Liver resection and liver transplantation are the treatment modalities with the greatest potentia... more Liver resection and liver transplantation are the treatment modalities with the greatest potential for curing hepatocellular carcinoma (HCC). Tumor recurrence after resection for HCC is, however, a major problem, and an increased rate of recurrence after living donor transplantation versus cadaveric whole liver transplantation has been suggested. Factors involved in liver regeneration may stimulate the growth of occult tumors. The aim of this project was to test the hypothesis that a microscopic HCC tumor in the setting of partial hepatectomy would show enhanced growth and signs of increased invasiveness corresponding to the size of the liver resection. Hepatectomy was performed to various degrees in groups of Buffalo rats with the concomitant implantation of a fixed number of hepatoma cells in the remnant liver; a control group underwent only resection. After 21 days, the sizes and numbers of the tumors and the expression of alpha-fetoprotein (AFP), cyclin D1, calpain small subunit 1 (CAPNS1), CD34 (a microvessel density marker), vascular endothelial growth factor (VEGF), and vascular endothelial growth factor receptor 2 (VEGFR2) were evaluated and compared between the groups. The tumor volume and number increased significantly with the size of the partial hepatectomy (P < 0.05). The largest resections were also associated with increased hepatoma cell infiltration in the lungs and significant up-regulation of cyclin D1, AFP, CAPNS1, CD34, VEGF, and VEGFR2. The results suggest that liver regeneration after partial hepatectomy facilitates the growth and malignant transformation of microscopic HCC, and this could be significant for liver resection and partial liver transplantation strategies for HCC. Liver Transpl 17:866-874,
To investigate the impact of brain death (BD) on the morphology and function of liver. Fifteen Ba... more To investigate the impact of brain death (BD) on the morphology and function of liver. Fifteen Ba-ma minipigs were randomly divided into 3 equal groups: brain death group (Group B) made into BD models by increasing the intracranial pressure; breviscapine pretreatment group (Group P), with breviscapine 2.5 mg x kg(-1) given intravenous drip 1-2 hours after the successful establishment of BD model; and control group (Group C) undergoing operation similar to that in Group B but without increasing the intracranial pressure. 3, 6, 12, 18, and 24 hours after the initial confirmation of BD blood samples were collected from the superior vena cava to detect the serum alanine transaminase (ALT), aspartate transaminase (AST), tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta, and IL-6, and a piece of liver tissues were collected to undergo light microscopy and electron microscopy, and immunohistochemistry to examine the expression of protein kinase (PKC)-alpha by RT-PCR. The levels of serum ALT and AST of Group B began to increase since 12 h after BD, and were both significantly higher than those of Group C 18 and 24 hours after BD (both P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.05). The levels of serum ALT and AST of Group P began to increase since 12 h after BD, and were both significantly lower than those of Group B (both P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.05). The levels of serum TNF-alpha, IL-1beta, and IL-6 of Group B and Group P began to increase gradually since 3 h after BD, however, those of Group B were all significantly higher than those of group P (all P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.05). PKC-alpha was only expressed in the plasma of a few normal liver cells. The PKC-alpha mRNA and protein levels of Groups B and P began to increase since 6 h after BD, however, those of Group B were all significantly higher than those of Group P (all P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.05). Light and electron microscopy showed that only mild edema of liver cells was seen in Group P, and since 12 h after BD swelling of mitochondria, edema of liver cells, etc. were seen in Group B, and the morphologic damages were more severe in Group B. Brain death evokes hepatic functional and morphological injuries. PKC-alpha may involve in the mechanism. Breviscapine inhibits the activation of PKC-alpha, thus reducing the damage in liver.
RESULTS: The levels of AST and ALT in groups B and P began to increase 12 hours after brain-death... more RESULTS: The levels of AST and ALT in groups B and P began to increase 12 hours after brain-death, while the values in group P were lower than those in group B (P<0.05). The levels of IL-1β, IL-6, and TNF-α in groups B and P at 3, 6, 12 and 18 hours were lower than those in group B (P<0.05).
Hepatobiliary & pancreatic diseases international : HBPD INT, 2007
Brain-dead donors are the main sources for organ transplantation, but many studies show that brai... more Brain-dead donors are the main sources for organ transplantation, but many studies show that brain-death affects the organ's function after transplantation. This study was undertaken to investigate liver injury after brain-death in BA-Ma mini pigs and the protective effects of breviscapine on hepatic function and on PKC-alpha mRNA and its protein expression. Fifteen BA-Ma mini pigs were equally divided into 3 groups at random: brain-dead (group B), breviscapine pretreated (group P), and control (group C). The brain-dead model was established by increasing intracranial pressure in a modified, slow and intermittent way. At 3, 6, 12, 18 and 24 hours after the initial brain-death, the levels of serum AST, ALT, TNF-alpha, IL-1beta, and IL-6 were determined. The changes in hepatic tissues were assessed, and the expression of PKC-alpha and PKC-alpha mRNA was detected by immunohistochemistry and RT-PCR, respectively. The levels of AST and ALT in groups B and P began to increase 12 hours...
World journal of gastroenterology : WJG, Jan 21, 2014
Liver regeneration after major surgery may activate occult micrometastases and facilitate tumor g... more Liver regeneration after major surgery may activate occult micrometastases and facilitate tumor growth, leading to liver tumor recurrence. Molecular changes during liver regeneration can provide a microenvironment that stimulates intrahepatic tumor propagation through alterations in cellular signaling pathways, where activation and proliferation of mature hepatocytes, hepatic progenitor cells, non-parenchymal liver cells might favor both liver regeneration and tumor growth. This review highlights recent advances of tumor growth and development in the regenerating liver, possible mechanisms and clinical implications.
Hepatobiliary & pancreatic diseases international : HBPD INT, 2006
Brain-dead donors have been the main sources in organ transplantation. But many studies show that... more Brain-dead donors have been the main sources in organ transplantation. But many studies show that brain-death affects the organ's function after transplantation. This study was undertaken to investigate liver injury after brain-death in rats and the protective effects of N-acetyleysteine (NAC) on liver injury. A total of 30 Wistar rats were randomized into 3 groups: normal control group (C), brain-dead group (B), and NAC pretreatment group (N). At 4 hours after the establishment of a brain-dead model, serum was collected to determine the levels of ALT, AST, TNF-alpha and hyaluronic acid (HA). Hepatic tissue was obtained for electron microscopic examination. At 4 hours, the levels of ALT, AST, TNF-alpha, and HA in group N were significantly higher than those in group C, but these parameters were significantly lower than those in group B. Electron microscopy showed activated Kupffer cells, denuded sinusoidal endothelial cells (SECs), and widened fenestration in group B, but elimin...
Hepatobiliary & pancreatic diseases international : HBPD INT, 2005
Morphological and functional changes commonly occur in livers of brain-death donors. Prevention o... more Morphological and functional changes commonly occur in livers of brain-death donors. Prevention of liver injury from brain-death will benefit the results of transplantation. This study was conducted to evaluate the protection effects of glycine on the liver of brain-death donor. Fourty-two male Wistar rats were randomly divided into brain-death donor (BDD) group (B), glycine pretreatment group with BDD (G), and strychnine pretreatment group with BDD(S). For these groups, brain death model was established in donor rats and liver transplantation was performed subsequently utilizing microsurgical techniques. After the establishment of the model and during cold rinsing of liver donors or liver reperfusion of recipients, glycine was given at a dose of 0.6 mmol, 25 micromol and 25 micromol in the group G, and a same dose of glycine and strychnine (1000 :1) was prescribed for the group S, but nothing for the group B. Before cold rinsing at 2 and 6 hours after portal vein(PV) reperfusion, b...
Objective. Liver regeneration following hepatectomy can stimulate the growth of hepatocellular ca... more Objective. Liver regeneration following hepatectomy can stimulate the growth of hepatocellular carcinoma (HCC), and major hepatectomy can be associated with activation of hepatic progenitor cells (HPCs). The aim of this study was to evaluate how HPCs influence the malignant potential of tumor cells in vitro and HCC tumor growth after surgery in a rodent model. Material and methods. Hepatoma cells (JM1) were cultured with conditioned medium (CM) from syngeneic HPCs (WB-F344). Growth rate, resistance to Adriamycin, and expression patterns for invasiveness and stemness were compared with naïve JM1. Microscopic HCC tumors from naïve JM1 or JM1 cultured with CM were inoculated in Fischer 344 rats undergoing 70% hepatectomy with or without simultaneous infusion of WB-F344. Tumor growth and invasiveness-related factors were compared. Buffalo rats were induced with Morris hepatoma cells. Liver tissue from both in vivo models was examined with regard to activation of cells with progenitor-like phenotype. Results. Co-culture with CM resulted in an increased resistance to Adriamycin and enhanced expressions of a-FP, MMP9, ABCG2, CD133, and SOX2, as well as the activation of ERK, AKT, WNT, and TGF-b1 pathways. Tumor size and metastases were significantly higher in groups with co-cultured cells or HPCs infusion. After 70% hepatectomy and tumor implantation, cells positive for a-FP, CK19, and CD133 were found, thus suggesting a progenitor-like phenotype in the setting of epithelial-mesenchymal transition. Conclusion. HPCs have a marked effect on HCC cells in vitro and appear to stimulate the growth and malignant potential of experimental HCC tumors.
Background: Post-operative liver regeneration may contribute to tumor recurrence. There is a theo... more Background: Post-operative liver regeneration may contribute to tumor recurrence. There is a theoretical need for an adjuvant therapy that can suppress tumor growth without adversely affecting post-operative liver regeneration. Objective: To evaluate the effect of RAF inhibitor Sorafenib on cell viability and proliferation of hepatoma cells and hepatocytes in vitro and in an in vivo rat model. Methods: Cell viability, DNA synthesis, and RAF/MAPK kinase activity in the primary hepatocyte and hepatoma cell lines were investigated after Sorafenib exposure. Sequence analysis of the B-RAF gene in hepatic cells was determined. Tumor markers were compared within the rats after 70% hepatectomy with or without daily oral gavages of Sorafenib. Liver regeneration was assessed by liver function tests and proliferation markers. Results: Primary hepatocytes showed higher cell viability, proliferation rate, and stronger RAF/MAPK kinase activity compared with hepatoma cell lines. The in vivo tumor volumes, size, and metastases were significantly decreased (P < 0.05) whereas no significant change in liver regeneration related to Sorafenib exposure was found (P > 0.05). B-RAF V600E mutation was not detected neither in the hepatic cells nor untransformed hepatocytes. Conclusions: The RAF targeted inhibitor can reduce tumor growth without retarding liver regeneration in this experiment.
Liver resection and liver transplantation are the treatment modalities with the greatest potentia... more Liver resection and liver transplantation are the treatment modalities with the greatest potential for curing hepatocellular carcinoma (HCC). Tumor recurrence after resection for HCC is, however, a major problem, and an increased rate of recurrence after living donor transplantation versus cadaveric whole liver transplantation has been suggested. Factors involved in liver regeneration may stimulate the growth of occult tumors. The aim of this project was to test the hypothesis that a microscopic HCC tumor in the setting of partial hepatectomy would show enhanced growth and signs of increased invasiveness corresponding to the size of the liver resection. Hepatectomy was performed to various degrees in groups of Buffalo rats with the concomitant implantation of a fixed number of hepatoma cells in the remnant liver; a control group underwent only resection. After 21 days, the sizes and numbers of the tumors and the expression of alpha-fetoprotein (AFP), cyclin D1, calpain small subunit 1 (CAPNS1), CD34 (a microvessel density marker), vascular endothelial growth factor (VEGF), and vascular endothelial growth factor receptor 2 (VEGFR2) were evaluated and compared between the groups. The tumor volume and number increased significantly with the size of the partial hepatectomy (P < 0.05). The largest resections were also associated with increased hepatoma cell infiltration in the lungs and significant up-regulation of cyclin D1, AFP, CAPNS1, CD34, VEGF, and VEGFR2. The results suggest that liver regeneration after partial hepatectomy facilitates the growth and malignant transformation of microscopic HCC, and this could be significant for liver resection and partial liver transplantation strategies for HCC. Liver Transpl 17:866-874,
To investigate the impact of brain death (BD) on the morphology and function of liver. Fifteen Ba... more To investigate the impact of brain death (BD) on the morphology and function of liver. Fifteen Ba-ma minipigs were randomly divided into 3 equal groups: brain death group (Group B) made into BD models by increasing the intracranial pressure; breviscapine pretreatment group (Group P), with breviscapine 2.5 mg x kg(-1) given intravenous drip 1-2 hours after the successful establishment of BD model; and control group (Group C) undergoing operation similar to that in Group B but without increasing the intracranial pressure. 3, 6, 12, 18, and 24 hours after the initial confirmation of BD blood samples were collected from the superior vena cava to detect the serum alanine transaminase (ALT), aspartate transaminase (AST), tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta, and IL-6, and a piece of liver tissues were collected to undergo light microscopy and electron microscopy, and immunohistochemistry to examine the expression of protein kinase (PKC)-alpha by RT-PCR. The levels of serum ALT and AST of Group B began to increase since 12 h after BD, and were both significantly higher than those of Group C 18 and 24 hours after BD (both P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.05). The levels of serum ALT and AST of Group P began to increase since 12 h after BD, and were both significantly lower than those of Group B (both P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.05). The levels of serum TNF-alpha, IL-1beta, and IL-6 of Group B and Group P began to increase gradually since 3 h after BD, however, those of Group B were all significantly higher than those of group P (all P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.05). PKC-alpha was only expressed in the plasma of a few normal liver cells. The PKC-alpha mRNA and protein levels of Groups B and P began to increase since 6 h after BD, however, those of Group B were all significantly higher than those of Group P (all P &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.05). Light and electron microscopy showed that only mild edema of liver cells was seen in Group P, and since 12 h after BD swelling of mitochondria, edema of liver cells, etc. were seen in Group B, and the morphologic damages were more severe in Group B. Brain death evokes hepatic functional and morphological injuries. PKC-alpha may involve in the mechanism. Breviscapine inhibits the activation of PKC-alpha, thus reducing the damage in liver.
RESULTS: The levels of AST and ALT in groups B and P began to increase 12 hours after brain-death... more RESULTS: The levels of AST and ALT in groups B and P began to increase 12 hours after brain-death, while the values in group P were lower than those in group B (P<0.05). The levels of IL-1β, IL-6, and TNF-α in groups B and P at 3, 6, 12 and 18 hours were lower than those in group B (P<0.05).
Hepatobiliary & pancreatic diseases international : HBPD INT, 2007
Brain-dead donors are the main sources for organ transplantation, but many studies show that brai... more Brain-dead donors are the main sources for organ transplantation, but many studies show that brain-death affects the organ's function after transplantation. This study was undertaken to investigate liver injury after brain-death in BA-Ma mini pigs and the protective effects of breviscapine on hepatic function and on PKC-alpha mRNA and its protein expression. Fifteen BA-Ma mini pigs were equally divided into 3 groups at random: brain-dead (group B), breviscapine pretreated (group P), and control (group C). The brain-dead model was established by increasing intracranial pressure in a modified, slow and intermittent way. At 3, 6, 12, 18 and 24 hours after the initial brain-death, the levels of serum AST, ALT, TNF-alpha, IL-1beta, and IL-6 were determined. The changes in hepatic tissues were assessed, and the expression of PKC-alpha and PKC-alpha mRNA was detected by immunohistochemistry and RT-PCR, respectively. The levels of AST and ALT in groups B and P began to increase 12 hours...
World journal of gastroenterology : WJG, Jan 21, 2014
Liver regeneration after major surgery may activate occult micrometastases and facilitate tumor g... more Liver regeneration after major surgery may activate occult micrometastases and facilitate tumor growth, leading to liver tumor recurrence. Molecular changes during liver regeneration can provide a microenvironment that stimulates intrahepatic tumor propagation through alterations in cellular signaling pathways, where activation and proliferation of mature hepatocytes, hepatic progenitor cells, non-parenchymal liver cells might favor both liver regeneration and tumor growth. This review highlights recent advances of tumor growth and development in the regenerating liver, possible mechanisms and clinical implications.
Hepatobiliary & pancreatic diseases international : HBPD INT, 2006
Brain-dead donors have been the main sources in organ transplantation. But many studies show that... more Brain-dead donors have been the main sources in organ transplantation. But many studies show that brain-death affects the organ's function after transplantation. This study was undertaken to investigate liver injury after brain-death in rats and the protective effects of N-acetyleysteine (NAC) on liver injury. A total of 30 Wistar rats were randomized into 3 groups: normal control group (C), brain-dead group (B), and NAC pretreatment group (N). At 4 hours after the establishment of a brain-dead model, serum was collected to determine the levels of ALT, AST, TNF-alpha and hyaluronic acid (HA). Hepatic tissue was obtained for electron microscopic examination. At 4 hours, the levels of ALT, AST, TNF-alpha, and HA in group N were significantly higher than those in group C, but these parameters were significantly lower than those in group B. Electron microscopy showed activated Kupffer cells, denuded sinusoidal endothelial cells (SECs), and widened fenestration in group B, but elimin...
Hepatobiliary & pancreatic diseases international : HBPD INT, 2005
Morphological and functional changes commonly occur in livers of brain-death donors. Prevention o... more Morphological and functional changes commonly occur in livers of brain-death donors. Prevention of liver injury from brain-death will benefit the results of transplantation. This study was conducted to evaluate the protection effects of glycine on the liver of brain-death donor. Fourty-two male Wistar rats were randomly divided into brain-death donor (BDD) group (B), glycine pretreatment group with BDD (G), and strychnine pretreatment group with BDD(S). For these groups, brain death model was established in donor rats and liver transplantation was performed subsequently utilizing microsurgical techniques. After the establishment of the model and during cold rinsing of liver donors or liver reperfusion of recipients, glycine was given at a dose of 0.6 mmol, 25 micromol and 25 micromol in the group G, and a same dose of glycine and strychnine (1000 :1) was prescribed for the group S, but nothing for the group B. Before cold rinsing at 2 and 6 hours after portal vein(PV) reperfusion, b...
Objective. Liver regeneration following hepatectomy can stimulate the growth of hepatocellular ca... more Objective. Liver regeneration following hepatectomy can stimulate the growth of hepatocellular carcinoma (HCC), and major hepatectomy can be associated with activation of hepatic progenitor cells (HPCs). The aim of this study was to evaluate how HPCs influence the malignant potential of tumor cells in vitro and HCC tumor growth after surgery in a rodent model. Material and methods. Hepatoma cells (JM1) were cultured with conditioned medium (CM) from syngeneic HPCs (WB-F344). Growth rate, resistance to Adriamycin, and expression patterns for invasiveness and stemness were compared with naïve JM1. Microscopic HCC tumors from naïve JM1 or JM1 cultured with CM were inoculated in Fischer 344 rats undergoing 70% hepatectomy with or without simultaneous infusion of WB-F344. Tumor growth and invasiveness-related factors were compared. Buffalo rats were induced with Morris hepatoma cells. Liver tissue from both in vivo models was examined with regard to activation of cells with progenitor-like phenotype. Results. Co-culture with CM resulted in an increased resistance to Adriamycin and enhanced expressions of a-FP, MMP9, ABCG2, CD133, and SOX2, as well as the activation of ERK, AKT, WNT, and TGF-b1 pathways. Tumor size and metastases were significantly higher in groups with co-cultured cells or HPCs infusion. After 70% hepatectomy and tumor implantation, cells positive for a-FP, CK19, and CD133 were found, thus suggesting a progenitor-like phenotype in the setting of epithelial-mesenchymal transition. Conclusion. HPCs have a marked effect on HCC cells in vitro and appear to stimulate the growth and malignant potential of experimental HCC tumors.
Background: Post-operative liver regeneration may contribute to tumor recurrence. There is a theo... more Background: Post-operative liver regeneration may contribute to tumor recurrence. There is a theoretical need for an adjuvant therapy that can suppress tumor growth without adversely affecting post-operative liver regeneration. Objective: To evaluate the effect of RAF inhibitor Sorafenib on cell viability and proliferation of hepatoma cells and hepatocytes in vitro and in an in vivo rat model. Methods: Cell viability, DNA synthesis, and RAF/MAPK kinase activity in the primary hepatocyte and hepatoma cell lines were investigated after Sorafenib exposure. Sequence analysis of the B-RAF gene in hepatic cells was determined. Tumor markers were compared within the rats after 70% hepatectomy with or without daily oral gavages of Sorafenib. Liver regeneration was assessed by liver function tests and proliferation markers. Results: Primary hepatocytes showed higher cell viability, proliferation rate, and stronger RAF/MAPK kinase activity compared with hepatoma cell lines. The in vivo tumor volumes, size, and metastases were significantly decreased (P < 0.05) whereas no significant change in liver regeneration related to Sorafenib exposure was found (P > 0.05). B-RAF V600E mutation was not detected neither in the hepatic cells nor untransformed hepatocytes. Conclusions: The RAF targeted inhibitor can reduce tumor growth without retarding liver regeneration in this experiment.
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