Effect of human growth hormone on human pancreatic carcinoma growth, protein, and cell cycle kinetics

Lawrence Harrison, David Blumberg, Russell Berman, Bruce Ng, Steve Hochwald, Murray F. Brennan, Michael Burt

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

The role of human growth hormone (hGH) as a nutritional adjunct for cancer patients is controversial because of its potential mitogenic effects on tumor growth. No studies to date have examined the effect of hGH on human tumor response in vivo. In Vitro: Athymic mice were injected (s.c.) daily with hGH (GH, n = 14) or saline (CTL, n = 14). On Day 10, serum was collected and added to human pancreatic carcinoma cells in culture. In Vivo: Athymic mice were inoculated (s.c.) with human pancreatic carcinoma cells. On Day 14, mice were randomized to receive daily either hGH (GH, n = 14) or saline (CTL, n = 12). On Day 29, animals received [3H]phenylalanine for tissue protein fractional synthetic rate (FSR) measurement. Tumors were excised and cell cycle kinetics analyzed. Data are expressed as mean ± SEM. Statistical analysis was performed by unpaired t test and/or ANOVA where appropriate. In Vitro: Serum from GH-treated animals had elevated IGF-1 levels (287 ± 34 ng/ml vs 157 ± 53 ng/ml, P < 0.001) and significantly stimulated cell growth (No. cells x 103/well) compared with CTL serum (925 ± 31 vs 747 ± 38, P < 0.001). In Vivo: Serum from GH-treated animals had elevated IGF-1 levels (287 ± 34 ng/ml vs 157 ± 53 ng/ml, P < 0.001) and significantly stimulated cell growth (No. cells x 103/well) compared with CTL serum (925 ± 31 vs 747 ± 38, P < 0.001). In Vivo: Growth hormone had no significant effect on tumor growth rate (mm3/day) (1.45 ± 0.47 CTL vs 1.57 ± 0.66 GH), final tumor weight (mg) (0.19 ± 0.15 CTL vs 0.17 ± 0.06 GH), DNA Index (1.5 ± 0.1 CTL vs 1.5 ± 0.1 GH), percent S phase (20.3 ± 3.3 CTL vs 22.1 ± 3.0 GH), or tumor FSR (%/day) (51.1 ± 17.8 CTL vs 70.2 ± 61.1 GH). Growth hormone significantly elevated serum IGF-1 levels (ng/ml) (176 ± 48 CTL vs 222 ± 53 GH, P < 0.005) and liver FSR (%/day) (62.8 ± 17.8 CTL vs 79.7 ± 12.7 GH, P < 0.005). Serum of GH-treated mice increased human pancreatic cell growth in vitro. In vivo, GH administration raised serum IGF-1 levels and increased liver protein FSR, without tumor growth, cell cycle kinetics, or protein FSR.

Original languageEnglish (US)
Pages (from-to)317-322
Number of pages6
JournalJournal of Surgical Research
Volume61
Issue number2
DOIs
StatePublished - Jan 1 1996
Externally publishedYes

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Cell Cycle Proteins
Human Growth Hormone
Growth
Serum
Insulin-Like Growth Factor I
Neoplasms
Nude Mice
Growth Hormone
Cell Cycle
Proteins
Pancreatic Carcinoma
Liver
Tumor Burden
Phenylalanine
S Phase
Analysis of Variance
Cell Culture Techniques
DNA

All Science Journal Classification (ASJC) codes

  • Surgery

Cite this

Harrison, Lawrence ; Blumberg, David ; Berman, Russell ; Ng, Bruce ; Hochwald, Steve ; Brennan, Murray F. ; Burt, Michael. / Effect of human growth hormone on human pancreatic carcinoma growth, protein, and cell cycle kinetics. In: Journal of Surgical Research. 1996 ; Vol. 61, No. 2. pp. 317-322.
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abstract = "The role of human growth hormone (hGH) as a nutritional adjunct for cancer patients is controversial because of its potential mitogenic effects on tumor growth. No studies to date have examined the effect of hGH on human tumor response in vivo. In Vitro: Athymic mice were injected (s.c.) daily with hGH (GH, n = 14) or saline (CTL, n = 14). On Day 10, serum was collected and added to human pancreatic carcinoma cells in culture. In Vivo: Athymic mice were inoculated (s.c.) with human pancreatic carcinoma cells. On Day 14, mice were randomized to receive daily either hGH (GH, n = 14) or saline (CTL, n = 12). On Day 29, animals received [3H]phenylalanine for tissue protein fractional synthetic rate (FSR) measurement. Tumors were excised and cell cycle kinetics analyzed. Data are expressed as mean ± SEM. Statistical analysis was performed by unpaired t test and/or ANOVA where appropriate. In Vitro: Serum from GH-treated animals had elevated IGF-1 levels (287 ± 34 ng/ml vs 157 ± 53 ng/ml, P < 0.001) and significantly stimulated cell growth (No. cells x 103/well) compared with CTL serum (925 ± 31 vs 747 ± 38, P < 0.001). In Vivo: Serum from GH-treated animals had elevated IGF-1 levels (287 ± 34 ng/ml vs 157 ± 53 ng/ml, P < 0.001) and significantly stimulated cell growth (No. cells x 103/well) compared with CTL serum (925 ± 31 vs 747 ± 38, P < 0.001). In Vivo: Growth hormone had no significant effect on tumor growth rate (mm3/day) (1.45 ± 0.47 CTL vs 1.57 ± 0.66 GH), final tumor weight (mg) (0.19 ± 0.15 CTL vs 0.17 ± 0.06 GH), DNA Index (1.5 ± 0.1 CTL vs 1.5 ± 0.1 GH), percent S phase (20.3 ± 3.3 CTL vs 22.1 ± 3.0 GH), or tumor FSR ({\%}/day) (51.1 ± 17.8 CTL vs 70.2 ± 61.1 GH). Growth hormone significantly elevated serum IGF-1 levels (ng/ml) (176 ± 48 CTL vs 222 ± 53 GH, P < 0.005) and liver FSR ({\%}/day) (62.8 ± 17.8 CTL vs 79.7 ± 12.7 GH, P < 0.005). Serum of GH-treated mice increased human pancreatic cell growth in vitro. In vivo, GH administration raised serum IGF-1 levels and increased liver protein FSR, without tumor growth, cell cycle kinetics, or protein FSR.",
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Effect of human growth hormone on human pancreatic carcinoma growth, protein, and cell cycle kinetics. / Harrison, Lawrence; Blumberg, David; Berman, Russell; Ng, Bruce; Hochwald, Steve; Brennan, Murray F.; Burt, Michael.

In: Journal of Surgical Research, Vol. 61, No. 2, 01.01.1996, p. 317-322.

Research output: Contribution to journalArticle

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