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Biochemistry Research and Pathology Departments, Roswell Park Memorial Institute, and the New York State Department of Health, Buffalo, New York 14203
The effect of recently derived rat transplantable mammary carcinomas (TMC), the Walker carcinoma 256 (W256) and the Walker carcinosarcoma R256 (WR256) upon the lipid composition of the host liver and muscle was determined. Sephadex column chromatography was employed to separate the nonlipid water-soluble substances and gangliosides from the total pure lipid of chloroform-methanol extracts of tissues; silicic acid column chromatography was used to separate the neutral and polar lipids and diethylaminoethyl cellulose to separate the acidic from the nonacidic phosphatides. The total lipid obtained from liver was increased significantly by the growth of TMC and W256. No change in total lipid resulted from the growth of WR256. The total lipid of muscle was decreased by 20 to 30 percent as a result of the growth of W256, but not by TMC and WR256. Sephadex column chromatography of chloroform-methanol extracts of liver also revealed that TMC and W256 tumors decreased the nonlipid water soluble materials significantly, whereas no change was produced by WR256. The nonlipid water soluble materials of muscle were unchanged for medium sized tumors, but when TMC reached 47 percent of the host body weight, the nonlipid water-soluble materials increased signally. WR256 produced no change in total lipid but induced an increase in the nonlipid water soluble materials. The level of neutral lipid of the liver of rats bearing W256 was increased, whereas TMC had no such effect. The amount of liver phosphatides was increased by TMC. The neutral lipid content of muscle was only decreased by W256. Neither tumor appreciably affected the proportions of muscle and liver phosphatides nor the percentages of acidic and nonacidic phosphatides. The alterations in liver and muscle lipid composition induced by W256 appear to be unique to this tumor.
1 This investigation was supported by Public Health Service Research Grant No. CA06107 and American Cancer Society Grant P-389A.
Received 11/17/67. Accepted 2/21/68.
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