Bombesin antagonist prevents CO2 laser-induced promotion of oral cancer

Mark F. Kozacko, Thomas S. Mang, Andrew V Schally, Roger L. Priore, Charles Liebow

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

We previously reported that CO2 laser incisions in carcinogen-initiated fields promoted cancer development and caused release of growth factors. Here we examined the quantitative and additive properties of this tumor-promoting event and examined whether this promotion could be nullified by treatment with a bombesin antagonist, which down-regulates epidermal growth factor receptors. The model used for cancer promotion was the hamster buccal cheek pouch that had been treated with a carcinogen (9,10-dimethyl-1,2- benzanthracene) for 6 weeks, producing premalignant lesions. These lesions would evolve into a cancer eventually without further treatment. Promotion was measured both by increased fluorescence in response to systemically administered Photofrin, measured noninvasively using an in vivo fluorescence photometer, and by the timing of appearance of clinical tumors. Laser incisions (0-3) were made into the hamster cheek 1 week apart, or three incisions were done 1 day apart. Another group of animals received bombesin antagonist RC-3095 for 4 weeks during the time incisions were made, again measuring promotion. Laser incisions 1 week apart produced additive promotion, whereas three incisions 1 day apart were not statistically different from the group receiving only one incision. RC-3095 treatment completely eliminated the promoting effects of incision and totally stopped promotion for the 4-week period of treatment. After discontinuing treatment with RC-3095, lesion progression resumed at the untreated control rate. This work confirms that the promoting event of a laser incision follows a comparable time course to release of growth factors after such an incision and that it can be eliminated by treatment with bombesin antagonists.

Original languageEnglish
Pages (from-to)2953-2957
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume93
Issue number7
DOIs
StatePublished - Apr 2 1996
Externally publishedYes

Fingerprint

Bombesin
Gas Lasers
Mouth Neoplasms
Cheek
Lasers
Neoplasms
Cricetinae
Carcinogens
Intercellular Signaling Peptides and Proteins
Fluorescence
Dihematoporphyrin Ether
9,10-Dimethyl-1,2-benzanthracene
Down-Regulation
Tpi(6)-Leu(13)-psi(CH2NH)-Leu(14)-bombesin (6-14)

Keywords

  • carcinogenesis
  • growth factors
  • hematoporphyrin
  • laser surgery
  • RC-3095

ASJC Scopus subject areas

  • Genetics
  • General

Cite this

Bombesin antagonist prevents CO2 laser-induced promotion of oral cancer. / Kozacko, Mark F.; Mang, Thomas S.; Schally, Andrew V; Priore, Roger L.; Liebow, Charles.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 93, No. 7, 02.04.1996, p. 2953-2957.

Research output: Contribution to journalArticle

Kozacko, Mark F. ; Mang, Thomas S. ; Schally, Andrew V ; Priore, Roger L. ; Liebow, Charles. / Bombesin antagonist prevents CO2 laser-induced promotion of oral cancer. In: Proceedings of the National Academy of Sciences of the United States of America. 1996 ; Vol. 93, No. 7. pp. 2953-2957.
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