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Cancer Prevention by Delay1 Commentary Re: J Vol. 8, 305–313, February 2002 Clinical Cancer Research 305 The Biology Behind Cancer Prevention by Delay1 Commentary re: J. A. O’Shaughnessy et al., Treatment and Prevention of Intraepithelial Neoplasia: An Important Target for Accelerated New Agent Development. Clin. Cancer Res., 8: 314–346, 2002. Scott M. Lippman and Waun Ki Hong2 elephant certainly encompasses the delay of cancer development Department of Clinical Cancer Prevention, Division of Cancer and all of the molecular biological complexity this implies. Prevention [S. M. L.], and Department of Thoracic/Head and Neck This commentary will present strong evidence for the bi- Medical Oncology, Division of Cancer Medicine [S. M. L., W. K. H.], ological basis and clinical benefit of delay. We hope it may The University of Texas M. D. Anderson Cancer Center, Houston, stimulate a new way of looking at cancer chemoprevention, Texas 77030 especially for readers who believe that prevention must be Introduction tantamount to a complete or permanent incidence reduction, which we heartily dispute. We also will outline the novel con- Chemoprevention only recently matured into a standard modality for controlling epithelial carcinogenesis. This maturity cept of delaying cancer by molecular detours. resulted from the landmark United States FDA3 approvals of tamoxifen for reducing breast cancer risk in three settings (1) Chemoprevention and Biological Considerations of and from FDA approvals of several agents for treating advanced Cancer Delay premalignancy, or IEN, most recently the NSAIDs diclofenac and celecoxib in the IEN settings of actinic keratosis and FAP Cancer chemoprevention can be defined in practical clini- (2, 3). We were privileged to serve on the AACR Task Force on cal terms as the reduction in the rate of cancer development, or IEN that prepared the Special Article “Treatment and Preven- incidence, by single or combined agents for the period of a tion of Intraepithelial Neoplasia: An Important Target for Ac- Phase III (cancer end point) trial (5), as seen in the BCPT (1). celerated New Agent Development,” which appears elsewhere Animal carcinogenesis studies suggest broadening this defini- in this issue (3). We now have the honor of writing “The tion by adding the concept of a rate reduction based on a fixed Biology Behind. ” commentary on this seminal report docu- number of cancers developing over a longer time (in treated menting the importance of IEN end points to the field of cancer versus control animals). Regarding the first definition, it is not chemoprevention. entirely clear whether the incidence reduction in the BCPT Although chemoprevention has come of age as a cancer- resulted from eradicating premalignant clones or delaying car- control modality (1–5), the biology behind cancer chemopre- cinogenic progression. It probably resulted from both. The sec- vention, including treating and/or preventing IEN, has been ond, animal-based definition, however, is the essence of cancer tinged with riddle. One researcher touches the tail and claims, delay. Evidence from both the clinic (discussed in a later sec- “It’s a snake of temporary inhibition.” Another touches the leg tion) and the laboratory (discussed below in this section) indi- and declares, “It’s a tree of permanent reversal.” A third re- cates that a substantial part of chemopreventive activity involves searcher touches the side and says, “It’s a wall of risk reduc- delay. tion.” As in the parable of the blind men and the elephant, most Implying that the preventive effect lasts for a finite period of us are blinded to one extent or another by our specialized (whether therapy is stopped or not), the concept of cancer or perspectives on cancer chemoprevention. Although possibly IEN delay is not new to chemoprevention (6–10), having been encompassing permanent or complete prevention, the whole addressed comprehensively in the laboratory with respect to the classic phases of chemical carcinogenesis. Delay terminology is used in describing the standard animal measures of chemopre- ventive efficacy, which include measures of decreases in the rate Received 12/21/01; revised 12/28/01; accepted 12/31/01. of tumor development, even if the incidence eventually returns 1 Supported in part by the Cancer Center Support Grant CA16672 from to that in the control group, and of overall decreases in the the National Cancer Institute, NIH. S. M. L. holds the Anderson Clinical incidence or number of tumors. The decreased rate of tumor Faculty Chair for Cancer Treatment and Research. W. K. H. is an development is measured by the increased time of tumor la- American Cancer Society Clinical Research Professor and Fellow Na- tional Foundation Cancer Research and holds the Charles A. LeMaistre tency, which is the time between carcinogen exposure and either Distinguished Chair in Thoracic Oncology, M. D. Anderson Cancer the first tumor or 50% of the overall tumor incidence. Active Center. chemopreventive agents can produce a several-month shift to 2 To whom requests for reprints should be addressed, at Department of the right in the curves of the time-to-tumor-development (laten- Thoracic/Head & Neck Medical Oncology, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Box 80, cy) and survival durations in rodents. Considering the large Houston, TX 77030. Email: [email protected]. ratios of human:rodent tumor latencies and life spans (e.g., 3 The abbreviations used are: FDA, Food and Drug Administration; ϳ50:1 for humans:mice), this shift could represent years or IEN, intraepithelial neoplasia; NSAID, nonsteroidal anti-inflammatory decades of increased time-to-cancer and survival in humans. drug; FAP, familial adenomatous polyposis; BCPT, Breast Cancer Pre- vention Trial (as reported in Ref. 13); APC, adenomatous polyposis coli; “Even a delay in [bladder] tumor development [by retinoids] of DCIS, ductal carcinoma in situ; SPT, second primary tumor. as little as 7 to 10 weeks in the rat,” stated Hicks (and echoed by Downloaded from clincancerres.aacrjournals.org on September 26, 2021. © 2002 American Association for Cancer Research. 306 Cancer Prevention by Delay Fig. 1 Leukoplakia-carcinoma progression models in the oral cavity. Top panels, the clinical progression of a patient’s white oral leukoplakia lesion (left) to an oral cancer (right) that developed 3 years after complete leukoplakia resection. Middle panels, histological progression from hyperplasia to invasive cancer. Bottom panels, a molecular progression model, in which the accumulation of genetic alterations is more important than the order. The apparent loss of heterozygosity at 11q may represent allelic imbalance via cyclin D1 amplification at 11q13. Some molecular alterations, such as an autocrine growth loop involving transforming growth factor-␣ (TGF-␣) and epidermal growth factor receptor (EGFR) overexpression, can occur in carcinogen-exposed histologically normal epithelium. Molecular alterations will differ depending on carcinogenic exposure [e.g., to cigarette smoke, betel nuts, or human papillomavirus (especially for oropharyngeal cancer)], and on genetic susceptibility (e.g., affected by certain glutathione S-transferase genotypes and by helicase defects involved with DNA-repair genes). FHIT, fragile histidine triad. Modified with permission of the Massachusetts Medical Society from a figure originally published in The New England Journal of Medicine (20). Copyright © 2001 Massachusetts Medical Society. All rights reserved. Moon et al.; Refs. 9, 10), “could equate to an extra 5 or 6 years for highly educated reflections on cancer delay in the clinical of symptom-free life for the human bladder-cancer patient.” setting. Sophisticated statistical models have been developed for The molecular basis of multistep carcinogenesis was first analyzing animal studies with respect to the carcinogenic phases illustrated by Vogelstein et al. (16) in studies of human adeno- and measures of drug efficacy (11, 12). The ability of these ma-carcinoma progression in the colon. The molecular biology models to assess delay is confounded by the usual termination of of multistep carcinogenesis subsequently has been worked out animal experiments before all of the possible latent tumors have in other epithelial sites, including the head and neck (Refs. developed in the treatment group and by forced carcinogenesis 17–21; Fig. 1), which exemplifies the molecular basis of cancer designed to produce a ϳ100% cancer incidence in control delay. Head and neck carcinogenesis involves accumulated mo- animals in a short time. lecular alterations that contribute to clonal expansion, intraepi- For decades, researchers studying animals have accepted thelial spread, lesion heterogeneity, and drug resistance. First the potential clinical impact of cancer delay. Within the clinical described 50 years ago as “field cancerization” in the setting of research and practice community, however, considerations of head and neck carcinogenesis (22), multifocal carcinogenesis is cancer delay gained prominence only recently and did so be- another fundamental concept of chemoprevention and involves cause of the dramatic trial results and FDA approvals of tamox- multiple genetically distinct clones and the lateral spread of ifen in breast cancer prevention (1, 5, 13–15). Needing many genetically related preinvasive clones (4, 20, 21). years or possibly decades of follow-up, it will be difficult, if not As indicated by advancing molecular studies, the lengthy impossible, to prove
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