Comparison of Neoplasms in Six Sources of Rats

Kenzie, W. F. Mac; Garner, F. M.

doi:10.1093/jnci/50.5.1243

Cited by 133 publications

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“…From lifetime studies, the incidence of spontaneous mammary tumors of Sprague-Dawley rats often approaches 50% in control animals, 17 and it usually varies 7-40% in studies from different sources. 18 This indicates that there is likely to be significant genetic variation over time, though dietary, hormonal and physiologic factors may have also played a role.…”

Section: Discussionmentioning

confidence: 99%

Strain‐specific mammary proliferative lesion development following lifetime oral administration of ochratoxin A in DA and Lewis rats

Son

Kamino

Lee

et al. 2003

Intl Journal of Cancer

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OTA, a potent nephrotoxin in several species, is a renal carcinogen in animals and is implicated in the etiology of BEN. The NTP classified OTA as having clear evidence of carcinogenic activity, based on uncommon tubular adenomas and tubular cell carcinomas of the kidney and multiple fibroadenomas of the mammary gland, seen in the rat. As shown previously (Castegnaro et al., Int J Cancer 1998;77:70 -5), induction of renal tumors by OTA is sex-and strain-specific in DA and Lewis rats, with DA males being most responsive and DA females being resistant; however, that report was confined to the kidney and urinary tract. To obtain OTAinduced tumorigenic information in rats, we administered OTA (0.4 mg/kg) by oral gavage to both DA and Lewis rats for their lifetimes and extended the investigation to complete histopathology of all tissues and organs. We also observed the characteristic renal tumor that is highly strainand sex-specific, and there were increased incidences of proliferative mammary lesions in Lewis rats but not in DA rats, indicating that these were also strain-specific. In view of the NTP report of OTA treatment-related mammary fibroadenoma in F344 rats, we observed increased mammary proliferative lesions in Lewis rats but not in DA rats. Our results suggest that OTA may play some role in mammary tumor development in some rat strains. OTA, a potent nephrotoxin in several species, is produced by storage fungi in the Aspergillus and Penicillium groups, causes endemic porcine nephropathy under natural conditions and is implicated in the etiology of BEN. 1 OTA has been found as a contaminant in a variety of cereal grains and foods, including coffee beans and ham. 2 Long-term animal studies have been conducted in rats and mice, and carcinogenic potential was reported in these species. [3][4][5] An NTP study in rats 6 reported that OTA induced uncommon tubular adenomas and tubular cell carcinomas of the kidney and multiple fibroadenomas of the mammary glands; on the basis of these results, the NTP classified OTA as having clear evidence of carcinogenic activity.Patients in the Balkan area who suffer from BEN have the EM profile for DB. 1 Accordingly, DA and Lewis rats were selected on the basis of their metabolic profiles as PMs and EMs, respectively, for DB in liver. 7 These different strains show genetic polymorphisms for the gene regulating DB in a manner thought to be analogous to human metabolism. Similarly, Castegnaro et al. 8 reported that OTA induction of renal tumors is markedly sex-and strain-specific in DA and Lewis rats, with DA males being most responsive and DA females being resistant. However, this previous report 8 was confined to the kidney and urinary tract and did not take account of other organs and tissues.To obtain more precise information on the systemic tumorigenic effects of OTA, we administered OTA to both DA and Lewis rats for their lifetimes and performed complete histopathology for all organs and tissues.Throughout the extended histopathology in our study, we first observed that OT...

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Section: Discussionmentioning

confidence: 99%

Strain‐specific mammary proliferative lesion development following lifetime oral administration of ochratoxin A in DA and Lewis rats

Son

Kamino

Lee

et al. 2003

Intl Journal of Cancer

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“…Spontaneous mammary tumors develop in females of various strains of rats such as August, Albany-Hooded, Copenhagen, Fisher, Lewis, Osborne-Mendel, SpragueDawley, Wistar, and Wistar/Furth (9,45,116,(119)(120)(121). Mammary tumors are third in incidence among spontaneous tumors found in the Fisher 344 rat used in the National Cancer Institute/National Toxicology Program (NCI/NTP) carcinogenicity bioassays (116).…”

Section: Spontaneous Rodent Mammary Tumorsmentioning

confidence: 99%

“…Data from continuously operating cancer registries, such as the one in the state of Connecticut and the Surveillance, Epidemiology, and End Results (SEER) program established by the National Cancer Institute in 1973 (which collects data from nine population-based cancer registries covering about 10% of the US population), reveal that the age-adjusted incidence of breast cancer rose at a rate of 1.2%/year from 1940 to 1980; it rose even more steeply in the next 7 years, reaching a peak of 112.4 cases/100,000 women in 1987, although it decreased to 104.6 cases/100,000 women by 1989 (3)(4)(5). The increased incidence of cancer has been pardy attributed to an improvement in early detection, as indicated by the progressively increased percentage of patients with early stage (0 to I) disease (from 45.2% in 1985-1986 to 53.1% in 1991) and decreased percentage of patients in stage II and III disease (6). Early diagnosis has improved the rates of cure and prolonged survival; however, stage-specific survival rates have increased only slightly since the mid1970s, and breast cancer remains only second to lung cancer as a cause of death, causing 46,000 deaths in 1994 (3)(4)(5).…”

mentioning

confidence: 97%

“…If these influences are not exerted in proper temporal, sequential, and quantitative relationships, normal development, differentiation, and function are adversely affected (41). The development of the mammary gland, in turn, cannot be separated from its aging, a process that markedly influences the incidence of spontaneous tumors in all strains of rats (8,45,46), as well as in mice infected with MMTV (10).…”

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confidence: 99%

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Mammary Gland Neoplasia in Long-Term Rodent Studies

Russo¹,

Russo²

1996

Environmental Health Perspectives

121

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“…Osteosarcoma was observed in the tibia, femur, lumbar vertebra, coxal bone, pubis/ischium, rib or thoracic vertebra (Table 7). Although osteosarcoma was also observed in the tibia in 1 animal in the 4.5 μg/kg group, this finding was considered to be spontaneous since spontaneous occurrence of osteosarcoma in SD rats has been reported (Imai and Yoshimura, 1988;Mac Kenzie and Garner, 1973;Nagayabu et al, 2000) and osteosarcoma was also observed in 1 animal each in the vehicle control group in Studies-3 and 4. No bone neoplasms other than osteosarcoma were observed in any group.…”

Section: Study-2mentioning

confidence: 83%

Osteosarcoma in Sprague-Dawley rats after long-term treatment with teriparatide (human parathyroid hormone (1-34))

Watanabe

Yoneyama²,

Nakajima

et al. 2012

J. Toxicol. Sci.

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-Teriparatide, a therapeutic agent for osteoporosis, has been reported to increase the incidences of bone neoplasms such as osteosarcoma when administered subcutaneously to Fischer 344 (F344) rats for a long term, but its non-carcinogenic dose level following 2-year daily administration has not been established. Here we report detailed studies on the carcinogenicity of teriparatide following longterm administration. When teriparatide was administered subcutaneously to male and female SpragueDawley (SD) rats daily for 2 years, the incidence of osteosarcoma was increased at 13.6 μg/kg/day. The non-carcinogenic dose level was 4.5 μg/kg/day for both males and females. The development of osteosarcoma in SD rats depends on the dose level of, and treatment duration with, teriparatide. Responses of the bones to teriparatide were similar between F344 and SD rats in many aspects. These results suggested that the carcinogenic potential of teriparatide in SD rats is essentially the same as in F344 rats.

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Comparison of Neoplasms in Six Sources of Rats

Cited by 133 publications

References 0 publications

Strain‐specific mammary proliferative lesion development following lifetime oral administration of ochratoxin A in DA and Lewis rats

Strain‐specific mammary proliferative lesion development following lifetime oral administration of ochratoxin A in DA and Lewis rats

Mammary Gland Neoplasia in Long-Term Rodent Studies

Osteosarcoma in Sprague-Dawley rats after long-term treatment with teriparatide (human parathyroid hormone (1-34))

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