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[Cancer Research 37, 3484-3489, October 1, 1977]
© 1977 American Association for Cancer Research

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Vascular Volume and Perfusion in Hamster Cheek Pouch Carcinomas and Tumor-bearing Cheek Pouches1

Alan G. Lurie2, Bethaney B. Nintzel and Robert M. Rippey

Department of Oral Radiology [A. G. L.] and Research in Health Education [R. M. R.] and School of Dental Medicine [B. B. N.], The University of Connecticut Health Center School of Dental Medicine, Farmington, Connecticut 06032

Blood volume and perfusion in 7,12-dimethylbenz[a]anthracene-induced hamster cheek pouch carcinomas, tumor-bearing pouch tissue, and normal pouch tissue were studied by distribution of 51Cr-labeled erythrocytes and 86RbCl. Squamous cell carcinomas were induced in male Syrian golden hamsters by repeated topical applications of 0.5% 7,12-dimethylbenz[a]anthracene in mineral oil. Normal and tumor-bearing hamsters received i.v. injections of 20 µCi 51Cr-labeled hamster erythrocytes, followed in 10 min by 50 µCi 86RbCl. Pouches and tumors were everted, clamped separately, and excised separately 90 sec after 86RbCl injection, and the tumor volumes were determined. Radioactivity was determined by scintillation spectrometry, and histopathological evaluations were subsequently performed. Tumor 51Cr and 86Rb activities were less than those of control pouches in small tumors (volume, < 10 cu mm) and rose steadily thereafter to levels above those of control pouches but less than those of tumor-bearing pouches. Tumors with volumes > 10 cu mm were squamous cell carcinomas except for one papilloma. Statistical analysis of the tumor isotopic distribution values showed correlations of tumor hemodynamic changes with tumor volume and histopathology. Histopathologically defined malignant changes and increasing tumor sizes were accompanied by increasing tumor volume and blood perfusion. Increases in blood volume and perfusion also occurred in tumor-bearing pouch tissue. These results support the concept of the relation of rapid tumor growth and malignant behavior to tumor neovascularization, initiated possibly by a chemical mediator such as tumor angiogenesis factor.

1 This work was supported by Grant PDT 18 from the American Cancer Society and by Special Dental Investigator Grant 5 R23 DE03996-03 from the National Institute of Dental Research, NIH.

2 To whom requests for reprints should be addressed, at Department of Oral Radiology. The University of Connecticut Health Center, Farmington, Conn. 06032.

Received 4/15/77. Accepted 6/24/77.







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Copyright © 1977 by the American Association for Cancer Research.