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[Cancer Research 49, 4289-4294, August 1, 1989]
© 1989 American Association for Cancer Research

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Postpromotional Effects of Dietary Marine or Safflower Oils on Large Bowel or Pulmonary Implants of CT-26 in Mice1

Francis Cannizzo, Jr. and Selwyn A. Broitman2

Departments of Pathology and Microbiology, Boston University, Boston, Massachusetts 02118

Marine oils containing n-3 fatty acids exhibit variable antineoplastic effects. Diets containing low (11.6% of kcal) or high (46.5% of kcal) levels of marine oils as the exclusive fat source were compared to diets containing identical amounts of safflower oil (n-6) in weanling, male BALB/c ByJ mice. All diets provided approximately 90 kcal/100 g body weight/day, and contained identical quantities of vitamins, minerals, protein, and fiber. The growth of transplantable colon carcinoma, CT-26, (106 cells/animal) implanted, subserosally, into the descending colon via laparotomy, was observed weekly over 28 days by necropsy in all dietary groups. At each time period animals fed safflower oil had larger tumors than those fed marine oil. Tumor volumes at 21 days postimplantation were as follows: low fat marine, 55 mm3 (5–196 mm3) [median (range)]; high fat marine, 70 (26–194); low fat safflower, 216 (32–800); high fat safflower, 247 (70–1352). Marine oil tumors were smaller than safflower oil tumors (P < 0.005 by analysis of variance; P < 0.01 by Scheffe test). Metastatic potential was assessed by pulmonary colonization. CT-26 was injected i.v. in tail veins (105 cells/animal). Mice were sacrificed and colonies were counted after 21 days. Mice fed low fat marine, high fat marine, and low fat safflower oil diets, 10–14 colonies; high fat safflower, 55 colonies (P < 0.001 by analysis of variance). Hence, dietary marine oil significantly suppressed growth of this colon carcinoma at all intake levels studied and inhibited pulmonary colonization at higher intakes relative to safflower oil.

1 This work was supported by American Cancer Society Grant BC-539, National Large Bowel Project Grant CA-38177, and Oncobiology Training Grant CA9423 of the National Cancer Institute, National Institutes of Health, Bethesda, MD, whom the authors gratefully acknowledge.

2 To whom requests for reprints should be addressed, at: Boston University School of Medicine, Department of Microbiology, 80 East Concord St., Boston, MA 02118.

Received 7/15/88. Revised 4/ 4/89. Accepted 5/ 1/89.




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
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Copyright © 1989 by the American Association for Cancer Research.