Acceleration of primary liver tumor growth rate in embolized hepatic lobe after portal vein embolization

2007 ◽  
Vol 48 (7) ◽  
pp. 721-727 ◽  
Author(s):  
S. Hayashi ◽  
Y. Baba ◽  
K. Ueno ◽  
M. Nakajo ◽  
F. Kubo ◽  
...  

Background: Portal vein embolization (PVE) is now widely accepted as a useful preoperative procedure in selected patients undergoing extended hepatectomy. However, the effect of PVE on the growth of liver tumors has not been fully elucidated. Purpose: To retrospectively evaluate the effects of PVE on the growth of liver tumors in the embolized lobes. Material and Methods: Eight patients with a primary liver tumor, six hepatocellular carcinomas (HCC) and two cholangiocellular carcinomas (CCC), were studied. The growth rates of the tumors in the embolized lobes and non-embolized liver parenchyma were calculated using the computed tomography (CT) volume values at the time of tumor identification, and before and after PVE. Result: The median tumor growth rate was 0.59 cm3/day (range 0.22–6.01 cm3/day) before PVE and 2.37 cm3/day (range 0.29–13.97 cm3/day) after PVE ( P = 0.018). The tumor growth acceleration ratios ranged from 1.50 to 7.46 (median 2.65) in the six HCCs, and were 1.00 and 1.32 in the two CCCs. There was no apparent correlation between the tumor growth rate after PVE and the growth rate of non-embolized liver parenchyma (median 6.00 cm3/day, range 1.24–11.0 cm3/day). Conclusion: Liver tumor growth in an embolized lobe accelerates after PVE, in patients with HCC.

2016 ◽  
Vol 101 (7-8) ◽  
pp. 338-346 ◽  
Author(s):  
Takaaki Osawa ◽  
Tsuyoshi Sano ◽  
Yoshiki Senda ◽  
Seiji Natsume ◽  
Yasuhiro Shimizu

This study aimed to clarify the predictive factors for bile leakage after hepatectomy for liver tumor in terms of the International Study Group of Liver Surgery (ISGLS) definition. Between August 2006 and July 2012, 242 patients with a diagnosis of liver tumor underwent hepatectomy in our department, and the total bilirubin level of peritoneal drainage fluid prior to removal of the abdominal drains was examined. The data on all of the patients were analyzed retrospectively to identify the factors that might significantly affect the postoperative bile leakage. There was no grade C bile leakage, and grade A was documented in 65 patients (26.9%) and grade B in 7 patients (2.9%) in terms of the ISGLS definition. Although there was no significant difference in postoperative hospital stay between grade A bile leakage only and those without bile leakage (P = 0.933), a significant difference was noted between grades A and B (median, 11.0 versus 21.0 days; P < 0.001). Multivariate analysis revealed 4 independent significant predictive factors: prolonged operation time (P = 0.040), cholecystectomy (P = 0.048), non–portal vein embolization (P = 0.010), and preoperative chemotherapy (P = 0.021). The ISGLS definition of bile leakage is clinically useful. Prolonged operation time, cholecystectomy, non–portal vein embolization, and preoperative chemotherapy were significant independent risk factors of bile leakage in this study.


2010 ◽  
Vol 53 (5) ◽  
pp. 1101-1108 ◽  
Author(s):  
Fernando Guimarães ◽  
Alessandra Soares Schanoski ◽  
Tereza Cristina Samico Cavalcanti ◽  
Priscila Bianchi Juliano ◽  
Ana Neuza Viera-Matos ◽  
...  

The present study aimed at characterizing the subcutaneous development of the Walker 256 (W256) AR tumor, a regressive variant of the rat W256 A tumor. Wistar rats were injected subcutaneously with 4x10(6) W256 A or W256 AR tumor cells. The development of tumors was evaluated daily by percutaneous measurements. None of the W256 A tumors (n=20) regressed, but 62% of the W256 AR tumor-bearing rats (n=21) underwent complete tumor regression within 35 days. Continuous growth of AR tumors was characterized by an increase of the tumor growth rate from day 12, which reached values above 1.0 g/day, and were significantly higher (p<0.05) than those of the regressive AR tumors. Immunosuppression by irradiation before subcutaneous injection of AR cells completely abrogated tumor regression and was associated with severe metastatic dissemination. Daily evaluation of the tumor growth rate enabled the discrimination, in advance, between continuously growing tumors and those that regressed later on.


Neurosurgery ◽  
2015 ◽  
Vol 79 (3) ◽  
pp. 481-491 ◽  
Author(s):  
Alexander E. Ropper ◽  
Xiang Zeng ◽  
Hariprakash Haragopal ◽  
Jamie E. Anderson ◽  
Zaid Aljuboori ◽  
...  

Abstract BACKGROUND There are currently no satisfactory treatments or experimental models showing autonomic dysfunction for intramedullary spinal cord gliomas (ISCG). OBJECTIVE To develop a rat model of ISCG and investigate whether genetically engineered human neural stem cells (F3.hNSCs) could be developed into effective therapies for ISCG. METHODS Immunodeficient/Rowett Nude rats received C6 implantation of G55 human glioblastoma cells (10K/each). F3.hNSCs engineered to express either cytosine deaminase gene only (i.e., F3.CD) or dual genes of CD and thymidine kinase (i.e., F3.CD-TK) converted benign 5-fluorocytosine and ganciclovir into oncolytic 5-fluorouracil and ganciclovir-triphosphate, respectively. ISCG rats received injection of F3.CD-TK, F3.CD, or F3.CD-TK debris near the tumor epicenter 7 days after G55 seeding, followed with 5-FC (500 mg/kg/5 mL) and ganciclovir administrations (25 mg/kg/1 mL/day × 5/each repeat, intraperitoneal injection). Per humane standards for animals, loss of weight-bearing stepping in the hindlimb was used to determine post-tumor survival. Also evaluated were autonomic functions and tumor growth rate in vivo. RESULTS ISCG rats with F3.CD-TK treatment survived significantly longer (37.5 ± 4.78 days) than those receiving F3.CD (21.5 ± 1.75 days) or F3.CD-TK debris (19.3 ± 0.85 days; n = 4/group; P &lt;.05, median rank test), with significantly improved autonomic function and reduced tumor growth rate. F3.DC-TK cells migrated diffusively into ISCG clusters to mediate oncolytic effect. CONCLUSION Dual gene-engineered human neural stem cell regimen markedly prolonged survival in a rat model that emulates somatomotor and autonomic dysfunctions of human cervical ISCG. F3.CD-TK may provide a novel approach to treating clinical ISCG.


2010 ◽  
Vol 6 (3) ◽  
pp. e1000712 ◽  
Author(s):  
Samuel Bernard ◽  
Branka Čajavec Bernard ◽  
Francis Lévi ◽  
Hanspeter Herzel

Author(s):  
Fonghsu Kuo ◽  
Timothy Kotyla ◽  
Thomas Wilson ◽  
Lydia Kifle ◽  
Thomai Panagiotou ◽  
...  

Haigan ◽  
2014 ◽  
Vol 54 (7) ◽  
pp. 937-946
Author(s):  
Shusuke Sone ◽  
Ryoichi Kondo ◽  
Keiko Ishii ◽  
Takayuki Honda ◽  
Kazuo Yoshida ◽  
...  

2016 ◽  
Vol 18 (7) ◽  
pp. 1021-1027 ◽  
Author(s):  
Michael Sommerauer ◽  
Jan-Karl Burkhardt ◽  
Karl Frontzek ◽  
Elisabeth Rushing ◽  
Alfred Buck ◽  
...  

Endocrinology ◽  
2016 ◽  
Vol 157 (9) ◽  
pp. 3577-3587 ◽  
Author(s):  
Shahrzad Jalali ◽  
Eric Monsalves ◽  
Toru Tateno ◽  
Gelareh Zadeh

Pituitary adenomas (PAs) are common intracranial lesions. Available medical therapies are limited in PAs, and therefore, it is essential to identify treatments that control PA growth when surgery is not an option. Fibroblast growth factor 4 is implicated in PA pathogenesis; therefore, in this study, we used an isogenic mammosomatotroph cell line (GH4C1) harboring different fibroblast growth factor receptor (FGFR)-4 genotypes to establish and characterize intracranial xenograft mouse models that can be used for preclinical drug testing. We show that proliferating GH4C1 tumors have an average latency of 3 weeks to form. Histological analysis revealed that prototypic FGFR4 (G388) tumors express increased prolactin and less GH, whereas tumors possessing the polymorphic variant of FGFR4 (R388) express increased GH relative to prolactin. All tumors show abundant mammalian target of rapamycin (mTOR) signaling as confirmed using phosphorylated (p)-S6 and p-4E-binding protein 1 as downstream regulators of this pathway. We subsequently demonstrate that the mTOR inhibitor RAD001 decreases tumor growth rate and reduces p-S6 but not p-4E-binding protein 1 activation, regardless of FGFR4 status. More importantly, GH activity was significantly reduced after mTOR inhibition in the R388 polymorphic variant tumors. This reduction was also associated with a concomitant reduction in serum IGF-1 levels in the R388 group. In summary, we demonstrate that the GH4C1 FGFR polymorphic xenograft is a useful model for examining PAs. Furthermore, we show that RAD001 can efficiently reduce tumor growth rate by a reduction in mTOR signaling and more importantly results in control of GH expression and IGF-1 secretion, providing further support for using mTOR inhibitors in PA patients, in particular GH-producing adenomas.


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