A Transplantable Rabbit Carcinoma Originating in a Virus-Induced Papilloma and Containing the Virus in Masked or Altered Form

Kidd, John G.; Rous, Peyton

doi:10.1084/jem.71.6.813

Cited by 207 publications

(92 citation statements)

References 20 publications

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“…Experimental animals Male Japanese White rabbits implanted with VX2-carcinoma 7) in the muscles of their right thigh were supplied by Tsukuba Animal Research Laboratories Co. (Tsukuba) and fed essential CR-3 (Clea, Tokyo) and water. When the VX2-carcinoma in the right thigh of the rabbits grew to more than 5 cm in diameter, it was resected, and cell suspensions (1×10 5 cells in 1 ml of 0.15 M NaCl) were injected intramuscularly into the right thigh of normal rabbits weighing about 3 kg.…”

Section: Methodsmentioning

confidence: 99%

Apoptosis of Muscle Cells Causes Weight Loss Prior to Impairment of DNA Synthesis in Tumor‐bearing Rabbits

Ishiko¹,

Sumi²,

Hirai³

et al. 2001

Japanese Journal of Cancer Research

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The mechanism of weight loss induced by the growth of malignant tumors is still unknown. We investigated it by focusing on apoptosis of skeletal muscle. VX2-tumor was implanted into rabbits and the apoptotic index (AI) of skeletal muscle was measured by in situ end-labeling assay. Plasma of the tumor-bearing rabbits was perfused repeatedly through non-coated charcoal resin. The AI reached 54.6% early after tumor implantation, when weight loss amounted to an 18% decrease in lean body mass (LBM) without change in muscle DNA synthesis or urinary 3-methylhistidine/ creatinine ratio (3-MH/Cr). When the decrease of LBM reached 30%, DNA synthesis was decreased by 48% and 3-MH/Cr was increased by 104%, whereas AI was only 4.7%. The plasma perfusion did not prevent apoptosis in muscle, but improved LBM, DNA synthesis, and 3-MH/Cr. There may be two mechanisms of muscle depletion during the tumor growth: apoptosis in the early stage and metabolic abnormalities in muscle in the late stage.Key words: Muscle cell -Apoptosis -DNA synthesis -Weightloss -Plasma perfusion The weight loss induced by the progression of malignant tumors is the symptom that has attracted the greatest attention among investigators attempting to identify the etiology of cancer cachexia, a condition that gives rise to a variety of symptoms. Cancer cachexia is generally considered to be characterized metabolically by proteolysis and lipolysis rates that exceed protein synthesis and lipogenesis, but no conclusion has been reached concerning how these metabolic abnormalities occur. Todorov et al. succeeded in purifying a cancer cachectic factor that induces skeletal muscle catabolism from mice transplanted with MAC16 tumors. 1) Other humoral factors such as cachectin, tumor-necrosis factor, interleukin (IL)-1, IL-6, interferon (IFN)-γ, leukemia-inhibitory factor (LIF), and lipid-mobilizing factor have also been reported to act as mediators inducing cancer cachexia.2-4) We purified an anemiainducing substance (AIS) that depresses erythrocyte and immunocompetent cell functions, as reported in our previous papers, 5,6) and AIS has been recently shown to have another biological action, i.e., lipolytic activity. As stated above, many substances have been reported to be causative agents of cancer cachexia, and at present it is difficult to discuss the etiology of this condition in a coherent fashion.In the present study using tumor-bearing rabbits, we examined the relationship between weight loss induced during the progression of malignant tumors and the morphological and energy metabolism changes in muscle tissue. MATERIALS AND METHODSExperimental animals Male Japanese White rabbits implanted with VX2-carcinoma 7) in the muscles of their right thigh were supplied by Tsukuba Animal Research Laboratories Co. (Tsukuba) and fed essential CR-3 (Clea, Tokyo) and water. When the VX2-carcinoma in the right thigh of the rabbits grew to more than 5 cm in diameter, it was resected, and cell suspensions (1×10 5 cells in 1 ml of 0.15 M NaCl) were injected intramuscularly in...

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Section: Methodsmentioning

confidence: 99%

Apoptosis of Muscle Cells Causes Weight Loss Prior to Impairment of DNA Synthesis in Tumor‐bearing Rabbits

Ishiko¹,

Sumi²,

Hirai³

et al. 2001

Japanese Journal of Cancer Research

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“…This tumour originates from a Shope virus-induced papilloma (Kidd and Rous, 1940). Small 0.5 × 0.5 cm 2 pieces were implanted intramuscularly in the right thigh.…”

Section: Tumour Assaymentioning

confidence: 99%

Combination oral antiangiogenic therapy with thalidomide and sulindac inhibits tumour growth in rabbits

et al. 1998

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Neovascularization facilitates tumour growth and metastasis formation. In our laboratory, we attempt to identify clinically available oral efficacious drugs for antiangiogenic activity. Here, we report which non-steroidal anti-inflammatory drugs (NSAIDs) can inhibit corneal neovascularization, induced by basic fibroblast growth factor (bFGF) or vascular endothelial growth factor (VEGF). This antiangiogenic activity may contribute to the known effects of NSAIDs on gastric ulcers, polyps and tumours. We found that sulindac was one of the most potent antiangiogenic NSAIDs, inhibiting bFGF-induced neovascularization by 50% and VEGF-induced neovascularization by 55%. Previously, we reported that thalidomide inhibited growth factor-induced corneal neovascularization. When we combined sulindac with thalidomide, we found a significantly increased inhibition of bFGF- or VEGF-induced corneal neovascularization (by 63% or 74% respectively) compared with either agent alone ( P < 0.01). Because of this strong antiangiogenic effect, we tested the oral combination of thalidomide and sulindac for its ability to inhibit the growth of V2 carcinoma in rabbits. Oral treatment of thalidomide or sulindac alone inhibited tumour growth by 55% and 35% respectively. When given together, the growth of the V2 carcinoma was inhibited by 75%. Our results indicated that oral antiangiogenic combination therapy with thalidomide and sulindac may be a useful non-toxic treatment for cancer. © 1999 Cancer Research Campaign

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“…However, in some cases, carcinomas appear at the same sites several months or years later. Some examples of naturally occurring papilloma virus-induced malignancies are the Shope rabbit carcinoma (Kidd & Rous, 1940;Ito, 1962), epidermodysplasia verruciformis, a rare human disease in which malignant transformation of some of the lesions is observed (Jablonska et al, 1972;Yabe & Sadakane, 1975), and possibly, human genital carcinomas associated with genital warts, condyloma acuminata .…”

Section: Introductionmentioning

confidence: 99%

Isolation and Characterization of the Major Capsid Protein of Bovine Papilloma Virus Type 1

Meinke

1981

Journal of General Virology

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SUMMARYThe major capsid protein of bovine papilloma virus type 1 (BPV-1) was isolated by gel filtration following disruption of purified virus particles with guanidine hydrochloride. The capsid protein, VP1, has a mol. wt. of about 53 500. Amino acid composition studies of VP1 showed that it is a highly acidic protein containing almost twice the average number of acidic residues than basic residues. Relatedness was observed between VP1 and the major capsid proteins of simian virus 40 (SV40) and polyoma virus.

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A Transplantable Rabbit Carcinoma Originating in a Virus-Induced Papilloma and Containing the Virus in Masked or Altered Form

Cited by 207 publications

References 20 publications

Apoptosis of Muscle Cells Causes Weight Loss Prior to Impairment of DNA Synthesis in Tumor‐bearing Rabbits

Apoptosis of Muscle Cells Causes Weight Loss Prior to Impairment of DNA Synthesis in Tumor‐bearing Rabbits

Combination oral antiangiogenic therapy with thalidomide and sulindac inhibits tumour growth in rabbits

Isolation and Characterization of the Major Capsid Protein of Bovine Papilloma Virus Type 1

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