Liver Neoplasms
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Publication
Journal: Nihon Naika Gakkai zasshi. The Journal of the Japanese Society of Internal Medicine
October/25/2004
Publication
Journal: Free radical research
October/20/2004
Abstract
Although capsaicin (8-methyl-N-vanillyl-6-nonenamide), a pungent ingredient in a variety of red peppers of the genus Capsicum, has been shown to induce apoptotic cell death in many cancer cells, the exact mechanism of this action of capsaicin is not completely understood. In this study, we investigated the possible mediation of the NADPH oxidase-modulated production of reactive oxygen species (ROS) in the apoptotic mechanism of capsaicin in HepG2 human hepatoblastoma cells. Capsaicin induced apoptotic cell death in a time- and dose-dependent manner. Capsaicin at the concentration of inducing apoptosis also markedly increased the level of ROS. The capsaicin-induced generation of ROS and apoptosis was significantly suppressed by treatment with antioxidants, DPPD and tocopherol. In addition, inhibitors of NADPH oxidase, diphenylene iodonium, apocynin and neopterine, profoundly blocked the capsaicin-induced ROS generation and apoptosis. The expression of Rac1N17, a dominant negative mutant of Rac1, also significantly inhibited the capsaicin-induced apoptosis. Activation of nuclear factor-kappaB, a transcription factor essentially involved in ROS-induced apoptosis, was also observed by treatment with capsaicin. Collectively, these results suggest that the NADPH oxidase-mediated generation of ROS may be essentially involved in the mechanism of capsaicin-induced apoptosis in HepG2 cells. These results further suggest that capsaicin may be a valuable agent for the therapeutic intervention of human hepatomas.
Publication
Journal: Journal of immunology (Baltimore, Md. : 1950)
November/1/2004
Abstract
alpha-Fetoprotein (AFP) is a tumor-associated Ag, and its serum level is elevated in patients with hepatocellular carcinoma (HCC). In vitro, AFP induces functional impairment of dendritic cells (DCs). This was demonstrated by the down-regulation of CD40 and CD86 molecules and the impairment of allostimulatory function. Also, AFP was found to induce significant apoptosis of DCs, and AFP-treated DCs produced low levels of IL-12 and TNF-alpha, a cytokine pattern that could hamper an efficient antitumor immune response. Ex vivo, APCs of patients with HCC and high levels of AFP produced lower levels of TNF-alpha than that of healthy individuals. In conclusion, these results illustrate that AFP induces dysfunction and apoptosis of APCs, thereby offering a mechanism by which HCC escapes immunological control.
Publication
Journal: Journal of registry management
April/21/2014
Abstract
Inaccuracies in primary liver cancer (ie, excluding intrahepatic bile duct [IHBD]) or IHBD cancer as the underlying cause of death on the death certificate vs the cancer site in a cancer registry should be considered in surveillance of mortality rates in the population. Concordance between cancer site on the death record (1999-2010) and diagnosis (1973-2010) in the database for 9 cancer registries of the Surveillance, Epidemiology, and End Results (SEER) Program was examined for decedents with only 1 cancer recorded. Overreporting of deaths coded to liver cancer (ie, lack of confirmation in SEER) was largely balanced by underreporting (ie, a cancer site other than liver cancer in SEER). For IHBD cancer, overreporting was much more frequent than underreporting. Using modified rates, based on the most accurate numerators available, had little impact on trends for liver cancer in the SEER population, which were similar to trends for the entire US population based on routine statistics. An increase in the death rate for IHBD cancer, however, was no longer evident after modification. The findings support the use of routine data on underlying cause of death for surveillance of trends in death rates for liver cancer but not for IHBD cancer. Additional population-based cancer registries could potentially be used for surveillance of recent and future trends in mortality rates from these cancers.
Publication
Journal: Turkish journal of medical sciences
January/21/2015
Abstract
OBJECTIVE
To evaluate the role of computed tomography (CT) perfusion imaging in patients with hepatocellular carcinoma (HCC).
METHODS
Seventeen patients (9 men, 8 women) with newly diagnosed HCC, proven by biopsy, were evaluated with 256-slice helical CT. Perfusion parameters of blood flow (BF), blood volume (BV), arterial perfusion (AP), portal perfusion (PP), and hepatic perfusion index (HPI) were calculated in the normal liver parenchyma and HCC samples.
RESULTS
A total of 21 histologically proven HCC lesions were evaluated from CT perfusion images. BF, BV, AP, and HPI values were shown to be significantly higher (P < 0.05) in the HCC lesions than in the normal liver parenchyma. Conversely, PP values were found to be significantly lower (P < 0.05) in HCC relative to liver parenchyma.
CONCLUSIONS
CT perfusion imaging has the ability to evaluate tumor assessment, characterization, and neoangiogenesis in HCC.
Publication
Journal: International journal of cancer
June/1/2015
Abstract
This study examined whether glycated hemoglobin A1C (HbA1C) and chronic liver diseases are associated with hepatocellular carcinoma (HCC) risk in Type 2 diabetic patients. A retrospective cohort study consisting of 51,705 patients with Type 2 diabetes aged 30 and over enrolled in the National Diabetes Care Management Program before 2004 was used in Cox proportional hazards models. HbA1C was independently associated with HCC incidence, and multivariate-adjusted hazard ratio (HR) of HCC was 1.20 (95% confidence interval, CI: 1.02-1.41) for patients with a level of HbA1c ≥ 9% compared with patients with a level of HbA1c <7% after multivariate adjustment. We observed a significant linear trend in HCC incidence with increasing HbA1c (p for trend = 0.02, HR = 1.07, 95% CI = 1.01-1.12 for every 1% increment in HbA1c). We observed significant HRs of HCC for patients with a level of HbA1c ≥ 9% with alcoholic liver damage, liver cirrhosis, HBV, HCV and any one of chronic liver diseases compared with patients with a level of HbA1c <9% and no counterpart comorbidity in the entire sample (HR = 8.63, 95% CI = 1.41-52.68; HR = 5.02, 95% CI = 3.10-8.12; HR = 2.53, 95% CI = 1.10-5.85; HR = 1.79, 95% CI = 1.01-3.17; and HR = 3.59, 95% CI = 2.56-5.02, respectively). Our results suggest significant joint associations of HbA1c ≥ 9% and chronic liver diseases. Lifestyle or treatment interventions such as maintaining a satisfactory glycemic control and chronic liver diseases may reduce the burden of HCC.
Publication
Journal: Current gastroenterology reports
April/20/2011
Abstract
Hepatocellular carcinoma (HCC) used to be considered a universally fatal disease. Today, however, we have tools to identify patients at risk for HCC with more accuracy. We are able to provide surveillance using ultrasonography that is sufficiently sensitive to detect small HCC lesions. Treatment of these lesions, whether by resection or by radiofrequency ablation, is highly effective. These advances mean that HCC is theoretically curable in the majority of patients, provided these tools are used. Microarray technology has been applied to the study of the genetic changes in HCC, and has defined several distinct genetic variants of this disease, as well as identifying gene signatures that predict poor outcome, and predict metastases. These techniques are now being used to identify new potential targets for therapy, and hold great promise for the future.
Publication
Journal: Journal of hepatology
April/24/2011
Abstract
OBJECTIVE
Human carbonyl reductase1 (CBR1) has been reported to protect cells against lipid peroxidation. Since human hepatocellular carcinoma (HCC) cells are under oxidative stress in hypoxic conditions, we tested if CBR1 is upregulated by hypoxia inducible factor (HIF)-1α, helps tumor growth under hypoxia, and renders chemoresistance to cisplatin and doxorubicin in HCC.
METHODS
Luciferase, EMSA, and chromatin immunoprecipitation (ChIP) assays were performed to analyze whether HIF-1α transactivates CBR1 promoter. CBR1 overexpression, siRNA, and inhibitors were used to study the role of CBR1 in tumor survival under hypoxia and chemoresistance to cisplatin and doxorubicin in HCC. FACS and Western blot analysis for oxidative stress markers were performed to measure ROS. Immunohistochemistry (IHC) was performed to analyze CBR1 expression in 78 cases of HCC and 123 cases of colon cancer tissues.
RESULTS
The CBR1 promoter was activated by HIF-1α. CBR1 overexpression enhanced cell survival by decreasing oxidative stress under hypoxia, cisplatin, and doxorubicin treatment. CBR1-siRNA increased apoptosis via increasing oxidative stress. Combinational therapy of CBR1 inhibitors with cisplatin or doxorubicin enhanced cell death in HCC cells. IHC showed CBR1 overexpression in 56 (72%) out of 78 HCC and 88 (72%) out of 123 colon cancer cases.
CONCLUSIONS
Overexpressed CBR1 by HIF-1α plays important roles in tumor growth under hypoxia and chemoresistance to anticancer drugs. The inhibition of CBR1 by specific inhibitors enhances anticancer drug efficacy in HCC. Therefore, we concluded that CBR1 is a good molecular target for the development of anticancer drugs for HCC patients.
Publication
Journal: Acta biochimica et biophysica Sinica
April/22/2010
Abstract
Hepatoma-derived growth factor (HDGF), a nuclear protein with both mitogenic and angiogenic activity, has been reported to be mainly involved in tumorigenesis and the progression of non-small cell lung cancer. In this study, the HDGF expression was knocked down by specific-shRNA with lentivirus expression vector targeting HDGF in lung squamous cell carcinoma 520 cells. HDGF knocked down by shRNA suppressed the cell proliferation significantly both in vitro and in vivo as indicated by MTT, plate clone and transplanted tumor model assays. In addition, the knocked-down expression of HDGF also inhibited cell migration and invasion as shown in transwell and Boyden experiments. We concluded that HDGF acts as an oncogene participating in the pathogenesis of squamous cell lung cancer, and HDGF may be a key therapeutic target for non-small cell lung cancer.
Publication
Journal: International journal of cancer
April/17/2006
Abstract
We previously observed that a chemokine, macrophage inflammatory protein-1 alpha/CCL3, and its receptor, CCR1, were aberrantly expressed in human hepatocellular carcinoma (HCC) tissues. Here, we show that CCL3 and CCR1 are also expressed in 2 different models of this cancer; N-nitrosodiethylamine (DEN)-induced HCC and HCC induced by hepatitis B virus surface (HBs) antigen-primed splenocyte transfer to myelo-ablated syngeneic HBs antigen transgenic mice. At 10 months after DEN treatment, foci number and sizes were remarkably reduced in CCR1- and CCL3-deficient mice, compared with those of wild-type (WT) mice, although tumor incidence were marginally, but significantly, higher in CCR1- and CCL3-deficient mice than in WT mice. Of note is that tumor angiogenesis was also markedly diminished in CCL3- and CCR1-deficient mice, with a concomitant reduction in the number of intratumoral Kupffer cells, a rich source of growth factors and matrix metalloproteinases (MMPs). Among growth factors and MMPs that we examined, only MMP9 and MMP13 gene expression was augmented progressively in liver of WT mice after DEN treatment. Moreover, MMP9, but not MMP13, gene expression was attenuated in CCR1- and CCL3-deficient mice, compared with that of WT mice. Furthermore, MMP9 was expressed mainly by mononuclear cells but not hepatoma cells, and MMP9-expressing cell numbers were decreased in CCR1- or CCL3-deficient mice, compared with WT mice. These observations suggest the contribution of the CCR1-CCL3 axis to HCC progression.
Publication
Journal: Hepatobiliary & pancreatic diseases international : HBPD INT
November/8/2004
Abstract
BACKGROUND
The molecular mechanism of hepatic metastasis of colorectal cancer is not well understood. The aim of this study was to assess the relations between phospholipid contents of cellular membrane and isoenzyme expression of protein kinase C (PKC) and their effects on hepatic metastasis of colorectal cancer.
METHODS
High performance liquid chromatography was used to detect contents of cell membrane phospholipids: phosphatidylinosital (PI), phosphatidylserine (PS), phosphatidylethanolamine (PE) and phosphatidylcholine (PC) in primary foci, paratumor mucosa and hepatic metastatic foci in patients with colorectal carcinoma. The mRNA expression levels of PKC-alpha, -betaII, -delta, -epsilon, -lambda, -zeta isoenzymes were detected with the QRT-PCR technique.
RESULTS
The levels of PI, PC and PE in primary foci and hepatic metastatic foci were higher than those in paratumor mucosa. The level of PE in hepatic metastatic foci was much higher than that in primary foci (t=98.88, P<0.01); but the levels of PI and PC were not significantly different between primary foci and hepatic metastatic foci (t=1.73, 1.36, P>0.05). The expression levels of PKC-betaII, -delta, -epsilon, -lambda, -zeta were enhanced in primary foci and hepatic metastatic foci, but the level of PKC-alpha in primary foci was decreased as compared with that in paratumor mucosa. The levels of PKC-delta, -epsilon, -lambda, -zeta in hepatic metastatic foci were higher than those in primary foci. A positive correlation was observed between the expression levels of PI, PC and PKC-betaII and also between those of PE and PKC-delta, -epsilon, -lambda, -zeta. However, there was a close negative correlation between PE and PKC-alpha.
CONCLUSIONS
Increased levels of PI and PC and decreased ratio of PKC-alpha to PKC-betaII are related to colorectal cancer genesis. Increased levels of PE, increased expression of PKC-delta, -epsilon, -lambda, -zeta isoenzymes and decreased level of PKC-alpha are related to hepatic metastasis in colorectal carcinoma.
Publication
Journal: Clinical cancer research : an official journal of the American Association for Cancer Research
January/4/2009
Abstract
OBJECTIVE
In pancreatic carcinoma, vascular endothelial growth factor (VEGF) expression at the primary site has been suggested to be a prognostic parameter. We quantitatively analyzed VEGF expression in liver metastases from pancreatic carcinoma and examined the correlation among VEGF expression in liver metastases, clinicopathologic factors, and clinical outcome.
METHODS
The subjects consisted of 23 patients with pancreatic adenocarcinoma who had liver metastases and were treated with S-1 and gemcitabine as the first-line treatment. VEGF expression was quantitated by enzyme immunoassay in biopsy specimens of liver metastases and nontumorous liver tissue, and in plasma. In 10 of the 23 patients, VEGF expression was also quantitated in biopsy specimens of the primary pancreatic tumor. All samples were collected before treatment.
RESULTS
The VEGF level in nontumorous liver tissue was 36.6 +/- 10.0 pg/mg protein versus 376.8 +/- 106.1 pg/mg protein in liver metastases (P = 0.0016). Pretreatment VEGF levels in plasma and in primary pancreatic carcinoma did not correlate with VEGF levels in the corresponding liver metastases. The median VEGF level in liver metastases (138.9 pg/mg protein) was used as the cutoff value between high and low VEGF expression in liver metastases. Patients showing high VEGF expression had a significantly longer progression-free survival and overall survival than patients showing low VEGF expression in liver metastases (P = 0.0219 and P = 0.0074, respectively).
CONCLUSIONS
Evaluation of VEGF levels in liver metastases might be useful in assessing the prognosis of patients with metastatic pancreatic carcinoma who are under systemic chemotherapy.
Publication
Journal: Archives of internal medicine (Chicago, Ill. : 1908)
March/17/2010
Publication
Journal: International journal of cancer
November/15/2004
Abstract
In animal models, explosive growth of metastases after removal of the primary tumor has been attributed to abolishment of angiogenesis inhibition. We investigated the influence of (removal of) the primary tumor on vascularization of liver metastases in human colorectal cancer patients. We analyzed vascular density in synchronous liver metastases from patients with the primary tumor in situ, in synchronous metastases from patients with the primary tumor resected and in metachronous metastases. In a limited number of cases, biopsies from metastases from the same patient before and within 3 months after resection were analyzed. In addition, vascular density in metastases was compared to the vascular density in the corresponding primary tumor. Peritumoral and intratumoral vascular density were determined by staining for endothelial antigens CD31 and CD34, respectively. Both peritumoral and intratumoral vascular density were elevated in synchronous metastases from patients with the primary tumor removed compared to synchronous metastases from patients with the primary tumor in situ. Comparable results were observed in patients with metachronous metastases. An increase in vascular density after resection of the colorectal malignancy was also observed in biopsies taken from the same patient before and after tumor resection. Remarkably, vascular density in the liver metastases was always lower than that in the corresponding primary tumor. Our data show for the first time in humans that the presence of a primary tumor is correlated with decreased vascularization of its distant metastases. Resection of the primary tumor results in an increased vascularization of metastatic lesions.
Publication
Journal: Clinical nuclear medicine
March/1/2010
Publication
Journal: Journal of the American College of Surgeons
April/23/2014
Publication
Journal: Nihon rinsho. Japanese journal of clinical medicine
October/17/2004
Publication
Journal: Medicina clinica
September/28/2011
Publication
Journal: Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology
January/8/2019
Abstract
Objective: To study the clinical value of transcatheter arterial chemoembolization (TACE) therapy for hepatocellular carcinoma with blood supply from right adrenal artery. Methods: An imaging and clinical data of HCC patients with blood supply from right adrenal artery were collected from 2012 to 2016 after TACE treatment in the Second Affiliated Hospital of Chongqing Medical University and the safety and therapeutic efficacy of complete embolization therapy was analyzed retrospectively. Results: Twenty hepatocellular carcinoma patients with blood supply from right adrenal artery had received 23 times treatment. All lesions had invaded and protruded from the exogenous development of liver capsule. There were 14 cases with lesions > 5 cm in diameter. Right adrenal artery was found to be involved in the blood supply of three cases of hepatocellular carcinoma during TACE treatment for the first time. In addition, the remaining 17 cases had also received TACE treatment for the second to sixth time. The superior, middle, and inferior adrenal arteries were involved in 13, 3, and 9 cases, respectively. Twenty-four right adrenal arteries (96.0%) superselectively cannulated were successfully embolized without any serious complications. The standard method for evaluating the efficacy of liver cancer in 20 solid tumors follow-up cases showed that three cases were completely relieved, nine cases were partially relieved, two cases were stable, and six cases were progressive. The effective rate of embolization with blood supply from right adrenal artery lesions was 60.0%, and the control rate of lesion development was 70.0%. Conclusion: The right adrenal artery is mainly located in the S5-S7 segments of the liver. TACE features are obvious to ascertain its safety and effectiveness in the treatment of right adrenal artery tumors.
Publication
Journal: Acta cytologica
March/12/2007
Abstract
BACKGROUND
Hepatocellular carcinoma (HCC) metastasizing to the orbit is extremely rare. In the 13 cases reported in the English-langnage literature, the diagnosis was confirmed by fine needle aspiration (FNA) cytology only once. This is the second such case to be diagnosed by FNA cytology and the first to be reported from the Indian subcontinent.
METHODS
A 76-year-old woman presented with progressive proptosis, bulging of the globe and loss of vision in the right eye. Clinical and radiologic evidence favored a primary orbital tumor with liver metastasis. Cytologic examination of aspirated material from the orbital and liver masses showed features similar to those of HCC.
CONCLUSIONS
Recognition of the cytologic features of HCC permits its diagnosis in metastatic sites. FNA can be employed as an effective tool for diagnosing HCC at metastatic sites, especially when biopsy is technically difficult.
Publication
Journal: Carcinogenesis
September/29/2011
Publication
Journal: Surgery
July/25/2013
Abstract
BACKGROUND
Simultaneous surgery for primary colorectal tumor with synchronous liver metastasis has been showed to be safe and effective. One-stage, totally laparoscopic colorectal and minor liver resections have been reported, but there are no data regarding patients requiring simultaneous major hepatectomies and colorectal surgery. We aimed to evaluate the safety, feasibility and short-term outcomes of a small cohort of highly selected patients treated by 1-stage, totally laparoscopic major hepatectomy and colorectal resection.
METHODS
From January 2009 to July 2011, 5 patients (3 women and 2 men) with primary colorectal neoplasm and synchronous monolobar liver metastasis requiring a major hepatectomy underwent attempt of 1-stage, totally laparoscopic approach after neoadjuvant chemotherapy. A retrospective analysis of prospective collected data was performed.
RESULTS
There were no conversions to open procedures. All the patients but 1 underwent a 1-stage laparoscopic resection. Among these, liver procedures were 3 right and 1 left hepatectomy; colonic procedures were 3 sigmoidectomies and 1 anterior resection of the rectum. Median operative time was 495 minutes, and duration of hospital stay, 6 days. Median estimated blood loss was 475 mL (range, 300-630) with no mortality observed. An R0 resection was always achieved. Median follow-up was 14 months (range, 7-20) with 1 recurrence observed in the liver.
CONCLUSIONS
In highly selected patients, a totally laparoscopic approach is a feasible and safe option to treat primary colorectal neoplasm with synchronous liver metastasis requiring major hepatectomies. These results need to be validated by larger, prospective, randomized studies.
Publication
Journal: HPB : the official journal of the International Hepato Pancreato Biliary Association
July/25/2013
Abstract
BACKGROUND
Resection of liver metastases from neuroendocrine cancer (NEC) prolongs survival and provides durable symptom relief. Not all hepatic lesions are amenable to resection, particularly when there is multifocal involvement. In this study, it was hypothesized that ablation of concomitant non-resectable NEC liver metastases is safe and salvages patients who would not have been selected for cytoreductive surgery.
METHODS
Patients who underwent adjuvant ablation of NEC liver metastases between 1995 and 2008 were reviewed. NEC was classified by patient and tumour characteristics. Regression and Kaplan-Meier models were used to compare variables and generate survival curves.
RESULTS
Ninety-four patients underwent hepatic resection and intra-operative ablation of metastatic NEC. The median number of lesions ablated was 3, and median size was 1.4 cm. One abscess occurred at an ablation site. Local recurrence was detected in four patients (3.8%). Overall survival was 80% and 59% at 5 and 10 years. Age, gender, tumour type, grade, primary site and need for repeat ablation had no significant association with survival. The Ki67 proliferative index was a significant predictor of decreased survival. Symptom-free survival was 34% at 3 years and 16% at 5 years, independent of the tumour grade.
CONCLUSIONS
Concurrent ablation of NEC metastases to the liver not amenable to resection is safe and increases the candidacy of patients for cytoreductive surgery. Ablation performed intra-operatively and repeated post-operatively as needed provides significant symptom control regardless of the tumour grade.
Publication
Journal: Medizinische Klinik (Munich, Germany : 1983)
September/26/2010
Abstract
METHODS
A 73-year-old male patient presented with upper gastrointestinal bleeding. The reason was an arterial hemorrhage from a duodenal tumor that could only be stopped by an angiographic intervention. In the further staging, there was evidence for a neuroendocrine carcinoma of the pancreatic head with infiltration of the duodenum and hepatic metastases. Due to good differentiation (G1) a systemic biotherapy with octreotide LAR was induced. After recurrent bleeding with arrosion of a branch of the superior mesenteric artery, a duodenum-preserving pancreatic head resection was performed. Afterwards, the systemic therapy was changed to a palliative chemotherapy with streptozotocin and 5-fluorouracil due to local progression of the disease and a Ki-67 index of 4% in the primary tumor.
CONCLUSIONS
In about 0.7% of patients with neuroendocrine tumors, the lesion is located in the pancreas. At this site these entities are very heterogeneous. The majority are nonfunctional tumors without secretion of bioactive substances and the associated symptoms. About 60% of the patients present with advanced metastasized disease. The therapy depends on the local spread and histological grading as well as symptoms of the patient. The only curative option represents surgical resection. However, even in a palliative situation, there can be benefit for the patient in case of a tumor mass reduction of > 90%. Alternative therapies in the palliative situation are somatostatin analogs, a classic systemic chemotherapy, or locoregional interventional procedures.
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