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PubMed1981

Triiodothyronine generation from thyroxine in human thyroid: enhanced conversion in Graves' thyroid tissue.

Conversion of T4 to T3 was studied in normal, Graves', and neoplastic thyroid tissues obtained at surgery. Homogenates of human thyroid follicular adenoma and carcinomas were incubated with [125I]T4 and dithiothreitol (DTT) at 37 C for 60 min under N2 gas. T3 formation was assessed by measuring [125I]T3 formed, using paper chromatography. In the second series of experiments, the suspensions of the 100,000 X g pellet of normal thyroid tissues adjacent to the tumor and Graves' thyroid tissues were incubated with unlabeled T4 and DTT at 37 C for 60 min under N2 gas. T3 generated was measured by RIA. T3 generation in the thyroid tissue was dependent on incubation time, amount of the tissue used, concentration of DTT, temperature, and pH. Propylthioracil inhibited T3 formation, while methimazole had no effect. A kinetic study with the homogenate of a thyroid adenoma and 100,000 X g pellet suspensions of two normal and three Graves' thyroids gave apparent Km values of 2.7, 4.9, and 4.1 microM for T4, respectively, and Vmax values of 0.8, 3.0, and 10.9 pmol T3/mg protein.min, respectively. Conversion of T4 to T3 was observed in two of three tumor tissues studied and was markedly enhanced in Graves' thyroid tissues (mean +/- SE, 11.9 +/- 2.0 pmol/mg protein.min) compared to that of normal thyroid tissues (3.2 +/- 0.6 pmol/mg protein.min; P less than 0.01). It is concluded that T4 is enzymatically converted to T3 in normal and Graves' thyroids and differentiated thyroid neoplasms. Moreover, enhanced conversion of T4 to T3 was found in Graves' thyroid tissue.

Adenoma↗
PubMed1977

Plasma thyroglobulin in detecting thyroid carcinoma after childhood head and neck irradiation.

The level of thyroglobulin in plasma was measured in 904 subjects with a history of head and neck irradiation during childhood to evaluate its potential value in screening for and differentiating thyroid neoplasms. Mean plasma thyroglobulin level was significantly elevated in subjects with nodular thyroid disease versus those without evidence of nodules (49.8 versus 27.0 ng/ml). However, the overlap with normal subjects does not allow thyroglobulin assays to serve as the only screening procedure. The mean levels in subjects with benign and malignant thyroid nodules were indistinguishable (48.8 versus 53.9 ng/ml). Thirteen percent of otherwise normal-appearing subjects had elevated values that may represent clinically inapparent thyroid disease. It is concluded that in screening large numbers of persons at risk for thyroid neoplasia, thyroglobulin assays are useful in combination with other modes of evaluation. The assay is without value in distinguishing benign from malignant disease.

Adult↗
PubMed1982

Castration induces a marked reduction in the incidence of thyroid cancers.

Although thyroid disease in humans predominates in females, the prognosis of thyroid cancer in males is much less favorable. To further explore the role of male sex hormones, we utilized the experimental model of radiation-induced follicular cancer in the rat, studying the effects of castration on tumor development. Microscopic evidence of tumor formation was correlated with the biochemical parameters serum thyroxine (T4), thyrotropin (TSH), and thyrocalcitonin (TC) at 24 months. The incidence of follicular carcinomas in intact males ws 58%, compared to 28% in comparable females. Castration of males caused a reduction in the incidence to 22%. Mean circulating levels of TSH were markedly elevated in all three irradiated groups. Mean T4 levels were reduced significantly only in irradiated castrated animals. TC levels were reduced in all irradiated groups. We conclude that although elevated levels of TSH probably play a significant role in the development of radioactive iodine-triggered follicular thyroid neoplasms in the rat, male sex hormone may also play an important role beyond their known effect on basal and thyrotropin-releasing hormone-stimulated TSH.

Adenocarcinoma↗
PubMedDate not supplied

Expression of Pax-8, p53 and bcl-2 in human benign and malignant thyroid diseases.

BACKGROUND: Immunohistochemical expression of the transcription factor Pax-8 in human thyroid diseases has never been investigated. The relationship between Pax-8, bcl-2 and p53 in thyroid neoplasms is also matter of interest. MATERIALS AND METHODS: Seventy-three thyroid tissue samples were evaluated for the expression of Pax-8, p53 and bcl-2 using the immunoperoxidase technique. The series included 11 follicular adenomas, 11 goitres, 23 papillary carcinomas, 16 follicular carcinomas, 6 undifferentiated carcinomas and 6 medullary carcinomas. RESULTS: The percentage of Pax-8 positive cells ranged from 14.9 to 27.1% and 10.1 to 39% in goitres and follicular adenomas, respectively. Among differentiated carcinomas, follicular histotype showed a Pax-8 immunoreactivity ranging from 0 to 26.5% of the neoplastic cells whereas in papillary carcinomas the percentage of positive cells ranged from 0 to 16.8%. None out of the six undifferentiated carcinomas showed Pax-8 immunoreactivity. The same negative pattern was noticed in medullary carcinomas. A statistically significant difference in Pax-8 expression was observed between non-malignant and malignant diseases (p < 0.0001). A different reactivity for Pax-8 was also noticed between differentiated carcinomas and undifferentiated carcinomas (p = 0.07). None of the benign tissues stained for p53 whereas among malignant specimens different percentages of p53 expression were observed with all undifferentiated carcinomas expressing the highest positivity (range 24.1-88.6%). Finally, when a combined analysis of bcl-2 and Pax-8 reactivity was carried out, some carcinomas proved to be Pax-8 negative and bcl-2 positive whereas others showed a similar immunoreactive pattern for both Pax-8 and bcl-2. CONCLUSIONS: Pax-8 is mainly expressed in benign rather than in malignant thyroid diseases and, among neoplasms, differentiated carcinomas express Pax-8 more frequently than undifferentiated carcinomas. An inverse pattern was observed for p53. Bcl-2 seems to be partially related to Pax-8 expression. However, a Pax-8 independent bcl-2 expression is also evident.

Adenocarcinoma, Follicular↗
PubMedDate not supplied

Thyroid carcinoma presenting as a parapharyngeal mass.

Nodal metastases from occult head and neck primaries presenting as a pharyngeal space mass are unusual. In this report, a patient with dysphagia and a large parapharyngeal mass was found to have metastases papillary thyroid carcinoma. Although it is common for such tumors to metastasize to regional lymph nodes, to our knowledge, this is the only reported case of a thyroid neoplasm masquerading as a primary parapharyngeal space tumor. It indicates upward lymphatic spread of tumor to involve the lateral retropharyngeal nodes. This pattern of spread is in keeping with Rouviere's description of a direct lymphatic pathway from the posterior surface of the superior thyroid lobe to the lateral retropharyngeal nodes. The case presentation is intended to alert the reader of this possibility and to emphasize the inclusion of regional metastatic nodal disease as a possible cause of parapharyngeal space masses.

Carcinoma, Papillary↗
PubMed2004

PAX8 and peroxisome proliferator-activated receptor gamma 1 gene expression status in benign and malignant thyroid tissues.

OBJECTIVE: Genetic alterations involving the thyroid transcription factor PAX8 and the peroxisome proliferator-activated receptor gamma 1 (PPARgamma1) genes have been described in thyroid neoplasms. We investigated in a series of thyroid samples, including 14 normal, 13 hyperfunctioning tissues, 26 follicular adenomas, 21 follicular and 41 papillary carcinomas, both the frequency of the PAX8-PPARgamma1 rearrangement and the expression of the PAX8 and PPARgamma transcripts. METHODS: Using RT-PCR followed by sequencing PCR products, PAX8-PPARgamma1 translocation was not detected in benign tissues nor in papillary carcinomas and was detected in 4 (19%) of 21 follicular carcinomas and in one (4%) of 26 follicular adenomas. RESULTS: Specific real-time quantitative RT-PCR (Q RT-PCR) methods detected high levels of PPARgamma transcripts in follicular carcinomas presenting the rearrangement. Interestingly, the level of PPARgamma transcripts was significantly decreased in papillary carcinomas in comparison with those found in benign adenomas and follicular carcinomas. Finally, PAX8 gene expression was decreased in both papillary and follicular thyroid carcinomas, and in these tumors to the same extent in the presence or absence of the rearrangement. These alterations in both PPARgamma and PAX8 gene expression may explain the poorly differentiated histotype of follicular carcinomas harboring the translocation. Immunohistochemistry showed that nuclear PPARgamma staining was weak in normal tissues, adenomas, papillary carcinomas and in some follicular carcinomas, and strong in the follicular carcinomas positive for the PAX8-PPARgamma1 translocation, but also in some follicular tumors in which no translocation could be evidenced. CONCLUSION: These observations confirm that the PAX8-PPARgamma1 translocation characterizes a subset of thyroid follicular carcinomas but is not a specific marker of carcinoma and that its frequency is lower than that initially reported. Finally, immunohistochemistry is not a reliable method for the specific detection of the translocation, that can be specifically evidenced by Q RT-PCR.

Adenocarcinoma, Follicular↗
PubMed1986

Recurrent medullary carcinoma of the thyroid demonstrated by thallium-201 scintigraphy.

Thallium-201 scintigraphy has been used in the evaluation of thyroid neoplasms, but uptake in recurrent or persistent medullary thyroid cancer has not been reported. We present two cases where focal 201TI activity localized superior mediastinal recurrences which were subsequently resected. Postoperative 201TI scans in both cases showed elimination of the focal uptake seen before surgery, as well as return of previously elevated serum calcitonin levels to normal. Scanning with 201TI may be useful in the preoperative localization of recurrent medullary thyroid cancer.

Adult↗
PubMed1996

Incidence of neoplasia in Hashimoto's thyroiditis: a fine-needle aspiration study.

There is a recognized association between Hashimoto's thyroiditis (HT) and thyroid neoplasms. We reviewed fine-needle aspirations (FNAs) from 90 patients with HT to assess the contribution of this procedure. For seven patients, FNA showed HT and follicular neoplasm (n = 6) or HT and papillary carcinoma (n = 1). Eighteen patients underwent thyroid resection. Three patients had follicular adenomas which were not detected by FNA, one patient had papillary carcinoma confirmed, and six patients with follicular neoplasm by FNA were negative for tumor. Thus, 4% of our patients had confirmed neoplasms, an incidence lower than usually reported. One reason for the lower rate of neoplasia in our series was misinterpretation of follicular neoplasia in the background of HT. The cytologic changes in the hyperplastic follicular and metaplastic oncocytic epithelium are similar to those seen in follicular neoplasm. Our study suggests that these processes may be indistinguishable, and thus, in the presence of HT, the diagnosis of follicular neoplasm probably should not be rendered.

Adenocarcinoma, Follicular↗
PubMed1995

Thyroid growth factors, signal transduction pathways, and oncogenes.

Growth of thyroid cancer cells is stimulated by various growth factors via signal transduction pathways. TSH, EGF, IGF, and TGF-alpha stimulate and TGF-beta inhibits thyroid cell growth. TSH stimulates thyroid cells via both the adenylate cyclase-PKA and the PLC-PKC-Ca signal transduction pathways. TSH-r, ras, gsp, ret, trk, and myc are oncogenes that are activated in some thyroid neoplasms. P53 and RB are tumor suppressor genes that are inactivated in some thyroid cancers.

Epidermal Growth Factor↗
PubMed1993

Increased phospholipase C activity in neoplastic thyroid membrane.

The phospholipase C (PLC)-protein kinase C (PKC) signal transduction pathway appears to be important for cellular growth of many normal and neoplastic tissues. Because alterations in the thyroid-stimulating hormone (TSH) receptor-adenylate cyclase-protein kinase A system in some thyroid tumors do not correlate with tumor size, invasiveness, or metastatic potential, we studied the PLC activity in both normal and neoplastic thyroid tissues from 11 patients. Five of these patients had follicular adenomas and 6 had papillary carcinomas. An 8,000 x g membrane fraction and a 105,000 x g cytosol fraction were prepared from the normal and neoplastic human thyroid tissues. PLC hydrolyzes phosphatidylinositol, 4,5-diphosphate (PIP2) to diacylglycerol (DAG) and inositol 1,4,5-triphosphate (IP3). Phospholipase C activity was determined measuring the hydrolysis of [3H]-PIP2. The activity of PLC in the neoplastic thyroid tissue membrane fraction (20.91 +/- 2.28 nmol PIP2 hydrolyzed/mg protein/120 min) was higher than that in normal thyroid membrane (14.27 +/- 0.82) (p < 0.05). In contrast, PLC activity was similar in the neoplastic (16.12 +/- 0.86 nmol PIP2 hydrolyzed/mg protein/120 min) and normal (16.66 +/- 0.60) cytosol. There was no difference between PLC activity in the membrane fraction from adenomas (21.21 +/- 3.71 nmol PIP2 hydrolyzed/mg protein/120 min) when compared with thyroid carcinomas (20.67 +/- 3.14). Neoplastic thyroid membranes have greater PLC activity than that found in normal thyroid membranes from the same patients. Although PLC activity in benign and malignant thyroid membranes was similar, the increased PLC activity in thyroid neoplasms may be responsible for or contribute to the enhanced growth of some thyroid tumors.

Adenoma↗
PubMed2006

CpG island methylation of tumor-related promoters occurs preferentially in undifferentiated carcinoma.

OBJECTIVE: To understand the role of epigenetic inactivation of tumor-related genes in the pathogenesis of thyroid cancer, we investigated the methylation profile of distinct thyroid neoplasms. DESIGN: We analyzed the methylation pattern of 17 gene promoters in nine thyroid cancer cell lines and in 38 primary thyroid carcinomas (13 papillary thyroid carcinoma [PTC], 10 follicular thyroid carcinoma [FTC], 9 undifferentiated thyroid carcinoma [UTC], 6 medullary thyroid carcinoma [MTC]), 12 goiters, and 10 follicular adenomas (FA) by methylation- specific polymerase chain reaction (PCR). Epigenetic inactivation was validated by expression analysis. MAIN OUTCOME: Twelve of these genes (RASSF1A, p16(INK4A), TSHR, MGMT, DAPK, ERalpha, ERbeta, RARbeta, PTEN, CD26, SLC5A8, and UCHL1) were frequently methylated in UTC (15%-86%) and thyroid cancer cell lines (25%-100%). In the more aggressive UTC, the mean methylation index (MI = 0.44) was the highest compared to other thyroid alterations PTC (MI = 0.29, p = 0.123), FTC (MI = 0.15, p = 0.005), MTC (MI = 0.13; p = 0.017), FA (MI = 0.27; p = 0.075) and goiters (MI = 0.23; p = 0.024). Methylation of TSHR, MGMT, UCHL1, and p16 occurred preferentially in UTC and this inactivation was reverted by a demethylating agent. CONCLUSIONS: Our results show that hypermethylation of several tumor-related gene promoters is a frequent event in UTC. The hypermethylation status may be reversed by DNA demethylating agents. Their clinical value remains to be investigated.

Carcinoma↗
PubMed1998

Absence of activating mutations of the genes encoding the alpha-subunits of G11 and Gq in thyroid neoplasia.

Activating mutations of the TSH receptor and alpha-subunit of Gs (G alpha s) that increase adenylyl cyclase activity have been identified in a subset of hyperfunctioning benign thyroid follicular adenomas and, less commonly, in hypofunctioning adenomas and carcinomas. In addition some thyroid tumors exhibit inappropriate activation of phospholipase C (PLC), a signaling pathway that has been implicated in the growth and dedifferentiation of thyroid cells. We therefore hypothesized that some thyroid tumors might be caused by somatic mutations in the genes encoding the alpha-chain of Gq or G11 that result in constitutive activation of the PLC pathway. We amplified regions of the alpha q and alpha 11 genes that encode amino acids, Q209 and R183, and we screened the DNA for mutations by sequence analysis and denaturing gradient gel electrophoresis. No mutations were identified after analysis of DNA from 38 thyroid tumors and 2 poorly differentiated thyroid carcinoma cell lines, including: 13 follicular adenomas, 10 follicular carcinomas, 5 papillary carcinomas, and 10 hyperplastic nodules from multinodular goiters. We conclude that activating mutations of alpha q and alpha 11 are absent or rare in hypofunctioning thyroid neoplasms and that other mechanisms must explain the elevated PLC activity reported in thyroid carcinoma.

Adenocarcinoma, Follicular↗
PubMed2003

Increased expression of phosphorylated p70S6 kinase and Akt in papillary thyroid cancer tissues.

Although a number of abnormalities in oncogenes have been reported in thyroid neoplasms, little information is available on the signal transduction pathway involved in neoplastic thyroid cell growth. Both p70S6 kinase (p70S6K) and Akt are kinases downstream of phosphatidylinositol 3 kinase (PI3K). These kinases are phosphorylated and activated by growth factors including IGF-1, EGF/TGF-alpha, and HGF in thyroid cells. Since the receptors for these growth factors are reportedly overexpressed in human thyroid cancer, we hypothesized that the PI3K-mediated signalings are overactivated in thyroid cancers. Tumorous and adjacent normal tissues of 20 patients with papillary thyroid cancer were obtained at surgery, and expression of p70S6K and Akt were measured by Western blot. Expression of the protein levels of p70S6K was increased in tumor tissues (T) compared to normal thyroid tissues (N), and expression of phosphorylated p70S6K was also significantly increased in tumor than in surrounding normal tissues. Overexpression of p70S6K in tumor tissues was further confirmed by immunohistochemistry. Strong immunoreactivity in the cytoplasm of thyroid cancer cells was seen in the majority of cases, whereas little immunoreactivity was found in the surrounding normal portion. Expression of phosphorylated Akt (pAkt) was also significantly higher in tumor tissues. Phosphorylation of Bad (pBad), a substrate of Akt, was also increased in the tumor tissues in association with activation of Akt, and the T/N ratio for pAkt positively correlated to the T/N ratio for pBad. The data presented here demonstrate that both p70S6K and Akt are activated in the majority of human papillary cancer cells. Activation of these signalings may be involved in the progression of papillary carcinoma by stimulating cell proliferation and/or preventing apoptosis.

Carcinoma, Papillary↗
PubMed1978

Bioassay of 1,5-naphthalenediamine for possible carcinogenicity.

A bioassay of 1,5-naphthalenediamine for possible carcinogenicity was conducted using Fischer 344 rats and B6C3F1 mice. 1,5-Naphthalenediamine was administered in the feed, at either of two concentrations, to groups of 50 male and 50 female animals of each species. The high and low dietary concentrations utilized in the chronic bioassay were, respectively, 0.1 and 0.05 percent for rats and 0.2 and 0.1 percent for mice. The compound was administered in the diet for 103 weeks, followed by up to 4 weeks of observation. Fifty mice of each sex and 25 rats of each sex were placed on test as controls. These animals were observed for up to 110 weeks. There were no significant positive associations between the administered concentrations of 1,5-naphthalenediamine and mortality in either sex of rats or mice. In all groups adequate numbers of animals survived sufficiently long to be at risk from late-developing tumors. Among dosed female rats, a statistically significant increase in endometrial stromal polyps was observed. Several of these tumors underwent malignant transformation to endometrial stromal sarcomas. The incidence of female rats having either adenoma or carcinoma of the clitoral gland was statistically significant. No neoplasms were observed at significantly increased incidences in dosed male rats. Based on lack of clinical signs or weight loss, the male rats may have been able to withstand a higher dose. In mice, dose-related increases in thyroid neoplasms were observed in both sexes. The incidence of thyroid C-cell carcinomas was significant for high dose female mice. The combined incidences of papillary adenomas, follicular-cell adenomas and papillary cystadenomas of the thyroid were significant for mice of both sexes. The incidence of hepatocellular carcinomas and the incidence of alveolar/bronchiolar adenomas were each significant for dosed female mice. Under the conditions of this bioassay, 1,5-naphthalenediamine was carcinogenic in female Fischer 344 rats, causing clitoral and uterine neoplasms. 1,5-Naphthalenediamine was also carcinogenic for B6C3F1 mice, producing thyroid neoplasms in males and neoplasms of the thyroid, liver, and lung in females. Insufficient evidence was provided for the carcinogenicity of the compound in male Fischer 344 rats.

Journal Article↗
PubMedDate not supplied

Use of immunohistochemistry in fine needle aspiration of thyroid nodules in patients with a history of malignancy. A report of two cases.

BACKGROUND: A history of a nonthyroid malignancy may present a diagnostic dilemma in the assessment of fine needle aspiration (FNA) of thyroid nodules. One reported series, on patients with prior malignancies and a thyroid nodule, indicated that in 17% of patients, the thyroid nodule represented metastatic malignancy, 6% were classified as primary thyroid cancers, and the remainder were benign or inconclusive lesions. The resolution of this problem is essential to patient management. CASES: We report two cases in which patients with a history of renal cell carcinoma presented with a thyroid nodule. The first patient was an 80-year-old female whose Papanicolaou-stained FNA demonstrated clusters of round to polygonal cells with round to ovoid, hyperchromatic nuclei and abundant, wispy cytoplasm. The second patient was a 55-year-old female with clusters and single cells with round to oval, eccentric nuclei and copious, granular, gray cytoplasm noted on Papanicolaou-stained material. In each case, the diagnosis was inconclusive on initial review of Papanicolaou-stained slides, and immunohistochemical staining was ordered to better characterize the lesions. Tumor cells from case 1 were positive for cytokeratin cocktail and vimentin and negative for thyroglobulin, epithelial membrane antigen and calcitonin, suggestive of metastatic renal cell carcinoma. In contrast, the tumor cells from case 2 expressed cytokeratin, thyroglobulin and vimentin, consistent with a primary thyroid neoplasm. In each case, the cytologic diagnoses were confirmed in the resected specimens. CONCLUSION: Immunohistochemistry is a helpful adjunct in the evaluation of thyroid nodules in patients with a past history of malignancy.

Adenocarcinoma, Papillary↗
PubMed1999

Involvement of protein kinase Cepsilon (PKCepsilon) in thyroid cell death. A truncated chimeric PKCepsilon cloned from a thyroid cancer cell line protects thyroid cells from apoptosis.

The protein kinase C (PKC) family has been implicated in the regulation of apoptosis. However, the contribution of individual PKC isozymes to this process is not well understood. We reported amplification of the chromosome 2p21 locus in 28% of thyroid neoplasms, and in the WRO thyroid carcinoma cell line. By positional cloning we identified a rearrangement and amplification of the PKCepsilon gene, that maps to 2p21, in WRO cells. This resulted in the overexpression of a chimeric/truncated PKCepsilon (Tr-PKCepsilon) mRNA, coding for N-terminal amino acids 1-116 of the isozyme fused to an unrelated sequence. Expression of the Tr-PKCepsilon protein in PCCL3 cells inhibited activation-induced translocation of endogenous PKCepsilon, but its kinase activity was unaffected, consistent with a dominant negative effect of the mutant protein on activation-induced translocation of wild-type PKCepsilon and/or displacement of the isozyme to an aberrant subcellular location. Cell lines expressing Tr-PKCepsilon grew to a higher saturation density than controls. Moreover, cells expressing Tr-PKCepsilon were resistant to apoptosis, which was associated with higher Bcl-2 levels, a marked impairment in p53 stabilization, and dampened expression of Bax. These findings point to a role for PKCepsilon in apoptosis-signaling pathways in thyroid cells, and indicate that a naturally occurring PKCepsilon mutant that functions as a dominant negative can block cell death triggered by a variety of stimuli.

Amino Acid Sequence↗
PubMedDate not supplied

Longevity, body weight, and neoplasia in ad libitum-fed and diet-restricted C57BL6 mice fed NIH-31 open formula diet.

Groups of C57BL6 mice of each sex were assigned to one of 2 dietary regimens, ad libitum (AL) or dietary restriction (DR), to study effects of food restriction on body weight, survival, and neoplasia. The AL and DR groups were subdivided into a scheduled sacrifice group for examination at 6-mo intervals, and a lifetime group to provide longevity data. Necropsies and microscopic examinations were conducted on 911 animals. In the lifetime group food consumption averaged 33.6 and 34.4 g per week by AL males and AL females, respectively; the DR counterparts were given 40% less. The diet contained 4.35 kcal/g. The average lifetime body weights were 34.8, 26.8, 22.6, and 21.6 g for AL males, AL females, DR males, and DR females, respectively, and their age at 50% survival was 27.5, 26.9, 31.7, and 33.5 mo. Maximal lifespan was increased 18% in DR males and females. Lifetime incidence of tumor-bearing mice was 89% and 86% for AL males and females, versus 64% for each sex of DR mice. Dramatic reduction occurred in female DR mice in lymphoma (9% vs 29%), pituitary neoplasms (1% vs 37%), and thyroid neoplasms (0.4% vs 8%). In males, hepatocellular tumors were reduced to 1% from 10% by DR. In contrast, the incidence of histiocytic sarcoma was increased in DR females and unaffected in DR males. Tumor onset was delayed in DR animals; 87% of all neoplasms in males and 95% in females had occurred in the AL mice by 24 mo, whereas the DR animals had only 52% and 39% of their lifetime incidence, respectively, by that age. This study provided comparative AL and DR data from C57BL6 mice examined randomly at 6-mo intervals (cross-sectional group) in parallel with data from animals in similar cohort that was unsampled and allowed to succumb naturally (longevity group). Dietary restriction reduced the lifetime percentage of tumor-bearing animals and the number of tumors per animal, and delayed the age at onset of most neoplasms.

Animals↗