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  • 1
    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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  • 2
    Electronic Resource
    Electronic Resource
    Introductory remarks: Development of chemopreventive agents for prostate cancer (1992)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 50 (1992), S. 1-8 
    Details
    ISSN: 0730-2312
    Keywords: chemoprevention ; clinical trials ; intermediate biomarkers ; prostate ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The term “cancer chemoprevention” refers to the prevention of cancer by intervening with drugs prior to the malignant (i.e., invasive) stage of carcinogenesis. The development of chemopreventive drugs is the major objective of the Chemoprevention Branch at the National Cancer Institute.The testing of drug for cancer chemoprevention differs from testing of those for cancer treatment. Chemopreventive drug trials involve healthy target populations, and the endpoints of reduced cancer incidence or mortality, reduced/eliminated precancerous lesions, or increased latency must be achieved with little or no drug toxicity.The design of cancer chemoprevention trials for prostate presents several problems, such as the age of the study population and undependable methods for detecting microscopic foci by sequential sampling. A major motivation for organizing this workshop is the development of strategies for the design of chemopreventive intervention trials for prostate cancer.One of the most difficult problems of chemoprevention drug testing is the necessity of lengthy trials due to the long developmental period of many cancers. This is especially true for prostate cancer. A major solution to the problem is the use of intermediate biomarkers, defined as morphological or molecular intraepithelial changes that can constitute short-term endpoints in chemoprevention clinical trials. They are categorized as histological, genetic, proliferation-related, and differentiation-related. Modulation of intermediate biomarkers, instead of cancer incidence, as trial endpoints would allow chemoprevention trials to be of shorter duration, to use fewer subjects, and to be of lower cost. Review of the current status of prostatic intermediate biomarkers, and methods for identifying and validating them, are also major reason for convening this workshop. © 1992 Wiley-Liss, Inc.
    Additional Material: 1 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240501203
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  • 3
    Electronic Resource
    Electronic Resource
    Chemoprevention of rat mammary carcinogenesis: Exceptional activity of dietary dehydroepiandrosterone (DHEA) (1993)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 53 (1993), S. 253-254 
    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: A major determinant of progress in human breast cancer prevention is the identification of agents with significant anticarcinogenic activity and acceptable levels of toxicity in experimental animals. Over the past 20 years, more than 50 experimental regimens have been shown to have significant chemopreventive activity in the rat mammary gland. The most effective approaches to mammary cancer chemoprevention in rats involve surgical endocrine ablations such as bilateral ovariectomy. However, prophylactic surgical ablations are unlikely to be acceptable to the majority of the general public. All chemicals evaluated to date are less effective, and none has been shown to reduce mammary cancer incidence to zero. As a result, efforts continue to identify chemical agents whose protective activity is comparable to that of endocrine ablation. DHEA is an adrenal steroid with chemopreventive activity in several animal models for human cancer. In the present studies, the chemopreventive efficacy of DHEA was evaluated in rats exposed to the mammary gland carcinogen, N-methyl-N-nitrosourea (MNU). Groups of 20 female Sprague-Dawley rats were fed an AIN-76A diet supplemented with 0, 400, or 800 mg DHEA per kg diet; one week later, all rats received a single i.p. injection of 35 mg MNU per kg body weight. Animals were palpated weekly to monitor mammary tumor development, and all mammary tumors were histologically confirmed. When administered at 800 mg/kg diet, DHEA reduced mammary cancer incidence in controls from 95% to 15%; carcinoma multiplicity in rats receiving 800 mg DHEA per kg diet was reduced by more than 85% from control levels. In a separate study, the 400 mg/kg diet dose of DHEA reduced the incidence of mammary cancer to 5% from 80% found in controls fed the basal diet. Reductions in mammary cancer incidence and multiplicity associated with DHEA administration were accompanied by large increases in cancer latency. Evaluation of mammary gland wholemounts from animals fed DHEA demonstrated a massive induction of lobuloalveolar differentiation. These results indicate the dietary supplementation with non-toxic dose levels of DHEA has chemopreventive efficacy approaching that of endocrine ablation. This protection may be mediated by the induction of differentiation in the mammary gland, during which sensitive mammary parenchymal structures (terminal end buds) are stimulated to develop into structures (alveolar buds) less sensitive to carcinogenic insult.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240531154
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  • 4
    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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  • 5
    Electronic Resource
    Electronic Resource
    Intermediate biomarkers of precancer and their application in chemoprevention (1992)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 50 (1992), S. 15-21 
    Details
    ISSN: 0730-2312
    Keywords: chemoprevention ; clinical trial ; drug development ; intermediate biomarker ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The Chemoprevention Branch of the National Cancer Institute has established a progam for the development of safe and effective cancer chemopreventive agents. This program includes identification of new agents, testing for efficacy in vitro and in animals, studies in animals to model clinical use, and preclinical toxicity and metabolism evaluation. Ultimately, the most promising agents progress to clinical trials. The long period required for cancer onset presents a significant challenge to the design of clinical trials for chemoprevention. Phase 111 trials in which cancer reduction is the endpoint require large subject group (tens of thousands) and follow-up duration of more than five years. Because of these requirements, the costs of such trials are high. The Chemoprevention Branch is addressing this challange by expansion of the preclinical and Phase II clinical efficacy efforts to include intermediate biomarkers of carcinogenesis as study endpoints.The Chemoprevention Branch's studies focus on the development of biomarkers with high reliability and predictive value for cancer. Both single markers and batteries of complementary and parallel markers are evaluated. Among the criteria for biomarkers for chemoprevention studies are the following: (1) differential expression in normal and high risk tissue, (2) appearance early in carcinogenesis (the earlier a reliable biomarker appears, the greater is the chance for successful intervention with a chemopreventive agent), (3) high sensitivity, specificity, and accuracy relative to cancer, (4) ease of measurement (use of non-invasive techniques and small tissue samples is preferable), (5) demonstration of modulation by chemopreventive agents, and (6) correlation of modulation with decreased cancer incidence. © 1992 Wiley-Liss, Inc.
    Additional Material: 1 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240501103
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  • 6
    Electronic Resource
    Electronic Resource
    Growth kinetics and chemoprevention of aberrant crypts in the rat colon (1992)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 50 (1992), S. 51-54 
    Details
    ISSN: 0730-2312
    Keywords: aberrant crypts ; azoxymethane ; chemoprevention ; colorectal cancer ; intermediate biomarker ; NSAID ; piroxicam ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Single and multiple colonic crypts exhibiting dysplasia that are detectable in situ by staining of rat colon with methylene blue are called aberrant crypts (AC) and may serve as an intermediate marker for colon cancer. In a characterization study, we have established the kinetics of AC growth and development over a period of 20 d following injection of rats with the carcinogen azoxymethane (AOM). AC are not present at 5 d post-injection, but are a constant feature at 10 d and thereafter. Multiple AC, presumably clonal, begin to evolve at 10 d and are consistent by 20 d, forming incipient microdenomata. We have examined 20 candidate chemopreventive agents for inhibition of AC. All agents were given in AIN-76diet, at two dose levels, with injections of AOM. AC were measured after 5 weeks of growth. Among the most active AC-inhibiting agents were BHA, DFMO, quercetin, diallyl sulfide, 18β-glycyrrhetinic acid, and ascorbyl palmitate. In a postinitiation study, the differentiating agent sodium butyrate was ineffective, but piroxicam was highly effective in modulating AC growth. Further, piroxicam inhibited AC development at all stages of growth from single to polycryptal clusters of AC. The AC assay shows marked sensitivity and specificity for screening agents for chemoprevention of colon cancer. © 1992 Wiley-Liss, Inc.
    Additional Material: 1 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240501110
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  • 7
    Electronic Resource
    Electronic Resource
    Development of chemopreventive agents for bladder cancer (1992)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 50 (1992), S. 1-12 
    Details
    ISSN: 0730-2312
    Keywords: bladder cancer ; chemoprevention ; intermediate biomarkers ; intermediate endpoint biomarkers ; surrogate endpoints ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The term cancer chemoprevention refers to the prevention of prolongation of carcinogenesis by intervention with drugs prior to the malignant (i.e., invasive) stage. The development of chemopreventive drugs is the major objective of the Chemoprevention Branch of the National Cancer Institute. Neoplastic lesions of the urinary bladder present a unique opportunity for evaluating chemopreventive agents because of (1) the accessibility of the lesions to observation and biopsy, and (2) those patients who have been successfully treated for a primary lesion represent a population at unusually high risk for recurrence and/or progression.Although 70-80% of bladder cancers initially present as superficial, papillary transitional cell neoplasms with limited potential for invasion, the incidence of recurrence is high after resection (60-75%). Recurrent tumors are highly unpredictable, and may be of higher grade of stage (progression). Although recurrence is responsible for high treatment-related morbidity, progression represents the greatest potential for mortality. Thus, potential chemopreventive agents considered here would modulate bladder carcinogenesis from initiation of normal-appearing tissue through progression of superficial tumors.Clinical trials of chemopreventive drugs involve healthy target populations, and the endpoints are reduced cancner incidence or mortality, reduced/eliminated precancerous lesions or increased latency, with none to minimal toxicity. Since cancers may not appear for 20-30 years, two of the most difficult aspects of testing these drugs in intervention trials are the long observation poeriods and large study populations required to measure cancer incidence reduction. However, observing the regression or recurrence of superficial bladder lesions (TIS, T1, Ta) requires relatively short time periods. Thus, these lesions lend themselves to the investigation of intermediate biomarkers, defined as morphologic and/or molecular alterations in tissue between initiation and tumor invasion. It is hypothesized that modulation of one or more biomarkers would interrupt carcinogenesis and result in a decrease in cancer incidence. Thus, evaluation of biomarkers as surrogate endpoints would allow bladder trials to be of even shorter duration, use fewer subjects and be lower in cost. In addition, intermediate biomarkers could predict which superficial lesions (or normal-appearing tissue) have the greatest potential for neoplastic progression. Development of strategies for the design of intrvention trials for bladder cancer and review of the current status of intermediate biomarkers in the bladder, and methods for their validation, are major objectives of this workshop.
    Additional Material: 1 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240501303
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  • 8
    Electronic Resource
    Electronic Resource
    The natural history of intraepithelial neoplasia: Relevance to the search for intermediate endpoint biomarkers (1992)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 50 (1992), S. 23-26 
    Details
    ISSN: 0730-2312
    Keywords: biomarkers ; chemoprevention ; clonal evolution ; dysplasia ; genomic instability ; intermediate biomarker ; intermediate endpoint biomarker ; intraepithelial neoplasia ; precancerous ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The development of carcinomas, definedas invasive epithelial neoplasma, is preceded by a preinvasive stage termed intraepithelial neoplasia that typically lasts for years. Intraepithelial neoplasia is the target tissue for the action of chmopreventive agents and the site where biomarkers frequently develop. the term “dysplasia” refers to the morphological alteration that characterize intraepithelial neoplasia and, according to many authors, consists of seven basic changes that are the same for the majority of epithelia. These are increased nuclear size, abnormal nuclear shape, increased nuclear stain uptake, nuclear pleomorphism (increased variation in size, shape, and stain uptake), increased mitoses, abnormal mitoses, and disordered or absent differentiation. Clonal evolution appears to begin early in the neoplastic process during intraepithelial neoplasia. The use of intraepithelial neoplasia as an intermediate endpoint biomarker requires that effective chemopreventive agents cause it to regress. Two examples are the regression of dysplastic oral leukoplakia produced by beta-carotene and the regression of colonic polyps in familial polyposis patients following treatment with the nonsteroidal antiinflammatory drug sulindac. There is a critical need to identify and develop biomarkers that correlate with the appearance and regression of intraepithelial neoplasia. © 1992 Wiley-Liss, Inc.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240501104
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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
    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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