week-old animals (4/group) were maintained on powdered AIN-76A diet with or without I3C (0.02% or 0.1%, w/w) for 58 days. PhIP (0.04%, w/w) was added to the diet from days 15 through 42. Animals were killed on days 43 and 58. DNA isolated from mammary epithelial cells (MECs), colon, liver, and white blood cells (WBCs) was analyzed for PhIP-DNA adducts by 32P-postlabeling assays. On day 43, adduct levels of the group receiving 0.1% dietary I3C decreased in MECs (91.9%), colon (67.2%), liver (69.2%), and WBCs (82.3%). On day 58, DNA adduct formation was inhibited in the colon (81.3-82.2%) at both dietary I3C concentrations, and in liver (46.8%) only in the animals fed 0.1% I3C. When incorporated in the diet after exposure to dietary PhIP (0.04% for 2 weeks), I3C (0.1%) had no effect on the rate of removal of PhIP-DNA adducts over the next 28 days. It is concluded that dietary I3C inhibits PhIP-DNA adduct formation in the female F344 rat but does not affect adduct removal. I3C may be a promising chemopreventive agent in PhIP-induced carcinogenesis in rats. J. Cell. Biochem. Suppl. 27:42-51. © 1998 Wiley-Liss, Inc.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
  • 6
    Electronic Resource
    Electronic Resource
    Chemoprevention of cancer of uterine cervix: A study on chemoprevention of Retinamide II from cervical precancerous lesions (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 140-143 
    Details
    ISSN: 0730-2312
    Keywords: chemoprevention ; precancerous lesions ; uterine cervix Retinamide II (RII) ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Dysplasia of the uterine cervix is a recognized precancerous condition. Because of the observed ability of retinoids to suppress various cell lines in vitro, a number of clinical studies have examined the effect these agents have on cervical dysplasia, with the object of developing a means of chemoprevention of cervical malignancies in women at risk. Three cervical cancer chemoprevention trials with Retinamide II (RII) have been conducted at the Cancer Institute, Chinese Academy of Medical Sciences, Beijing, China.A pilot study used RII to intervene in cases of precancerous cervical dysplasia. Twenty-seven women with mild, moderate, or servere cervical dysplasia, pathologically confirmed, were treated by RII suppositories, 10 mg QD, given intravaginally for 6 months (each course lasting 3 months). The results indicated that after the second course, the overall response rate was 96.29% and the complete response rate was 88.89%. In general, side effects were mild. A little cervical and vaginal irritation was well tolerated. In the second double-blind study, patients with precancerous cervical lesions were randomized into two groups, one treated with RII suppository intravaginally and the other with a placebo, once daily for 50 days in two courses. Precancerous lesions in 68.76% of patients in the treatment arm disappeared, with an overall effective rate of 74.29% after two courses of treatment with RII. Its curative effect was approximately that of laser beam radiation and electrocautery (P 〉 0.05), and differed significantly (P 〈0.01) from that of traditional antiinflammatories. RII can be a major measure in prevention and treatment of cervical cancer in high-incidence areas in China. In the third trial, we are conducting a randomized double-blind study placebo controlled, in a high-incidence area of cervical cancer (Xiang-Yuan county, Shang Xi Province, China). At present, the patients are being followed up and the study will be completed after 2 years. J. Cell. Biochem. Suppls. 28/29:140-143. © 1998 Wiley-Liss, Inc.
    Additional Material: 9 Tab.
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
  • 7
    Electronic Resource
    Electronic Resource
    Inhibitory effects of curcumin on tumorigenesis in mice (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 26-34 
    Details
    ISSN: 0730-2312
    Keywords: anti-inflammatory agent ; antioxidant ; chemoprevention ; Curcuminoid ; cyclooxygenase inhibitor ; food coloring agent ; lipoxygenase inhibitor ; plant phenol ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Curcumin (diferuloylmethane), the naturally occurring yellow pigment in turmeric and curry, is isolated from the rhizomes of the plant Curcuma longa Linn. Curcumin inhibits tumorigenesis during both initiation and promotion (post-initiation) periods in several experimental animal models. Topical application of curcumin inhibits benzo[a]pyrene (B[a]P)-mediated formation of DNA-B[a]P adducts in the epidermis. It also reduces 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced increases in skin inflammation, epidermal DNA synthesis, ornithine decarboxylase (ODC) mRNA level, ODC activity, hyperplasia, formation of c-Fos, and c-Jun proteins, hydrogen peroxide, and the oxidized DNA base 5-hydroxymethyl-2′-deoxyuridine (HmdU). Topical application of curcumin inhibits TPA-induced increases in the percent of epidermal cells in synthetic (S) phase of the cell cycle. Curcumin is a strong inhibitor of arachidonic acid-induced edema of mouse ears in vivo and epidermal cyclooxygenase and lipoxygenase activities in vitro. Commercial curcumin isolated from the rhizome of the plant Curcuma longa Linn contains 3 major curcuminoids (approximately 77% curcumin, 17% demethoxycurcumin, and 3% bisdemethoxycurcumin). Commercial curcumin, pure curcumin, and demethoxycurcumin are about equipotent as inhibitors of TPA-induced tumor promotion in mouse skin, whereas bisdemethoxycurcumin is somewhat less active. Topical application of curcumin inhibits tumor initiation by B[a]P and tumor promotion by TPA in mouse skin. Dietary curcumin (commercial grade) inhibits B[a]P-induced forestomach carcinogenesis, N-ethyl-N′-nitro-N-nitrosoguanidine (ENNG)-induced duodenal carcinogenesis, and azoxymethane (AOM)-induced colon carcinogenesis. Dietary curcumin had little or no effect on 4-(methylnitosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung carcinogenesis and 7,12-dimethylbenz[a]anthracene (DMBA)-induced breast carcinogenesis in mice. Poor circulating bioavailability of curcumin may account for the lack of lung and breast carcinogenesis inhibition. J. Cell. Biochem. Suppl. 27:26-34. © 1998 Wiley-Liss, Inc.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
  • 8
    Electronic Resource
    Electronic Resource
    Chemoprevention by naturally occurring and synthetic agents in oral, liver, and large bowel carcinogenesis (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 35-41 
    Details
    ISSN: 0730-2312
    Keywords: chemoprevention ; tongue ; liver ; large bowel ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: A number of naturally occurring compounds and several related synthetic agents were confirmed to exert chemopreventive properties against carcinogenesis in the digestive organs. Phenolic compounds, widely distributed as plant constituents, possess chemopreventive activities in tongue, liver, and large bowel of rodents. Of them, a simple phenolic protocatechuic acid seems to be a promising compound. Organosulfur compounds contained in the cruciferous vegetables and known to activate detoxifying enzymes are regarded as a candidate group for cancer preventive agents. We proved a strong protective effect of S-methylmethanethiosulfonate, a constituent in these vegetables, on azoxymethane (AOM)-induced large bowel carcinogenesis. Some oxygenated carotenoids (xanthophylls) are reported to have antitumor effects. Naturally occurring xanthophylls astaxanthin and canthaxanthin have considerable preventive activities on 4-nitroquinoline-1-oxide (4-NQO)-induced tongue carcinogenesis and AOM-induced large bowel carcinogenesis. A novel synthesized retinoidal butenolide, KYN-54, which suppresses large bowel as well as tongue carcinogenesis, could be a useful agent for prevention of digestive organ cancers. Some trace elements are known to have anticarcinogenic effects. Magnesium hydroxide, a protective agent in colorectal carcinogenesis, inhibits c-myc expression and ornithine decarboxylase activity in the mucosal epithelium of the intestine. Our results show that many agents with preventive effects in tongue, liver, and large bowel control carcinogen-induced hyperproliferation of cells in these organs. Carcinogens used to induce large bowel cancers also induce apoptosis in the target sites. Telomerase activity is increased in the tissues of preneoplastic as well as neoplastic lesions in experimental models such as dimethylbenz[a]anthracene-induced oral carcinogenesis in hamsters. These could be useful biomarkers in studies for cancer chemoprevention. J. Cell. Biochem. Suppl. 27:35-41. Published 1998 Wiley-Liss, Inc.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
  • 9
    Electronic Resource
    Electronic Resource
    Effect of early vs. late administration of 4-Hydroxyphenylretinamide (4-HPR) on N-Methyl-N-Nitrosourea (MNU)-induced mammary tumorigenesis (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 92-99 
    Details
    ISSN: 0730-2312
    Keywords: chemoprevention ; H-ras ; PCNA ; rat ; retinoid ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Mammary tumors were induced in 48-52-day-old female Sprague-Dawley rats in metestrus or diestrus with a single jugular injection of MNU (50 mg/kg). Control rats received the saline vehicle (Group 4 n = 9). Rats were fed 4% Teklad diet containing either 0 (Group 3, n = 20) or 782 mg 4-HPR/kg diet. 4-HPR supplementation was initiated either 1 week prior to (Group 1, n = 14) or 4 weeks following MNU administration (Group 2, n = 19). Neither body weight nor food intake differed significantly between treatment groups. Feeding of 4-HPR 1 week prior to tumor induction reduced the number of tumors (0.8±.2) when compared to MNU control rats (2.1±.4). Immunohistochemical staining of mammary tumor sections for PCNA was quantitated by microdensitometry and expressed as an HSCORE. No differences in HSCORE were observed between tumor groups although the percentage of nuclear area occupied by intermediate and darkly stained nuclei was reduced in the late 4-HPR group. GC→AT transitions in codon 12 of the H-ras gene were detected in 50% (12/24) of MNU control tumors, 60% (6/10) of early 4-HPR tumors, and 38% (6/16) of late 4-HPR tumors. Mutation rates did not differ significantly between groups. 4-HPR appears to be a more effective chemopreventive when fed during the initiation period. J. Cell. Biochem. Suppl. 27:92-99. © 1998 Wiley-Liss, Inc.
    Additional Material: 2 Ill.
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
  • 10
    Electronic Resource
    Electronic Resource
    Dose-ranging study of Indole-3-Carbinol for breast cancer prevention (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 111-116 
    Details
    ISSN: 0730-2312
    Keywords: chemoprevention ; estrogen metabolites ; surrogate endpoint biomarker ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Sixty women at increased risk for breast cancer were enrolled in a placebo-controlled, double-blind dose-ranging chemoprevention study of indole-3-carbinol (I3C). Fifty-seven of these women with a mean age of 47 years (range 22-74) completed the study. Each woman took a placebo capsule or an I3C capsule daily for a total of 4 weeks; none of the women experienced any significant toxicity effects. The urinary estrogen metabolite ratio of 2-hydroxyestrone to 16α-hydroxyestrone, as determined by an ELISA assay, served as the surrogate endpoint biomarker (SEB). Perturbation in the levels of SEB from baseline was comparable among women in the control (C) group and the 50, 100, and 200 mg low-dose (LD) group. Similarly, it was comparable among women in the 300 and 400 mg high-dose (HD) group. Regression analysis showed that peak relative change of SEB for women in the HD group was significantly greater than that for women in the C and LD groups by an amount that was inversely related to baseline ratio; the difference at the median baseline ratio was 0.48 with 95 % confidence interval (0.30, 0.67). No other factors, such as age and menopausal status, were found to be significant in the regression analysis. The results in this study suggest that I3C at a minimum effective dose schedule of 300 mg per day is a promising chemopreventive agent for breast cancer prevention. A larger study to validate these results and to identify an optimal effective dose schedule of I3C for long-term breast cancer chemoprevention will be necessary. J. Cell. Biochem. Suppls. 28/29:111-116. © 1998 Wiley-Liss, Inc.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
  • 11
    Electronic Resource
    Electronic Resource
    Chemopreventive effect of green tea (Camellia sinensis) against cigarette smoke-induced mutations (SCE) in humans (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 68-75 
    Details
    ISSN: 0730-2312
    Keywords: cigarette smoke ; lung cancer ; green tea ; SCE ; chemoprevention ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Green tea (Camellia sinensis) is consumed daily between the meals or after meals in Japan and other Asian countries. In recent years, green tea and its major polyphenolics have been demonstrated to prevent chemically induced tumors in a variety of experimental animal models system. The exact mechanism(s) of its anticarcinogenic activity remains to be elucidated, but green tea polyphenolics have demonstrated antimutagenic, anticarcinogenic, antioxidant, and antipromotional effects, including inhibition of Phase I and inducing Phase II enzymes. Enzyme activities of glutathione peroxidase, catalase, and quinone reductase, and glutathione S-transferase are also induced. However, a paucity of green tea effects in humans prompted us to investigate antimutagenic effects of green tea against smoke-induced mutation in humans. Chemopreventive effects of green tea and coffee among cigarette smokers were examined in 52 clinically healthy male subjects between 20-51 years of age. Blood specimens were obtained from non-smokers (Group I), smokers (II), smokers consuming green tea (III), and smoker/coffee drinkers (IV). The mean years of cigarette smoking ( 〉 10 cigarettes/day) of Groups II, III, and IV ranged from 13.4-14.7 years. Daily intake of green tea and coffee was 3 cups/day/6 months (III and IV). The frequencies of sister-chromatid exchange (SCE) in mitogen-stimulated peripheral lymphocytes from each experimental group were determined and statistically analyzed. SCE rates were significantly elevated in smokers (9.46 ± 0.46) vs. non-smokers (7.03 ± 0.33); however, the frequency of SCE in smokers who consumed green tea (7.94 ± 0.31) was comparable to that of non-smokers, implying that green tea can block the cigarette-induced increase in SCE frequency. Coffee, by contrast, did not exhibit a significant inhibitory effect on smoking-induced SCE. J. Cell. Biochem. Suppl. 27:68-75. © 1998 Wiley-Liss, Inc.
    Additional Material: 2 Ill.
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
  • 12
    Electronic Resource
    Electronic Resource
    Genetic markers for early detection of lung cancer and outcome measures for response to chemoprevention (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 64-73 
    Details
    ISSN: 0730-2312
    Keywords: lung cancer ; chemoprevention ; genetic alterations ; sputum cytology ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Lung cancer is one of the leading causes of cancer death in the world. The high mortality rate for lung cancer probably results, at least in part, from the absence of standard clinical procedures for diagnosis of the disease at early and more treatable stages compared to breast, prostate, and colon cancers. The delineation of genetic alterations that occur in lung tumorigenesis may aid in both developing molecular markers for early detection and predicting of response to chemoprevention/chemotherapy. Cytogenetic and molecular genetic studies have shown that mutations in protooncogenes and tumor suppressor genes (TSGs) are critical in the multi-step development and progression of lung tumors. Inactivation of TSGs are by far the most common mutational events documented during the development of lung cancer. For example, loss of function of the Rb and/or p53 genes has been detected in both small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC). In addition, allelic loss analyses have implicated the existence of other tumor suppressor gene loci on 9p as well as on 3p, 5q, 8p, 9q, 11p, 11q, and 17q. We examined the short arm of chromosomes 3 and 9 for TSG loci by analyzing 23 squamous cell carcinomas of the lung with numerous microsatellite markers. On chromosome 9p, loss of heterozygosity was detected in all of the 23 tumors and homozygous deletions of the p16/CDKN2 locus were detected in 6 of the 23 (26%) tumors. In addition, a novel region of homozygous deletion was detected in 6 of the tumors (26%) at D9S126. The homozygous deletion of D9S126 was confirmed by fluorescent in situ hybridization (FISH) analysis of tumor tissue touch preparations and isolated nuclei using P1 and cosmid probes that contain D9S126. Only one tumor harbored a homozygous deletion at both the p16/CDKN2 locus and the D9S126 locus. The data identify a region of homozygous loss on the short arm of chromosome 9, suggesting the presence of a novel TSG locus approximately 2.5 cM proximal to p16/CDKN2. On chromosome 3p, a similar high percentage of the tumors exhibited loss of heterozygosity. Also, homozygous deletions were detected in several tumors at 3p21.3. Thus, FISH analysis with probes containing the D9S126 or p16 locus could be used as molecular markers to assay sputum samples for premalignant cells exfoliated from the bronchial epithelium. Probes from other chromosome regions such as 3p21 could be used in a similar manner. J. Cell. Biochem. Suppls. 28/29:64-73. © 1998 Wiley-Liss, Inc.
    Additional Material: 3 Tab.
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
  • 13
    Electronic Resource
    Electronic Resource
    Molecular cytogenetic alterations in the early stage at human bronchial epithelial cell carcinogenesis (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 74-80 
    Details
    ISSN: 0730-2312
    Keywords: bronchial epithelium ; carcinogenesis ; lung cancer ; molecular cytogenetic alterations ; chemoprevention ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Lung carcinogenesis is a multi-step process involving activation of oncogenes and inactivation of tumor suppress genes. Many molecular and cytogenetic alterations occur in the early stages of carcinogenesis. We have developed an effective culture system for human bronchial epithelial cells and lung cancer cells. Four immortalized human bronchial epithelial cell lines were established by transfecting the epithelial cells with plasmid DNA containing the early region of SV40. Some molecular and cytogenetic alterations, such as 3p-, 2q-, 9p-, c-myc translocation t(8;14) (q23; q32), were found in one immortalized bronchial epithelial cell line M when approaching malignant transformation. An increase in cell proliferation and decrease of apoptosis were noted in the late passages of the immortalized cell line M. Some molecular cytogenetic alterations were also observed in human primary non-small cell lung cancers. Molecular cytogenetic alterations during the early stage of carcinogenesis of human bronchial epithelial cells may be useful as biomarkers for both diagnosis and intermediate endpoint of chemoprevention of lung cancer. J. Cell. Biochem. Suppls. 28/29:74-80. © 1998 Wiley-Liss, Inc.
    Additional Material: 2 Tab.
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
  • 14
    Electronic Resource
    Electronic Resource
    Chemopreventive effect of difluoromethylornithine (DMFO) on mouse skin squamous cell carcinomas induced by Benzo(a)pyrene (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 81-89 
    Details
    ISSN: 0730-2312
    Keywords: chemoprevention ; benzo-(a)pyrene ; squamous cell carcinoma ; skin tumor markers ; difluoromethyl-ornithine ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The effect of the chemopreventive agent D, L-α-difluoromethylornithine (DFMO) on the incidence of skin squamous cell carcinoma was studied in SENCAR mice treated weekly with topical applications of benzo(a)pyrene (B(a)P) (0.15 mmol, 2×/week) on the dorsal skin. Animals were randomized to receive either chow or chow supplemented with DFMO (1 g/1 kg) and studied at 10, 15, 20, 25, and 30 weeks of B(a)P treatment. Morphometric analyses at each timepoint evaluated the epidermal thickness (ET) and the number of epidermal nucleated layers (NL). The ET increased from 12-17 μm as early as 10 weeks after B(a)P treatment, reaching 22 μm at 20 weeks, and 27 μm at 25 weeks (130% increase). The NL also increased markedly. A relatively modest increase in ET was observed in animals treated with B(a)P and DFMO (16% at 15 weeks, 53% at 20 weeks, and 85% at 25 weeks) as compared to controls. The relative increase in NL showed a similar pattern. Although extensive epidermal hyperplasia was seen early, clear-cut focal premalignant lesions were not identifiable before week 20 of B(a)P treatment. At 20 weeks, the most frequently noted focal premalignant lesions in carcinogen-treated animals (without DFMO) were moderate dysplasias. At 25 and 30 weeks, a large increase was seen in the incidence of more advanced dysplastic lesions and invasive carcinomas. In the group treated with B(a)P and DFMO, a marked reduction in the number of carcinomas was observed at 25 and 30 weeks. At 25 weeks, DFMO reduced tumor yield from 5.8 to 3.2 carcinomas per mouse. At 30 weeks, the reduction was from 13.1 to 5.7 carcinomas per mouse (57% reduction). Collectively, these data emphasize the strong chemopreventive effect of DFMO against tumors in the mouse skin complete carcinogenesis model, as indicated by the reduction of overall skin tumor incidence and the decreased epidermal hyperplasia in DFMO-treated animals. Morphometrically defined increases in ET and NL can be used as early biomarkers of DFMO chemoprevention in mouse skin tumorigenesis. J. Cell. Biochem. Suppls. 28/29:81-89. © 1998 Wiley-Liss, Inc.
    Additional Material: 1 Ill.
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...