Correspondence to: Maarten C. Bosland, D.V.Sc., Ph.D., Department of Environmental Medicine, New York University School of Medicine, 550 First Ave., New York, NY 10016 (e-mail: maarten.bosland{at}med.nyu.edu).
I thank Dr. Pretlow for pointing out an error in the fourth sentence from the end of our editorial stating that "the Dunning R3327-H tumor caused serious disease in its human host" (1). The word "human" was erroneously included in the final draft and should be deleted. The Dunning R3327-H tumor grows only in rats of the COP strain or F1 crosses of the COP and F344 strains (2,3). In the context of our editorial, this erroneous statement should not be construed to be a "most extravagant claim," as stated by Dr. Pretlow in his letter.
The purpose of our editorial was to discuss the findings of Mukherjee et al. (4) who used the Dunning R3327-H tumor model and LNCaP cells xenografted into nude mice to study the effects of dietary fat and caloric intake and to put their findings in perspective. We did not intend to claim that these two models are the only ones generally available, and we did not intend to include a detailed discussion of currently available models of prostate cancer. We are fully aware of the availability of the important androgen-sensitive CWR22 model through the generosity of Dr. Pretlow who has developed this model with his associates. We are also aware of the diversity in opinions about the origin of the Dunning tumor and its relevance to prostate cancer (5). A discussion of the relevance of the Dunning tumor and the value of the CWR22 tumor as a model of localized human prostate cancer was clearly beyond the scope of our editorial. However, Dr. Pretlow's letter gives me reason to make two additional points. First, Dr. Dunning's initial report on the R3327 tumor (2) suggests a gross appearance of the tumor similar to that commonly observed in prostate cancer induction model rats. These tumors are, in my experience, typically not attached to other pelvic or abdominal tissues than the accessory sex glands, such as the bladder, rectum, or other parts of the intestinal tract. Thus, in contrast to what Dr. Pretlow states, the primary R3327 tumor most likely originated from one of the accessory sex glands, which is consistent with its androgen sensitivity (3). Also, unlike what Dr. Pretlow states, Dr. Dunning indicated that the tumor was histologically examined by a pathologist (and was found to be a papillary adenocarcinoma) (2). Second, Dr. Pretlow's statement that Dr. Michael Sporn and others have demonstrated that a high proportion of accessory sex gland tumors in rodents are tumors of the seminal vesicles and do not originate from the prostate is incorrect in the sense that this is only the case for the so-called Pollard model in Lobund-Wistar rats (5,6). In most, if not all, other rat models of prostate cancer, prostate lobes and not the seminal vesicles are the primary sites of tumor development (5,7).
REFERENCES
1
Bosland MC, Oakley-Girvan I, Whittemore AS. Dietary fat,
calories, and prostate cancer risk. J Natl Cancer Inst 1999;91:489-91.
2 Dunning WF. Prostate cancer in the rat. J Natl Cancer Inst Monograph 1963;12:351-70.
3 Isaacs JT. Development and characteristics of the available animal model systems for the study of prostatic cancer. In: Coffey DS, Bruchovsky N, Gardner WA, Resnick MI, Karr JP, editors. Current concepts and approaches to the study of prostate cancer. New York (NY): Alan R. Liss; 1987. p. 513-76.
4
Mukherjee P, Sotnikov AV, Mangian HJ, Zhou JR, Visek WJ,
Clinton SK. Energy intake and prostate tumor growth, angiogenesis, and vascular endothelial
growth factor expression. J Natl Cancer Inst 1999;91:512-23.
5 Lucia SM, Bostwick DG, Bosland M, Cockett AT, Knapp DW, Leav I, et al. Workgroup I: rodent models of prostate cancer. Prostate 1998;36:49-55.[Medline]
6 Tamano S, Rehm S, Waalkes MP, Ward JM. High incidence and histogenesis of seminal vesicle adenocarcinoma and lower incidence of prostate carcinoma in the Lobund-Wistar prostate cancer rat model using N-nitrosomethylurea and testosterone. Vet Pathol 1996;33:557-67.[Abstract]
7 Bosland MC. Chemical and hormonal induction of prostate cancer in animal models. Urol Oncol 1996;2:103-10.
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