Effect of somatostatin and tamoxifen on the growth of human pancreatic cancers in nude mice

G. J. Poston, Courtney Townsend, S. Rajaraman, J. C. Thompson, Pomila Singh

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

We studied the effects of SMS 201-995 (SMS), a somatostatin analog, and tamoxifen, an antagonist of estrogenic actions, on the growth of human pancreatic cancers (SKI and PGER) in vivo. Male nude mice were inoculated with either SKI or PGER by passage of tumor chunks (3 mm2) to the scapular region. Mice from each tumor group were randomly allocated to one of four treatment groups: group 1, control group; group 2, SMS (100 μg/kg t.i.d.); group 3, tamoxifen (10 mg/kg three times a week); and group 4, SMS (100 μg/kg t.i.d.) + tamoxifen (10 mg/kg three times a week). The somatostatin analog, SMS, given alone or as a combined regimen with tamoxifen, significantly reduced (a) the rate of growth of SKI, and (b) DNA, RNA, and protein content of the tumors. On the other hand, in the case of PGER tumors, none of the treatment regimes significantly influenced the growth of PGER in vivo. Despite showing no significant effects during the study, PGER tumors in mice receiving tamoxifen alone had significantly lower total DNA, RNA, and protein contents compared to control tumors; this was reversed on combined treatment with SMS. None of the growth parameters of PGER was effected by SMS alone. We conclude that, in the case of SKI, SMS with or without tamoxifen was effective as a growth inhibitory agent, whereas in the case of PGER, tamoxifen alone was effective. This finding suggests that independent pathways mediate the growth-inhibitory effects of tamoxifen and SMS, and that different pancreatic cancers may respond to the two agents differently, some with inhibition, some not.

Original languageEnglish (US)
Pages (from-to)151-157
Number of pages7
JournalPancreas
Volume5
Issue number2
StatePublished - 1990

Fingerprint

Tamoxifen
Somatostatin
Pancreatic Neoplasms
Nude Mice
Growth
Neoplasms
RNA
Octreotide
DNA
Proteins
Control Groups

Keywords

  • Pancreatic cancer
  • Somatostatin
  • Tamoxifen

ASJC Scopus subject areas

  • Endocrinology
  • Gastroenterology

Cite this

Effect of somatostatin and tamoxifen on the growth of human pancreatic cancers in nude mice. / Poston, G. J.; Townsend, Courtney; Rajaraman, S.; Thompson, J. C.; Singh, Pomila.

In: Pancreas, Vol. 5, No. 2, 1990, p. 151-157.

Research output: Contribution to journalArticle

Poston, G. J. ; Townsend, Courtney ; Rajaraman, S. ; Thompson, J. C. ; Singh, Pomila. / Effect of somatostatin and tamoxifen on the growth of human pancreatic cancers in nude mice. In: Pancreas. 1990 ; Vol. 5, No. 2. pp. 151-157.
@article{c8e4d2bea3954021aa777b4604c0c7e3,
title = "Effect of somatostatin and tamoxifen on the growth of human pancreatic cancers in nude mice",
abstract = "We studied the effects of SMS 201-995 (SMS), a somatostatin analog, and tamoxifen, an antagonist of estrogenic actions, on the growth of human pancreatic cancers (SKI and PGER) in vivo. Male nude mice were inoculated with either SKI or PGER by passage of tumor chunks (3 mm2) to the scapular region. Mice from each tumor group were randomly allocated to one of four treatment groups: group 1, control group; group 2, SMS (100 μg/kg t.i.d.); group 3, tamoxifen (10 mg/kg three times a week); and group 4, SMS (100 μg/kg t.i.d.) + tamoxifen (10 mg/kg three times a week). The somatostatin analog, SMS, given alone or as a combined regimen with tamoxifen, significantly reduced (a) the rate of growth of SKI, and (b) DNA, RNA, and protein content of the tumors. On the other hand, in the case of PGER tumors, none of the treatment regimes significantly influenced the growth of PGER in vivo. Despite showing no significant effects during the study, PGER tumors in mice receiving tamoxifen alone had significantly lower total DNA, RNA, and protein contents compared to control tumors; this was reversed on combined treatment with SMS. None of the growth parameters of PGER was effected by SMS alone. We conclude that, in the case of SKI, SMS with or without tamoxifen was effective as a growth inhibitory agent, whereas in the case of PGER, tamoxifen alone was effective. This finding suggests that independent pathways mediate the growth-inhibitory effects of tamoxifen and SMS, and that different pancreatic cancers may respond to the two agents differently, some with inhibition, some not.",
keywords = "Pancreatic cancer, Somatostatin, Tamoxifen",
author = "Poston, {G. J.} and Courtney Townsend and S. Rajaraman and Thompson, {J. C.} and Pomila Singh",
year = "1990",
language = "English (US)",
volume = "5",
pages = "151--157",
journal = "Pancreas",
issn = "0885-3177",
publisher = "Lippincott Williams and Wilkins",
number = "2",

}

TY - JOUR

T1 - Effect of somatostatin and tamoxifen on the growth of human pancreatic cancers in nude mice

AU - Poston, G. J.

AU - Townsend, Courtney

AU - Rajaraman, S.

AU - Thompson, J. C.

AU - Singh, Pomila

PY - 1990

Y1 - 1990

N2 - We studied the effects of SMS 201-995 (SMS), a somatostatin analog, and tamoxifen, an antagonist of estrogenic actions, on the growth of human pancreatic cancers (SKI and PGER) in vivo. Male nude mice were inoculated with either SKI or PGER by passage of tumor chunks (3 mm2) to the scapular region. Mice from each tumor group were randomly allocated to one of four treatment groups: group 1, control group; group 2, SMS (100 μg/kg t.i.d.); group 3, tamoxifen (10 mg/kg three times a week); and group 4, SMS (100 μg/kg t.i.d.) + tamoxifen (10 mg/kg three times a week). The somatostatin analog, SMS, given alone or as a combined regimen with tamoxifen, significantly reduced (a) the rate of growth of SKI, and (b) DNA, RNA, and protein content of the tumors. On the other hand, in the case of PGER tumors, none of the treatment regimes significantly influenced the growth of PGER in vivo. Despite showing no significant effects during the study, PGER tumors in mice receiving tamoxifen alone had significantly lower total DNA, RNA, and protein contents compared to control tumors; this was reversed on combined treatment with SMS. None of the growth parameters of PGER was effected by SMS alone. We conclude that, in the case of SKI, SMS with or without tamoxifen was effective as a growth inhibitory agent, whereas in the case of PGER, tamoxifen alone was effective. This finding suggests that independent pathways mediate the growth-inhibitory effects of tamoxifen and SMS, and that different pancreatic cancers may respond to the two agents differently, some with inhibition, some not.

AB - We studied the effects of SMS 201-995 (SMS), a somatostatin analog, and tamoxifen, an antagonist of estrogenic actions, on the growth of human pancreatic cancers (SKI and PGER) in vivo. Male nude mice were inoculated with either SKI or PGER by passage of tumor chunks (3 mm2) to the scapular region. Mice from each tumor group were randomly allocated to one of four treatment groups: group 1, control group; group 2, SMS (100 μg/kg t.i.d.); group 3, tamoxifen (10 mg/kg three times a week); and group 4, SMS (100 μg/kg t.i.d.) + tamoxifen (10 mg/kg three times a week). The somatostatin analog, SMS, given alone or as a combined regimen with tamoxifen, significantly reduced (a) the rate of growth of SKI, and (b) DNA, RNA, and protein content of the tumors. On the other hand, in the case of PGER tumors, none of the treatment regimes significantly influenced the growth of PGER in vivo. Despite showing no significant effects during the study, PGER tumors in mice receiving tamoxifen alone had significantly lower total DNA, RNA, and protein contents compared to control tumors; this was reversed on combined treatment with SMS. None of the growth parameters of PGER was effected by SMS alone. We conclude that, in the case of SKI, SMS with or without tamoxifen was effective as a growth inhibitory agent, whereas in the case of PGER, tamoxifen alone was effective. This finding suggests that independent pathways mediate the growth-inhibitory effects of tamoxifen and SMS, and that different pancreatic cancers may respond to the two agents differently, some with inhibition, some not.

KW - Pancreatic cancer

KW - Somatostatin

KW - Tamoxifen

UR - http://www.scopus.com/inward/record.url?scp=0025055752&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025055752&partnerID=8YFLogxK

M3 - Article

VL - 5

SP - 151

EP - 157

JO - Pancreas

JF - Pancreas

SN - 0885-3177

IS - 2

ER -