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  • 1
    Electronic Resource
    Electronic Resource
    Effects of vitamin D and parathyroid hormone on cyclic AMP production by bone cells isolated from rat calvariae (1984)
    Springer
    Calcified tissue international 36 (1984), S. 320-326 
    Details
    ISSN: 1432-0827
    Keywords: Calcium ; Vitamin D deficiency ; 1,25(OH)2D3 ; Parathyroidectomy ; Parathyroid hormone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Studies presented here were designed to investigate further the basis for an impaired cAMP response to parathyroid hormone (PTH) in osteoblastlike calvarial bone cells isolated from vitamin D-deficient rat pups. The goal was to perturb Ca, PTH, and vitamin Din vivo in order to see which factors might be responsible for the impairedin vitro bone cell cAMP response. Pups either were parathyroidectomized (PTX) 3–5 days, implanted with osmotic minipumps delivering high doses of PTH, given repeated, high doses of 1,25(OH)2D3, or were D-deficient (-D, i.e., born and suckled by D-deficient mothers). Osteoblastlike bone cells, isolated by sequential enzyme digestion and centrifugation, were exposed to PTH for 5 min in the presence of a phosphodiesterase inhibitor. In bone cells isolated from -D rat pups, both basal and PTH-induced cAMP accumulation were significantly lower than in +D bone cells. Earlier, we had shown that two daily injections of -D pups with 50 ng 1,25(OH)2D3 restores this reduced bone cAMP response of -D pups toward normal. In the present study, neither basal nor PTH-induced bone cell cAMP accumulation was affected by subjecting D-replete pups to PTX, PTH infusion, or repeated high doses of 1,25(OH)2D3 despite the fact that each treatment markedly changed serum Ca or serum immunoreactive PTH. The results indicate that the impaired bone cell cAMP response seen in -D pups is not a direct result of chronic hypocalcemia and that the “heterologous desensitization” seenin vitro with added 1,25(OH)2D3 could not be duplicated byin vivo treatment of +D pups with supraphysiologic doses of 1,25(OH)2D3. Finally the lack of alteration in the bone cell cAMP response to PTHin vitro after chronic PTH infusionin vivo fails to support the notion that the impaired response in -D bone cells can be explained entirely by “homologous desensitization” induced by high circulating levels of PTH in the hypocalcemic, -D rat pup.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02405337
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  • 2
    Electronic Resource
    Electronic Resource
    Development of Breast Cancer Chemopreventive Drugs (1995)
    Oxford, UK : Blackwell Publishing Ltd
    The @breast journal 1 (1995), S. 0 
    Details
    ISSN: 1524-4741
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Chemoprevention, or intervention with chemical agents at the precancer stage to avoid or slow the development of the carcinogenic process, is one strategy to reduce both the incidence of breast cancer and its mortality. Systematic development of cancer chemopreventive drugs calls for evaluation of pre-clinical efficacy in well-characterized in vitro screens and animal cancer models. Highly promising agents are also included in traditional pre-clinical toxicity tests performed in two species. The most promising and least toxic agents enter clinical trials, including both phase I safety and pharmacokinetics evaluations and phase II and III efficacy studies. The use of populations with defined, measurable biologic alterations in tissue occurring prior to cancer development, i.e. intermediate biomarkers, is important to successful phase II chemoprevention trials. The intermediate biomarkers may be of several types, such as histological/premalignant lesions, proliferative, genetic/regulatory, differentiation-related, or biochemical. For example, ductal and lobular carcinoma in situ are premalignant lesions in the human breast. These lesions are tissue at very high risk of malignant progression and also have the potential to be modulated by chemopreventive agents. In addition, other types of biomarkers may be identified within the lesions. These biomarkers could then serve as surrogate trial end-points, instead of cancer incidence, for use in shorter, less costly trials.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1524-4741.1995.tb00250.x
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  • 3
    Electronic Resource
    Electronic Resource
    Difluoromethylornithine in combination with tamoxifen in female rats: 13-week oral toxicity study (1999)
    Springer
    Cancer chemotherapy and pharmacology 44 (1999), S. 475-483 
    Details
    ISSN: 1432-0843
    Keywords: Key words Tamoxifen ; Difluoromethylornithine ; Rats ; Reproductive system toxicity ; GI toxicity ; Dermal toxicity ; Ornithine decarboxylase ; Estrogen
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Purpose: Cancer chemoprevention is the use of pharmacologic or natural agents to inhibit the development of cancer. Difluoromethylornithine (DFMO) is an irreversible inhibitor of ornithine decarboxylase, the rate-limiting enzyme in the biosynthesis of polyamines. DFMO has demonstrated chemopreventive efficacy in animal models of tumorigenesis. Tamoxifen (TAM) is currently used for treatment of estrogen receptor-positive breast carcinoma and has demonstrated efficacy in chemoprevention of breast cancer in women at high risk for the disease. The administration of tamoxifen with DFMO is being considered for development by the National Cancer Institute as a potential drug regimen for the chemoprevention of breast carcinoma. Methods: The toxicity of DFMO in combination with TAM was evaluated in female rats following 13 weeks of daily administration by gavage. Dose groups were vehicle control, DFMO (1000 mg/kg per day), low TAM (0.25 mg/kg per day), high TAM (2.5 mg/kg per day), low combination (1000 + 0.25) and high combination (1000 + 2.5). Results: No mortalities occurred in the study. Clinical signs of toxicity were limited to dermal lesions consisting of scab formation and abrasions produced by DFMO. Administration of either DFMO or TAM resulted in decreased body weight gains, with coadministration having an additive effect. Serum albumin, total protein, cholesterol and triglyceride levels were decreased in all drug-treated dose groups, although histologic evidence of liver lesions were not seen. TAM resulted in increased numbers of red blood cells, whereas DFMO produced a slightly anemic response. DFMO produced lesions in the small intestine consisting of necrosis of crypt epithelium and crypt microabscess, which were enhanced by TAM coadministration. Administration of TAM resulted in histologic changes in the ovaries, fallopian tube, vagina, cervix and uterus, indicating that inhibition of ovulation and reproductive cycle arrest in the proestrus stage had occurred. Coadministration with DFMO did not affect the changes to the reproductive system induced by TAM. Conclusions: Coadministration of DFMO with tamoxifen did not result in toxicity unique to the combination drug regimen, but rather toxicity resulted from administration of each drug. Under the conditions of the study, the overall toxicity produced by dual administration of DFMO with tamoxifen was additive with respect to the toxicity associated with each agent alone.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002800051121
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  • 4
    Electronic Resource
    Electronic Resource
    Thirteen-week oral toxicity study of difluoromethylornithine in combination with tamoxifen citrate in female dogs (1999)
    Springer
    Cancer chemotherapy and pharmacology 43 (1999), S. 479-488 
    Details
    ISSN: 1432-0843
    Keywords: Key words Tamoxifen ; Difluoromethylornithine ; Dogs ; Reproductive system toxicity ; GI toxicity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Purpose: Cancer chemoprevention is the use of pharmacologic or natural agents to inhibit the development of cancer. Difluoromethylornithine (DFMO) is an irreversible inhibitor of ornithine decarboxylase, the rate-limiting enzyme in the biosynthesis of polyamines. DFMO has demonstrated chemopreventive efficacy in animal models of tumorigenesis. Tamoxifen (TAM), a nonsteroidal antiestrogen, is approved for use in the treatment of estrogen receptor-positive breast carcinoma and has demonstrated efficacy in chemoprevention of breast cancer in women at high risk for the disease. The administration of TAM with DFMO is being considered for development by the National Cancer Institute as a potential drug regimen for the chemoprevention of breast carcinoma. Methods: The toxicity of DFMO in combination with TAM was evaluated in female Beagle dogs following 13 weeks of daily oral administration by capsule. Dose levels in milligrams per kilogram body weight per day were: 0 (vehicle control), 100 DFMO, 0.1 TAM, 1.0 TAM, 0.1 TAM + 100 DFMO and 1.0 TAM + 100 DFMO. Results: No mortalities occurred. Diarrhea was produced by TAM and vaginal discharge, due to reproductive tract lesions, was produced by both DFMO and TAM, either alone or in combination. DFMO decreased reticulocyte counts and TAM increased counts of mature neutrophils. DFMO alone resulted in lesions to the intestines and ovaries, and cornified epithelium of vagina and cervix. TAM produced cornified epithelium of vagina and cervix, and numerous lesions in the ovaries, fallopian tube, uterus, cervix and vagina which were likely due to an estrogen agonist effect. Coadministration of DFMO increased the incidence and/or severity of these reproductive tract lesions. Each compound alone produced ovarian atrophy, and antral follicles and corpora lutea were completely absent in the 1.0 TAM + 100 DFMO group. Conclusions: Coadministration of DFMO and TAM resulted in additive toxicity involving the female reproductive system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002800050927
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  • 5
    Electronic Resource
    Electronic Resource
    The perception of heading during eye movements (1992)
    [s.l.] : Nature Publishing Group
    Nature 360 (1992), S. 583-585 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Experiment 1 reproduced the conditions of Warren and Han-non13 except we used constant, faster rotation rates (actual or simulated) from 0 to 5 deg s"1 and a vertical axis of rotation. In addition, the fixation point was positioned slightly above the horizon and moved independently of the ground ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/360583a0
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  • 6
    Electronic Resource
    Electronic Resource
    Preclinical efficacy evaluation of potential chemopreventive agents in animal carcinogenesis models: Methods and results from the NCI chemoprevention drug development program (1994)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 56 (1994), S. 32-54 
    Details
    ISSN: 0730-2312
    Keywords: Animal models ; carcinogenesis ; chemoprevention ; drug development ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: In the NCI, Chemoprevention Branch drug development program, potential chemopreventive agents are evaluated for efficacy against chemical carcinogen-induced tumors in animal models. This paper summarizes the results of 144 agents in 352 tests using various animal efficacy models. Of these results, 146 were positive, representing 85 different agents.The target organs selected for the animals model are representative of high-incidence human cancers. The assays include inhibition of tumors induced by MNU in hamster trachea, DEN in hamster lung, AOM in rat colon (including inhibition of AOM-induced aberrant crypts), MAM in mouse colon, DMBA and MNU in rat mammary glands, DMBA promoted by TPA in mouse skin, and OH-BBN in mouse bladder.The agents tested may be classified into various pharmacological and chemical structural categories that are relevant to their chemopreventive potential. These categories include antiestrogens, antiinflammatories (e. g., NSAIDs), antioxidants, arachidonic acid metabolism inhibitors, GST and GSH enhancers, ODC inhibitors, protein kinase C inhibitors, retinoids and carotenoids, organosulfur compounds, calcium compounds, vitamin D3 and analogs, and phenolic compounds (e. g., flavonoids). The various categories of compounds have different spectra of efficacy in animal models. In hamster lung, GSH-enhancing agents and antioidants appear to have high potential for inhibiting carcinogenesis. In the colon, NSAIDs and other antiinflammatory agents appear particularly promising. Likewise, NSAIDs are very active in mouse bladder. In rat mammary glands, retinoids and antiestrogens (as would be expected) are efficacious. Several of the chemicals evaluated also appear to be promising chemopreventive agents based on their activity in several of the animal models. Particularly, the ODC inhibitor DFMO was active in the colon, mammary glands, and bladder models, while the dithiolthione, oltipraz, was efficacious in all the models listed above (i. e., lung, colon, mammary glands, skin, and bladder). 1994 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 Tab.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240560905
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  • 7
    Electronic Resource
    Electronic Resource
    Guidance for development of chemopreventive agents (1994)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 56 (1994), S. 25-31 
    Details
    ISSN: 0730-2312
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Additional Material: 4 Tab.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240560904
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  • 8
    Electronic Resource
    Electronic Resource
    Strategy and planning for chemopreventive drug development: Clinical development plans (1994)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 56 (1994), S. 55-62 
    Details
    ISSN: 0730-2312
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: At the National Cancer Institute, Division of Cancer Prevention and Control, the Chemoprevention Branch and Agent Development Committee develop strategies for efficiently identifying, procuring, and advancing the most promising drugs into clinical trials. Scientific expertise is applied at each phase of development to critically review the testing methods and results, and to establish and apply criteria for evaluating the agents for further development. The Clinical Development Plan, prepared by the Chemoprevention Branch and the Agent Development Committee, is a summary of the status of the agent regarding evidence for safety and chemopreventive efficacy in preclinical and clinical studies. It also contains the strategy for further development of the drug that addresses pharmacodynamics, drug effect measurements, intermediate biomarkers for monitoring efficacy, toxicity, supply and formulation, regulatory approval, and proposed clinical trials. Sixteen Clinical Development Plans are presented here: N-acetyl-l-cysteine (NAC), aspirin, calcium, β-carotene, 2-difluoromethylornithine (DFMO), DHEA analog 8354, 18β-glycyrrhetinic acid, N-(4-hydroxyphenyl)retinamide (4-HPR), ibuprofen, oltipraz, piroxicam, Proscar®, sulindac, tamoxifen, vitamin D3 and analogs and vitamin E. The objective of publishing these plans is to stimulate interest and thinking among the scientific community on the prospects for developing chemopreventive drugs. 1994 Wiley-Liss, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240560906
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  • 9
    Electronic Resource
    Electronic Resource
    Development of breast cancer chemopreventive drugs (1993)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 53 (1993), S. 2-13 
    Details
    ISSN: 0730-2312
    Keywords: β-carotene ; breast cancer ; chemoprevention ; clinical trials ; ductal carcinoma in situ ; 4-HPR ; intermediate biomarkers ; lobular carcinoma in situ ; surrogate endpoints ; tamoxifen ; vitamin E ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Breast cancer is the second highest cause of cancer mortality (19%) estimated for U.S. women in 1993 and accounts for the highest proportion of new cancer cases (32%) in this population. The rate of documented cases increased during the early 1970s and again in 1980-87, probably due to early mammographic detection. Increased knowledge of personal risk may also have been a consideration; however, 60% of women diagnosed with breast cancer have no known risk factor(s), such as family history, early age at menarche, late age at menopause, nulliparity, late age at first live birth, socioeconomic status, contraceptive use, postmenopausal estrogen replacement, or high fat intake. To prevent cancer, one strategy undertaken by the NCI is cancer chemoprevention, or intervention with chemical agents at the precancer stage to halt or slow the carcinogenic process.An objective of the NCI, DCPC is to develop promising cancer chemopreventive chemical agents as drugs for human use. Briefly, the process begins with identification of potential agents (e.g., pharmaceuticals, natural products, minor dietary constituents) from surveillance and analysis of the literature and from in vitro prescreen assays. Data on both efficacy (i.e., biological activities that either directly or indirectly indicate inhibition of carcinogenesis) and toxicity are gathered these sources. Various criteria are used to select and prioritize agents for entry into the NCI, DCPC preclinical testing program. The program begins with battery of in vitro efficacy screens using both animal and human cells to select agents for further testing; agents positive in these assays are considered for further testing. In the assay used for breat cancer chemoprevention, 7,12-dimethylbenz(a)anthracene (DMBA)-induced mouse mammary organ culture, 64 chemicals have inhibited formation of hyperplastic alveolar-like nodules. A panel of organ-specific animal screening assays are then used to assess efficacy in vivo. Two assays relevant for breast cancer chemoprevention are inhibition of N-methyl-N-nitrosourea- and DMBA-induced rat mammary gland carcinogenesis. Of 89 agents tested, 29 have inhibited cancer incidence, multiplicity, or both in at least one of the mammary assays; 21 agents are currently on test. Highly promising agents are then placed in traditional preclinical toxicity tests performed in two species. Finally, the most promising and least toxic agents enter clinical trials. Phase I clinical trials are designed to investigate human dose-related safety and pharmacokinetics of the drug. Phase II trials are small scale, placebo-controlled studies designed to determine chemopreventive efficacy and optimal dosing regimens. Three Phase II trials are in progress or in the planning stage investigating tamoxifen citrate or N-(4-hydroxyphenyl)retinamide (4-HPR) as single agents; also, both Phase I and Phase II trials evaluating the combination of 4-HPR and tamoxifen are in the planning stage. Phase III trials involve a large target population, with cancer incidence reduction as the endpoint. Tamoxifen citrate is being tested as a breast cancer chemopreventive in high-risk women in a Phase III trial funded by NCI and under the direction of the National Surgical Adjuvant Breast and Bowel Project. Prevention by 4-HPR of a second primary in the contralateral breat of women surgically treated for Stage I/II breat cancer is being evaluated in a Phase III trial in Italy. Finally, the efficacy of β-carotene or vitamin E in decreasing the incidence of breast, lung, and colon cancer is being determined in a Phase III trial involving nurses 45 years of age or older.Essential to the completion of Phase II clinical trials is the use of populations with defined, measurable biological alterations in tissue occurring prior to malignancy (i.e., intermediate biomarkers) which can serve as surrogate trial endpoints, instead of the more time-consuming and costly endpoint of cancer incidence. Intermediate biomarkers may be of several types, including histological/premalignant lesions, or those based on genetic, biochemical, proliferative, or differentiation-related properties. The only well-established premalignant lesions in the human breast are ductal and lobular carcinoma in situ (CIS). In 1993, an estimated 25,000 new cases of CIS will be diagnosed. These lesions are at high risk of progression to invasive cancer and may be amenable to modulation by a chemopreventive agent. In addition, other types of biomarkers could be identified within the lesions. The goal of this workshop is to identify and discuss the best chemopreventive agents and intermediate biomarkers for use as surrogate endpoints in short-term Phase II breast cancer chemoprevention trials, as well as to design protocols for such trials.
    Additional Material: 2 Tab.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240531103
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  • 10
    Electronic Resource
    Electronic Resource
    Mechanistic considerations in chemopreventive drug development (1994)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 56 (1994), S. 1-24 
    Details
    ISSN: 0730-2312
    Keywords: Chemoprevention ; drug development ; mechanism of action ; cancer ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: This overview of the potential mechanisms of chemopreventive activity will provide the conceptual groundwork for chemopreventive drug discovery, leading to structure-activity and mechanistic studies that identify and evaluate new agents. Possible mechanisms of chemopreventive activity with examples of promising agents include carcinogen blocking activities such as inhibition of carcinogen uptake (calcium), inhibition of formation or activation of carcinogen (arylalkyl isothiocyanates, DHEA, NSAIDs, polyphenols), deactivation or detoxification of carcinogen (oltipraz, other GSH-enhancing agents), preventing carcinogen binding to DNA (oltipraz, polyphenols), and enhancing the level or fidelity of DNA repair (NAC, protease inhibitors). Chemopreventive antioxidant activities include scavenging reactive electrophiles (GSH-enhancing agents), scavenging oxygen radicals (polyphenols, vitamin E), and inhibiting arachidonic acid metabolism (glycyrrhetinic acid, NAC, NSAIDs, polyphenols, tamoxifen). Antiproliferation/antiprogression activities include modulation of signal transduction (glycyrrhetinic acid, NSAIDs, polyphenols, retinoids, tamoxifen), modulation of hormonal and growth factor activity (NSAIDs, retinoids, tamoxifen), inhibition of aberrant oncogene activity (genistein, NSAIDs, monoterpenes), inhibition of polyamine metabolism (DFMO, retinoids, tamoxifen), induction of terminal differentiation (calcium, retinoids, vitamin D3), restoration of immune response (NSAIDs, selenium, vitamin E), enhancing intercellular communication (carotenoids, retinoids), restoration of tumor suppressor function, induction of programmed cell death (apoptosis) (butyric acid, genistein, retinoids, tamoxifen), correction of DNA methylation imbalances (folic acid), inhibition of angiogenesis (genistein, retionoids, tamoxifen), inhibition of basement membrane degradation (protease inhibitors), and activation of antimetastasis genes.A systematic drug development program for chemopreventive agents is only possible with continuing research into mechanisms of action and thoughtful application of the mechanisms to new drug design and discovery. One approach is to construct pharmacological activity profiles for promising agents. These profiles are compared among the promising agents and with untested compounds to identify similarities. Classical structure-activity studies are used to find optimal agents (high efficacy with low toxicity) based on good lead agents. Studies evaluating tissue-specific and pharmacokinetic parameters are very important. A final approach is design of mechanism-based assays and identification of mechanism-based intermediate biomarkers for evaluation of chemopreventive efficacy. 1994 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 Tab.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240560903
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