| Material . | Method . | Study summary . | Reference . |
|---|---|---|---|
| normal liver tissue | RNA and protein | High GHR expression, very low GH expression | (210) |
| patient samples | RNA and protein | GH overexpression in ∼50% samples, | (228) |
| HCC cell lines, patient samples | RNA and protein, clinical correlations | GH expression increased compared to normal liver, higher GH correlates with poorer survival | (222) |
| HCC cell lines, patient samples | RNA and protein, clinical correlations | GHR expression is decreased compared to normal liver, lower GHR correlates with poorer survival | (212-218, 220) |
| human cell lines | autocrine GH | increased proliferation | (95, 237) |
| cell line with autocrine GH | nude mice xenograft | increased tumor growth in vivo | (222) |
| human cell lines | autocrine GH | induces EMT, promotes migration-invasion, metastasis | (237) |
| human and mouse cell lines | exogenous GH +/− GHR knockdown | increased ABC transporters and drug efflux, resistance to doxorubicin and sorafenib | (211) |
| AxC rats + hepatocarcinogen | GH administration | increase in liver tumorigenesis | (223) |
| Wistar rats + hepatocarcinogen | GH infusion | increase in liver tumorigenesis | (224) |
| GH transgenic animals | liver pathology | hyperplasia, hypertrophy, age-associated hepatocarcinogenesis | (95, 229-236) |
| ovine GH transgenic vs control mice | + hepatocarcinogen | increase in liver tumorigenesis | (225) |
| lit/lit vs control mice | + hepatocarcinogen | decrease in liver tumorigenesis and growth | (226) |
| GHRKO vs control mice | + hepatocarcinogen | decrease in liver tumorigenesis and growth | (227) |
| liver-GHRKO vs control mice | + hepatocarcinogen | decrease in liver tumorigenesis and growth | (227) |
| GHA mice | syngeneic allograft | increased ABC transporters, resistance to targeted therapy (sorafenib) | (211) |
| cell line with autocrine GH in nude mice | GHRA (hGH-G120R) treatment | suppressed tumor growth in vivo | (222) |
| human xenograft in nude mice + sorafenib | + pegvisomant | pegvisomant improves sorafenib efficacy | (228) |
| mouse allograft in GHA vs control mice | + sorafenib | transgenic GHR antagonist improves sorafenib efficacy | (211) |
| human HCC patients + sorafenib | + pegvisomant | disease stabilization | (228) |
| human HCC patients + immunotherapy | correlation of serum GH—treatment response | high serum GH correlates with poorer immunotherapy response and survival | (238) |
| Material . | Method . | Study summary . | Reference . |
|---|---|---|---|
| normal liver tissue | RNA and protein | High GHR expression, very low GH expression | (210) |
| patient samples | RNA and protein | GH overexpression in ∼50% samples, | (228) |
| HCC cell lines, patient samples | RNA and protein, clinical correlations | GH expression increased compared to normal liver, higher GH correlates with poorer survival | (222) |
| HCC cell lines, patient samples | RNA and protein, clinical correlations | GHR expression is decreased compared to normal liver, lower GHR correlates with poorer survival | (212-218, 220) |
| human cell lines | autocrine GH | increased proliferation | (95, 237) |
| cell line with autocrine GH | nude mice xenograft | increased tumor growth in vivo | (222) |
| human cell lines | autocrine GH | induces EMT, promotes migration-invasion, metastasis | (237) |
| human and mouse cell lines | exogenous GH +/− GHR knockdown | increased ABC transporters and drug efflux, resistance to doxorubicin and sorafenib | (211) |
| AxC rats + hepatocarcinogen | GH administration | increase in liver tumorigenesis | (223) |
| Wistar rats + hepatocarcinogen | GH infusion | increase in liver tumorigenesis | (224) |
| GH transgenic animals | liver pathology | hyperplasia, hypertrophy, age-associated hepatocarcinogenesis | (95, 229-236) |
| ovine GH transgenic vs control mice | + hepatocarcinogen | increase in liver tumorigenesis | (225) |
| lit/lit vs control mice | + hepatocarcinogen | decrease in liver tumorigenesis and growth | (226) |
| GHRKO vs control mice | + hepatocarcinogen | decrease in liver tumorigenesis and growth | (227) |
| liver-GHRKO vs control mice | + hepatocarcinogen | decrease in liver tumorigenesis and growth | (227) |
| GHA mice | syngeneic allograft | increased ABC transporters, resistance to targeted therapy (sorafenib) | (211) |
| cell line with autocrine GH in nude mice | GHRA (hGH-G120R) treatment | suppressed tumor growth in vivo | (222) |
| human xenograft in nude mice + sorafenib | + pegvisomant | pegvisomant improves sorafenib efficacy | (228) |
| mouse allograft in GHA vs control mice | + sorafenib | transgenic GHR antagonist improves sorafenib efficacy | (211) |
| human HCC patients + sorafenib | + pegvisomant | disease stabilization | (228) |
| human HCC patients + immunotherapy | correlation of serum GH—treatment response | high serum GH correlates with poorer immunotherapy response and survival | (238) |
Abbreviations: GH, growth hormone; GHA mice, mice transgenic for growth hormone receptor antagonist; GHR, growth hormone receptor; GHRA, growth hormone receptor antagonist; HCC, hepatocellular carcinoma.
| Material . | Method . | Study summary . | Reference . |
|---|---|---|---|
| normal liver tissue | RNA and protein | High GHR expression, very low GH expression | (210) |
| patient samples | RNA and protein | GH overexpression in ∼50% samples, | (228) |
| HCC cell lines, patient samples | RNA and protein, clinical correlations | GH expression increased compared to normal liver, higher GH correlates with poorer survival | (222) |
| HCC cell lines, patient samples | RNA and protein, clinical correlations | GHR expression is decreased compared to normal liver, lower GHR correlates with poorer survival | (212-218, 220) |
| human cell lines | autocrine GH | increased proliferation | (95, 237) |
| cell line with autocrine GH | nude mice xenograft | increased tumor growth in vivo | (222) |
| human cell lines | autocrine GH | induces EMT, promotes migration-invasion, metastasis | (237) |
| human and mouse cell lines | exogenous GH +/− GHR knockdown | increased ABC transporters and drug efflux, resistance to doxorubicin and sorafenib | (211) |
| AxC rats + hepatocarcinogen | GH administration | increase in liver tumorigenesis | (223) |
| Wistar rats + hepatocarcinogen | GH infusion | increase in liver tumorigenesis | (224) |
| GH transgenic animals | liver pathology | hyperplasia, hypertrophy, age-associated hepatocarcinogenesis | (95, 229-236) |
| ovine GH transgenic vs control mice | + hepatocarcinogen | increase in liver tumorigenesis | (225) |
| lit/lit vs control mice | + hepatocarcinogen | decrease in liver tumorigenesis and growth | (226) |
| GHRKO vs control mice | + hepatocarcinogen | decrease in liver tumorigenesis and growth | (227) |
| liver-GHRKO vs control mice | + hepatocarcinogen | decrease in liver tumorigenesis and growth | (227) |
| GHA mice | syngeneic allograft | increased ABC transporters, resistance to targeted therapy (sorafenib) | (211) |
| cell line with autocrine GH in nude mice | GHRA (hGH-G120R) treatment | suppressed tumor growth in vivo | (222) |
| human xenograft in nude mice + sorafenib | + pegvisomant | pegvisomant improves sorafenib efficacy | (228) |
| mouse allograft in GHA vs control mice | + sorafenib | transgenic GHR antagonist improves sorafenib efficacy | (211) |
| human HCC patients + sorafenib | + pegvisomant | disease stabilization | (228) |
| human HCC patients + immunotherapy | correlation of serum GH—treatment response | high serum GH correlates with poorer immunotherapy response and survival | (238) |
| Material . | Method . | Study summary . | Reference . |
|---|---|---|---|
| normal liver tissue | RNA and protein | High GHR expression, very low GH expression | (210) |
| patient samples | RNA and protein | GH overexpression in ∼50% samples, | (228) |
| HCC cell lines, patient samples | RNA and protein, clinical correlations | GH expression increased compared to normal liver, higher GH correlates with poorer survival | (222) |
| HCC cell lines, patient samples | RNA and protein, clinical correlations | GHR expression is decreased compared to normal liver, lower GHR correlates with poorer survival | (212-218, 220) |
| human cell lines | autocrine GH | increased proliferation | (95, 237) |
| cell line with autocrine GH | nude mice xenograft | increased tumor growth in vivo | (222) |
| human cell lines | autocrine GH | induces EMT, promotes migration-invasion, metastasis | (237) |
| human and mouse cell lines | exogenous GH +/− GHR knockdown | increased ABC transporters and drug efflux, resistance to doxorubicin and sorafenib | (211) |
| AxC rats + hepatocarcinogen | GH administration | increase in liver tumorigenesis | (223) |
| Wistar rats + hepatocarcinogen | GH infusion | increase in liver tumorigenesis | (224) |
| GH transgenic animals | liver pathology | hyperplasia, hypertrophy, age-associated hepatocarcinogenesis | (95, 229-236) |
| ovine GH transgenic vs control mice | + hepatocarcinogen | increase in liver tumorigenesis | (225) |
| lit/lit vs control mice | + hepatocarcinogen | decrease in liver tumorigenesis and growth | (226) |
| GHRKO vs control mice | + hepatocarcinogen | decrease in liver tumorigenesis and growth | (227) |
| liver-GHRKO vs control mice | + hepatocarcinogen | decrease in liver tumorigenesis and growth | (227) |
| GHA mice | syngeneic allograft | increased ABC transporters, resistance to targeted therapy (sorafenib) | (211) |
| cell line with autocrine GH in nude mice | GHRA (hGH-G120R) treatment | suppressed tumor growth in vivo | (222) |
| human xenograft in nude mice + sorafenib | + pegvisomant | pegvisomant improves sorafenib efficacy | (228) |
| mouse allograft in GHA vs control mice | + sorafenib | transgenic GHR antagonist improves sorafenib efficacy | (211) |
| human HCC patients + sorafenib | + pegvisomant | disease stabilization | (228) |
| human HCC patients + immunotherapy | correlation of serum GH—treatment response | high serum GH correlates with poorer immunotherapy response and survival | (238) |
Abbreviations: GH, growth hormone; GHA mice, mice transgenic for growth hormone receptor antagonist; GHR, growth hormone receptor; GHRA, growth hormone receptor antagonist; HCC, hepatocellular carcinoma.
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