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1. Song Y, Wang LH, He J, Wang JW: [Treatment and prognosis of primary esophageal small cell carcinoma: a report of 151 cases]. Ai Zheng; 2009 Mar;28(3):303-7
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  • [Title] [Treatment and prognosis of primary esophageal small cell carcinoma: a report of 151 cases].
  • BACKGROUND AND OBJECTIVE: The treatment and prognosis of primary esophageal small cell carcinoma (PESC), an uncommon esophageal malignant tumor, have seldom been reported.
  • [MeSH-major] Carcinoma, Small Cell / surgery. Esophageal Neoplasms / surgery. Esophagectomy / methods
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chemotherapy, Adjuvant. Female. Follow-Up Studies. Humans. Liver Neoplasms / secondary. Lung Neoplasms / secondary. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Staging. Neoplastic Cells, Circulating / pathology. Proportional Hazards Models. Radiotherapy, Adjuvant. Survival Rate

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  • (PMID = 19619447.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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2. Fan ZH, Chen MH, Dai Y, Wang YB, Yan K, Wu W, Yang W, Yin SS: Evaluation of primary malignancies of the liver using contrast-enhanced sonography: correlation with pathology. AJR Am J Roentgenol; 2006 Jun;186(6):1512-9
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  • [Title] Evaluation of primary malignancies of the liver using contrast-enhanced sonography: correlation with pathology.
  • OBJECTIVE: Our purpose was to investigate the correlation of contrast-enhanced sonographic patterns with the histopathology of primary malignancies of the liver.
  • RESULTS: All 65 moderately to poorly differentiated hepatocellular carcinomas (HCCs) enhanced in the arterial phase, and 96.9% (63 lesions) of them quickly washed out in the portal venous phase.
  • Seventy-five percent of the clear cell carcinomas (12/16) enhanced in the arterial phase, 25% (4/16) did not enhance until the portal venous phase, and 31.3% (5/16) of the clear cell carcinomas washed out slowly during the late phase.
  • The enhancement and washout times of clear cell carcinomas were significantly different than those of moderately to poorly differentiated HCCs (p < 0.05).
  • CONCLUSION: Our study showed that the enhancement manifestations of primary malignancies of the liver are related to pathologic types and grades.
  • Contrast-enhanced sonograms may provide the histopathologic information for malignant tumors of the liver.
  • [MeSH-major] Carcinoma, Hepatocellular / pathology. Carcinoma, Hepatocellular / ultrasonography. Contrast Media. Liver Neoplasms / pathology. Liver Neoplasms / ultrasonography. Phospholipids. Sulfur Hexafluoride
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged

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  • (PMID = 16714638.001).
  • [ISSN] 1546-3141
  • [Journal-full-title] AJR. American journal of roentgenology
  • [ISO-abbreviation] AJR Am J Roentgenol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media; 0 / Phospholipids; 0 / contrast agent BR1; WS7LR3I1D6 / Sulfur Hexafluoride
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3. Lekoubou Looti AZ, Kengne AP, Djientcheu Vde P, Kuate CT, Njamnshi AK: Patterns of non-traumatic myelopathies in Yaounde (Cameroon): a hospital based study. J Neurol Neurosurg Psychiatry; 2010 Jul;81(7):768-70
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  • Aetiologies were dominated by primary and secondary spinal tumours (mainly prostate carcinoma, lymphoma and liver carcinoma) that each accounted for 24.5% of cases.
  • Other causes included spinal tuberculosis (12.9%), tropical spastic paraparesis (five positive for human T cell lymphotrophic virus (HTLV)-I and one for HTLV-II) (4.8%), spinal degenerative disease (4.1%), acute transverse myelitis (4.1%), HIV myelopathy (1.4%), vitamin B12 deficiency myelopathy and multiple sclerosis (0.7%).
  • Metastasis is a leading cause of spinal cord compression with liver carcinoma being more frequent than reported elsewhere.
  • [MeSH-minor] Adult. Anal Canal / pathology. Cameroon / epidemiology. Female. Hospitals. Humans. Infection / complications. Infection / epidemiology. Liver Neoplasms / complications. Liver Neoplasms / pathology. Male. Middle Aged. Neoplasm Metastasis. Paraplegia / etiology. Paraplegia / pathology. Quadriplegia / etiology. Quadriplegia / pathology. Sensation. Sex Factors. Spinal Cord Compression / complications. Spinal Cord Compression / pathology

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  • (PMID = 20581141.001).
  • [ISSN] 1468-330X
  • [Journal-full-title] Journal of neurology, neurosurgery, and psychiatry
  • [ISO-abbreviation] J. Neurol. Neurosurg. Psychiatry
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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4. He F, Yan Q, Fan L, Liu Y, Cui J, Wang J, Wang L, Wang Y, Wang Z, Guo Y, Huang G: PBK/TOPK in the differential diagnosis of cholangiocarcinoma from hepatocellular carcinoma and its involvement in prognosis of human cholangiocarcinoma. Hum Pathol; 2010 Mar;41(3):415-24
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  • [Title] PBK/TOPK in the differential diagnosis of cholangiocarcinoma from hepatocellular carcinoma and its involvement in prognosis of human cholangiocarcinoma.
  • The increased expression of PDZ binding kinase/lymphokine-activated killer T-cell-originated protein kinase (PBK/TOPK) is associated with some human malignant tumors.
  • In this study, we analyzed PBK/TOPK expression in hepatic primary tumor and explored its role in cholangiocarcinoma biology.
  • Seventy-four cholangiocarcinomas, 33 hepatocellular carcinomas, and 10 normal liver tissues were prepared from paraffin-embedded specimens.
  • The protein, mRNA of PBK/TOPK, and cell cycle of cholangiocarcinoma cell line after PBK/TOPK suppression with small interfere RNA were studied by Western blot, semiquantitative reverse transcriptase-polymerase chain reaction, and flow cytometry, respectively.
  • PBK/TOPK was usually expressed in normal bile duct epithelial cells and much more frequently expressed in cholangiocarcinoma (68/74) but never expressed in hepatocytes and hepatocellular carcinomas (0/33).
  • PBK/TOPK protein could serve as a useful indicator for histopathologic differentiation between cholangiocarcinoma and hepatocellular carcinomas and the low expression of PBK/TOPK is predicative of poor survival in cholangiocarcinoma patients.
  • [MeSH-major] Carcinoma, Hepatocellular / diagnosis. Cholangiocarcinoma / diagnosis. Liver Neoplasms / diagnosis. Protein-Serine-Threonine Kinases / metabolism
  • [MeSH-minor] Adult. Aged. Bile Ducts / metabolism. Blotting, Western. Cell Cycle / physiology. Cell Line, Tumor. Cells, Cultured. Diagnosis, Differential. Epithelial Cells / metabolism. Female. Flow Cytometry. Gene Silencing. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. Mitogen-Activated Protein Kinase Kinases. Prognosis. Proportional Hazards Models. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Sex Factors

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 19954816.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; EC 2.7.12.2 / PDZ-binding kinase
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5. Liu LX, Lee NP, Chan VW, Xue W, Zender L, Zhang C, Mao M, Dai H, Wang XL, Xu MZ, Lee TK, Ng IO, Chen Y, Kung HF, Lowe SW, Poon RT, Wang JH, Luk JM: Targeting cadherin-17 inactivates Wnt signaling and inhibits tumor growth in liver carcinoma. Hepatology; 2009 Nov;50(5):1453-63
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  • [Title] Targeting cadherin-17 inactivates Wnt signaling and inhibits tumor growth in liver carcinoma.
  • Hepatocellular carcinoma (HCC) is a lethal malignancy for which there are no effective therapies.
  • Here, we show that cadherin-17 (CDH17) adhesion molecule is up-regulated in human liver cancers and can transform premalignant liver progenitor cells to produce liver carcinomas in mice.
  • RNA interference-mediated knockdown of CDH17 inhibited proliferation of both primary and highly metastatic HCC cell lines in vitro and in vivo.
  • The antitumor mechanisms underlying CDH17 inhibition involve inactivation of Wnt signaling, because growth inhibition and cell death were accompanied by relocalization of beta-catenin to the cytoplasm and a concomitant reduction in cyclin D1 and an increase in retinoblastoma.
  • [MeSH-major] Cadherins / metabolism. Carcinoma, Hepatocellular / pathology. Cell Proliferation. Liver Neoplasms / pathology. Signal Transduction / physiology. Wnt Proteins / metabolism
  • [MeSH-minor] Adult. Aged. Animals. Cell Line, Tumor. Female. Gene Knockdown Techniques. Humans. Male. Mice. Mice, Nude. Middle Aged. Phenotype. Transplantation, Heterologous. beta Catenin / antagonists & inhibitors. beta Catenin / metabolism

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  • [Cites] Apoptosis. 2006 Jul;11(7):1215-29 [16699959.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 2005;70:251-61 [16869761.001]
  • [Cites] Cell Mol Life Sci. 2006 Jul;63(13):1564-73 [16791429.001]
  • [Cites] Clin Cancer Res. 2006 Sep 1;12(17):5248-52 [16951245.001]
  • [Cites] Ann Surg Oncol. 2007 Jan;14(1):94-9 [17063305.001]
  • [Cites] J Mol Biol. 2007 Jul 6;370(2):220-30 [17512947.001]
  • [Cites] Hepatology. 2007 Jul;46(1):200-8 [17596871.001]
  • [Cites] Bioinformatics. 2007 Jul 1;23(13):i450-8 [17646330.001]
  • [Cites] Dis Colon Rectum. 2007 Nov;50(11):1873-80 [17828401.001]
  • [Cites] Curr Opin Oncol. 2008 Jan;20(1):90-6 [18043262.001]
  • [Cites] Br J Cancer. 2008 Jan 15;98(1):4-8 [18182973.001]
  • [Cites] J Mol Biol. 2008 Apr 18;378(1):44-54 [18342884.001]
  • [Cites] Clin Oncol (R Coll Radiol). 2008 May;20(4):275-83 [18353622.001]
  • [Cites] Gastroenterology. 2008 May;134(6):1752-63 [18471552.001]
  • [Cites] Proteomics. 2008 May;8(10):2136-49 [18425728.001]
  • [Cites] Mutat Res. 2008 May 31;653(1-2):6-13 [18467159.001]
  • [Cites] Cell. 2008 Nov 28;135(5):852-64 [19012953.001]
  • [Cites] Cell. 2006 Jun 30;125(7):1253-67 [16814713.001]
  • [Cites] Cell. 2009 Mar 20;136(6):1136-47 [19303855.001]
  • [Cites] Hepatology. 2000 Jan;31(1):173-81 [10613743.001]
  • [Cites] Gut. 2001 Jul;49(1):73-81 [11413113.001]
  • [Cites] World J Gastroenterol. 2001 Oct;7(5):630-6 [11819844.001]
  • [Cites] Cancer Sci. 2003 May;94(5):425-30 [12824888.001]
  • [Cites] Int J Cancer. 2003 Sep 1;106(3):334-41 [12845670.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Nov 21;311(3):618-24 [14623315.001]
  • [Cites] Cancer Genet Cytogenet. 2004 Jan 1;148(1):80-4 [14697646.001]
  • [Cites] Liver Transpl. 2004 Feb;10(2 Suppl 1):S39-45 [14762838.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Jun 25;319(2):562-8 [15178443.001]
  • [Cites] Cancer Lett. 2004 Aug 30;212(2):253-9 [15279905.001]
  • [Cites] J Clin Microbiol. 1987 Nov;25(11):2140-4 [2447120.001]
  • [Cites] Science. 1994 Apr 15;264(5157):430-3 [8153632.001]
  • [Cites] J Cell Biol. 1994 Jun;125(6):1353-69 [8207063.001]
  • [Cites] Clin Cancer Res. 2005 Jan 15;11(2 Pt 1):483-9 [15701831.001]
  • [Cites] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078.001]
  • [Cites] Virchows Arch. 2005 Oct;447(4):717-22 [16044349.001]
  • [Cites] J Clin Invest. 2006 Jun;116(6):1582-95 [16710476.001]
  • [ErratumIn] Hepatology. 2010 Jan;51(1):358
  • (PMID = 19676131.001).
  • [ISSN] 1527-3350
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] eng
  • [Grant] United States / Howard Hughes Medical Institute / / ; United States / NCI NIH HHS / CA / P01 CA013106; United States / NCI NIH HHS / CA / P30 CA008748; United States / NCI NIH HHS / CA / CA13106
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDH17 protein, human; 0 / Cadherins; 0 / Cdh17 protein, mouse; 0 / Wnt Proteins; 0 / beta Catenin
  • [Other-IDs] NLM/ HHMIMS353854; NLM/ PMC3328302
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6. Duan YW, Huang Y, Cai LQ, Duan Q, Zhu YS: Inhibition of tumor growth and tumor metastasis by a Chinese herbal formula--ZYD88, in an animal model with metastatic Lewis lung carcinoma. Oncol Rep; 2007 Jun;17(6):1391-7
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  • [Title] Inhibition of tumor growth and tumor metastasis by a Chinese herbal formula--ZYD88, in an animal model with metastatic Lewis lung carcinoma.
  • In the present study, we determined the effectiveness of ZYD88, a Chinese herbal formula, in the inhibition of tumor growth and distant tumor metastases to the lung and liver in an animal model with metastatic Lewis lung carcinoma (LLC).
  • Treatment with ZYD88 in adult C57BL/6 mice with metastatic LLC produced dose-dependent deceases in primary tumor weight, the mitotic tumor cell number, microvessel density, distant tumor metastases and red blood cell immune complexes, while it significantly increased tumor necrosis, thymus cortical thickness, the thymus medullar reticular epithelial cell (REC) number, and the activity of red blood cell C3b receptors.
  • Although cyclophosphamide inhibited tumor growth, it had no significant effects on distant tumor metastases, thymus cortical thickness, the thymus medullar REC number, red blood cell C3b receptor activity and red blood cell immune complexes.
  • [MeSH-major] Carcinoma, Lewis Lung / prevention & control. Carcinoma, Lewis Lung / secondary. Drugs, Chinese Herbal / therapeutic use. Liver Neoplasms / prevention & control. Liver Neoplasms / secondary. Neovascularization, Pathologic / prevention & control
  • [MeSH-minor] Animals. Capillaries / drug effects. Cell Proliferation / drug effects. Disease Models, Animal. Immunity / drug effects. Mice. Mice, Inbred C57BL. Xenograft Model Antitumor Assays

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  • (PMID = 17487396.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Drugs, Chinese Herbal; 0 / ZYD88 herbal formula
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7. Kuo FY, Swanson PE, Yeh MM: Pancreatic acinar tissue in liver explants: a morphologic and immunohistochemical study. Am J Surg Pathol; 2009 Jan;33(1):66-71
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  • [Title] Pancreatic acinar tissue in liver explants: a morphologic and immunohistochemical study.
  • BACKGROUND: Pancreatic acini-like tissue is occasionally seen in the liver.
  • To gain further insight into this issue, we performed a pathologic and immunohistochemical study in liver explants to identify pancreatic acinar tissue.
  • DESIGN: A total of 382 liver explants transplanted from 1995 to 2000 were examined.
  • RESULTS: Sixteen (4.2%) of 382 liver explants contained pancreatic acini-like tissue.
  • Fifteen of these were cirrhotic livers due to cryptogenic cirrhosis (n=1), primary biliary cirrhosis (n=3), primary sclerosing cholangitis (n=1), chronic hepatitis C-related cirrhosis (n=5), and cirrhosis with hepatitis C and hepatocellular carcinoma (n=5).
  • CONCLUSIONS: Our results collectively indicate that pancreatic acini-like tissue in liver represent aggregates of pancreatic acinar cells admixed with small intra-acinar terminal ductules.
  • [MeSH-major] Cell Transdifferentiation / physiology. Choristoma / etiology. Choristoma / pathology. Liver Diseases / pathology. Pancreas
  • [MeSH-minor] Adult. Aged. Female. Humans. Immunohistochemistry. Middle Aged

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  • (PMID = 18987542.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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8. Fishman M, Hunter TB, Soliman H, Thompson P, Dunn M, Smilee R, Farmelo MJ, Noyes DR, Mahany JJ, Lee JH, Cantor A, Messina J, Seigne J, Pow-Sang J, Janssen W, Antonia SJ: Phase II trial of B7-1 (CD-86) transduced, cultured autologous tumor cell vaccine plus subcutaneous interleukin-2 for treatment of stage IV renal cell carcinoma. J Immunother; 2008 Jan;31(1):72-80
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  • [Title] Phase II trial of B7-1 (CD-86) transduced, cultured autologous tumor cell vaccine plus subcutaneous interleukin-2 for treatment of stage IV renal cell carcinoma.
  • Vaccination consisted of autologous cells cultured from primary tumor or resected metastasis, transduced to express B7.1 surface molecule and then irradiated.
  • [MeSH-major] Antigens, CD80 / immunology. Cancer Vaccines / therapeutic use. Carcinoma, Renal Cell / therapy. Interleukin-2 / therapeutic use. Kidney Neoplasms / therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Interferon-gamma / metabolism. Leukocytes, Mononuclear / drug effects. Leukocytes, Mononuclear / immunology. Leukocytes, Mononuclear / metabolism. Liver / drug effects. Liver / immunology. Liver / pathology. Male. Middle Aged. Neoplasm Staging. Skin / drug effects. Skin / immunology. Skin / pathology. Survival Analysis. Transfection. Treatment Outcome. Tumor Cells, Cultured

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  • (PMID = 18157014.001).
  • [ISSN] 1524-9557
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R03 CA 82059-01
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD80; 0 / Cancer Vaccines; 0 / Interleukin-2; 82115-62-6 / Interferon-gamma
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9. Savelov NA, Petrovichev NN, Anurova OA, Pavlovskaia AI, Tatosian AG: [Immunohistochemical diagnosis of metastases of small round cell carcinomas with undetected primary focus]. Arkh Patol; 2006 Mar-Apr;68(2):16-9
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  • [Title] [Immunohistochemical diagnosis of metastases of small round cell carcinomas with undetected primary focus].
  • 17 small round cell tumors of unkown primary site were studied.
  • One of the following diagnosis was obtained in 14 cases (82.4%): small cell carcinoma, Merkel cell carcinoma, melanoma, Ewing sarcoma family tumor.
  • [MeSH-major] Brain Neoplasms / secondary. Carcinoma, Small Cell / secondary. Liver Neoplasms / secondary. Neoplasms, Unknown Primary / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Biomarkers, Tumor. Carcinoma, Merkel Cell / diagnosis. Carcinoma, Merkel Cell / secondary. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Lymphoma / pathology. Male. Middle Aged. Sarcoma, Ewing / diagnosis. Sarcoma, Ewing / secondary

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  • (PMID = 16752503.001).
  • [ISSN] 0004-1955
  • [Journal-full-title] Arkhiv patologii
  • [ISO-abbreviation] Arkh. Patol.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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10. Andrle J, Schartinger VH, Schwentner I, Deibl M, Sprinzl GM: Initial staging examinations for head and neck squamous cell carcinoma: are they appropriate? J Laryngol Otol; 2009 Aug;123(8):885-8
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  • [Title] Initial staging examinations for head and neck squamous cell carcinoma: are they appropriate?
  • OBJECTIVES: The presence of distant metastases affects the therapeutic regime in patients with head and neck squamous cell carcinoma.
  • This study evaluated the necessity to undertake bone scanning, chest computed tomography and abdominal ultrasonography in patients presenting with primary advanced head and neck squamous cell carcinoma.
  • METHODS: One hundred and sixty-three patients with head and neck squamous cell carcinoma who were scheduled for major surgery underwent screening for distant metastases.
  • Only one patient with primary liver metastases was detected by abdominal ultrasonography; this patient also had pulmonary metastases.
  • CONCLUSIONS: Computed tomography of the thorax is the most important technique for screening patients with head and neck squamous cell carcinoma.
  • [MeSH-major] Bone Neoplasms / secondary. Carcinoma, Squamous Cell / secondary. Head and Neck Neoplasms. Lung Neoplasms / secondary. Neoplasms, Second Primary / diagnosis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Bone and Bones / radionuclide imaging. Female. Humans. Male. Middle Aged. Neoplasm Staging / methods. Retrospective Studies. Tomography, X-Ray Computed / methods


11. Suenaga M, Matsushita K, Kawamata N, Kukita T, Hamakawa Y, Gejima K, Onodera R, Sato T, Yamaguchi A, Inoue H, Arimura K, Arima N, Yoshida H, Tei C: True malignant histiocytosis with trisomy 9 following primary mediastinal germ cell tumor. Acta Haematol; 2006;116(1):62-6
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  • [Title] True malignant histiocytosis with trisomy 9 following primary mediastinal germ cell tumor.
  • A diagnosis of mediastinal germ cell tumor, mixed type involving seminoma, immature teratoma and embryonal carcinoma, was made by transthoracic needle biopsy.
  • Examination of bone marrow revealed increased atypical large histiocytes (5.6%) with hemophagocytosis, and thus, hemophagocytic syndrome related to germ cell tumor was diagnosed.
  • Chemotherapies for germ cell tumor and hemophagocytic syndrome were performed without any improvement, and he died of diffuse alveolar damage.
  • Autopsy revealed diffuse infiltration of immature histiocytes with hemophagocytosis in the liver, spleen and bone marrow.
  • The atypical histiocytes were positive for CD68 and lysozyme and negative for lymphoid markers, and the diagnosis of true malignant histiocytosis associated with mediastinal germ cell tumor was made.
  • [MeSH-major] Chromosomes, Human, Pair 9. Histiocytic Sarcoma / pathology. Lymphohistiocytosis, Hemophagocytic / pathology. Mediastinal Neoplasms / pathology. Neoplasms, Germ Cell and Embryonal / pathology. Neoplasms, Second Primary / pathology. Trisomy
  • [MeSH-minor] Adult. Antigens, CD. Antigens, Differentiation, Myelomonocytic. Biopsy, Needle. Bone Marrow / pathology. Histiocytes / pathology. Humans. Japan. Liver / pathology. Male. Muramidase. Pulmonary Alveoli / pathology. Time Factors. Treatment Failure

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  • (PMID = 16809892.001).
  • [ISSN] 0001-5792
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD68 antigen, human; EC 3.2.1.17 / Muramidase
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12. Radfar L, Fatahzadeh M: Neuroendocrine carcinoma of the oral cavity: a case report and review of the literature. Gen Dent; 2008 Nov-Dec;56(7):714-8
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  • [Title] Neuroendocrine carcinoma of the oral cavity: a case report and review of the literature.
  • Neuroendocrine (NE) carcinoma is a rare disease originating from the NE cell system, which is considered to be the third division of the nervous system.
  • Based on their biological characteristics, NE carcinomas are classified into three subtypes: well-differentiated NE carcinoma (typical carcinoid tumor), moderately differentiated NE carcinoma (atypical carcinoid tumor), and poorly differentiated carcinoma (small cell carcinoma).
  • Among the primary tumors, the propensity for disease to spread to the oral region varies.
  • This case report describes a patient with an unknown primary NE malignancy that led to metastatic lesions in both the liver and mandibular soft tissues.
  • [MeSH-major] Carcinoma, Neuroendocrine / secondary. Mandibular Neoplasms / secondary. Neoplasms, Unknown Primary
  • [MeSH-minor] Adult. Brain Neoplasms / secondary. Fatal Outcome. Humans. Liver Neoplasms / secondary. Lymphatic Metastasis / pathology. Male

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  • (PMID = 19014033.001).
  • [ISSN] 0363-6771
  • [Journal-full-title] General dentistry
  • [ISO-abbreviation] Gen Dent
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 42
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13. Sha D, He YJ: [Expression and clinical significance of VEGF and its receptors Flt-1 and KDR in nasopharyngeal carcinoma]. Ai Zheng; 2006 Feb;25(2):229-34
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  • [Title] [Expression and clinical significance of VEGF and its receptors Flt-1 and KDR in nasopharyngeal carcinoma].
  • This study was to explore the correlations of VEGF, Flt-1 and KDR expression to clinical features and prognosis of nasopharyngeal carcinoma (NPC) patients.
  • VEGF expression was related to primary tumor site, lymph node metastasis, and clinical stage (P=0.04, P<0.01, P=0.02, respectively); KDR expression was related to primary tumor site (P=0.03); all of them were related to local recurrence and/or distal metastasis (P<0.01, P<0.01, P=0.01, respectively), and poor overall survival (P<0.01, P=0.01, P=0.03, respectively).
  • [MeSH-major] Carcinoma, Squamous Cell / metabolism. Nasopharyngeal Neoplasms / metabolism. Vascular Endothelial Growth Factor A / metabolism. Vascular Endothelial Growth Factor Receptor-1 / metabolism. Vascular Endothelial Growth Factor Receptor-2 / metabolism
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Bone Neoplasms / metabolism. Bone Neoplasms / secondary. Female. Follow-Up Studies. Humans. Liver Neoplasms / metabolism. Liver Neoplasms / secondary. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Recurrence, Local. Neoplasm Staging. Prognosis. Proportional Hazards Models. Survival Rate

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  • (PMID = 16480593.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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14. Jang HS, Kang KM, Choi BO, Chai GY, Hong SC, Ha WS, Jirtle RL: Clinical significance of loss of heterozygosity for M6P/IGF2R in patients with primary hepatocellular carcinoma. World J Gastroenterol; 2008 Mar 7;14(9):1394-8
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  • [Title] Clinical significance of loss of heterozygosity for M6P/IGF2R in patients with primary hepatocellular carcinoma.
  • AIM: To investigate the relationship between loss of heterozygosity (LOH) for mannose 6-phosphate/insulin-like growth factor 2 receptor (M6P/IGF2R) and the outcomes for primary HCC patients treated with partial hepatectomy.
  • METHODS: The LOH for M6P/IGF2R in primary HCC patients was assessed using six different gene-specific nucleotide polymorphisms.
  • CONCLUSION: These results show M6P/IGF2R LOH predicts poor clinical outcomes in surgically resected primary HCC patients.
  • [MeSH-major] Biomarkers, Tumor / genetics. Carcinoma, Hepatocellular / genetics. Liver Neoplasms / genetics. Loss of Heterozygosity / genetics. Receptor, IGF Type 2 / genetics
  • [MeSH-minor] Adult. Aged. Female. Hepatectomy. Humans. Male. Middle Aged. Polymorphism, Genetic / genetics. Predictive Value of Tests. Prognosis. Retrospective Studies. Survival Analysis. Treatment Outcome

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  • [Cites] Bioessays. 2000 Mar;22(3):274-85 [10684587.001]
  • [Cites] Oncogene. 2006 Jun 8;25(24):3463-70 [16449974.001]
  • [Cites] Bioessays. 2000 May;22(5):452-9 [10797485.001]
  • [Cites] Semin Cancer Biol. 2000 Jun;10(3):185-200 [10936068.001]
  • [Cites] Cell. 2000 Oct 27;103(3):491-500 [11081635.001]
  • [Cites] Nat Genet. 2001 Feb;27(2):153-4 [11175780.001]
  • [Cites] Exp Cell Res. 2001 Apr 1;264(2):388-96 [11262195.001]
  • [Cites] Development. 2001 May;128(10):1881-7 [11311167.001]
  • [Cites] Hum Mol Genet. 2001 Aug 15;10(17):1721-8 [11532981.001]
  • [Cites] Genes Dev. 2001 Nov 15;15(22):2917-21 [11711426.001]
  • [Cites] Hepatology. 2002 May;35(5):1153-63 [11981765.001]
  • [Cites] BMC Cancer. 2002 Jul 30;2:18 [12149131.001]
  • [Cites] Genomics. 1988 Oct;3(3):224-9 [2852162.001]
  • [Cites] Nature. 1991 Jan 3;349(6304):84-7 [1845916.001]
  • [Cites] Cancer Res. 1994 Apr 1;54(7 Suppl):1907s-1911s [8137310.001]
  • [Cites] Development. 1993 Jul;118(3):731-6 [8076514.001]
  • [Cites] Oncogene. 1995 May 4;10(9):1725-9 [7753549.001]
  • [Cites] Nat Genet. 1995 Dec;11(4):447-9 [7493029.001]
  • [Cites] Oncogene. 1996 May 2;12(9):2003-9 [8649861.001]
  • [Cites] Nat Genet. 1996 Nov;14(3):255-7 [8896552.001]
  • [Cites] Cancer Res. 1997 May 15;57(10):1851-4 [9157973.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Sep 16;94(19):10351-5 [9294214.001]
  • [Cites] Nature. 1997 Sep 11;389(6647):122-3 [9296483.001]
  • [Cites] Exp Cell Res. 1999 Apr 10;248(1):18-24 [10094809.001]
  • [Cites] Oncogene. 1999 Jul 15;18(28):4063-8 [10435587.001]
  • [Cites] Cell Growth Differ. 1999 Aug;10(8):591-600 [10470859.001]
  • [Cites] World J Gastroenterol. 2005 Jul 7;11(25):3850-4 [15991281.001]
  • [Cites] Oncogene. 2000 Mar 16;19(12):1572-8 [10734317.001]
  • (PMID = 18322954.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Receptor, IGF Type 2
  • [Other-IDs] NLM/ PMC2693688
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15. Tanioka M, Katsumata N, Sasajima Y, Ikeda S, Kato T, Onda T, Kasamatsu T, Fujiwara Y: Clinical characteristics and outcomes of women with stage IV endometrial cancer. Med Oncol; 2010 Dec;27(4):1371-7
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  • Neither surgery as primary therapy nor optimal cytoreduction was significantly related to overall survival in either the 28 patients in whom stage IV was diagnosed preoperatively or in all 41 patients.
  • [MeSH-major] Carcinoma, Endometrioid / surgery. Endometrial Neoplasms / surgery. Neoplasm, Residual / surgery
  • [MeSH-minor] Adenocarcinoma / secondary. Adenocarcinoma / surgery. Adult. Aged. Aged, 80 and over. Bone Neoplasms / secondary. Bone Neoplasms / surgery. Carcinoma, Small Cell / secondary. Carcinoma, Small Cell / surgery. Cystadenocarcinoma, Serous / secondary. Cystadenocarcinoma, Serous / surgery. Female. Humans. Liver Neoplasms / secondary. Liver Neoplasms / surgery. Lung Neoplasms / secondary. Lung Neoplasms / surgery. Middle Aged. Neoplasm Staging. Retrospective Studies. Survival Rate. Treatment Outcome

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  • [Cites] Gynecol Oncol. 2004 Jan;92(1):4-9 [14751130.001]
  • [Cites] Gynecol Oncol. 2000 Aug;78(2):85-91 [10926785.001]
  • [Cites] Gynecol Oncol. 2007 Nov;107(2):285-91 [17688923.001]
  • [Cites] Gynecol Oncol. 1997 Oct;67(1):56-60 [9345357.001]
  • [Cites] Gynecol Oncol. 2005 Jun;97(3):755-63 [15913742.001]
  • [Cites] Int J Gynecol Cancer. 2002 Sep-Oct;12(5):448-53 [12366661.001]
  • [Cites] Gynecol Oncol. 2007 Aug;106(2):325-33 [17532033.001]
  • [Cites] Gynecol Oncol. 2004 Jan;92(1):10-4 [14751131.001]
  • [Cites] Gynecol Oncol. 1994 Feb;52(2):237-40 [8314145.001]
  • [Cites] J Clin Oncol. 2006 Jan 1;24(1):36-44 [16330675.001]
  • [Cites] Int J Gynaecol Obstet. 2006 Nov;95 Suppl 1:S105-43 [17161155.001]
  • [Cites] Gynecol Oncol. 2004 Oct;95(1):133-8 [15385122.001]
  • [Cites] Gynecol Oncol. 2004 May;93(2):345-52 [15099944.001]
  • (PMID = 20024630.001).
  • [ISSN] 1559-131X
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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16. Zhu H, Chen XP, Zhang WG, Luo SF, Zhang BX: Expression and significance of new inhibitor of apoptosis protein survivin in hepatocellular carcinoma. World J Gastroenterol; 2005 Jul 7;11(25):3855-9
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  • [Title] Expression and significance of new inhibitor of apoptosis protein survivin in hepatocellular carcinoma.
  • AIM: To investigate expression and significance of inhibitor of apoptosis protein survivin in hepatocellular carcinoma (HCC).
  • METHODS: The expression of survivin and vascular endothelial growth factor (VEGF) was investigated in 38 cases of HCC tissues and 38 liver cirrhosis tissues by immunohistochemistry and Western blot.
  • RESULTS: Survivin protein was detected in 23 (60.5%) of 38 HCCs and 3 (7.9%) of 38 liver cirrhosis tissues.
  • In liver cirrhosis tissues, the expression of VEGF was as follows: 24 cases were negative, 10 cases were weak positive and 4 cases were strong positive.
  • The expression of survivin in the primary lesion is very useful as an indicator for metastasis and prognosis of HCC.
  • [MeSH-major] Apoptosis. Carcinoma, Hepatocellular / physiopathology. Liver Neoplasms / physiopathology. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism
  • [MeSH-minor] Adult. Aged. Antigens, Neoplasm / metabolism. Female. Humans. Inhibitor of Apoptosis Proteins. Male. Middle Aged

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  • (PMID = 15991282.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins
  • [Other-IDs] NLM/ PMC4504885
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17. Perera GK, Child FJ, Heaton N, O'Grady J, Higgins EM: Skin lesions in adult liver transplant recipients: a study of 100 consecutive patients. Br J Dermatol; 2006 May;154(5):868-72
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  • [Title] Skin lesions in adult liver transplant recipients: a study of 100 consecutive patients.
  • OBJECTIVES: The primary objective was to determine the different types of cutaneous lesions encountered in the adult liver transplant population.
  • METHODS: Two dermatologists examined 100 consecutive liver transplant recipients (LTRs) attending the transplant outpatient department.
  • Four patients developed skin cancers; among them there were a total of seven skin cancers (one squamous cell carcinoma, six basal cell carcinomas).
  • The relatively low prevalence of skin cancer in our liver transplant population may in part be explained by the relatively high percentage of recipients on dual and monotherapy (48% and 17% respectively), and the shorter duration of therapy.
  • [MeSH-major] Liver Transplantation / immunology. Skin Diseases / etiology
  • [MeSH-minor] Adult. Carcinoma, Basal Cell / etiology. Carcinoma, Basal Cell / immunology. Carcinoma, Squamous Cell / immunology. Carcinoma, Squamous Cell / radiotherapy. Female. Humans. Immunocompromised Host. Immunosuppressive Agents / adverse effects. Keratosis / etiology. Keratosis / immunology. Liver Failure / etiology. Liver Failure / surgery. Male. Middle Aged. Risk Factors. Skin Diseases, Infectious / etiology. Skin Diseases, Infectious / immunology. Skin Neoplasms / etiology. Skin Neoplasms / immunology. Sunlight / adverse effects

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  • (PMID = 16634888.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunosuppressive Agents
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18. Ding T, Xu J, Wang F, Shi M, Zhang Y, Li SP, Zheng L: High tumor-infiltrating macrophage density predicts poor prognosis in patients with primary hepatocellular carcinoma after resection. Hum Pathol; 2009 Mar;40(3):381-9
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  • [Title] High tumor-infiltrating macrophage density predicts poor prognosis in patients with primary hepatocellular carcinoma after resection.
  • This study attempted to investigate the prognostic values of tumor-infiltrating macrophages in patients with hepatocellular carcinoma after resection, paying particular attention to their tissue microlocalization.
  • The CD68(+) macrophages were assessed by immunohistochemistry in tissues from 137 patients with hepatocellular carcinoma.
  • Our results demonstrate that high macrophage infiltration predicts poor prognosis in patients with hepatocellular carcinoma.
  • [MeSH-major] Carcinoma, Hepatocellular / pathology. Liver Neoplasms / pathology. Macrophages / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Antigens, CD / metabolism. Antigens, Differentiation, Myelomonocytic / metabolism. Cell Count. Cell Line, Tumor. Cell Movement. Disease-Free Survival. Female. Humans. Immunoenzyme Techniques. Male. Middle Aged. Prognosis. Survival Rate. Young Adult

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  • (PMID = 18992916.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD68 antigen, human
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19. Cui Y, Bi M, Su T, Liu H, Lu SH: Molecular cloning and characterization of a novel esophageal cancer related gene. Int J Oncol; 2010 Dec;37(6):1521-8
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  • Pulse-chase experiments showed that ECRG2 protein was detected in both cell lysates and culture medium, indicating that the ECRG2 protein was extracellularly secreted after the post-translational cleavage.
  • Northern blot analysis revealed the presence of the major band corresponding to a size of 569 kb throughout the fetal skin, thymus, esophagus, brain, lung, heart, stomach, liver, spleen, colon, kidney, testis, muscle, cholecyst tissues and adult esophageal mucosa, brain, thyroid tissue and mouth epithelia.
  • However, ECRG2 gene was significantly down-regulated in primary esophageal cancer tissues.
  • [MeSH-major] Carcinoma, Squamous Cell / genetics. Esophageal Neoplasms / genetics. Proteinase Inhibitory Proteins, Secretory / genetics
  • [MeSH-minor] Adult. Amino Acid Sequence. Base Sequence. Chromosome Mapping. Cloning, Molecular. Computational Biology. DNA, Complementary / analysis. DNA, Complementary / isolation & purification. Gene Expression Regulation, Neoplastic. Genes, Neoplasm. Humans. Models, Molecular. Molecular Sequence Data. Neoplasm Invasiveness. Sequence Analysis, DNA

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  • (PMID = 21042721.001).
  • [ISSN] 1791-2423
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / Proteinase Inhibitory Proteins, Secretory; 0 / SPINK7 protein, human
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20. Jarufe N, McMaster P, Mayer AD, Mirza DF, Buckels JA, Orug T, Tekin K, Bramhall SR: Surgical treatment of metastases to the pancreas. Surgeon; 2005 Apr;3(2):79-83
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  • There were seven cases of renal cell carcinomas, three colorectal carcinomas, two sarcomas and one lung carcinoma.
  • A prolonged disease-free interval from primary surgery was characteristic for renal cell carcinoma cases (median = 10.8 years).
  • Median survival for renal cell carcinoma was 30.5 months and for non-renal cell carcinoma was 26.4 months (p = 0.76).
  • [MeSH-major] Carcinoma / secondary. Carcinoma / surgery. Pancreatic Neoplasms / secondary. Pancreatic Neoplasms / surgery. Sarcoma / secondary. Sarcoma / surgery
  • [MeSH-minor] Adult. Aged. Colorectal Neoplasms / pathology. Female. Humans. Kidney Neoplasms / pathology. Lung Neoplasms / pathology. Male. Middle Aged. Pancreatectomy. Survival Rate. Treatment Outcome

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  • (PMID = 15861941.001).
  • [ISSN] 1479-666X
  • [Journal-full-title] The surgeon : journal of the Royal Colleges of Surgeons of Edinburgh and Ireland
  • [ISO-abbreviation] Surgeon
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Scotland
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21. Moghimi-Dehkordi B, Safaee A, Ghiasi S, Zali MR: Survival in gastric cancer patients: univariate and multivariate analysis. East Afr J Public Health; 2009 Apr;6 Suppl(1):41-4
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  • METHODS: Retrospective study of overall patients diagnosed with gastric cancer registered in the cancer registry center of Research Center for Gastroenterology and Liver Disease (RCGLD), Shahid Beheshti University, M.C, Tehran, Iran, between Dec.
  • CONCLUSIONS: According to results, early detection of cancer in lower ages and in primary grades of tumor is important to increase patient's life expectancy.
  • [MeSH-major] Adenocarcinoma / mortality. Carcinoma, Signet Ring Cell / mortality. Stomach Neoplasms / mortality
  • [MeSH-minor] Adult. Age Factors. Aged. Aged, 80 and over. Female. Humans. Iran / epidemiology. Kaplan-Meier Estimate. Male. Middle Aged. Multivariate Analysis. Prognosis. Proportional Hazards Models. Retrospective Studies. Survival Rate. Time Factors

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  • (PMID = 20084985.001).
  • [ISSN] 0856-8960
  • [Journal-full-title] East African journal of public health
  • [ISO-abbreviation] East Afr J Public Health
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Tanzania
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22. Lacornerie T, Mirabel X, Lartigau E: [The Cyberknife: experience of centre OSCAR-Lambret]. Cancer Radiother; 2009 Sep;13(5):391-8
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  • The program has been developed around specific clinical indications: head and neck reirradiation, liver.
  • [MeSH-major] Algorithms. Carcinoma, Hepatocellular / surgery. Head and Neck Neoplasms / surgery. Liver Neoplasms / surgery. Radiosurgery / methods. Robotics / methods
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antineoplastic Agents / therapeutic use. Cancer Care Facilities. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / surgery. Cetuximab. Colorectal Neoplasms. Equipment Design. Female. France. Humans. Male. Middle Aged. Movement. Neoplasm Recurrence, Local / surgery. Neoplasms, Second Primary / surgery. Phantoms, Imaging. Quality Control. Respiration. Retreatment. Young Adult

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  • (PMID = 19640759.001).
  • [ISSN] 1769-6658
  • [Journal-full-title] Cancer radiothérapie : journal de la Société française de radiothérapie oncologique
  • [ISO-abbreviation] Cancer Radiother
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; PQX0D8J21J / Cetuximab
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23. Kinoshita Y, Tajiri T, Souzaki R, Tatsuta K, Higashi M, Izaki T, Takahashi Y, Taguchi T: Diagnostic value of lectin reactive alpha-fetoprotein for neoinfantile hepatic tumors and malignant germ cell tumors: preliminary study. J Pediatr Hematol Oncol; 2008 Jun;30(6):447-50
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  • [Title] Diagnostic value of lectin reactive alpha-fetoprotein for neoinfantile hepatic tumors and malignant germ cell tumors: preliminary study.
  • BACKGROUND AND PURPOSE: The serum alpha-fetoprotein (AFP) level has been used as a tumor marker for hepatoblastoma, and malignant germ cell tumors in pediatric patients.
  • The AFP has 3 isoforms (L1, L2, L3), and the usefulness of the L3 fraction as a diagnostic marker for the adult hepatocellular carcinoma is well known.
  • MATERIALS AND METHODS: From 2003 to 2006, two cases of hepatoblastoma, and 5 cases of germ cell tumor, all of which were neoinfantile, were treated in our department.
  • DISCUSSION: Our results indicated that the level of the L3 fraction accurately confirmed the existence, or the malignant potential of hepatic tumor or germ cell tumor.
  • [MeSH-major] Biomarkers, Tumor / blood. Hepatoblastoma / blood. Liver Neoplasms / blood. Neoplasms, Germ Cell and Embryonal / blood. alpha-Fetoproteins / analysis


24. Zhong XG, He S, Yin W, Deng JY, Chen B: [Tropism of adult liver stem cells toward hepatocellular carcinoma cells in vitro]. Zhonghua Gan Zang Bing Za Zhi; 2005 Sep;13(9):644-7
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  • [Title] [Tropism of adult liver stem cells toward hepatocellular carcinoma cells in vitro].
  • OBJECTIVE: To explore the biological behavior of adult liver stem cells in a co-cultured system of them with hepatocellular carcinoma (HCC) cells without direct contact between the two kinds of cells.
  • METHODS: WB-F344, a kind of rat adult liver stem cell, and rat embryonic fibroblasts (REF) from a primary culture were engineered to express enhanced green fluorescent protein (EGFP) by recombinant adenoviral-mediated methods.
  • After the HCC cells grew to 40%-60% confluence in the culture dish with a 10-mm cell-free area, a similar number of WB-EGFP and REF-EGFP were placed in the blank areas respectively.
  • Their appearance was found not only when WB-EGFP cells were seeded into the cell-free area at the center of the dish, but also when seeded into the blank area at the extreme edge of the plate.
  • CONCLUSIONS: The results mean that adult liver stem cells have a biological behavior of selective tropism toward HCC cells in vitro, and suggest a possibility of using migratory liver stem cells as a delivery vehicle for gene therapy for HCC.
  • [MeSH-major] Carcinoma, Hepatocellular / pathology. Liver / cytology. Liver Neoplasms / pathology. Stem Cells / cytology

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  • (PMID = 16174449.001).
  • [ISSN] 1007-3418
  • [Journal-full-title] Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology
  • [ISO-abbreviation] Zhonghua Gan Zang Bing Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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25. Marrinucci D, Bethel K, Bruce RH, Curry DN, Hsieh B, Humphrey M, Krivacic RT, Kroener J, Kroener L, Ladanyi A, Lazarus NH, Nieva J, Kuhn P: Case study of the morphologic variation of circulating tumor cells. Hum Pathol; 2007 Mar;38(3):514-9
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  • We report a detailed cytomorphologic evaluation of the circulating component of widely metastatic breast carcinoma.
  • Wide local excision revealed a 1.7-cm infiltrating ductal adenocarcinoma, BSR score 7/9 with angiolymphatic invasion, and 4/20 lymph nodes positive for carcinoma.
  • Five years later, a bone marrow biopsy revealed involvement of bone marrow by metastatic breast carcinoma, and shortly thereafter, metastases were identified in the liver and lung hilum.
  • She enrolled in a clinical investigation for the detection of circulating tumor cells (CTCs) in breast carcinoma.
  • In addition, in comparison with her tumor cells in other sites, the full morphologic spectrum of cancer cells present in primary and metastatic tumor is also present in peripheral blood circulation.
  • [MeSH-major] Bone Neoplasms / secondary. Breast Neoplasms / pathology. Carcinoma, Ductal, Breast / pathology. Neoplastic Cells, Circulating / pathology
  • [MeSH-minor] Adult. Cytophotometry. Fatal Outcome. Female. Fiber Optic Technology. Humans. Optical Fibers


26. Granci V, Bibeau F, Kramar A, Boissière-Michot F, Thézénas S, Thirion A, Gongora C, Martineau P, Del Rio M, Ychou M: Prognostic significance of TRAIL-R1 and TRAIL-R3 expression in metastatic colorectal carcinomas. Eur J Cancer; 2008 Oct;44(15):2312-8
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  • Drug resistance is believed to cause treatment failure in patients with metastatic colorectal carcinoma (CRC).
  • Resistance to chemotherapy can involve different processes, including apoptosis, whose extrinsic pathway is regulated by expression of death-inducing TRAIL-R1 and -R2 and inhibitory TRAIL-R3 and -R4 cell surface receptors.
  • We analysed TRAIL-R 1, -2, -3 and -4 expression by immuno-histochemistry in CRC, using tissue micro arrays, and found that concomitant low/medium TRAIL-R1 and high TRAIL-R3 expression in primary CRC is significantly associated with a poor response to 5-FU-based first-line chemotherapy and with shorter progression-free survival.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antimetabolites, Antineoplastic / therapeutic use. Disease Progression. Disease-Free Survival. Female. Fluorouracil / therapeutic use. GPI-Linked Proteins. Humans. Liver Neoplasms / drug therapy. Liver Neoplasms / metabolism. Liver Neoplasms / secondary. Male. Middle Aged. Neoplasm Proteins / metabolism. Prognosis. Treatment Outcome. Tumor Necrosis Factor Decoy Receptors / metabolism

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  • (PMID = 18755584.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Biomarkers, Tumor; 0 / GPI-Linked Proteins; 0 / Neoplasm Proteins; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / TNFRSF10C protein, human; 0 / Tumor Necrosis Factor Decoy Receptors; U3P01618RT / Fluorouracil
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27. Yang MH, Chen CL, Chau GY, Chiou SH, Su CW, Chou TY, Peng WL, Wu JC: Comprehensive analysis of the independent effect of twist and snail in promoting metastasis of hepatocellular carcinoma. Hepatology; 2009 Nov;50(5):1464-74
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  • [Title] Comprehensive analysis of the independent effect of twist and snail in promoting metastasis of hepatocellular carcinoma.
  • In this study we investigated the expression profiles of the EMT markers, the relationship between EMT markers and patient/tumor/viral factors, and the interplay between major EMT regulators in human hepatocellular carcinoma (HCC).
  • Reduced E-cadherin and nonmembranous beta-catenin expression, the hallmarks of EMT, were shown in 60.2% and 51.5% of primary HCC samples, respectively.
  • Overexpression of Snail, Twist, or Slug, the major regulators of EMT, was identified in 56.9%, 43.1%, and 51.4% of primary HCCs, respectively.
  • HCC cell lines with increased Snail and Twist expression (e.g., Mahlavu) exhibited a greater capacity for invasiveness/metastasis than cells with low endogenous Twist/Snail expression (e.g., Huh-7).
  • [MeSH-major] Biomarkers, Tumor / metabolism. Carcinoma, Hepatocellular / pathology. Liver Neoplasms / pathology. Neoplasm Metastasis / pathology. Nuclear Proteins / metabolism. Transcription Factors / metabolism. Twist Transcription Factor / metabolism
  • [MeSH-minor] Adult. Aged. Animals. Cadherins / metabolism. Cell Differentiation / physiology. Cell Line, Tumor. Epithelial Cells / metabolism. Epithelial Cells / pathology. Female. Humans. Male. Mesoderm / metabolism. Mesoderm / pathology. Mice. Mice, Nude. Middle Aged. Retrospective Studies. Transforming Growth Factor beta / metabolism. Transplantation, Heterologous. Vimentin / metabolism. beta Catenin / metabolism. gamma Catenin / metabolism

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  • [CommentIn] Hepatology. 2009 Nov;50(5):1344-6 [19877297.001]
  • (PMID = 19821482.001).
  • [ISSN] 1527-3350
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cadherins; 0 / Nuclear Proteins; 0 / TWIST1 protein, human; 0 / Transcription Factors; 0 / Transforming Growth Factor beta; 0 / Twist Transcription Factor; 0 / Vimentin; 0 / beta Catenin; 0 / gamma Catenin; 0 / snail family transcription factors
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28. Chamuleau RA, Deurholt T, Hoekstra R: Which are the right cells to be used in a bioartificial liver? Metab Brain Dis; 2005 Dec;20(4):327-35
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  • [Title] Which are the right cells to be used in a bioartificial liver?
  • Because of the xenotransplantation-related disadvantages of porcine cells and the shortage of primary human hepatocytes, other sources of bio-components have to be explored.
  • The future lies in the development of one or more human hepatocyte cell lines, which will have minimal immunogenicity, no risk of xeno-zoonosis, and the requested functionality and availability.
  • Primary sources for the development of such human cell lines are liver-tumor-derived cell lines, immortalized fetal or adult hepatocytes, and stem cells of hepatic, hematopoietic, or embryonic origin.
  • At present the most promising results for BAL application have been obtained by immortalization of human fetal liver cells by reconstitution of telomerase activity.
  • However, in all cell types tested so far, the in vitro differentiation cannot be stimulated to such an extent that their functionality reaches that of primary human hepatocytes.
  • [MeSH-major] Liver / cytology. Liver, Artificial
  • [MeSH-minor] Animals. Carcinoma, Hepatocellular / pathology. Cell Line, Tumor. Fetus / cytology. Hematopoietic Stem Cells / physiology. Hepatocytes / physiology. Humans. Stem Cell Transplantation

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  • [Cites] Nature. 2003 Oct 30;425(6961):968-73 [14555960.001]
  • [Cites] Cell Transplant. 2003;12(5):469-73 [12953920.001]
  • [Cites] Hepatology. 1996 Dec;24(6):1446-51 [8938179.001]
  • [Cites] Diabetes. 2004 Jan;53(1):105-12 [14693704.001]
  • [Cites] Surgery. 2002 Aug;132(2):384-90 [12219039.001]
  • [Cites] Fukuoka Igaku Zasshi. 2001 Aug;92(8):299-305 [11586514.001]
  • [Cites] Hepatology. 1989 Mar;9(3):367-72 [2563984.001]
  • [Cites] Int J Artif Organs. 1999 Nov;22(11):769-77 [10612305.001]
  • [Cites] Nat Med. 2004 Jan;10(1):55-63 [14702635.001]
  • [Cites] Science. 2000 Feb 18;287(5456):1258-62 [10678831.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Oct 10;97(21):11307-12 [11027332.001]
  • [Cites] Ann Surg. 2004 May;239(5):660-7; discussion 667-70 [15082970.001]
  • [Cites] Lancet. 2000 Aug 19;356(9230):621-7 [10968434.001]
  • [Cites] Mech Dev. 2003 Jan;120(1):117-30 [12490302.001]
  • [Cites] Gastroenterology. 2004 Apr;126(4):1147-56 [15057753.001]
  • [Cites] Nat Med. 2000 Nov;6(11):1229-34 [11062533.001]
  • [Cites] Int J Artif Organs. 2002 Oct;25(10):1001-5 [12456042.001]
  • [Cites] Liver Transpl. 2001 Jan;7(1):2-10 [11150414.001]
  • [Cites] Nat Med. 2004 Jul;10(7):744-8 [15195088.001]
  • [Cites] Ann Surg. 1994 Jul;220(1):59-67 [8024360.001]
  • [Cites] Hepatology. 2000 Jul;32(1):11-6 [10869283.001]
  • [Cites] J Clin Invest. 2002 May;109(10):1291-302 [12021244.001]
  • [Cites] Ann Surg. 2004 Aug;240(2):216-30 [15273544.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Jan;85(1):160-4 [2893372.001]
  • [Cites] Transplant Proc. 2001 Feb-Mar;33(1-2):1935 [11267578.001]
  • [Cites] Dev Dyn. 2004 Feb;229(2):243-58 [14745950.001]
  • [Cites] Gastroenterology. 2003 Feb;124(2):432-44 [12557149.001]
  • [Cites] ASAIO J. 1993 Jul-Sep;39(3):M242-6 [8268536.001]
  • [Cites] Int J Artif Organs. 1997 Aug;20(8):418-21 [9323503.001]
  • [Cites] Tissue Eng. 2004 Jul-Aug;10(7-8):1113-24 [15363168.001]
  • [Cites] Nature. 2003 Apr 24;422(6934):897-901 [12665832.001]
  • [Cites] Science. 1999 May 14;284(5417):1168-70 [10325227.001]
  • [Cites] J Hepatol. 1997 Jun;26(6):1379-92 [9210627.001]
  • [Cites] Transplant Proc. 1997 Feb-Mar;29(1-2):964-5 [9123610.001]
  • [Cites] Nature. 2000 Jul 20;406(6793):257 [10917519.001]
  • [Cites] Gastroenterology. 2003 Jun;124(7):1891-900 [12806622.001]
  • [Cites] Cell Transplant. 2004;13(3):197-211 [15191158.001]
  • [Cites] Cell Transplant. 2001;10(4-5):429-33 [11549067.001]
  • [Cites] Nat Biotechnol. 2001 Oct;19(10):971-4 [11581665.001]
  • [Cites] Science. 1999 Aug 20;285(5431):1236-41 [10455044.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Mar 19;99(6):3639-44 [11904425.001]
  • [Cites] Int J Artif Organs. 2002 Mar;25(3):182-91 [11999190.001]
  • (PMID = 16382343.001).
  • [ISSN] 0885-7490
  • [Journal-full-title] Metabolic brain disease
  • [ISO-abbreviation] Metab Brain Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 42
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29. Peschel C, Hartmann JT, Schmittel A, Bokemeyer C, Schneller F, Keilholz U, Buchheidt D, Millan S, Izquierdo MA, Hofheinz RD: Phase II study of plitidepsin in pretreated patients with locally advanced or metastatic non-small cell lung cancer. Lung Cancer; 2008 Jun;60(3):374-80
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  • [Title] Phase II study of plitidepsin in pretreated patients with locally advanced or metastatic non-small cell lung cancer.
  • OBJECTIVE: To evaluate the progression-free rate (PFR) at 3 months (13+/-1 weeks), antitumor response, time-to-event efficacy endpoints, and toxicity profile of plitidepsin administered as a 3-h continuous i.v. infusion at a dose of 5mg/m(2), every 2 weeks, to patients with chemotherapy pretreated advanced non-small cell lung cancer (NSCLC).
  • PFR (primary efficacy endpoint) and objective response rate (secondary efficacy endpoint) were evaluated according to RECIST, while the toxic profile of plitidepsin was assessed using the NCI-CTC, version 2.0.
  • One patient was responder for the primary (PFR at 13+/-1 weeks) and secondary efficacy endpoint (stable disease according to RECIST).
  • Other two patients were non-responders for the primary efficacy endpoint, but had stable disease (not confirmed at weeks 13+/-1 due to previous withdrawal due to adverse events).
  • The most common side effects were anemia, and asymptomatic and non-cumulative increases of gamma-glutamyltransferase (GGT) and liver transaminase levels.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / pathology. Depsipeptides / administration & dosage. Lung Neoplasms / drug therapy. Lung Neoplasms / pathology. Urochordata
  • [MeSH-minor] Adult. Aged. Anemia / chemically induced. Animals. Disease Progression. Disease-Free Survival. Female. Humans. Infusions, Intravenous. Male. Middle Aged. Neoplasm Metastasis. Neoplasm Staging. Transaminases / blood. gamma-Glutamyltransferase / blood


30. Shengbing Z, Feng LJ, Bin W, Lingyun G, Aimin H: Expression of KiSS-1 gene and its role in invasion and metastasis of human hepatocellular carcinoma. Anat Rec (Hoboken); 2009 Aug;292(8):1128-34
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  • [Title] Expression of KiSS-1 gene and its role in invasion and metastasis of human hepatocellular carcinoma.
  • KiSS-1 has been identified as a putative metastasis-suppressor gene in human melanomas and breast cancer cell lines.
  • The expression of KiSS-1 protein in HCC and intrahepatic metastasis lesions was significantly lower (P < 0.01) when compared with non-tumor liver tissue and normal liver tissue.
  • Loss of KiSS-1 in intrahepatic metastasis versus primary carcinomas was statistically significant (P<0.01).
  • We conclude that loss of KiSS-1 during HCC metastasis, along with a concomitant upregulation of MMP-9 suggests a possible mechanism for cell motility and invasion during HCC metastasis, with KiSS-1 emerging as a possible therapeutic target during HCC metastasis.
  • [MeSH-major] Biomarkers, Tumor / physiology. Carcinoma, Hepatocellular / metabolism. Liver Neoplasms / metabolism. Tumor Suppressor Proteins / physiology
  • [MeSH-minor] Adult. Aged. Disease Progression. Down-Regulation. Female. Gene Expression. Humans. Kisspeptins. Male. Matrix Metalloproteinase 9 / metabolism. Middle Aged. Neoplasm Invasiveness. Neoplasm Metastasis. Neoplasm Staging. Prognosis

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19645016.001).
  • [ISSN] 1932-8494
  • [Journal-full-title] Anatomical record (Hoboken, N.J. : 2007)
  • [ISO-abbreviation] Anat Rec (Hoboken)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / KISS1 protein, human; 0 / Kisspeptins; 0 / Tumor Suppressor Proteins; EC 3.4.24.35 / Matrix Metalloproteinase 9
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31. Chahal P, Baron TH, Poterucha JJ, Rosen CB: Endoscopic retrograde cholangiography in post-orthotopic liver transplant population with Roux-en-Y biliary reconstruction. Liver Transpl; 2007 Aug;13(8):1168-73
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  • [Title] Endoscopic retrograde cholangiography in post-orthotopic liver transplant population with Roux-en-Y biliary reconstruction.
  • Its effectiveness in post-orthotopic liver transplantation (OLT) patients with Roux-en-Y biliary reconstruction has not been reported.
  • The indication for liver transplant was end-stage liver disease or occurrence of cholangiocarcinoma from primary sclerosing cholangitis in 28 patients and a case each of chronic hepatitis C, alcoholic liver disease, and metastatic islet cell carcinoma.
  • ERC indications were both diagnostic and therapeutic and included the following: evaluation of increased liver biochemistries and fever in 12 patients, dilation of anastomotic biliary strictures in 10 patients, removal of fractured biliary tube or retained biliary stent in 6 patients, and in 1 patient each, biliary stone removal, management of bile leak, and jejunal tube extension placement for nutritional purpose.
  • [MeSH-major] Anastomosis, Roux-en-Y / methods. Biliary Tract Diseases / surgery. Biliary Tract Diseases / therapy. Biliary Tract Surgical Procedures / methods. Cholangiography / methods. Endoscopy / methods. Liver Transplantation / methods. Reconstructive Surgical Procedures
  • [MeSH-minor] Adolescent. Adult. Aged. Bile Duct Diseases / surgery. Bile Duct Diseases / therapy. Child. Child, Preschool. Female. Humans. Infant. Male. Middle Aged

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  • [Copyright] Copyright (c) 2007 AASLD.
  • (PMID = 17663414.001).
  • [ISSN] 1527-6465
  • [Journal-full-title] Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society
  • [ISO-abbreviation] Liver Transpl.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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32. Galetta D, Giotta F, Rosati G, Gebbia V, Manzione L, Di Bisceglie M, Borsellino N, Colucci G: Carboplatin in combination with raltitrexed in recurrent and metastatic head and neck squamous cell carcinoma: A multicentre phase II study of the Gruppo Oncologico Dell'Italia Meridionale (G.O.I.M.). Anticancer Res; 2005 Nov-Dec;25(6C):4445-9
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  • [Title] Carboplatin in combination with raltitrexed in recurrent and metastatic head and neck squamous cell carcinoma: A multicentre phase II study of the Gruppo Oncologico Dell'Italia Meridionale (G.O.I.M.).
  • BACKGROUND: The combination of cisplatin (CDDP) and 5-Fluorouracil (5-FU) is a standard regimen for the treatment of recurrent and metastatic head and neck squamous cell carcinoma (HNSCC).
  • Patients had to be >18 years old with ECOG PS of 0-2 and adequate bone marrow, renal and liver functions.
  • The oral cavity/oropharynx were the primary site in 20 patients and the larynx in 10 patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Squamous Cell / drug therapy. Head and Neck Neoplasms / drug therapy. Neoplasm Recurrence, Local / drug therapy
  • [MeSH-minor] Adult. Aged. Carboplatin / administration & dosage. Carboplatin / adverse effects. Female. Humans. Male. Middle Aged. Quinazolines / administration & dosage. Quinazolines / adverse effects. Survival Rate. Thiophenes / administration & dosage. Thiophenes / adverse effects

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  • (PMID = 16334124.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Quinazolines; 0 / Thiophenes; BG3F62OND5 / Carboplatin; FCB9EGG971 / raltitrexed
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33. Dong-Dong L: Up-regulation expression of MLC1 in human liver cancer tissue and enhanced SMMC7721 cell tumorigenesis in vivo and vitro. Hepatogastroenterology; 2005 Jul-Aug;52(64):1186-90
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  • [Title] Up-regulation expression of MLC1 in human liver cancer tissue and enhanced SMMC7721 cell tumorigenesis in vivo and vitro.
  • BACKGROUND/AIMS: We screened a novel gene MLC1 in human liver cancer tissue by differential display, and its cDNA full-length is 1600bp.
  • The purpose of this study is to find expression of MLC1 gene in human liver cancer tissue and the affect to SMMC7721 cell tumorigenesis in vivo and vitro.
  • METHODOLOGY: 250 cases of primary HCC tissue samples were studied for MLC1 mRNA and protein expression using RT-PCR, western blot, immunohistochemistry, MLC1 stable transfection into SMMC771, and SMMC7721 cells growth curve was analyzed by MTT method and SMMC7721 cells tumorigenesis in vivo.
  • CONCLUSIONS: MLC1 gene showed up-regulation expression at both the mRNA and protein levels in HCC tissues and that MLC1 plays an important role in the growth of hepatoma cell SMMC7721 in vitro and vivo.
  • [MeSH-major] Carcinoma, Hepatocellular / etiology. Carcinoma, Hepatocellular / metabolism. Liver Neoplasms / etiology. Liver Neoplasms / metabolism. Membrane Proteins / metabolism
  • [MeSH-minor] Adult. Animals. Cell Culture Techniques. Cell Line, Tumor. Female. Humans. Male. Mice. Mice, Inbred BALB C. Middle Aged. RNA, Messenger / metabolism. Transfection. Up-Regulation

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  • (PMID = 16001658.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / MLC1 protein, human; 0 / Membrane Proteins; 0 / Mlc1 protein, mouse; 0 / RNA, Messenger
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34. Ceafalan L, Vidulescu C, Radu E, Regalia T, Popescu I, Pana M, Serghei L, Voiculescu B, Popescu LM: [Expression of stem cell markers on fetal and tumoral human liver cells in primary culture]. Rev Med Chir Soc Med Nat Iasi; 2005 Jan-Mar;109(1):96-104
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  • [Title] [Expression of stem cell markers on fetal and tumoral human liver cells in primary culture].
  • We have identified populations expressing these markers in both fetal and tumoral human liver by flow cytometry, using monoclonal antibodies against CD90, CD117, CD34, and HLA-DR.
  • In tumoral liver CD117+/CD90+ cells were found in decreasing number from the neoplastic (2.48 +/- 0.67) and peritumoral region (0.88 +/- 0.12) to the area of para-tumoral (normal) parenchyma (0.13 +/- 0.04).
  • Using the same markers on fetal liver cells we have also identified small populations of CD117+/CD90+ cells (0.28 +/- 0.07%) and CD117+/CD34+ cells (1.13 +/- 0.24%), presumably resident stem cells or hematopoietic stem cells.
  • Immunomagnetic negative separation was then performed on fetal liver cells using monoclonal antibodies against specific markers of hematopoietic lineages such as CD3, 14, 16, 19, 22, and CD56 to eliminate this population.
  • Isolation using appropriate markers and initiation of primary cultures is a first step to the therapeutic use of fetal stem cells and for the study of adult liver stem cells involvement in carcinogenesis.
  • [MeSH-major] Biomarkers / analysis. Biomarkers, Tumor / analysis. Carcinoma, Hepatocellular / immunology. Fetus. Hepatocytes / immunology. Liver Neoplasms / immunology. Stem Cells
  • [MeSH-minor] Adult. Antigens, CD34 / analysis. Antigens, Thy-1 / analysis. Flow Cytometry. HLA-DR Antigens / analysis. Humans. Immunomagnetic Separation. Microscopy, Fluorescence. Proto-Oncogene Proteins c-kit / analysis. Stem Cell Transplantation / methods

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  • (PMID = 16607835.001).
  • [ISSN] 0048-7848
  • [Journal-full-title] Revista medico-chirurgicală̆ a Societă̆ţ̜ii de Medici ş̧i Naturaliş̧ti din Iaş̧i
  • [ISO-abbreviation] Rev Med Chir Soc Med Nat Iasi
  • [Language] rum
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Antigens, Thy-1; 0 / Biomarkers; 0 / Biomarkers, Tumor; 0 / HLA-DR Antigens; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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35. Kunimura T, Yoshida T, Sugiyama T, Morohoshi T: The Relationships Between Loss of Standard CD44 Expression and Lymph Node, Liver Metastasis in T3 Colorectal Carcinoma. J Gastrointest Cancer; 2009;40(3-4):115-8
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  • [Title] The Relationships Between Loss of Standard CD44 Expression and Lymph Node, Liver Metastasis in T3 Colorectal Carcinoma.
  • MATERIALS AND METHODS: CD44s expression was measured on immunohistochemistry in tumors from 65 patients with primary colorectal carcinomas.
  • However, the CD44s expression showed significantly adverse relationship with lymph node metastasis (p < 0.05) and liver metastasis (p < 0.01), respectively.
  • CONCLUSION: The loss of CD44s expression in cancer cells in the deepest invaded area is a good marker for predicting potential metastasis to lymph nodes and liver in T3 CRC.
  • [MeSH-major] Antigens, CD44 / biosynthesis. Carcinoma / metabolism. Carcinoma / secondary. Colorectal Neoplasms / metabolism. Colorectal Neoplasms / pathology. Liver Neoplasms / secondary
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Female. Humans. Immunohistochemistry. Lymphatic Metastasis / pathology. Male. Middle Aged. Neoplasm Staging

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  • [Cites] Scand J Gastroenterol. 1998 Mar;33(3):301-9 [9548625.001]
  • [Cites] Dis Colon Rectum. 2000 Sep;43(9):1250-4; discussion 1254-5 [11005492.001]
  • [Cites] J Cell Biol. 1993 Jan;120(1):227-33 [8416989.001]
  • [Cites] Cancer Res. 1994 Jul 15;54(14):3922-8 [7518345.001]
  • [Cites] Pathol Int. 2009 Apr;59(4):241-6 [19351367.001]
  • [Cites] Cell. 1991 Apr 5;65(1):13-24 [1707342.001]
  • [Cites] Cancer Invest. 2004;22(6):878-85 [15641486.001]
  • [Cites] Mol Pathol. 1998 Aug;51(4):191-200 [9893744.001]
  • [Cites] Arch Pathol Lab Med. 2000 Feb;124(2):212-5 [10656728.001]
  • [Cites] Cell. 1989 Mar 24;56(6):1057-62 [2466575.001]
  • [Cites] Histopathology. 2005 Jan;46(1):24-30 [15656882.001]
  • [Cites] Oral Oncol. 2000 Nov;36(6):545-9 [11036249.001]
  • [Cites] J Craniofac Surg. 2002 Jan;13(1):85-9 [11887001.001]
  • [Cites] Am J Pathol. 1996 Oct;149(4):1147-55 [8863664.001]
  • (PMID = 19937401.001).
  • [ISSN] 1941-6636
  • [Journal-full-title] Journal of gastrointestinal cancer
  • [ISO-abbreviation] J Gastrointest Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / Biomarkers, Tumor
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36. Liu ZZ, Huang WY, Lin JS, Li XS, Lan X, Cai XK, Liang KH, Zhou HJ: Cell survival curve for primary hepatic carcinoma cells and relationship between SF(2) of hepatic carcinoma cells and radiosensitivity. World J Gastroenterol; 2005 Nov 28;11(44):7040-3
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  • [Title] Cell survival curve for primary hepatic carcinoma cells and relationship between SF(2) of hepatic carcinoma cells and radiosensitivity.
  • AIM: To establish the cell survival curve for primary hepatic carcinoma cells and to study the relationship between SF(2) of primary hepatic carcinoma cells and radiosensitivity.
  • METHODS: Hepatic carcinoma cells were cultured in vitro using 39 samples of hepatic carcinoma at stages II-IV.
  • After these cells were radiated with different dosages, the cell survival ratio and SF(2) were calculated by clonogenic assay and SF(2) model respectively.
  • After X-ray radiation of the fifth generation cells with 0, 2, 4, 6, 8 Gy, the cell survival rate was 41%, 36.5%, 31.0%, 26.8%, and 19%, respectively.
  • There was a negative correlation between cell survival and irradiation dosage (r = -0.973, P<0.05).
  • SF(2) ranged 0.28-0.78 and correlated with the clinical stage and pathological grade of hepatic carcinoma (P<0.05).
  • CONCLUSION: SF(2) correlates with the clinical stage and pathological grade of hepatic carcinoma and is a marker for predicting the radiosensitivity of hepatic carcinomas.
  • [MeSH-major] Carcinoma, Hepatocellular / pathology. Carcinoma, Hepatocellular / radiotherapy. Cell Survival. Liver Neoplasms / pathology. Liver Neoplasms / radiotherapy. Radiation Tolerance
  • [MeSH-minor] Adult. Aged. Animals. Cell Culture Techniques. Dose-Response Relationship, Radiation. Humans. Middle Aged. Neoplasm Staging. Tumor Cells, Cultured

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  • (PMID = 16437614.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Other-IDs] NLM/ PMC4717052
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37. Staehler MD, Kruse J, Haseke N, Stadler T, Roosen A, Karl A, Stief CG, Jauch KW, Bruns CJ: Liver resection for metastatic disease prolongs survival in renal cell carcinoma: 12-year results from a retrospective comparative analysis. World J Urol; 2010 Aug;28(4):543-7
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  • [Title] Liver resection for metastatic disease prolongs survival in renal cell carcinoma: 12-year results from a retrospective comparative analysis.
  • The value of surgical resection of renal cell carcinoma (RCC) liver metastases still remains unclear.
  • OBJECTIVE: Of our study was to evaluate the efficacy of liver resection by comparing patients who could have undergone metastasectomy due to limited disease, but refused surgery.
  • MATERIALS AND METHODS: Eighty-eight patients were identified with liver metastases and indication of surgery between 1995 and 2006.
  • In 68 patients, liver resection was performed, 20 patients denied surgery and served as comparison group.
  • Median amount of liver metastases was 2 (range 1-30).
  • Low-grade primary RCC had a MS of 155 (95% CI 123-187) months compared to 29 (95% CI 8-50) months without resection (P = 0.0036).
  • CONCLUSIONS: Liver metastasectomy is an independent valuable tool in the treatment of metastatic RCC and significantly prolongs patient's survival, even if further systemic treatment is necessary.
  • With the evidence given, patients may benefit from liver metastasis resection if technically feasible.
  • [MeSH-major] Carcinoma, Renal Cell. Kidney Neoplasms / mortality. Kidney Neoplasms / pathology. Liver / surgery. Liver Neoplasms
  • [MeSH-minor] Adolescent. Adult. Aged. Databases, Factual. Female. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Proportional Hazards Models. Retrospective Studies. Young Adult


38. Luo DL, Liu YH, Zhuang HG, Luo XL: [Tumors showing perivascular epithelioid cell differentiation: a clinicopathologic study of 39 cases]. Zhonghua Yi Xue Za Zhi; 2007 Nov 6;87(41):2909-13
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  • [Title] [Tumors showing perivascular epithelioid cell differentiation: a clinicopathologic study of 39 cases].
  • OBJECTIVE: To investigate the clinicopathologic features of tumors showing perivascular epithelioid cell differentiation (PEComas).
  • METHODS: The clinicopathologic data of 39 cases pf angiomyolipoma (AML), 17 males and 22 females, with the primary focus in the kidney on 30 cases, in the liver in 4 cases, in the lung, uterus and broad ligament, abdominal wall, retroperitoneum, and nasal cavity in 1 case respectively, were analyzed.
  • RESULTS: Pathological examination showed branched capillaries or arterioles, often thick-walled similar to those in the renal cell carcinoma, and the cancerous cells consisting of the mixture of epithelial cells and spindle cells.
  • [MeSH-minor] Adult. Aged. Antigens, CD34 / analysis. Cell Differentiation. Desmin / analysis. Female. Humans. Immunohistochemistry. Keratins / analysis. Liver Neoplasms / metabolism. Liver Neoplasms / pathology. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Male. Middle Aged. Nose Neoplasms / metabolism. Nose Neoplasms / pathology. Proto-Oncogene Proteins c-kit / analysis. Retrospective Studies. S100 Proteins / analysis. Vimentin / analysis

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  • (PMID = 18261305.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Desmin; 0 / S100 Proteins; 0 / Vimentin; 68238-35-7 / Keratins; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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39. Mudali SV, Fu B, Lakkur SS, Luo M, Embuscado EE, Iacobuzio-Donahue CA: Patterns of EphA2 protein expression in primary and metastatic pancreatic carcinoma and correlation with genetic status. Clin Exp Metastasis; 2006;23(7-8):357-65
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  • [Title] Patterns of EphA2 protein expression in primary and metastatic pancreatic carcinoma and correlation with genetic status.
  • EphA2 is a transmembrane receptor tyrosine kinase that functions in the regulation of cell growth, survival, angiogenesis, and migration and EphA2 targeting has been proposed as a novel therapeutic strategy for neoplasms that overexpress this protein.
  • EphA2 overexpression has been correlated with increased invasive and metastatic ability in pancreatic cancer cell lines.
  • We collected clinicopathologic data and paraffin-embedded materials from 98 patients with primary and/or metastatic pancreatic cancer and performed immunohistochemical labeling for EphA2 protein.
  • When evaluated specifically for labeling intensity, primary and metastatic carcinomas were more strongly positive compared to benign ducts and PanIN lesions (P < 0.00001 and P < 0.01, respectively) and poorly differentiated carcinomas were more strongly positive for EphA2 than well and moderately differentiated tumors (P < 0.005).
  • When primary carcinomas without metastatic disease were specifically compared to carcinomas with associated metastatic disease, the advanced carcinomas showed relatively less strong positive labeling for EphA2 (P < 0.008).
  • Moreover, decreased EphA2 labeling was more commonly found in liver (P < 0.002), lung (P < 0.004) or peritoneal metastases (P < 0.01) as compared to distant lymph node metastases (P < 0.01).

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  • [Cites] Am J Physiol. 1997 Oct;273(4 Pt 1):G824-32 [9357823.001]
  • [Cites] Cell Growth Differ. 1999 Sep;10(9):629-38 [10511313.001]
  • [Cites] Cancer Gene Ther. 2004 Nov;11(11):757-66 [15359289.001]
  • [Cites] Clin Cancer Res. 2005 Jan 1;11(1):226-31 [15671550.001]
  • [Cites] Oncogene. 2005 Apr 14;24(16):2684-94 [15829979.001]
  • [Cites] Anticancer Res. 2005 Jul-Aug;25(4):2943-50 [16080548.001]
  • [Cites] Cancer Biol Ther. 2005 May;4(5):548-54 [15846069.001]
  • [Cites] Cancer Genet Cytogenet. 2005 Oct 1;162(1):63-7 [16157202.001]
  • [Cites] J Biol Chem. 2005 Oct 7;280(40):34008-18 [16051609.001]
  • [Cites] Neoplasia. 2005 Aug;7(8):717-22 [16207473.001]
  • [Cites] Gynecol Oncol. 2005 Nov;99(2):278-86 [16061279.001]
  • [Cites] Adv Surg. 2005;39:223-44 [16250554.001]
  • [Cites] Mol Cancer Res. 2005 Oct;3(10):541-51 [16254188.001]
  • [Cites] FASEB J. 2005 Nov;19(13):1884-6 [16166198.001]
  • [Cites] Oncogene. 2005 Nov 24;24(53):7859-68 [16103880.001]
  • [Cites] J Biol Chem. 2005 Dec 23;280(51):42375-82 [16236711.001]
  • [Cites] Clin Cancer Res. 2006 Jan 15;12(2):353-60 [16428472.001]
  • [Cites] CA Cancer J Clin. 2006 Mar-Apr;56(2):106-30 [16514137.001]
  • [Cites] Oncogene. 2000 Nov 20;19(49):5614-9 [11114742.001]
  • [Cites] Oncol Rep. 2001 Jan-Feb;8(1):89-92 [11115575.001]
  • [Cites] Cancer Res. 2001 Mar 1;61(5):1833-8 [11280733.001]
  • [Cites] Cancer Res. 2001 Mar 1;61(5):2301-6 [11280802.001]
  • [Cites] Virchows Arch. 2001 Dec;439(6):798-802 [11787853.001]
  • [Cites] Cancer Res. 2002 Feb 1;62(3):819-26 [11830538.001]
  • [Cites] Cancer Res. 2002 May 15;62(10):2840-7 [12019162.001]
  • [Cites] J Biol Chem. 2002 Oct 18;277(42):39274-9 [12167657.001]
  • [Cites] Oncogene. 2002 Oct 31;21(50):7690-9 [12400011.001]
  • [Cites] Mol Cancer Res. 2002 Nov;1(1):79-87 [12496371.001]
  • [Cites] Clin Cancer Res. 2003 Feb;9(2):613-8 [12576426.001]
  • [Cites] Am J Pathol. 2003 Apr;162(4):1037-42 [12651595.001]
  • [Cites] Science. 2003 May 9;300(5621):949 [12738854.001]
  • [Cites] Oncol Rep. 2004 Mar;11(3):605-11 [14767510.001]
  • [Cites] Oncogene. 2004 Feb 19;23(7):1448-56 [14973554.001]
  • [Cites] Clin Chem. 2004 Mar;50(3):490-9 [14726470.001]
  • [Cites] Am J Clin Pathol. 2004 Feb;121(2):226-30 [14983936.001]
  • [Cites] J Cell Sci. 2004 Apr 15;117(Pt 10):2037-49 [15054110.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Aug 6;320(4):1096-102 [15249202.001]
  • [Cites] Clin Cancer Res. 2004 Aug 1;10(15):5145-50 [15297418.001]
  • [Cites] Gynecol Oncol. 2004 Aug;94(2):312-9 [15297167.001]
  • [Cites] Nat Genet. 2004 Sep;36(9):979-83 [15300251.001]
  • [Cites] Mol Cell Biol. 1990 Dec;10(12):6316-24 [2174105.001]
  • [Cites] Cancer. 1992 Apr 1;69(7):1674-81 [1551052.001]
  • [Cites] Science. 1994 Nov 4;266(5186):816-9 [7973638.001]
  • [Cites] Science. 1995 Apr 28;268(5210):567-9 [7536959.001]
  • [Cites] Cancer Res. 1995 Jun 1;55(11):2394-9 [7757992.001]
  • (PMID = 17146615.001).
  • [ISSN] 0262-0898
  • [Journal-full-title] Clinical & experimental metastasis
  • [ISO-abbreviation] Clin. Exp. Metastasis
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA106610-04; United States / NCI NIH HHS / CA / P50 CA062924; United States / NCI NIH HHS / CA / CA62924; United States / NCI NIH HHS / CA / K08 CA106610-04; United States / NCI NIH HHS / CA / CA106610; United States / NCI NIH HHS / CA / K08 CA106610
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, EphA2
  • [Other-IDs] NLM/ NIHMS147177; NLM/ PMC2755224
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40. Leyvraz S, Pampallona S, Martinelli G, Ploner F, Perey L, Aversa S, Peters S, Brunsvig P, Montes A, Lange A, Yilmaz U, Rosti G, Solid Tumors Working Party of the European Group for Blood and Marrow Transplantation: A threefold dose intensity treatment with ifosfamide, carboplatin, and etoposide for patients with small cell lung cancer: a randomized trial. J Natl Cancer Inst; 2008 Apr 16;100(8):533-41
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  • [Title] A threefold dose intensity treatment with ifosfamide, carboplatin, and etoposide for patients with small cell lung cancer: a randomized trial.
  • A randomized trial was performed to test the impact of such dose intensification on the long-term survival of patients with small cell lung cancer (SCLC).
  • The primary outcome was 3-year survival.
  • Comparisons between response rates and toxic effects within subgroups (limited or extensive disease, liver metastases or no liver metastases, Eastern Cooperative Oncology Group performance status of 0 or 1, normal or abnormal lactate dehydrogenase levels) were also performed.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Small Cell / drug therapy. Lung Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents, Alkylating / administration & dosage. Antineoplastic Agents, Alkylating / adverse effects. Antineoplastic Agents, Phytogenic / administration & dosage. Antineoplastic Agents, Phytogenic / adverse effects. Carboplatin / administration & dosage. Carboplatin / adverse effects. Dose-Response Relationship, Drug. Drug Administration Schedule. Etoposide / administration & dosage. Etoposide / adverse effects. Female. Hematologic Diseases / chemically induced. Humans. Ifosfamide / administration & dosage. Ifosfamide / adverse effects. Incidence. Male. Middle Aged. Odds Ratio. Prognosis. Research Design. Survival Analysis. Treatment Outcome

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  • [CommentIn] J Natl Cancer Inst. 2009 Jan 7;101(1):67; author reply 67-8 [19116385.001]
  • [CommentIn] J Natl Cancer Inst. 2008 Apr 16;100(8):520-1 [18398099.001]
  • (PMID = 18398095.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase III; Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Antineoplastic Agents, Phytogenic; 6PLQ3CP4P3 / Etoposide; BG3F62OND5 / Carboplatin; UM20QQM95Y / Ifosfamide
  • [Investigator] Aversa S; Brunsvig P; Buxhofer V; Crown J; De Bock R; Demirer T; Kühr T; Lange A; Leyvraz S; Martinelli G; Montes A; Piazza E; Ploner F; Rosti G; Rudolf C; Schneider CP; van Klaveren R; Yilmaz U; Parmar M; Thatcher N; Hansen H
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41. Zoller H, McFarlane I, Theurl I, Stadlmann S, Nemeth E, Oxley D, Ganz T, Halsall DJ, Cox TM, Vogel W: Primary iron overload with inappropriate hepcidin expression in V162del ferroportin disease. Hepatology; 2005 Aug;42(2):466-72
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  • [Title] Primary iron overload with inappropriate hepcidin expression in V162del ferroportin disease.
  • In the index case, the disorder is characterized by abundant deposition of hemosiderin in all tissues investigated (mesenteric lymph node, liver, gastric and duodenal mucosa, and also in squamous cell carcinoma of the lung).
  • Despite a significant burden of iron, no features of chronic liver disease were found in affected members of the family, including individuals aged up to 80 years.
  • In conclusion, the systemic iron burden in ferroportin disease is not a sufficient cause for chronic liver disease.
  • In patients with most, but not all, ferroportin mutations, retention of iron in macrophages of the liver and other organs may protect against damage to parenchymal cells.
  • [MeSH-minor] Adolescent. Adult. Aged. Ferritins / blood. Hepcidins. Humans. Liver / pathology. Male. Middle Aged

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  • (PMID = 15986403.001).
  • [ISSN] 0270-9139
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimicrobial Cationic Peptides; 0 / Cation Transport Proteins; 0 / HAMP protein, human; 0 / Hepcidins; 0 / Protein Precursors; 0 / metal transporting protein 1; 9007-73-2 / Ferritins
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42. Lee YC, Pan HW, Peng SY, Lai PL, Kuo WS, Ou YH, Hsu HC: Overexpression of tumour-associated trypsin inhibitor (TATI) enhances tumour growth and is associated with portal vein invasion, early recurrence and a stage-independent prognostic factor of hepatocellular carcinoma. Eur J Cancer; 2007 Mar;43(4):736-44
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  • [Title] Overexpression of tumour-associated trypsin inhibitor (TATI) enhances tumour growth and is associated with portal vein invasion, early recurrence and a stage-independent prognostic factor of hepatocellular carcinoma.
  • Tumour-associated trypsin inhibitor (TATI) overexpresses in various tumours, but its clinicopathological significance in hepatocellular carcinoma (HCC) is unclear.
  • By RT-PCR in the linear range, TATI was found to be overexpressed in 176 of 258 unifocal primary HCCs (68%).
  • Ectopic expression of TATI led to enhanced anchorage-independent tumour cell growth in vitro.
  • We conclude that TATI overexpression contributes to cell growth advantage, enhances the metastatic potential of tumours and leads to advanced HCC with PV invasion.
  • [MeSH-major] Carcinoma, Hepatocellular / metabolism. Liver Neoplasms / metabolism. Neoplasm Proteins / metabolism. Portal Vein. Trypsin Inhibitor, Kazal Pancreatic / metabolism
  • [MeSH-minor] Adult. Aged. Disease Progression. Female. HeLa Cells / metabolism. Humans. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Recurrence, Local / metabolism. Neoplasm Recurrence, Local / pathology. Osteopontin / metabolism. Prognosis. Survival Analysis. alpha-Fetoproteins / metabolism

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  • (PMID = 17267202.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / alpha-Fetoproteins; 106441-73-0 / Osteopontin; 50936-63-5 / Trypsin Inhibitor, Kazal Pancreatic
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43. Lao XM, Zhang YQ, Jin X, Lin XJ, Guo RP, Li GH, Li JQ: Primary clear cell carcinoma of liver--clinicopathologic features and surgical results of 18 cases. Hepatogastroenterology; 2006 Jan-Feb;53(67):128-32
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  • [Title] Primary clear cell carcinoma of liver--clinicopathologic features and surgical results of 18 cases.
  • BACKGROUND/AIMS: Primary clear cell carcinoma of the liver (PCCCL) is a subgroup of hepatocellular carcinoma.
  • The differentiation degree ranged from grade 1 to 3, liver cirrhosis or/and chronic hepatitis was present in paratumorous tissues.
  • The clinical characteristics of the PCCCL are similar to those of conventional hepatocellular carcinoma.
  • [MeSH-major] Carcinoma, Hepatocellular / pathology. Carcinoma, Hepatocellular / surgery. Liver Neoplasms / pathology. Liver Neoplasms / surgery
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Humans. Male. Middle Aged

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  • (PMID = 16506391.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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44. Rubie C, Frick VO, Pfeil S, Wagner M, Kollmar O, Kopp B, Graber S, Rau BM, Schilling MK: Correlation of IL-8 with induction, progression and metastatic potential of colorectal cancer. World J Gastroenterol; 2007 Oct 7;13(37):4996-5002
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  • AIM: To investigate the expression profile of IL-8 in inflammatory and malignant colorectal diseases to evaluate its potential role in the regulation of colorectal cancer (CRC) and the development of colorectal liver metastases (CRLM).
  • METHODS: IL-8 expression was assessed by quantitative real-time PCR (Q-RT-PCR) and the enzyme-linked immunosorbent assay (ELISA) in resected specimens from patients with ulcerative colitis (UC, n = 6) colorectal adenomas (CRA, n = 8), different stages of colorectal cancer (n = 48) as well as synchronous and metachronous CRLM along with their corresponding primary colorectal tumors (n = 16).
  • Most interestingly, IL-8 up-regulation was most enhanced in synchronous and metachronous CRLM, if compared with the corresponding primary CRC tissues.
  • CONCLUSION: Our results strongly suggest an association between IL-8 expression, induction and progression of colorectal carcinoma and the development of colorectal liver metastases.
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / metabolism. Disease Progression. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Neoplasm Metastasis. Neoplasm Staging

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  • (PMID = 17854143.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Interleukin-8
  • [Other-IDs] NLM/ PMC4434624
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45. Agarwal R, Levinson AW, Schowinsky J, Su LM: Large mixed epithelial and stromal tumor of the kidney masquerading as metastatic renal cell carcinoma. Urology; 2007 Nov;70(5):1008.e17-9
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  • [Title] Large mixed epithelial and stromal tumor of the kidney masquerading as metastatic renal cell carcinoma.
  • We report the case of a 39-year-old woman with a large right renal mass 20 cm in size with heterogeneous solid and cystic components as well as concurrent liver lesions suspicious for metastatic renal cell carcinoma.
  • Surgical extirpation of the renal mass and liver lesions was performed laparoscopically with the pathological analysis revealing a rare renal neoplasm--mixed epithelial and stromal tumor of the kidney--and adenomas of the liver.
  • [MeSH-major] Carcinoma, Renal Cell / pathology. Kidney Neoplasms / pathology. Liver Neoplasms / pathology. Neoplasms, Multiple Primary / pathology
  • [MeSH-minor] Adult. Diagnosis, Differential. Female. Humans


46. Mancini V, Battaglia M, Lucarelli G, Di Lorenzo V, Ditonno P, Bettocchi C, Selvaggi FP: Unusual solitary metastasis of the ciliary body in renal cell carcinoma. Int J Urol; 2008 Apr;15(4):363-5
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  • [Title] Unusual solitary metastasis of the ciliary body in renal cell carcinoma.
  • Renal cell carcinoma (RCC) usually metastasizes to the lung, liver, bone; ocular metastasis is uncommon.
  • Ocular metastasis of RCC is rare, can appear years after treating the primary tumor and should not be excluded in RCC follow-up.
  • [MeSH-major] Carcinoma, Renal Cell / secondary. Ciliary Body / pathology. Kidney Neoplasms / pathology. Uveal Neoplasms / secondary
  • [MeSH-minor] Adult. Humans. Male

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  • (PMID = 18380830.001).
  • [ISSN] 1442-2042
  • [Journal-full-title] International journal of urology : official journal of the Japanese Urological Association
  • [ISO-abbreviation] Int. J. Urol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
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47. Turato C, Ruvoletto MG, Biasiolo A, Quarta S, Tono N, Bernardinello E, Beneduce L, Fassina G, Cavalletto L, Chemello L, Merkel C, Gatta A, Pontisso P: Squamous cell carcinoma antigen-1 (SERPINB3) polymorphism in chronic liver disease. Dig Liver Dis; 2009 Mar;41(3):212-6
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  • [Title] Squamous cell carcinoma antigen-1 (SERPINB3) polymorphism in chronic liver disease.
  • BACKGROUND: The serpin squamous cell carcinoma antigen (SCCA, SERPINB3) has been found over-expressed in primary liver cancer and at lower extent in cirrhosis and chronic hepatitis.
  • AIM: To explore SCCA-1 polymorphism in patients with HCV infection as single etiologic factor and different extent of liver disease.
  • CONCLUSIONS: The newly identified SCCA-PD variant was more frequently found in liver cirrhosis, suggesting that patients carrying this polymorphism are more prone to develop progressive liver fibrosis.
  • [MeSH-major] Antigens, Neoplasm / genetics. Liver Diseases / genetics. Polymorphism, Restriction Fragment Length. Serpins / genetics
  • [MeSH-minor] Adult. Case-Control Studies. Chronic Disease. Female. Humans. Immunoglobulin M / blood. Male. Middle Aged

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  • (PMID = 18657489.001).
  • [ISSN] 1878-3562
  • [Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
  • [ISO-abbreviation] Dig Liver Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Immunoglobulin M; 0 / Serpins; 0 / squamous cell carcinoma-related antigen
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48. Ward SC, Huang J, Tickoo SK, Thung SN, Ladanyi M, Klimstra DS: Fibrolamellar carcinoma of the liver exhibits immunohistochemical evidence of both hepatocyte and bile duct differentiation. Mod Pathol; 2010 Sep;23(9):1180-90
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  • [Title] Fibrolamellar carcinoma of the liver exhibits immunohistochemical evidence of both hepatocyte and bile duct differentiation.
  • Fibrolamellar carcinoma is a rare malignant primary liver neoplasm with characteristic histological features that typically arises in young patients without viral hepatitis or cirrhosis.
  • In contrast to classical hepatocellular carcinoma, individual cases of fibrolamellar carcinoma have been reported to express cytokeratin 7.
  • In addition, ultrastructural and serological studies have suggested that fibrolamellar carcinoma may show neuroendocrine differentiation.
  • The cellular differentiation of fibrolamellar carcinoma has not been studied and little is reported about its immunohistochemical profile.
  • We studied 26 cases of fibrolamellar carcinoma and 62 cases of classical hepatocellular carcinoma by immunohistochemistry for HepPar1, glypican-3, pCEA, CD10, alpha-fetoprotein, cytokeratin 20, neuroendocrine markers, and surrogate markers for biliary differentiation (cytokeratin 7, cytokeratin 19, epithelial membrane antigen, EpCAM, mCEA, B72.3, and CA19.9).
  • Tumor cells of fibrolamellar carcinoma and hepatocellular carcinoma showed positive signals for albumin mRNA by in situ hybridization in all cases.
  • Both tumor types stained uniformly positively with HepPar1 and most showed a canalicular staining pattern for pCEA, confirming their hepatocellular differentiation.
  • In addition, 39% of hepatocellular carcinoma cases and 59% of fibrolamellar carcinoma cases were positive for glypican-3.
  • All 22 fibrolamellar carcinoma cases tested showed positive staining for cytokeratin 7 and epithelial membrane antigen, whereas less than one-third of hepatocellular carcinoma cases were positive for these markers (P<0.0001).
  • Further, 36% of fibrolamellar carcinoma cases showed staining for B72.3, cytokeratin 19, EpCAM, or mCEA.
  • Therefore, cytokeratin 7 and epithelial membrane antigen may be useful to differentiate between fibrolamellar carcinoma and hepatocellular carcinoma.
  • On the basis of immunohistochemistry, fibrolamellar carcinoma seems to show both hepatocellular and bile duct differentiation.
  • [MeSH-major] Bile Ducts / pathology. Hepatocytes / pathology. Liver Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Carcinoma, Hepatocellular / metabolism. Carcinoma, Hepatocellular / pathology. Cell Differentiation. Female. Humans. Immunohistochemistry. In Situ Hybridization. Male. Middle Aged. Tissue Array Analysis

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  • (PMID = 20495535.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; Fibrolamellar hepatocellular carcinoma
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49. Bex A, Van der Veldt AA, Blank C, Meijerink MR, Boven E, Haanen JB: Progression of a caval vein thrombus in two patients with primary renal cell carcinoma on pretreatment with sunitinib. Acta Oncol; 2010 May;49(4):520-3
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  • [Title] Progression of a caval vein thrombus in two patients with primary renal cell carcinoma on pretreatment with sunitinib.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Carcinoma, Renal Cell / complications. Carcinoma, Renal Cell / drug therapy. Indoles / therapeutic use. Kidney Neoplasms / complications. Kidney Neoplasms / drug therapy. Neoadjuvant Therapy / methods. Nephrectomy. Pyrroles / therapeutic use. Vena Cava, Inferior. Venous Thrombosis / etiology
  • [MeSH-minor] Adult. Bone Neoplasms / secondary. Disease Progression. Fatal Outcome. Humans. Liver Neoplasms / secondary. Middle Aged. Time Factors. Tomography, X-Ray Computed

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  • (PMID = 20105087.001).
  • [ISSN] 1651-226X
  • [Journal-full-title] Acta oncologica (Stockholm, Sweden)
  • [ISO-abbreviation] Acta Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Indoles; 0 / Pyrroles; 0 / sunitinib
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50. Pawlik TM, Gleisner AL, Bauer TW, Adams RB, Reddy SK, Clary BM, Martin RC, Scoggins CR, Tanabe KK, Michaelson JS, Kooby DA, Staley CA, Schulick RD, Vauthey JN, Abdalla EK, Curley SA, Choti MA, Elias D: Liver-directed surgery for metastatic squamous cell carcinoma to the liver: results of a multi-center analysis. Ann Surg Oncol; 2007 Oct;14(10):2807-16
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  • [Title] Liver-directed surgery for metastatic squamous cell carcinoma to the liver: results of a multi-center analysis.
  • BACKGROUND: The role of hepatic resection for metastatic squamous cell carcinoma (SCC) remains unknown.
  • The current study evaluates the role of hepatic resection in patients with metastatic SCC to the liver.
  • RESULTS: Primary SCC site was anal (n = 27), head/neck (n = 12), lung (n = 4), esophagus (n = 2), and other (n = 7).
  • Treatment of primary SCC was chemotherapy +/- radiotherapy alone (n = 29), chemotherapy +/- radiotherapy + surgery (n = 15), or surgery alone (n = 8).
  • Factors associated with reduced DFS were liver tumor size > 5 cm (hazard ratio (HR) = 2.02) and positive surgical margin (HR = 2.33).
  • Long-term survival, however, can be achieved following surgical resection of SCC liver metastasis, especially in patients who present with limited metachronous disease amenable to margin negative resection.
  • [MeSH-major] Anus Neoplasms / surgery. Carcinoma, Squamous Cell / secondary. Electrocoagulation. Esophageal Neoplasms / surgery. Head and Neck Neoplasms / surgery. Hepatectomy. Liver Neoplasms / secondary. Lung Neoplasms / surgery
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Combined Modality Therapy. Disease-Free Survival. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Recurrence, Local / mortality. Prognosis. Retreatment. United States


51. Thanapprapasr D, Nartthanarung A, Likittanasombut P, Na Ayudhya NI, Charakorn C, Udomsubpayakul U, Subhadarbandhu T, Wilailak S: Bone metastasis in cervical cancer patients over a 10-year period. Int J Gynecol Cancer; 2010 Apr;20(3):373-8
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  • Bone is the third most common site of distant metastasis after the lungs and liver.
  • Most patients had squamous cell carcinoma (80.48%) and received radiation therapy alone as their primary treatment (58.53%).
  • Common sites were the bone beyond the radiation field of their primary treatment.
  • [MeSH-major] Adenocarcinoma / secondary. Bone Neoplasms / secondary. Carcinoma, Adenosquamous / secondary. Carcinoma, Small Cell / secondary. Carcinoma, Squamous Cell / secondary. Uterine Cervical Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Female. Humans. Incidence. Middle Aged. Neoplasm Staging. Prognosis. Survival Rate. Time Factors


52. Wakasa T, Wakasa K, Shutou T, Hai S, Kubo S, Hirohashi K, Umeshita K, Monden M: A histopathological study on combined hepatocellular and cholangiocarcinoma: cholangiocarcinoma component is originated from hepatocellular carcinoma. Hepatogastroenterology; 2007 Mar;54(74):508-13
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  • [Title] A histopathological study on combined hepatocellular and cholangiocarcinoma: cholangiocarcinoma component is originated from hepatocellular carcinoma.
  • BACKGROUND/AIMS: Combined hepatocellular and cholangiocarcinoma of the liver is relatively infrequent, and its pathogenesis remains obscure.
  • METHODOLOGY: In this study, we investigated the histopathological features, Ki-67 labeling index, and p53 immunohistochemistry of 18 surgically resected cases of combined hepatocellular and cholangiocarcinoma among 1102 consecutive cases of surgically resected primary liver cancers.
  • Microscopically, we classified the cases into the following three categories according to the arrangement of the hepatocellular carcinoma and cholangiocarcinoma components;.
  • (1) Type I in which hepatocellular carcinoma and cholangiocarcinoma formed nodules that could easily be distinguished from each other, (2) Type II in which the both components were finely mixed, so that the two components were almost indistinguishable, and (3) Type III in which the tumors had lobular structures with hepatocellular carcinomas existing centrally and cholangiocarcinomas existing peripherally.
  • In one case of type I, well differentiated hepatocellular carcinoma demonstrated cholangiocarcinoma in "nodules-in-nodules" fashion.
  • The average of Ki-67 labeling index of hepatocellular carcinoma component of combined hepatocellular and cholangiocarcinoma was 4.4 +/- 3.4% and the index of cholangiocarcinoma component was 11.0 +/- 8.5%, which is significantly higher than that of the hepatocellular carcinoma component.
  • In one case, the cholangiocarcinoma component was positive for p53, but the hepatocellular carcinoma component was negative.
  • In the other 4 cases, both the hepatocellular carcinoma and cholangiocarcinoma components were positive.
  • Metaplasia of hepatocellular carcinoma to intrahepatic cholangiocarcinoma is assumed to be one of the pathogenic pathways of combined hepatocellular and cholangiocarcinoma.
  • [MeSH-major] Bile Duct Neoplasms / pathology. Bile Ducts, Intrahepatic / pathology. Carcinoma, Hepatocellular / pathology. Cholangiocarcinoma / pathology. Liver Neoplasms / pathology. Neoplasms, Multiple Primary / pathology
  • [MeSH-minor] Adult. Aged. Cell Division / physiology. Cell Transformation, Neoplastic / pathology. Female. Hepatitis B, Chronic / pathology. Hepatitis C, Chronic / pathology. Humans. Immunoenzyme Techniques. Ki-67 Antigen / analysis. Liver / pathology. Male. Metaplasia. Middle Aged. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 17523309.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
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53. Yin S, Li J, Hu C, Chen X, Yao M, Yan M, Jiang G, Ge C, Xie H, Wan D, Yang S, Zheng S, Gu J: CD133 positive hepatocellular carcinoma cells possess high capacity for tumorigenicity. Int J Cancer; 2007 Apr 1;120(7):1444-50
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  • [Title] CD133 positive hepatocellular carcinoma cells possess high capacity for tumorigenicity.
  • Recently increasing reported data have suggested that only a small subset of cancer cells possess capability to initiate malignancies including leukemia and solid tumors, which was based on investigation in these cells displaying a distinct surface marker pattern within the primary cancers.
  • CD133 is a putative hematopoietic and neuronal stem-cell marker, which was also considered as a tumorigenic marker in brain and prostate cancer.
  • We hypothesized that CD133 was a marker closely correlated with tumorigenicity, since it was reported that CD133 expressed in human fetal liver and repairing liver tissues, which tightly associated with hepatocarcinogenesis.
  • Our findings showed that a small population of CD133 positive cells indeed exists in human hepatocellular carcinoma (HCC) cell lines and primary HCC tissues.
  • From SMMC-7721 cell line, CD133+ cells isolated by MACS manifested high tumorigenecity and clonogenicity as compared with CD133- HCC cells.
  • [MeSH-major] Antigens, CD / metabolism. Carcinoma, Hepatocellular / metabolism. Glycoproteins / metabolism. Liver Neoplasms / metabolism. Peptides / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Animals. Biomarkers, Tumor / metabolism. Female. Humans. Immunoenzyme Techniques. Liver Cirrhosis / metabolism. Male. Mice. Mice, Congenic. Mice, Inbred NOD. Mice, SCID. Middle Aged. Neoplasm Proteins / metabolism. Tumor Cells, Cultured

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 17205516.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Biomarkers, Tumor; 0 / Glycoproteins; 0 / Neoplasm Proteins; 0 / Peptides
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54. Guillouzo A, Corlu A, Aninat C, Glaise D, Morel F, Guguen-Guillouzo C: The human hepatoma HepaRG cells: a highly differentiated model for studies of liver metabolism and toxicity of xenobiotics. Chem Biol Interact; 2007 May 20;168(1):66-73
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  • [Title] The human hepatoma HepaRG cells: a highly differentiated model for studies of liver metabolism and toxicity of xenobiotics.
  • Although they have several important limitations primary human hepatocytes still represent the in vitro gold standard model for xenobiotic metabolism and toxicity studies.
  • The large use of human liver cell lines either from tumoral origin or obtained by oncogenic immortalisation is prevented by the loss of various liver-specific functions, especially many cytochrome P450 (CYP)-related enzyme activities.
  • We review here recent results obtained with a new human hepatoma cell line, named HepaRG, derived from a human hepatocellular carcinoma.
  • Moreover contrary to other human hepatoma cell lines including HepG2 cells, HepaRG cells express various CYPs (CYP1A2, 2B6, 2C9, 2E1, 3A4) and the nuclear receptors constitutive androstane receptor (CAR) and pregnane X receptor (PXR) at levels comparable to those found in cultured primary human hepatocytes.
  • They also express various other functions such phase 2 enzymes, apical and canalicular ABC transporters and basolateral solute carrier transporters, albumin, haptoglobin as well as aldolase B that is a specific marker of adult hepatocytes.
  • HepaRG cells could represent a surrogate to primary human hepatocytes for xenobiotic metabolism and toxicity studies and even more, a unique model system for analysing genotoxic compounds.
  • [MeSH-major] Carcinoma, Hepatocellular / metabolism. Liver Neoplasms / metabolism. Models, Biological. Xenobiotics / toxicity
  • [MeSH-minor] Aflatoxin B1 / poisoning. Biomarkers / metabolism. Cell Differentiation. Cell Line, Tumor. Cytochrome P-450 Enzyme System / genetics. Cytochrome P-450 Enzyme System / metabolism. Female. Hepatocytes / cytology. Hepatocytes / drug effects. Hepatocytes / metabolism. Humans. Inhibitory Concentration 50. Metabolic Detoxication, Phase I. Metabolic Detoxication, Phase II. RNA, Messenger / analysis. Receptors, Cytoplasmic and Nuclear / genetics. Receptors, Cytoplasmic and Nuclear / metabolism. Receptors, Steroid / genetics. Receptors, Steroid / metabolism. Transcription Factors / genetics. Transcription Factors / metabolism

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  • (PMID = 17241619.001).
  • [ISSN] 0009-2797
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Biomarkers; 0 / RNA, Messenger; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Steroid; 0 / Transcription Factors; 0 / Xenobiotics; 0 / constitutive androstane receptor; 0 / pregnane X receptor; 9035-51-2 / Cytochrome P-450 Enzyme System; 9N2N2Y55MH / Aflatoxin B1
  • [Number-of-references] 23
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55. Wang ZP, Liu YT, Yang J: [Classification and regression tree analysis of 154 patients with cancer of unknown primary]. Zhonghua Zhong Liu Za Zhi; 2010 Sep;32(9):690-3
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  • [Title] [Classification and regression tree analysis of 154 patients with cancer of unknown primary].
  • OBJECTIVE: To explore the prognostic factors and their impact on survival of patients with cancer of unknown primary (CUP).
  • [MeSH-major] Adenocarcinoma / secondary. Bone Neoplasms / secondary. Neoplasms, Unknown Primary / classification
  • [MeSH-minor] Adult. Aged. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / secondary. Female. Follow-Up Studies. Humans. Liver Neoplasms / secondary. Lymphatic Metastasis. Male. Middle Aged. Multivariate Analysis. Regression Analysis. Survival Rate

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  • (PMID = 21122385.001).
  • [ISSN] 0253-3766
  • [Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]
  • [ISO-abbreviation] Zhonghua Zhong Liu Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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56. Paret C, Hildebrand D, Weitz J, Kopp-Schneider A, Kuhn A, Beer A, Hautmann R, Zöller M: C4.4A as a candidate marker in the diagnosis of colorectal cancer. Br J Cancer; 2007 Oct 22;97(8):1146-56
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  • In addition, tumour cell lines released C4.4A by vesicle shedding and proteolytic cleavage.
  • C4.4A was expressed in over 80% of primary colorectal cancer and liver metastasis with negligible expression in adjacent colonic mucosa, inflamed colonic tissue and liver.
  • C4.4A expression was only observed in about 50% of pancreatic cancer and renal cell carcinoma.
  • [MeSH-major] Biomarkers, Tumor / analysis. Cell Adhesion Molecules / metabolism. Colorectal Neoplasms / diagnosis. Colorectal Neoplasms / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Blotting, Western. Cell Line, Tumor. Female. Flow Cytometry. GPI-Linked Proteins. Humans. Immunohistochemistry. Immunoprecipitation. Male. Middle Aged. Neoplasm Staging

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  • [Cites] Eur J Biochem. 1992 Sep 1;208(2):397-404 [1325906.001]
  • [Cites] Int J Cancer. 1993 Feb 20;53(4):651-6 [8436439.001]
  • [Cites] FEBS Lett. 1994 Aug 1;349(2):163-8 [8050560.001]
  • [Cites] J Biol Chem. 1994 Aug 19;269(33):20807-10 [8063692.001]
  • [Cites] J Biol Chem. 1994 Dec 23;269(51):32380-8 [7528215.001]
  • [Cites] Cancer. 1995 Jun 15;75(12):2818-26 [7773932.001]
  • [Cites] Clin Exp Metastasis. 1995 Jul;13(4):277-86 [7606890.001]
  • [Cites] Cell Growth Differ. 1996 May;7(5):663-78 [8732676.001]
  • [Cites] Eur J Cancer. 1997 May;33(6):867-72 [9291807.001]
  • [Cites] Clin Chem. 1997 Oct;43(10):1868-76 [9342006.001]
  • [Cites] J Natl Cancer Inst. 1998 Jan 21;90(2):118-23 [9450571.001]
  • [Cites] Cancer Res. 1998 May 1;58(9):1843-9 [9581823.001]
  • [Cites] J Cancer Res Clin Oncol. 1999 Aug-Sep;125(8-9):461-74 [10480338.001]
  • [Cites] Eur J Biochem. 1999 Sep;264(2):281-6 [10491072.001]
  • [Cites] J Cell Biol. 1999 Oct 4;147(1):89-104 [10508858.001]
  • [Cites] Thromb Haemost. 2005 Feb;93(2):192-8 [15711732.001]
  • [Cites] Clin Cancer Res. 2005 Apr 15;11(8):2840-52 [15837731.001]
  • [Cites] Int J Cancer. 2005 Jul 10;115(5):724-33 [15729693.001]
  • [Cites] Oncol Rep. 2005 Sep;14(3):777-82 [16077991.001]
  • [Cites] Anticancer Res. 2005 Jul-Aug;25(4):3117-21 [16080575.001]
  • [Cites] Clin Exp Metastasis. 2005;22(1):11-24 [16132574.001]
  • [Cites] Int J Cancer. 2006 May 1;118(9):2210-9 [16331622.001]
  • [Cites] Int J Cancer. 2007 Apr 1;120(7):1511-7 [17192896.001]
  • [Cites] Int J Cancer. 2007 May 15;120(10):2135-47 [17278103.001]
  • [Cites] Am J Physiol Lung Cell Mol Physiol. 2007 May;292(5):L1263-72 [17237151.001]
  • [Cites] Mol Cancer Res. 2007 Jun;5(6):553-67 [17579117.001]
  • [Cites] Cancer Res. 2000 May 15;60(10):2584-8 [10825125.001]
  • [Cites] FEBS Lett. 2000 Jun 9;475(1):52-6 [10854857.001]
  • [Cites] Cancer Res. 2001 Jan 1;61(1):400-5 [11196194.001]
  • [Cites] Gene. 2001 Jan 10;262(1-2):35-41 [11179665.001]
  • [Cites] J Invest Dermatol. 2001 Feb;116(2):344-7 [11180013.001]
  • [Cites] Cancer Res. 2001 Feb 15;61(4):1678-85 [11245483.001]
  • [Cites] J Biol Chem. 2002 Aug 2;277(31):27982-90 [12034711.001]
  • [Cites] Br J Cancer. 2003 Feb 24;88(4):579-85 [12592373.001]
  • [Cites] Cancer. 2003 Apr 15;97(8):1849-58 [12673710.001]
  • [Cites] Mod Pathol. 2003 May;16(5):491-504 [12748256.001]
  • [Cites] Cancer Biol Ther. 2003 Jul-Aug;2(4):320-6 [14508099.001]
  • [Cites] Exp Dermatol. 2003 Oct;12(5):537-45 [14705793.001]
  • [Cites] Cancer Metastasis Rev. 2004 Jan-Jun;23(1-2):77-99 [15000151.001]
  • [Cites] Biochem J. 2004 Jun 15;380(Pt 3):845-57 [15012588.001]
  • [Cites] Br J Cancer. 1978 Jan;37(1):61-6 [619957.001]
  • [Cites] Cancer Res. 1981 Feb;41(2):405-9 [7448785.001]
  • [Cites] Cancer Res. 1987 Jun 1;47(11):2883-91 [3552208.001]
  • [Cites] J Cell Biol. 1988 Mar;106(3):761-71 [2450098.001]
  • [Cites] Cancer Res. 1989 Mar 1;49(5):1294-9 [2917359.001]
  • [Cites] Hybridoma. 1989 Aug;8(4):481-91 [2777278.001]
  • [Cites] Dev Biol (N Y 1985). 1986;3:33-57 [3077969.001]
  • [Cites] Blood. 1991 Jul 15;78(2):264-76 [2070064.001]
  • [Cites] Oncogene. 1998 Oct 15;17(15):1989-2002 [9788443.001]
  • [Cites] Electrophoresis. 1999 Feb;20(2):362-71 [10197444.001]
  • [Cites] Prostate. 1999 May;39(2):123-9 [10221568.001]
  • [Cites] J Natl Cancer Inst. 1999 May 19;91(10):869-74 [10340907.001]
  • [Cites] EMBO J. 1999 Jun 1;18(11):3013-23 [10357814.001]
  • [Cites] Int J Oncol. 1999 Jul;15(1):143-8 [10375607.001]
  • [Cites] J Cell Physiol. 1999 Aug;180(2):225-35 [10395292.001]
  • (PMID = 17912244.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cell Adhesion Molecules; 0 / GPI-Linked Proteins; 0 / LYPD3 protein, human
  • [Other-IDs] NLM/ PMC2360445
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57. Mucha K, Foroncewicz B, Zieniewicz K, Nyckowski P, Krawczyk M, Cyganek A, Paczek L: Patient with liver epithelioid hemangioendothelioma treated by transplantation: 3 years' observation. Transplant Proc; 2006 Jan-Feb;38(1):231-3
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  • [Title] Patient with liver epithelioid hemangioendothelioma treated by transplantation: 3 years' observation.
  • Epithelioid hemangioendothelioma (EHE) is a rare neoplasm of vascular origin, but unknown etiology that occurs in the liver, lungs and other organs.
  • Surgical resection or liver transplantation (OLT) has been recommended after diagnosis.
  • We present a 30-year-old woman with primary HEHE of the liver treated by OLT in 2002.
  • Her medical history started 3 years prior when an abdominal ultrasound examination revealed multiple focal changes in the liver.
  • The histopathological diagnosis from a needle biopsy was carcinoma cholangiogenes desmoplasticum.
  • After 3 years observation the patient presented with good liver function and no signs of tumor recurrence.
  • We concluded that immunohistochemical staining for characteristic endothelial cell markers may facilitate the correct diagnosis of HEHE.
  • [MeSH-major] Hemangioendothelioma, Epithelioid / surgery. Liver Neoplasms / surgery. Liver Transplantation / methods
  • [MeSH-minor] Adult. Female. Follow-Up Studies. Humans. Treatment Outcome


58. Cho S, Lee JH, Cho SB, Yoon KW, Park SY, Lee WS, Park CH, Joo YE, Kim HS, Choi SK, Rew JS: Epigenetic methylation and expression of caspase 8 and survivin in hepatocellular carcinoma. Pathol Int; 2010 Mar;60(3):203-11
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  • [Title] Epigenetic methylation and expression of caspase 8 and survivin in hepatocellular carcinoma.
  • Caspase 8 and survivin are known as key molecules of apoptosis in hepatocellular carcinoma (HCC).
  • Promoter methylation of the caspase 8 and survivin gene was analyzed in 73 primary HCC using methylation-specific polymerase chain reaction.
  • [MeSH-major] Carcinoma, Hepatocellular / genetics. Caspase 8 / genetics. DNA Methylation / genetics. Liver Neoplasms / genetics. Microtubule-Associated Proteins / genetics
  • [MeSH-minor] Adult. Aged. Analysis of Variance. Apoptosis / genetics. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Cell Count. Cell Proliferation. Chi-Square Distribution. Epigenesis, Genetic / genetics. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Inhibitor of Apoptosis Proteins. Male. Middle Aged. Prognosis. Promoter Regions, Genetic / genetics

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  • (PMID = 20403046.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; EC 3.4.22.- / Caspase 8
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59. Lin GH, Wang J, Li SH, Wang J, Xu L, Li SP: Relationship and clinical significance of TGF-beta1 expression with Treg cell infiltration in hepatocellular carcinoma. Chin J Cancer; 2010 Apr;29(4):403-7
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  • [Title] Relationship and clinical significance of TGF-beta1 expression with Treg cell infiltration in hepatocellular carcinoma.
  • BACKGROUND AND OBJECTIVE: There are few studies about origins of regulatory T (Treg) cells increased in primary hepatocellular carcinoma (HCC) tissue.
  • Studies showed that Treg cells could be induced by transforming growth factor-beta1 (TGF-beta1), but the relation between TGF-beta1 expression and Treg cell infiltration is unclear in HCC tissue.
  • METHODS: Envision immunohistochemistry was used to detect the expression of TGF-beta1 and Foxp3 in 102 specimens of HCC tissue and paired adjacent non-tumor liver tissue.
  • Average Foxp3+ cell density in HCC was 2.98 cells/HP, but there was very few or no expression of Foxp3 in adjacent non-tumor liver tissue.
  • TGF-beta1 and Foxp3 expression had no correlations with tumor diameter, tumor capsule, liver cirrhosis, and so on.
  • The 5-year survival rate was not different between HCC tissues with high and low TGF-beta1 expression (P = 0.790); however, it was significantly lower in HCC tissues with high Treg cell infiltration than in those low infiltration (25% vs. 44%, P = 0.007).
  • [MeSH-major] Carcinoma, Hepatocellular. Liver Neoplasms. T-Lymphocytes, Regulatory / pathology. Transforming Growth Factor beta1 / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Follow-Up Studies. Forkhead Transcription Factors / metabolism. Humans. Lymphocyte Count. Male. Middle Aged. Neoplasm Invasiveness. Proportional Hazards Models. Survival Rate. Young Adult. alpha-Fetoproteins / metabolism

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  • (PMID = 20346216.001).
  • [ISSN] 1000-467X
  • [Journal-full-title] Chinese journal of cancer
  • [ISO-abbreviation] Chin J Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Transforming Growth Factor beta1; 0 / alpha-Fetoproteins
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60. Alexopoulou A, Koskinas J, Deutsch M, Delladetsima J, Kountouras D, Dourakis SP: Acute liver failure as the initial manifestation of hepatic infiltration by a solid tumor: report of 5 cases and review of the literature. Tumori; 2006 Jul-Aug;92(4):354-7
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  • [Title] Acute liver failure as the initial manifestation of hepatic infiltration by a solid tumor: report of 5 cases and review of the literature.
  • BACKGROUND: Acute liver failure is a rare complication of metastatic liver disease with a high mortality.
  • Recognition of malignant infiltration of the liver as the cause of acute liver failure could be a diagnostic challenge.
  • PATIENTS: The medical files of 5 patients with acute liver failure due to metastatic liver disease collected over a 4-year period (1997-2000) in our department were reviewed.
  • Liver imaging studies in 2 of the 5 patients were nondiagnostic and the malignant liver infiltration was confirmed postmortem.
  • Liver histology in all cases showed massive tumoral infiltration of the hepatic sinusoids with diffuse replacement of hepatocytes.
  • The primary tumors were colon, gastric, small cell lung, pancreas and cancer of unknown origin.
  • CONCLUSIONS: Malignant infiltration of the liver should be taken into account in the differential diagnosis of rapidly progressive liver failure.
  • Although effective chemotherapy has improved the survival of patients with metastatic liver disease, there has been no change in the course and outcome of acute liver failure due to malignant infiltration of the liver over the last 2 decades.
  • A proper diagnosis by liver biopsy is mandatory to prevent such patients from being considered for liver transplant.
  • [MeSH-major] Adenocarcinoma / secondary. Carcinoma, Small Cell / secondary. Liver Failure, Acute / etiology. Liver Neoplasms / complications. Liver Neoplasms / secondary
  • [MeSH-minor] Adult. Aged, 80 and over. Biopsy. Female. Hepatic Encephalopathy / etiology. Humans. Jaundice / etiology. Liver Function Tests. Lung Neoplasms / pathology. Male. Medical Records. Middle Aged. Retrospective Studies

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  • (PMID = 17036530.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 23
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61. Bergmann F, Wandschneider F, Sipos B, Moldenhauer G, Schniewind B, Welsch T, Schirrmacher P, Klöppel G, Altevogt P, Schäfer H, Sebens Müerköster S: Elevated L1CAM expression in precursor lesions and primary and metastastic tissues of pancreatic ductal adenocarcinoma. Oncol Rep; 2010 Oct;24(4):909-15
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  • [Title] Elevated L1CAM expression in precursor lesions and primary and metastastic tissues of pancreatic ductal adenocarcinoma.
  • Recently, we identified L1CAM expression in pancreatic ductal adenocarcinoma (PDAC) cells accounting for chemoresistance and increased cell migration.
  • L1CAM expression was determined by immunohistochemistry in tissues of 123 patients including tissues of 110 primary PDACs, 15 lymph node metastases and 14 liver metastases.
  • The immunohistochemical analyses revealed L1CAM expression in 92.7% of primary PDACs, 80% of lymph node metastases and 100% of liver metastases.
  • Furthermore, its broad expression in primary tumors as well as in metastases of PDAC patients provide a rationale to further explore the value of L1CAM as a therapeutic target in the treatment of this highly malignant tumor.
  • [MeSH-major] Carcinoma in Situ / metabolism. Carcinoma, Pancreatic Ductal / metabolism. Neural Cell Adhesion Molecule L1 / biosynthesis. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Metastasis / pathology. Neoplasm Staging. Prognosis

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  • (PMID = 20811670.001).
  • [ISSN] 1791-2431
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neural Cell Adhesion Molecule L1
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62. Kim J, Hong SJ, Lim EK, Yu YS, Kim SW, Roh JH, Do IG, Joh JW, Kim DS: Expression of nicotinamide N-methyltransferase in hepatocellular carcinoma is associated with poor prognosis. J Exp Clin Cancer Res; 2009;28:20
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  • [Title] Expression of nicotinamide N-methyltransferase in hepatocellular carcinoma is associated with poor prognosis.
  • BACKGROUND: Hepatocellular carcinoma (HCC) is the most common tumor in the adult liver, with high relapse and mortality rates despite diverse treatment modalities.
  • METHODS: Frozen tumors and non-cancerous surrounding tissues from 120 patients with primary HCC were studied.
  • [MeSH-major] Carcinoma, Hepatocellular / enzymology. Liver Neoplasms / enzymology. Nicotinamide N-Methyltransferase / biosynthesis
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / biosynthesis. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Cohort Studies. Disease-Free Survival. Female. Gene Expression. Humans. Male. Middle Aged. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate. Young Adult

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  • [Cites] Jpn J Cancer Res. 1991 Nov;82(11):1277-83 [1836457.001]
  • [Cites] Clin Chim Acta. 1990 Jan 31;186(3):359-74 [2311261.001]
  • [Cites] J Biol Chem. 1994 May 20;269(20):14835-40 [8182091.001]
  • [Cites] J Hepatol. 1994 Jan;20(1):138-42 [8201215.001]
  • [Cites] Cancer. 1954 May;7(3):462-503 [13160935.001]
  • [Cites] Oncol Res. 2004;14(10):491-9 [15559763.001]
  • [Cites] Mol Endocrinol. 2005 Feb;19(2):527-39 [15486044.001]
  • [Cites] J Pathol. 2005 Feb;205(3):377-87 [15682440.001]
  • [Cites] Toxicol Pathol. 2005;33(1):175-80 [15805069.001]
  • [Cites] Semin Liver Dis. 2005;25(2):212-25 [15918149.001]
  • [Cites] Clin Cancer Res. 2005 Sep 15;11(18):6550-7 [16166432.001]
  • [Cites] J Urol. 2006 Nov;176(5):2248-54 [17070307.001]
  • [Cites] Exp Mol Med. 2006 Oct 31;38(5):455-65 [17079861.001]
  • [Cites] BMC Bioinformatics. 2007;8:66 [17326819.001]
  • [Cites] J Cancer Res Clin Oncol. 2008 May;134(5):551-9 [17922140.001]
  • [Cites] Clin Cancer Res. 2008 Aug 1;14(15):4814-20 [18676753.001]
  • [Cites] N Engl J Med. 2008 Nov 6;359(19):1995-2004 [18923165.001]
  • [Cites] Oncogene. 2008 Nov 6;27(52):6679-89 [18724390.001]
  • [Cites] Cancer Res. 2008 Nov 15;68(22):9167-75 [19010888.001]
  • [Cites] Physiol Genomics. 2001 Feb 7;5(1):21-33 [11161003.001]
  • [Cites] Cancer Res. 2001 Mar 1;61(5):2129-37 [11280777.001]
  • [Cites] Oncogene. 2001 Jul 27;20(33):4568-75 [11494152.001]
  • [Cites] J Neuropathol Exp Neurol. 2002 Feb;61(2):111-24 [11853016.001]
  • [Cites] Hepatology. 2002 May;35(5):1237-46 [11981774.001]
  • [Cites] Cancer Res. 2002 Jul 15;62(14):3939-44 [12124323.001]
  • [Cites] Nat Genet. 2002 Aug;31(4):339-46 [12149612.001]
  • [Cites] Genome Biol. 2002 Jun 18;3(7):RESEARCH0034 [12184808.001]
  • [Cites] J Hepatol. 2003;38 Suppl 1:S136-49 [12591191.001]
  • [Cites] Neurosci Lett. 2003 May 15;342(1-2):13-6 [12727306.001]
  • [Cites] Curr Mol Med. 2003 Sep;3(6):573-88 [14527088.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Oct;88(10):4990-6 [14557485.001]
  • [Cites] Cancer Cell. 2004 Aug;6(2):129-37 [15324696.001]
  • [Cites] Gastroenterology. 2004 Nov;127(5 Suppl 1):S5-S16 [15508102.001]
  • [Cites] Gastroenterology. 2004 Nov;127(5 Suppl 1):S51-5 [15508103.001]
  • [Cites] Gastroenterology. 1981 Oct;81(4):668-75 [7262512.001]
  • [Cites] Hepatology. 1988 Jan-Feb;8(1):65-8 [3338721.001]
  • [Cites] Arch Biochem Biophys. 1988 Feb 1;260(2):601-8 [2963591.001]
  • [Cites] Tumour Biol. 1994;15(1):7-16 [8146531.001]
  • (PMID = 19216803.001).
  • [ISSN] 1756-9966
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; EC 2.1.1.1 / NNMT protein, human; EC 2.1.1.1 / Nicotinamide N-Methyltransferase
  • [Other-IDs] NLM/ PMC2657806
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63. Basile J, Caldwell S, Nolan N, Hammerle C: Clear cell hepatocellular carcinoma arising 25 years after the successful treatment of an infantile hepatoblastoma. Ann Hepatol; 2010 Oct-Dec;9(4):465-7
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  • [Title] Clear cell hepatocellular carcinoma arising 25 years after the successful treatment of an infantile hepatoblastoma.
  • Primary liver tumors in children are rare with hepatoblastoma (HB) being the most common malignancy.
  • Clear cell carcinoma, a variant of hepatocellular carcinoma (HCC), is another rare tumor of the liver that tends to affect adults.
  • We describe the diagnosis and management of the only known documented case of a primary clear cell HCC arising twenty-five years after the patient was successfully treated with chemotherapy and surgical resection for a malignant HB as an infant.
  • Further knowledge of liver tumorigenesis will help elucidate the complicated genetic, molecular, and environmental factors involved in the development of these two rare hepatic malignancies.
  • [MeSH-major] Carcinoma, Hepatocellular / diagnosis. Hepatoblastoma / drug therapy. Hepatoblastoma / surgery. Liver Neoplasms / diagnosis
  • [MeSH-minor] Adult. Biopsy. Combined Modality Therapy. Genetic Predisposition to Disease / genetics. Humans. Magnetic Resonance Imaging. Male. Time Factors. Treatment Outcome

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  • (PMID = 21057168.001).
  • [ISSN] 1665-2681
  • [Journal-full-title] Annals of hepatology
  • [ISO-abbreviation] Ann Hepatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Mexico
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64. Kou T, Marusawa H, Kinoshita K, Endo Y, Okazaki IM, Ueda Y, Kodama Y, Haga H, Ikai I, Chiba T: Expression of activation-induced cytidine deaminase in human hepatocytes during hepatocarcinogenesis. Int J Cancer; 2007 Feb 1;120(3):469-76
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  • Activation-induced cytidine deaminase (AID) plays a role as a genome mutator in activated B cells, and inappropriate expression of AID has been implicated in the immunopathological phenotype of human B-cell malignancies.
  • Notably, we found that the transgenic mice overexpressing AID developed lung adenocarcinoma and hepatocellular carcinoma (HCC), suggesting that ectopic expression of AID can lead to tumorigenesis in epithelial tissues as well.
  • To examine the involvement of AID in the development of human HCC, we analyzed the AID expression and its correlation with mutation frequencies of the p53 gene in liver tissues from 51 patients who underwent resection of primary HCCs.
  • Only trace amounts of AID transcripts were detected in the normal liver; however, endogenous AID was significantly upregulated in both HCC and surrounding noncancerous liver tissues with underlying chronic hepatitis or liver cirrhosis (p < 0.05).
  • Most liver tissues with underlying chronic inflammation with endogenous AID upregulation already contained multiple genetic changes in the p53 gene.
  • In both hepatoma cell lines and cultured human primary hepatocytes, the expression of AID was substantially induced by TGF-beta stimulation.
  • Our findings suggest that the aberrant expression of AID is observed in human hepatocytes with several pathological settings, including chronic liver disease and HCC, which might enhance the genetic susceptibility to mutagenesis leading to hepatocarcinogenesis.
  • [MeSH-major] Carcinoma, Hepatocellular / genetics. Cytidine Deaminase / genetics. Hepatocytes / metabolism. Liver Neoplasms / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Amino Acid Sequence. Base Sequence. Cell Line, Tumor. Cells, Cultured. Enzyme Activation. Female. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Hepatitis, Viral, Human / physiopathology. Humans. Immunoblotting. Male. Middle Aged. Mutation / genetics. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Transforming Growth Factor beta / pharmacology. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 17066440.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Transforming Growth Factor beta; 0 / Tumor Suppressor Protein p53; EC 3.5.4.5 / Cytidine Deaminase
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65. Chang Q, Zhang Y, Beezhold KJ, Bhatia D, Zhao H, Chen J, Castranova V, Shi X, Chen F: Sustained JNK1 activation is associated with altered histone H3 methylations in human liver cancer. J Hepatol; 2009 Feb;50(2):323-33
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  • [Title] Sustained JNK1 activation is associated with altered histone H3 methylations in human liver cancer.
  • BACKGROUND/AIMS: Aberrant c-Jun N-terminal kinase (JNK) activation has been linked to hepatocellular carcinoma (HCC) in mouse models.
  • METHODS: The JNK activation, global gene expression, and the status of histone H3 methylations were measured in 31 primary human hepatocellular carcinoma (HCC) samples paired with the adjacent non-cancerous (ANC) tissues.
  • In addition, an association of JNK1 activation with the histone H3 lysines 4 and 9 tri-methylation was observed in the HCC tissues, which leads to an elevated expression of genes regulating cell growth and a decreased expression of the genes for cell differentiation and the p450 family members in HCC.

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  • (PMID = 19041150.001).
  • [ISSN] 0168-8278
  • [Journal-full-title] Journal of hepatology
  • [ISO-abbreviation] J. Hepatol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 5R01CA116697; United States / NCI NIH HHS / CA / R01 CA119028; United States / NCI NIH HHS / CA / R01 CA116697; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / 5R01CA119028
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Histones; 0 / Transcription Factors; EC 2.1.1.43 / EZH2 protein, human; EC 2.1.1.43 / Polycomb Repressive Complex 2; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 8
  • [Other-IDs] NLM/ NIHMS546011; NLM/ PMC4417500
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66. Salguero FJ, Richard A, Gough J, Long A, Weyer U, Cooley WA, Chambers MA, Lesellier S: Pelioid hepatocellular carcinoma in an adult Eurasian badger (Meles meles). J Comp Pathol; 2010 Feb-Apr;142(2-3):208-12
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  • [Title] Pelioid hepatocellular carcinoma in an adult Eurasian badger (Meles meles).
  • A mass was identified within the left lateral lobe of the liver of a 10-year-old Eurasian badger (Meles meles).
  • The histological appearance was consistent with hepatocellular carcinoma (HCC).
  • [MeSH-major] Carcinoma, Hepatocellular / veterinary. Liver / pathology. Liver Neoplasms / veterinary. Mustelidae

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  • [Copyright] Crown Copyright 2009. Published by Elsevier Ltd. All rights reserved.
  • (PMID = 19683720.001).
  • [ISSN] 1532-3129
  • [Journal-full-title] Journal of comparative pathology
  • [ISO-abbreviation] J. Comp. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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67. Nakanuma S, Tajima H, Okamoto K, Hayashi H, Nakagawara H, Onishi I, Takamura H, Kitagawa H, Fushida S, Tani T, Fujimura T, Kayahara M, Ohta T, Wakayama T, Iseki S, Harada S: Tumor-derived trypsin enhances proliferation of intrahepatic cholangiocarcinoma cells by activating protease-activated receptor-2. Int J Oncol; 2010 Apr;36(4):793-800
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  • In primary malignant liver tumors, trypsinogen-immunoreactivity was present in 70% of intrahepatic cholangiocarcinoma (ICC) specimens, but absent in hepatocellular carcinoma (HCC) specimens.
  • The purpose of this study was to investigate the secretion of tumor-derived trypsin and the expression of its specific receptor, protease-activated receptor-2 (PAR-2), in ICC using cell lines and surgical specimens.
  • The expression of trypsinogen-1 mRNA was observed in three of four ICC cell lines, but none of three HCC cell lines.
  • Western blot analysis detected trypsinogen-1 in serum-free conditioned medium from one of the ICC cell lines positive for the mRNA.
  • PAR-2 mRNA and protein were observed in ICC cell lines.
  • [MeSH-major] Bile Duct Neoplasms / enzymology. Bile Ducts, Intrahepatic / enzymology. Cell Proliferation. Cholangiocarcinoma / enzymology. Receptor, PAR-2 / metabolism. Trypsin / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Carcinoma, Hepatocellular / enzymology. Carcinoma, Hepatocellular / pathology. Culture Media, Serum-Free / metabolism. Dose-Response Relationship, Drug. Female. Fibroblasts / enzymology. Fibroblasts / pathology. Gabexate / pharmacology. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Hep G2 Cells. Humans. Liver Neoplasms / enzymology. Liver Neoplasms / pathology. Male. Middle Aged. RNA, Messenger / metabolism. Serine Proteinase Inhibitors / pharmacology

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  • (PMID = 20198321.001).
  • [ISSN] 1791-2423
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Culture Media, Serum-Free; 0 / RNA, Messenger; 0 / Receptor, PAR-2; 0 / Serine Proteinase Inhibitors; 4V7M9137X9 / Gabexate; EC 3.4.21.4 / PRSS1 protein, human; EC 3.4.21.4 / Trypsin
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68. Smith CM, Graham RA, Krol WL, Silver IS, Negishi M, Wang H, Lecluyse EL: Differential UGT1A1 induction by chrysin in primary human hepatocytes and HepG2 Cells. J Pharmacol Exp Ther; 2005 Dec;315(3):1256-64
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  • [Title] Differential UGT1A1 induction by chrysin in primary human hepatocytes and HepG2 Cells.
  • Chrysin, a dietary flavonoid, has been shown to markedly induce UGT1A1 expression and activity in HepG2 and Caco-2 cell lines; thus, it has been suggested to have clinical utility in the treatment of UGT1A1-mediated deficiencies, such as unconjugated hyperbilirubinemia or the prevention of 7-ethyl-10-hydroxycamptothecin (SN-38) toxicity.
  • However, little is known about its induction potential in a more physiologically relevant model system, such as primary hepatocyte culture.
  • In this study, induction of UGT1A1 expression (mRNA, protein, and activity) was investigated in primary human hepatocyte cultures after treatment with chrysin and other prototypical inducers.
  • Endogenous nuclear receptor-mediated UGT1A1 induction was studied using transient transfection reporter assays in primary human hepatocytes and HepG2 cells.
  • Subsequent experiments to determine whether the differential response was due to its metabolic stability revealed strikingly different elimination rate constants between the two cell systems (half-life of 13 min in human hepatocytes versus 122 min in HepG2 cell suspensions).
  • [MeSH-minor] Adolescent. Adult. African Continental Ancestry Group / genetics. Aged. Carcinogens / pharmacology. Carcinoma, Hepatocellular / metabolism. Carcinoma, Hepatocellular / pathology. Cell Line, Tumor. Cells, Cultured. Child, Preschool. Dose-Response Relationship, Drug. Drug Interactions. Enzyme Induction / drug effects. European Continental Ancestry Group / genetics. Female. Genes, Reporter. Humans. Liver Neoplasms / metabolism. Liver Neoplasms / pathology. Luciferases / metabolism. Male. Methylcholanthrene / pharmacology. Middle Aged. RNA, Messenger / analysis

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  • (PMID = 16135700.001).
  • [ISSN] 0022-3565
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK061652
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Flavonoids; 0 / RNA, Messenger; 3CN01F5ZJ5 / chrysin; 56-49-5 / Methylcholanthrene; EC 1.13.12.- / Luciferases; EC 2.4.1.17 / Glucuronosyltransferase
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69. Chan KY, Wong N, Lai PB, Squire JA, Macgregor PF, Beheshti B, Albert M, To KF, Johnson PJ: Transcriptional profiling on chromosome 19p indicated frequent downregulation of ACP5 expression in hepatocellular carcinoma. Int J Cancer; 2005 May 10;114(6):902-8
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  • [Title] Transcriptional profiling on chromosome 19p indicated frequent downregulation of ACP5 expression in hepatocellular carcinoma.
  • Chromosomal rearrangements unraveled by spectral karyotyping (SKY) indicated frequent chromosome 19 translocations in hepatocellular carcinoma (HCC).
  • In an effort to characterize the aberrant 19 rearrangements in HCC, we performed positional mapping by fluorescence in-situ hybridization (FISH) in 10 HCC cell lines.
  • SKY analysis indicated structural rearrangements of chromosome 19 in 6 cell lines, 4 of which demonstrated recurring 19p translocations with different partner chromosomes.
  • Quantitative RT-PCR confirmed the reduced expression of ACP5 and indicated a strong correlation of its repressed expression only in cell lines that contain a 19p rearrangement (p = 0.004).
  • We further examined the expression of ACP5 in a cohort of 82 primary tumors and 74 matching nonmalignant liver tissues.
  • In the primary HCC examined, a reduction of ACP5 transcripts by 2 to as much as 1,000-fold was suggested in 67% of tumors (55/82 cases).
  • Functional examination of ACP5 ectopic expression in HCC cells further demonstrated a significant growth inhibitory effect of ACP5 on tumor cell survival (p < 0.001).
  • [MeSH-major] Acid Phosphatase / biosynthesis. Carcinoma, Hepatocellular / genetics. Chromosomes, Human, Pair 19 / genetics. Down-Regulation. Gene Expression Profiling. Isoenzymes / biosynthesis. Liver Neoplasms / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Female. Gene Expression Regulation, Neoplastic. Humans. Karyotyping. Liver Cirrhosis. Male. Middle Aged. Tumor Cells, Cultured

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  • (PMID = 15645427.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Isoenzymes; EC 3.1.3.- / tartrate-resistant acid phosphatase; EC 3.1.3.2 / Acid Phosphatase
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70. Kosmidis PA, Kalofonos HP, Christodoulou C, Syrigos K, Makatsoris T, Skarlos D, Bakogiannis C, Nicolaides C, Bafaloukos D, Bamias A, Samantas E, Xiros N, Boukovinas I, Fountzilas G, Dimopoulos MA: Paclitaxel and gemcitabine versus carboplatin and gemcitabine in patients with advanced non-small-cell lung cancer. A phase III study of the Hellenic Cooperative Oncology Group. Ann Oncol; 2008 Jan;19(1):115-22
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  • [Title] Paclitaxel and gemcitabine versus carboplatin and gemcitabine in patients with advanced non-small-cell lung cancer. A phase III study of the Hellenic Cooperative Oncology Group.
  • BACKGROUND: This phase III study was designed to compare the combination paclitaxel (Taxol)-gemcitabine (PG) versus carboplatin-gemcitabine (CG) in patients with advanced inoperable non-small-cell lung cancer.
  • Primary end point was overall survival (OS).

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  • (PMID = 17938425.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Clinical Trial, Phase III; Comparative Study; Journal Article; Randomized Controlled Trial
  • [Publication-country] England
  • [Chemical-registry-number] 0W860991D6 / Deoxycytidine; 4AF302ESOS / Ondansetron; 7S5I7G3JQL / Dexamethasone; 80061L1WGD / Cimetidine; 8GTS82S83M / Diphenhydramine; B76N6SBZ8R / gemcitabine; BG3F62OND5 / Carboplatin; P88XT4IS4D / Paclitaxel
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71. Fu XM, Yang QX, Shao CK, Feng ZY: [Expressions of h-TERT, c-myc, PCNA and cell apoptosis in liver carcinogenesis]. Nan Fang Yi Ke Da Xue Xue Bao; 2006 Jun;26(6):821-3
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  • [Title] [Expressions of h-TERT, c-myc, PCNA and cell apoptosis in liver carcinogenesis].
  • OBJECTIVE: To investigate the expressions of human telomerase reverse transcriptase (h-TERT), c-myc, and proliferating cell nuclear antigen (PCNA) in chronic viral hepatitis (CVH), liver cirrhosis and primary hepatocellular carcinoma (HCC) and understand their possible role in liver carcinogenesis.
  • METHODS: Totally 157 liver disease specimens were collected, including 56 CVH, 52 liver cirrhosis and 49 primary HCC specimens.
  • In situ hybridization was performed on these specimens to examine the expressions of h-TRET and c-myc mRNA, and immunohistochemistry carried out for PCNA detection, with the cell apoptosis detected with in situ ending labeling.
  • RESULTS: In the CVH, liver cirrhosis and primary HCC specimens, h-TERT expression was detected at the frequencies of 11/56 (19.6%), 43/52 (82.7%) and 44/47 (93.6%), c-myc expression at 7/56 (12.5%), 21/52 (40.4%) and 26/47 (55.3%), with apoptotic index of (27.3-/+4.7)%, (16.5-/+2.6)% and (8.7-/+1.3)% and PCNA expression rate of (17.1-/+2.9)%, (49.3-/+7.8)% and (62.5-/+9.1)%, respectively.
  • CONCLUSION: Liver carcinogenesis may involve increased h-TERT, c-myc, and PCNA expressions and suppressed cell apoptosis.
  • [MeSH-major] Apoptosis. Liver Neoplasms / pathology. Proliferating Cell Nuclear Antigen / biosynthesis. Proto-Oncogene Proteins c-myc / genetics. Telomerase / genetics
  • [MeSH-minor] Adult. Carcinoma, Hepatocellular / genetics. Carcinoma, Hepatocellular / metabolism. Carcinoma, Hepatocellular / pathology. Cell Transformation, Neoplastic. Female. Hepatitis B, Chronic / genetics. Hepatitis B, Chronic / metabolism. Hepatitis B, Chronic / pathology. Humans. Immunohistochemistry. Liver Cirrhosis / genetics. Liver Cirrhosis / metabolism. Liver Cirrhosis / pathology. Male. Middle Aged. RNA, Messenger / genetics. RNA, Messenger / metabolism

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  • (PMID = 16793609.001).
  • [ISSN] 1673-4254
  • [Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University
  • [ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Proliferating Cell Nuclear Antigen; 0 / Proto-Oncogene Proteins c-myc; 0 / RNA, Messenger; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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72. Balta Z, Sauerbruch T, Hirner A, Büttner R, Fischer HP: [Primary neuroendocrine carcinoma of the liver. From carcinoid tumor to small-cell hepatic carcinoma: case reports and review of the literature]. Pathologe; 2008 Feb;29(1):53-60
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  • [Title] [Primary neuroendocrine carcinoma of the liver. From carcinoid tumor to small-cell hepatic carcinoma: case reports and review of the literature].
  • Primary hepatic neuroendocrine tumors are rare neoplasms.
  • While primary hepatic carcinoid tumors (PHCT) are well-differentiated tumors, primary hepatic small-cell carcinomas (PHSCC) represent the poorly differentiated end of the spectrum of neuroendocrine carcinomas.
  • The second patient suffered from small-cell carcinoma of the liver.
  • There were no risk factors for a hepatocellular carcinoma.
  • An extensive preoperative and postoperative diagnostic investigation could rule out an extrahepatic primary site.
  • After neoadjuvant cytostatic treatment the carcinoma was completely extirpated and 18 months after treatment the patient is healthy.PHCT and PHSCC have to be clearly separated from hepatocellular and cholangiocellular carcinomas.
  • Exclusion of an extrahepatic primary site requires an accurate and synoptic analysis of clinical, radiologic and pathologic findings.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoid Tumor / pathology. Carcinoma / drug therapy. Carcinoma / pathology. Carcinoma, Neuroendocrine / pathology. Liver Neoplasms / drug therapy. Liver Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Adult. Aged. Carboplatin / administration & dosage. Cell Differentiation. Etoposide / administration & dosage. Female. Follow-Up Studies. Humans. Rectal Neoplasms / pathology. Risk Factors. Treatment Outcome

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  • [Cites] Radiat Med. 1993 May-Jun;11(3):102-6 [8372237.001]
  • [Cites] Br J Surg. 1989 Mar;76(3):248-9 [2655808.001]
  • [Cites] Dig Dis Sci. 2003 Aug;48(8):1665-7 [12924666.001]
  • [Cites] Clin Nucl Med. 2005 Jul;30(7):530-1 [15965342.001]
  • [Cites] Dtsch Med Wochenschr. 1989 Apr 21;114(16):623-7 [2707129.001]
  • [Cites] Radiat Med. 1995 Jul-Aug;13(4):183-5 [8539446.001]
  • [Cites] Hepatogastroenterology. 1999 Jul-Aug;46(28):2547-50 [10522038.001]
  • [Cites] Surgery. 1992 Dec;112(6):1039-46; discussion 1046-7 [1455307.001]
  • [Cites] J Chin Med Assoc. 2003 Apr;66(4):247-51 [12854878.001]
  • [Cites] Ultrastruct Pathol. 1986;10(4):331-6 [3739044.001]
  • [Cites] Jpn J Clin Oncol. 1999 May;29(5):252-5 [10379337.001]
  • [Cites] Abdom Imaging. 2002 May-Jun;27(3):325-8 [12173364.001]
  • [Cites] Ultrastruct Pathol. 1992 Nov-Dec;16(6):667-72 [1448886.001]
  • [Cites] Med Sci Monit. 2001 Jul-Aug;7(4):746-50 [11433205.001]
  • [Cites] Hepatol Res. 2002 Apr;22(4):313-321 [11929717.001]
  • [Cites] J Comput Assist Tomogr. 1992 Jan-Feb;16(1):99-102 [1729316.001]
  • [Cites] Digestion. 1999 Mar-Apr;60(2):110-6 [10095151.001]
  • [Cites] Abdom Imaging. 2005 May-Jun;30(3):281-5 [15785908.001]
  • [Cites] Am J Clin Pathol. 1988 Apr;89(4):561-4 [3354510.001]
  • [Cites] Ann Surg. 2004 Feb;239(2):210-9 [14745329.001]
  • [Cites] J Comput Tomogr. 1986 Oct;10 (4):313-7 [3780258.001]
  • [Cites] Surgery. 1998 Dec;124(6):1145-52 [9854596.001]
  • [Cites] Pathol Int. 2001 Nov;51(11):874-8 [11844054.001]
  • [Cites] Virchows Arch. 2006 May;448(5):655-8 [16541281.001]
  • [Cites] J Gastroenterol. 1999 Feb;34(1):123-7 [10204622.001]
  • [Cites] Korean J Hepatol. 2005 Sep;11(3):289-92 [16177556.001]
  • [Cites] Radiat Med. 1998 Sep-Oct;16(5):371-3 [9862161.001]
  • [Cites] J Gastroenterol Hepatol. 2002 Oct;17(10):1119-24 [12201876.001]
  • [Cites] Cancer. 1993 Apr 15;71(8):2660-5 [8453589.001]
  • [Cites] Hepatogastroenterology. 2005 Jul-Aug;52(64):1218-20 [16001665.001]
  • [Cites] Surg Today. 2003;33(3):214-8 [12658390.001]
  • [Cites] Am J Surg Pathol. 1992 Aug;16(8):802-7 [1497121.001]
  • [Cites] Histopathology. 1996 Nov;29(5):449-53 [8951490.001]
  • [Cites] Med Princ Pract. 2005 Jul-Aug;14 (4):288-91 [15961944.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8078-83 [12048252.001]
  • [Cites] Pathol Int. 1998 Jun;48(6):481-5 [9702863.001]
  • [Cites] J Korean Med Sci. 1998 Jun;13(3):317-20 [9681813.001]
  • [Cites] Ann Surg Oncol. 2003 Dec;10(10):1171-5 [14654473.001]
  • [Cites] Pathol Oncol Res. 1999;5(1):67-9 [10079384.001]
  • [Cites] Surgery. 1988 Dec;104(6):1080-9 [3194834.001]
  • [Cites] Int J Gastrointest Cancer. 2005;35(2):147-51 [15879630.001]
  • [Cites] Acta Chir Belg. 1999 Dec;99(6):299-302 [10674133.001]
  • [Cites] J Surg Oncol. 1996 Jul;62(3):218-21 [8667631.001]
  • [Cites] Cancer. 1990 Mar 1;65(5):1211-8 [2302669.001]
  • [Cites] Am J Clin Pathol. 1991 Feb;95(2):172-5 [1704179.001]
  • [Cites] J Clin Gastroenterol. 1996 Jul;23(1):60-2 [8835904.001]
  • [Cites] J Clin Ultrasound. 2005 Jul-Aug;33(6):302-4 [16134160.001]
  • [Cites] Am J Gastroenterol. 1993 Jun;88(6):958-61 [8389095.001]
  • [Cites] Br J Radiol. 1999 Feb;72(854):207-9 [10365076.001]
  • [Cites] Cancer. 1980 Sep 1;46(5):1146-51 [7194135.001]
  • [Cites] Intern Med. 2005 Sep;44(9):958-62 [16258211.001]
  • [Cites] Acta Pathol Jpn. 1993 Dec;43(12):783-9 [8109257.001]
  • [Cites] J Clin Endocrinol Metab. 2001 May;86(5):2227-30 [11344231.001]
  • [Cites] Jpn J Clin Oncol. 1992 Feb;22(1):54-9 [1374135.001]
  • [Cites] Pathol Int. 1999 Apr;49(4):318-24 [10365851.001]
  • [Cites] Hepatogastroenterology. 2000 Mar-Apr;47(32):528-30 [10791229.001]
  • (PMID = 18210116.001).
  • [ISSN] 1432-1963
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 6PLQ3CP4P3 / Etoposide; BG3F62OND5 / Carboplatin
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73. Burri E, Steuerwald M, Cathomas G, Mentha G, Majno P, Rubbia-Brandt L, Meier R: Hepatocellular carcinoma in a liver-cell adenoma within a non-cirrhotic liver. Eur J Gastroenterol Hepatol; 2006 Apr;18(4):437-41
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  • [Title] Hepatocellular carcinoma in a liver-cell adenoma within a non-cirrhotic liver.
  • Liver-cell adenomas are benign lesions of the liver occurring predominantly in young women.
  • Hepatocellular carcinomas in most of the cases arise in a cirrhotic liver during the fifth or sixth decade.
  • Tests for chronic liver diseases were negative.
  • The tumour was surgically removed and a hepatocellular carcinoma arising within a liver-cell adenoma in a non-cirrhotic liver was found.
  • Malignant transformation of liver-cell adenoma has only been reported in a few case reports.
  • [MeSH-major] Adenoma, Liver Cell / pathology. Carcinoma, Hepatocellular / pathology. Liver Neoplasms / pathology. Neoplasms, Multiple Primary / pathology
  • [MeSH-minor] Adult. Female. Humans

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  • (PMID = 16538118.001).
  • [ISSN] 0954-691X
  • [Journal-full-title] European journal of gastroenterology & hepatology
  • [ISO-abbreviation] Eur J Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 42
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74. Xu J, Chen X: Expression of twist gene in primary liver cancer. J Huazhong Univ Sci Technolog Med Sci; 2007 Dec;27(6):668-70
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  • [Title] Expression of twist gene in primary liver cancer.
  • In order to investigate the possibility of overexpression of Twist in primary liver cancer (PLC), the Twist expression was detected by using immunohistochemical analysis and RT-PCR assay in 45 patients with PLC.
  • Control tissues were obtained from 9 patients with liver hemangioma.
  • In noncancerous adjacent areas and control liver tissues, the expression of Twist was 57.8% and 22.2% respectively.
  • [MeSH-major] Carcinoma, Hepatocellular / genetics. Liver Neoplasms / genetics. Nuclear Proteins / genetics. Twist-Related Protein 1 / genetics
  • [MeSH-minor] Adult. Aged. Female. Humans. Immunohistochemistry. Male. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction. Up-Regulation. Young Adult

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  • [Cites] Cancer Res. 2003 Apr 15;63(8):1906-13 [12702582.001]
  • [Cites] Nat Genet. 1997 Jan;15(1):42-6 [8988167.001]
  • [Cites] Dev Biol. 1995 Nov;172(1):280-92 [7589808.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Jan 3;300(1):178-81 [12480539.001]
  • [Cites] Cell. 2004 Jun 25;117(7):927-39 [15210113.001]
  • [Cites] J Biol Chem. 2005 Jan 21;280(3):2294-9 [15545268.001]
  • [Cites] Hum Mutat. 2005 Jun;25(6):550-6 [15880747.001]
  • [Cites] Mol Cell Biol. 2001 Nov;21(21):7416-28 [11585922.001]
  • [Cites] Nucleic Acids Res. 1987 Apr 24;15(8):3439-53 [3106932.001]
  • [Cites] Clin Genet. 2004 May;65(5):396-9 [15099347.001]
  • [Cites] Ann Surg Oncol. 2005 Jun;12 (6):488-96 [15864483.001]
  • [Cites] Genes Dev. 1995 Mar 15;9(6):686-99 [7729687.001]
  • [Cites] Nature. 2000 Sep 14;407(6801):249-57 [11001068.001]
  • [Cites] Cell. 2003 Jan 24;112(2):169-80 [12553906.001]
  • [Cites] J Clin Invest. 2002 Sep;110(5):633-41 [12208864.001]
  • [Cites] Nat Med. 2003 Jun;9(6):653-60 [12778163.001]
  • [Cites] Dev Biol. 1997 Sep 15;189(2):205-14 [9299114.001]
  • [Cites] Genes Dev. 1999 Sep 1;13(17 ):2207-17 [10485844.001]
  • [Cites] Am J Pathol. 2002 Nov;161(5):1881-91 [12414534.001]
  • (PMID = 18231738.001).
  • [ISSN] 1672-0733
  • [Journal-full-title] Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban
  • [ISO-abbreviation] J. Huazhong Univ. Sci. Technol. Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Nuclear Proteins; 0 / TWIST1 protein, human; 0 / Twist-Related Protein 1
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75. Chalermchai T, Suwanrusme H, Chantranuwat P, Voravud N, Sriuranpong V: Retrospective review of extra-pulmonary small cell carcinoma at King Chulalongkorn memorial hospital cases during 1998-2005. Asia Pac J Clin Oncol; 2010 Jun;6(2):111-5
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  • [Title] Retrospective review of extra-pulmonary small cell carcinoma at King Chulalongkorn memorial hospital cases during 1998-2005.
  • OBJECTIVE: The aim of this study was to review cases of extra-pulmonary small cell carcinoma (EPSCC), including their clinical manifestations and treatment outcomes.
  • The most common primary sites were the gastrointestinal organs and the nasal cavity.
  • EPSCC of pancreas demonstrated a favorable clinical outcome with treatment, whereas primary EPSCC of the liver, esophagus and rectum had an aggressive natural history and a poor response to treatment.
  • CONCLUSION: Our report suggests that EPSCC may have a different biology from that of pulmonary small cell carcinoma.
  • [MeSH-major] Carcinoma, Small Cell / pathology. Carcinoma, Small Cell / therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Combined Modality Therapy. Female. Gastrointestinal Neoplasms / drug therapy. Gastrointestinal Neoplasms / pathology. Gastrointestinal Neoplasms / surgery. Humans. Male. Middle Aged. Neoplasms, Unknown Primary / drug therapy. Neoplasms, Unknown Primary / pathology. Neoplasms, Unknown Primary / surgery. Nose Neoplasms / drug therapy. Nose Neoplasms / pathology. Nose Neoplasms / radiotherapy. Prognosis. Retrospective Studies. Survival Analysis. Treatment Outcome. Urogenital Neoplasms / drug therapy. Urogenital Neoplasms / pathology. Urogenital Neoplasms / surgery. Young Adult

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  • (PMID = 20565423.001).
  • [ISSN] 1743-7563
  • [Journal-full-title] Asia-Pacific journal of clinical oncology
  • [ISO-abbreviation] Asia Pac J Clin Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Number-of-references] 15
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76. Nan KJ, Ruan ZP, Jing Z, Qin HX, Wang HY, Guo H, Xu R: Expression of fragile histidine triad in primary hepatocellular carcinoma and its relation with cell proliferation and apoptosis. World J Gastroenterol; 2005 Jan 14;11(2):228-31
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  • [Title] Expression of fragile histidine triad in primary hepatocellular carcinoma and its relation with cell proliferation and apoptosis.
  • AIM: To evaluate the expression of fragile histidine triad (FHIT) gene protein, product of a candidate tumor suppressor, and to investigate the relationship between FHIT, cell apoptosis and proliferation, and pathological features of primary hepatocellular carcinoma (HCC).
  • METHODS: Forty-seven HCC and ten normal liver specimens were collected during surgical operation between 2001 and 2003.
  • FHIT and proliferating cell nuclear antigen (PCNA) expression were detected by immunohistochemistry, and apoptotic level was evaluated by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay on the tissue sections.
  • RESULTS: All normal liver tissues showed a strong expression of FHIT, whereas 28 of 47 (59.6%) carcinomas showed a significant loss or absence of FHIT expression (P = 0.001).
  • Apoptotic incidence in advanced TNM stage carcinoma and those with positive FHIT expression was higher than that in early stage carcinoma (P = 0.030) and in those with negative FHIT expression (P = 0.044) respectively.
  • The proliferating potential of hepatocellular carcinoma was associated with FHIT expression (P = 0.016) and the aggressive feature (P = 0.019).
  • [MeSH-major] Acid Anhydride Hydrolases / genetics. Apoptosis / genetics. Carcinoma, Hepatocellular / genetics. Carcinoma, Hepatocellular / pathology. Cell Division / genetics. Genes, Tumor Suppressor. Histidine / genetics. Liver Neoplasms / genetics. Liver Neoplasms / pathology. Neoplasm Proteins / genetics
  • [MeSH-minor] Adult. Female. Humans. Liver / physiology. Male. Middle Aged. Neoplasm Metastasis. Neoplasm Staging. Reference Values

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  • (PMID = 15633221.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / fragile histidine triad protein; 4QD397987E / Histidine; EC 3.6.- / Acid Anhydride Hydrolases
  • [Other-IDs] NLM/ PMC4205407
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77. Gulley JL, Arlen PM, Tsang KY, Yokokawa J, Palena C, Poole DJ, Remondo C, Cereda V, Jones JL, Pazdur MP, Higgins JP, Hodge JW, Steinberg SM, Kotz H, Dahut WL, Schlom J: Pilot study of vaccination with recombinant CEA-MUC-1-TRICOM poxviral-based vaccines in patients with metastatic carcinoma. Clin Cancer Res; 2008 May 15;14(10):3060-9
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  • [Title] Pilot study of vaccination with recombinant CEA-MUC-1-TRICOM poxviral-based vaccines in patients with metastatic carcinoma.
  • The primary end point of this study was vaccine safety, with immunologic and clinical responses as secondary end points.
  • A patient with clear cell ovarian cancer and symptomatic ascites had a durable (18-month) clinical response radiographically and biochemically, and one breast cancer patient had a confirmed decrease of >20% in the size of large liver metastasis.
  • [MeSH-minor] Adjuvants, Immunologic / metabolism. Adjuvants, Immunologic / therapeutic use. Adult. Aged. Antigens, CD58 / immunology. Antigens, CD58 / therapeutic use. Antigens, CD80 / immunology. Antigens, CD80 / therapeutic use. Female. Genetic Vectors. Humans. Intercellular Adhesion Molecule-1 / immunology. Intercellular Adhesion Molecule-1 / therapeutic use. Male. Middle Aged. Pilot Projects. Vaccines, Synthetic / immunology. Vaccines, Synthetic / therapeutic use

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  • [Cites] Cancer Res. 1999 Nov 15;59(22):5800-7 [10582702.001]
  • [Cites] Cancer Res. 2004 Nov 1;64(21):7985-94 [15520206.001]
  • [Cites] Cancer Immunol Immunother. 2006 Jan;55(1):63-7 [15864588.001]
  • [Cites] J Exp Med. 2005 Dec 19;202(12):1691-701 [16365148.001]
  • [Cites] Cancer Immunol Immunother. 2005 Mar;54(3):254-64 [15372205.001]
  • [Cites] J Clin Oncol. 2005 Feb 1;23(4):720-31 [15613691.001]
  • [Cites] Blood. 2005 Apr 1;105(7):2862-8 [15591121.001]
  • [Cites] J Immunol. 2005 May 15;174(10):5994-6004 [15879092.001]
  • [Cites] Clin Cancer Res. 2005 Jun 15;11(12):4430-6 [15958627.001]
  • [Cites] Clin Cancer Res. 2006 Feb 1;12(3 Pt 1):869-77 [16467101.001]
  • [Cites] Clin Cancer Res. 2006 Feb 1;12(3 Pt 1):878-87 [16467102.001]
  • [Cites] Clin Cancer Res. 2006 Feb 15;12(4):1260-9 [16489082.001]
  • [Cites] J Exp Med. 2006 May 15;203(5):1259-71 [16636135.001]
  • [Cites] J Clin Oncol. 2006 Jul 1;24(19):3089-94 [16809734.001]
  • [Cites] Expert Opin Investig Drugs. 2006 Nov;15(11):1395-410 [17040199.001]
  • [Cites] Expert Opin Biol Ther. 2007 Apr;7(4):543-54 [17373905.001]
  • [Cites] Vaccine. 2007 Sep 27;25 Suppl 2:B89-96 [17573164.001]
  • [Cites] Int J Cancer. 2000 Mar 15;85(6):829-38 [10709104.001]
  • [Cites] Surgery. 2000 Apr;127(4):383-9 [10776428.001]
  • [Cites] J Natl Cancer Inst. 2000 Aug 2;92(15):1228-39 [10922408.001]
  • [Cites] J Clin Oncol. 2000 Dec 1;18(23):3964-73 [11099326.001]
  • [Cites] Cancer Immunol Immunother. 2000 Dec;49(10):517-29 [11129322.001]
  • [Cites] Cancer Res. 2001 Jan 1;61(1):206-14 [11196163.001]
  • [Cites] Cancer Res. 2001 May 1;61(9):3689-97 [11325840.001]
  • [Cites] Clin Cancer Res. 2001 May;7(5):1181-91 [11350882.001]
  • [Cites] Cancer Res. 2001 Jun 1;61(11):4497-505 [11389081.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jul 17;98(15):8809-14 [11427731.001]
  • [Cites] J Immunother. 2002 Mar-Apr;25(2):97-138 [12074049.001]
  • [Cites] Prostate. 2002 Oct 1;53(2):109-17 [12242725.001]
  • [Cites] Clin Cancer Res. 2002 Oct;8(10):3219-25 [12374692.001]
  • [Cites] J Clin Oncol. 2003 Apr 1;21(7):1232-7 [12663709.001]
  • [Cites] Clin Cancer Res. 2003 May;9(5):1837-49 [12738742.001]
  • [Cites] J Clin Oncol. 2003 May 15;21(10 Suppl):187s-193s [12743133.001]
  • [Cites] J Immunol. 2003 Jun 15;170(12):6338-47 [12794167.001]
  • [Cites] Br J Radiol. 2004 Jan;77(913):74-5 [14988145.001]
  • [Cites] J Natl Cancer Inst. 2004 Mar 17;96(6):487-8 [15026475.001]
  • [Cites] Clin Cancer Res. 2004 Mar 15;10(6):2139-49 [15041735.001]
  • [Cites] J Immunother. 2004 May-Jun;27(3):240-53 [15076142.001]
  • [Cites] J Clin Oncol. 2004 Jun 1;22(11):2122-32 [15169798.001]
  • [Cites] J Immunol. 1987 Aug 15;139(4):1113-9 [3038997.001]
  • [Cites] Cancer Res. 1991 Jul 15;51(14):3657-62 [1712245.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Apr 15;90(8):3539-43 [8097319.001]
  • [Cites] J Exp Med. 1994 Apr 1;179(4):1109-18 [8145033.001]
  • [Cites] J Natl Cancer Inst. 1995 Jul 5;87(13):982-90 [7629885.001]
  • [Cites] J Clin Oncol. 1996 May;14(5):1545-51 [8622070.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Oct 1;93(20):10972-7 [8855293.001]
  • [Cites] Vaccine. 1997 Apr-May;15(6-7):759-68 [9178479.001]
  • [Cites] Cancer Res. 1997 Oct 15;57(20):4570-7 [9377571.001]
  • [Cites] J Immunol. 1998 Apr 1;160(7):3363-73 [9531296.001]
  • [Cites] J Clin Oncol. 1998 Jul;16(7):2401-8 [9667257.001]
  • [Cites] BMC Immunol. 2005;6:17 [16026627.001]
  • (PMID = 18483372.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 BC010425-09
  • [Publication-type] Case Reports; Clinical Trial; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Antigens, CD58; 0 / Antigens, CD80; 0 / Cancer Vaccines; 0 / Carcinoembryonic Antigen; 0 / MUC1 protein, human; 0 / Mucin-1; 0 / Vaccines, Synthetic; 126547-89-5 / Intercellular Adhesion Molecule-1
  • [Other-IDs] NLM/ NIHMS106857; NLM/ PMC2673097
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78. Huang JH, Gao F, Gu YK, Li WQ, Lu LW: Combined treatment of hepatocellular carcinoma with partial splenic embolization and transcatheter hepatic arterial chemoembolization. World J Gastroenterol; 2007 Dec 28;13(48):6593-7
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  • [Title] Combined treatment of hepatocellular carcinoma with partial splenic embolization and transcatheter hepatic arterial chemoembolization.
  • AIM: To prospectively evaluate the efficacy and safety of partial splenic embolization (PSE) combined with transcatheter hepatic arterial chemoembolization (TACE) in treatment of hepatocellular carcinoma (HCC).
  • METHODS: Fifty patients suffering from primary HCC associated with hypersplenism caused by cirrhosis were randomly assigned to 2 groups: group A receiving PSE combined with TACE (n = 26) and group B receiving TACE alone (n = 24).
  • RESULTS: Prior to treatment, there was no significant difference in sex, age, Child-Pugh grade, tumor diameter, mass pathology type and peripheral blood cell counts between the 2 groups.
  • [MeSH-major] Carcinoma, Hepatocellular / therapy. Chemoembolization, Therapeutic / methods. Embolization, Therapeutic / methods. Hepatic Artery. Liver Neoplasms / therapy
  • [MeSH-minor] Adult. Blood Cell Count. Combined Modality Therapy. Female. Humans. Male. Middle Aged. Prospective Studies. Treatment Outcome

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  • (PMID = 18161933.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial
  • [Publication-country] China
  • [Other-IDs] NLM/ PMC4611302
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79. Long KB, Srivastava A, Hirsch MS, Hornick JL: PAX8 Expression in well-differentiated pancreatic endocrine tumors: correlation with clinicopathologic features and comparison with gastrointestinal and pulmonary carcinoid tumors. Am J Surg Pathol; 2010 May;34(5):723-9
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  • PAX (paired box) genes encode a family of transcription factors that regulate organogenesis and cell-lineage specification in multiple organ systems.
  • In the pancreas, PAX proteins play a critical role in islet cell differentiation.
  • In total, 190 tumors were evaluated: 156 primary WDNETs (63 PETs, 31 ileal, 5 duodenal, 5 gastric, 19 appendiceal, 13 rectal, and 20 pulmonary carcinoid tumors) and 34 liver metastases (18 PETs and 16 ileal carcinoid tumors).
  • PAX8 was positive in 42/63 (67%) primary PETs.
  • Expression of PAX8 was significantly associated with WHO category 1.1 ("benign" behavior) compared with category 1.2 (uncertain behavior) or 2 (well-differentiated endocrine carcinoma) (positive in 100%, 64%, and 52% of tumors, respectively; P<0.05).
  • PAX8-positive PETs were also significantly smaller and more often clinically functional; PAX8-negative tumors were more frequently associated with liver metastases.
  • Among the liver metastases, PAX8 was positive in 9/18 (50%) metastatic PETs compared with 0/16 (0%) metastatic ileal carcinoid tumors.
  • In summary, PAX8 is expressed in normal pancreatic islet cells and in a high proportion of primary and metastatic PETs.
  • PAX8 immunostaining may be helpful in determining the primary site for a WDNET metastatic to the liver, as ileal (PAX8 negative) and pancreatic (PAX8 positive) tumors most often present as a metastasis from an occult primary.
  • [MeSH-major] Adenoma, Islet Cell / pathology. Carcinoid Tumor / pathology. Carcinoma, Islet Cell / secondary. Gastrointestinal Neoplasms / pathology. Lung Neoplasms / pathology. Paired Box Transcription Factors / metabolism. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Female. Humans. Immunohistochemistry. Islets of Langerhans / metabolism. Islets of Langerhans / pathology. Liver Neoplasms / metabolism. Liver Neoplasms / secondary. Lymph Nodes / pathology. Male. Middle Aged

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  • [CommentIn] Am J Surg Pathol. 2011 Dec;35(12):1906-8 [22067332.001]
  • (PMID = 20414099.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / PAX8 protein, human; 0 / Paired Box Transcription Factors
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80. Pozharisskiĭ KM, Granov DA, Ten VP, Kubaĭbergenova AG, Leenman EE, Rasskazov AI: [The significance of immunohistochemistry in the investigation of liver neoplasms: differential diagnosis, prognostic markers]. Vopr Onkol; 2008;54(4):417-33
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  • [Title] [The significance of immunohistochemistry in the investigation of liver neoplasms: differential diagnosis, prognostic markers].
  • The immunohistochemical investigation used 55 primary hepatic tumors (hepatocellular carcinoma (HCC)--32, cholangiocellular carcinoma (CCC)--23).
  • Wide panels of such antibodies as hepatocytic marker (Hep Par--1) CK-8, CK-19, polyclonal CEA, CD10, alpha-fetoprotein, TTF-1 as well as proliferative features of HCC (Ki-67) including regulators of stage-to-stage transition through mitoses of tumor cells (cyclin-D1 and A, genes p53 and RB), unrestricted tumor cell mitosis (telomerases), and intercellular adhesion marker (beta-catenin) were employed for differential diagnosis of neoplasia.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carcinoma, Hepatocellular / chemistry. Carcinoma, Hepatocellular / diagnosis. Immunohistochemistry. Liver Neoplasms / chemistry. Liver Neoplasms / diagnosis
  • [MeSH-minor] Adult. Aged. Bile Duct Neoplasms / diagnosis. Bile Ducts, Intrahepatic. Calcium-Binding Proteins / analysis. Carcinoembryonic Antigen / analysis. Cholangiocarcinoma / diagnosis. Cyclin A / analysis. Cyclin D. Cyclins / analysis. DNA-Binding Proteins / analysis. Diagnosis, Differential. Disease-Free Survival. Female. Gene Expression Regulation, Neoplastic. Genes, Retinoblastoma. Genes, p53. Humans. Keratin-19. Keratin-8. Ki-67 Antigen / analysis. Male. Microfilament Proteins / analysis. Middle Aged. Neprilysin / analysis. Prognosis. Risk Factors. Survival Analysis. alpha-Fetoproteins / analysis. beta Catenin / analysis

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  • (PMID = 18942395.001).
  • [ISSN] 0507-3758
  • [Journal-full-title] Voprosy onkologii
  • [ISO-abbreviation] Vopr Onkol
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / AFP protein, human; 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / Calcium-Binding Proteins; 0 / Carcinoembryonic Antigen; 0 / Cyclin A; 0 / Cyclin D; 0 / Cyclins; 0 / DNA-Binding Proteins; 0 / Keratin-19; 0 / Keratin-8; 0 / Ki-67 Antigen; 0 / Microfilament Proteins; 0 / TTF1 protein, human; 0 / alpha-Fetoproteins; 0 / beta Catenin; 0 / calponin; EC 3.4.24.11 / Neprilysin
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81. West J, Wood H, Logan RF, Quinn M, Aithal GP: Trends in the incidence of primary liver and biliary tract cancers in England and Wales 1971-2001. Br J Cancer; 2006 Jun 5;94(11):1751-8
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  • [Title] Trends in the incidence of primary liver and biliary tract cancers in England and Wales 1971-2001.
  • In the last two decades, mortality from primary liver cancer has increased in the UK.
  • We calculated directly age-standardised incidence rates (using the European standard population) by subsite and histological type for all cancers of the liver, gallbladder and biliary tract in England and Wales from 1971 to 2001, using cancer registry data.
  • The incidence of cancers of the liver, gallbladder and biliary tract increased, with the greatest rise, around 12-fold, in intrahepatic bile duct cancers.
  • The rate of liver cell cancer increased by around 45% in males, but by <10% in females.
  • Cholangiocarcinoma increased around 16-fold and became the most common type of primary liver cancer in females, while hepatocellular carcinoma remained the commonest type in males.
  • The age-specific incidence rates showed that intrahepatic bile duct cancer continued to increase throughout the 1990s in those aged 75 and over, while liver cell cancer decreased in the older age groups.
  • In conclusion, there were increases in the incidence of primary liver cancer, which have been particularly dramatic for intrahepatic bile duct cancer, over the last three decades of the 20th century in England and Wales.
  • [MeSH-major] Biliary Tract Neoplasms / epidemiology. Liver Neoplasms / epidemiology
  • [MeSH-minor] Adult. Aged. England / epidemiology. Female. Humans. Incidence. Male. Middle Aged. Registries. Sex Characteristics. Wales / epidemiology

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  • [Cites] Gut. 2005 Apr;54(4):533-9 [15753540.001]
  • [Cites] Health Stat Q. 2004 Autumn;(23):7-17 [15704380.001]
  • [Cites] Gut. 2001 Jun;48(6):816-20 [11358902.001]
  • [Cites] Hepatology. 2001 Jun;33(6):1353-7 [11391522.001]
  • [Cites] N Engl J Med. 1999 Mar 11;340(10):745-50 [10072408.001]
  • [Cites] Gastroenterology. 2005 Mar;128(3):620-6 [15765398.001]
  • [Cites] Gut. 1989 May;30(5):695-700 [2731765.001]
  • [Cites] Popul Trends. 1996 Winter;(86):29-35 [8987096.001]
  • [Cites] Lancet. 1997 Oct 18;350(9085):1142-3 [9343506.001]
  • [Cites] J Hepatol. 2004 Mar;40(3):472-7 [15123362.001]
  • [Cites] Gastrointest Endosc. 1988 May-Jun;34(3):277-8 [3292346.001]
  • (PMID = 16736026.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2361300
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82. Kim KH, Kim SH, Kim SH, Back JH, Park MJ, Kim JM: Cyclooxygenase-2 and inducible nitric oxide synthase expression in thyroid neoplasms and their clinicopathological correlation. J Korean Med Sci; 2006 Dec;21(6):1064-9
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  • To evaluate the expressions of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) in thyroid neoplasms in a Korean population, we studied a total of 154 cases: papillary carcinoma of classical type (PTC), 86; follicular adenoma (FA), 21; follicular carcinoma (FC), 35; medullary carcinoma (MC), 3; undifferentiated carcinoma (UC), 5; and Hurthle cell neoplasm (HN), 4.
  • In PTC, COX-2 and iNOS were significantly overexpressed in patients over 45 yr of age (p=0.029, p=0.041), and iNOS expression was increased in patients with a large primary tumor (p=0.028).
  • [MeSH-minor] Adult. Aged. Female. Gene Expression Profiling. Humans. Male. Middle Aged. Reproducibility of Results. Sensitivity and Specificity. Statistics as Topic. Tissue Distribution

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  • [Cites] FASEB J. 1998 Sep;12(12):1063-73 [9737710.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 1998;38:97-120 [9597150.001]
  • [Cites] Thyroid. 1999 Feb;9(2):113-7 [10090309.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2001 Sep;281(3):G688-96 [11518681.001]
  • [Cites] J Clin Gastroenterol. 2001 Nov-Dec;33(5):383-8 [11606854.001]
  • [Cites] Ann Clin Lab Sci. 2001 Oct;31(4):325-48 [11688844.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Jan;87(1):358-63 [11788675.001]
  • [Cites] J Pathol. 2002 Feb;196(2):171-9 [11793368.001]
  • [Cites] Laryngoscope. 2002 Feb;112(2):238-42 [11889377.001]
  • [Cites] Am J Clin Pathol. 2002 Apr;117(4):546-51 [11939728.001]
  • [Cites] Prostate. 2002 Nov 1;53(3):232-40 [12386924.001]
  • [Cites] Clin Cancer Res. 2003 Mar;9(3):961-8 [12631593.001]
  • [Cites] Endocr Pathol. 2002 Winter;13(4):331-40 [12665651.001]
  • [Cites] Histopathology. 2003 May;42(5):492-7 [12713627.001]
  • [Cites] Clin Cancer Res. 2003 May;9(5):1604-10 [12738712.001]
  • [Cites] Pathol Int. 2003 Jul;53(7):434-9 [12828608.001]
  • [Cites] Korean J Intern Med. 2003 Dec;18(4):225-9 [14717230.001]
  • [Cites] Histopathology. 2004 May;44(5):490-7 [15139997.001]
  • [Cites] Br J Pharmacol. 1993 Mar;108(3):833-7 [7682140.001]
  • [Cites] Cancer Res. 1994 Mar 1;54(5):1352-4 [7509718.001]
  • [Cites] Cell. 1994 Sep 23;78(6):915-8 [7522969.001]
  • [Cites] Gastroenterology. 1994 Oct;107(4):1183-8 [7926468.001]
  • [Cites] Cancer Res. 1995 Feb 15;55(4):727-30 [7531613.001]
  • [Cites] Cell. 1996 Nov 29;87(5):803-9 [8945508.001]
  • [Cites] J Clin Invest. 1997 Jun 1;99(11):2625-34 [9169492.001]
  • [Cites] Mod Pathol. 1997 Jul;10(7):645-9 [9237172.001]
  • [Cites] Cancer Res. 2000 Sep 1;60(17):4926-31 [10987308.001]
  • [Cites] BJU Int. 2000 Oct;86(6):736-41 [11069387.001]
  • [Cites] Cancer Res. 2001 Jan 1;61(1):303-8 [11196178.001]
  • [Cites] Antioxid Redox Signal. 2001 Apr;3(2):231-48 [11396478.001]
  • [Cites] Int J Urol. 2001 Jul;8(7):S35-9 [11442675.001]
  • [Cites] J Immunol. 1997 Sep 1;159(5):2445-51 [9278337.001]
  • [Cites] J Biol Chem. 1997 Dec 5;272(49):31138-48 [9388267.001]
  • [Cites] Cancer Metastasis Rev. 1998 Mar;17(1):107-18 [9544426.001]
  • [Cites] Laryngoscope. 1999 Jan;109(1):148-52 [9917057.001]
  • (PMID = 17179688.001).
  • [ISSN] 1011-8934
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.99.1 / Cyclooxygenase 2
  • [Other-IDs] NLM/ PMC2721930
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83. Guo Q, Tang W, Inagaki Y, Midorikawa Y, Kokudo N, Sugawara Y, Nakata M, Konishi T, Nagawa H, Makuuchi M: Clinical significance of subcellular localization of KL-6 mucin in primary colorectal adenocarcinoma and metastatic tissues. World J Gastroenterol; 2006 Jan 7;12(1):54-9
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  • [Title] Clinical significance of subcellular localization of KL-6 mucin in primary colorectal adenocarcinoma and metastatic tissues.
  • AIM: To assess subcellular localization of KL-6 mucin and its clinicopathological significance in colorectal carcinoma as well as metastatic lymph node and liver tissues.
  • METHODS: Colorectal carcinoma tissues as well as metastatic lymph node and liver tissues were collected from 82 patients who underwent colorectomy or hepatectomy.
  • RESULTS: Of the 82 colorectal carcinoma patients, 6 showed no staining, 29 showed positive staining only in the apical membrane, and 47 showed positive staining in the circumferential membrane and/or cytoplasm.
  • Statistical analysis between clinicopathological factors and subcellular localization of KL-6 mucin showed that KL-6 localization in the circumferential membrane and/or cytoplasm was significantly associated with the presence of venous invasion (P = 0.0003), lymphatic invasion (P<0.0001), lymph node metastasis (P<0.0001), liver metastasis (P = 0.058), and advanced histological stage (P<0.0001).
  • Positive staining was observed in all metastatic lesions tested as well as in the primary colorectal carcinoma tissues.
  • CONCLUSION: The subcellular staining pattern of KL-6 in colorectal adenocarcinoma may be an important indicator for unfavorable behaviors such as lymph node and liver metastasis, as well as for the prognosis of patients.
  • [MeSH-minor] Adult. Aged. Antigens, Neoplasm. Female. Humans. Immunohistochemistry. Lymphatic Metastasis. Male. Middle Aged. Mucin-1. Survival Rate

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  • [Cites] J Biol Chem. 1988 Mar 25;263(9):4215-22 [3346246.001]
  • [Cites] World J Gastroenterol. 2005 Sep 21;11(35):5450-4 [16222735.001]
  • [Cites] J Biol Chem. 1990 Sep 5;265(25):15286-93 [1697589.001]
  • [Cites] Int J Oncol. 2000 Mar;16(3):455-9 [10675475.001]
  • [Cites] Am J Physiol Lung Cell Mol Physiol. 2000 Mar;278(3):L625-9 [10710536.001]
  • [Cites] Cancer. 2001 Jun 1;91(11):1973-82 [11391575.001]
  • [Cites] Am J Surg Pathol. 2002 Apr;26(4):466-71 [11914624.001]
  • [Cites] World J Gastroenterol. 2001 Jun;7(3):425-30 [11819805.001]
  • [Cites] Biochem Biophys Res Commun. 2002 May 17;293(4):1183-90 [12054500.001]
  • [Cites] Histopathology. 2003 Mar;42(3):239-45 [12605643.001]
  • [Cites] Cancer Res. 2003 Aug 15;63(16):5011-20 [12941828.001]
  • [Cites] Nat Rev Cancer. 2004 Jan;4(1):45-60 [14681689.001]
  • [Cites] World J Gastroenterol. 2004 Oct 15;10(20):3044-7 [15378790.001]
  • [Cites] Hybridoma. 1984 Fall;3(3):223-32 [6094338.001]
  • [Cites] J Biol Chem. 1990 Sep 5;265(25):15294-9 [2394722.001]
  • [Cites] J Clin Oncol. 1991 Jul;9(7):1113-23 [2045853.001]
  • [Cites] Cancer Res. 1992 Apr 15;52(8):2318-24 [1559234.001]
  • [Cites] Cancer Res. 1992 May 1;52(9):2563-8 [1373671.001]
  • [Cites] Cancer. 1993 Apr 1;71(7):2191-9 [8384065.001]
  • [Cites] Gastroenterology. 1994 Feb;106(2):353-61 [7905449.001]
  • [Cites] J Clin Endocrinol Metab. 1994 Feb;78(2):337-42 [8106621.001]
  • [Cites] J Cell Biol. 1995 Apr;129(1):255-65 [7698991.001]
  • [Cites] Annu Rev Physiol. 1995;57:607-34 [7778880.001]
  • [Cites] J Surg Oncol. 1996 Jul;62(3):171-6 [8667623.001]
  • [Cites] Nat Med. 1998 Jan;4(1):43-9 [9427605.001]
  • [Cites] Oncology. 1998 Jul-Aug;55(4):307-19 [9663420.001]
  • [Cites] Dis Colon Rectum. 1998 Oct;41(10):1262-72 [9788390.001]
  • [Cites] Hepatogastroenterology. 2005 Jan-Feb;52(61):67-71 [15782996.001]
  • [Cites] Jpn J Clin Oncol. 1988 Sep;18(3):203-16 [3411786.001]
  • (PMID = 16440417.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens; 0 / Antigens, Neoplasm; 0 / Glycoproteins; 0 / MUC1 protein, human; 0 / Mucin-1; 0 / Mucins
  • [Other-IDs] NLM/ PMC4077483
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84. Manon R, O'Neill A, Knisely J, Werner-Wasik M, Lazarus HM, Wagner H, Gilbert M, Mehta M, Eastern Cooperative Oncology Group: Phase II trial of radiosurgery for one to three newly diagnosed brain metastases from renal cell carcinoma, melanoma, and sarcoma: an Eastern Cooperative Oncology Group study (E 6397). J Clin Oncol; 2005 Dec 1;23(34):8870-6
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  • [Title] Phase II trial of radiosurgery for one to three newly diagnosed brain metastases from renal cell carcinoma, melanoma, and sarcoma: an Eastern Cooperative Oncology Group study (E 6397).
  • PATIENTS AND METHODS: Patients with renal cell carcinoma, melanoma, or sarcoma; one to three brain metastases; and performance status of 0 to 2 were enrolled.
  • Exclusion criteria were leptomeningeal disease; metastases in medulla, pons, or midbrain; or liver metastases.
  • The primary end point was 3- and 6-month intracranial progression.
  • [MeSH-minor] Adult. Brain / pathology. Brain / physiopathology. Brain / surgery. Carcinoma, Renal Cell / secondary. Carcinoma, Renal Cell / surgery. Cognition / physiology. Female. Follow-Up Studies. Humans. Kidney Neoplasms / pathology. Male. Melanoma / pathology. Neoplasm Recurrence, Local. Neoplasm Staging. Prospective Studies. Sarcoma / pathology. Survival Analysis. Survival Rate. Time Factors. Treatment Outcome

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  • (PMID = 16314647.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
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85. Mizukami Y, Kono K, Maruyama T, Watanabe M, Kawaguchi Y, Kamimura K, Fujii H: Downregulation of HLA Class I molecules in the tumour is associated with a poor prognosis in patients with oesophageal squamous cell carcinoma. Br J Cancer; 2008 Nov 4;99(9):1462-7
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  • [Title] Downregulation of HLA Class I molecules in the tumour is associated with a poor prognosis in patients with oesophageal squamous cell carcinoma.
  • In this study, we investigated HLA class I expression in oesophageal squamous cell carcinoma (ESCC) (n=70) and in their metastatic lesions (lymph nodes (n=40) and liver (n=3)), by immunohistochemistry with anti-HLA class I monoclonal antibody (EMR8-5).
  • As a result, the downregulation of HLA class I expression in primary lesions of ESCC was observed in 43%, and that in metastatic lymph nodes was noted in 90%.
  • Furthermore, patients with preserved HLA class I expression in primary tumours showed a better survival in comparison to those with downregulated HLA class I molecules (P<0.01).
  • Furthermore, multivariate analysis using Cox's proportional hazards model revealed that the downregulated expression of HLA class I in primary lesions was an independent, unfavourable prognostic factor (P<0.01).
  • In conclusion, the downregulation of HLA class I expression frequently occurred in primary tumour and, to a greater extent, in metastatic lesions of patients with ESCC and was associated with patient survival.
  • [MeSH-major] Carcinoma, Squamous Cell / immunology. Esophageal Neoplasms / immunology. Histocompatibility Antigens Class I / analysis
  • [MeSH-minor] Adult. Aged. Down-Regulation. Female. Humans. Immunohistochemistry. Male. Middle Aged. Multivariate Analysis. Prognosis

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  • [Cites] Int J Cancer Suppl. 1991;6:95-100 [2066187.001]
  • [Cites] Cancer Res. 1991 Jan 15;51(2):729-36 [1985791.001]
  • [Cites] J Clin Pathol. 1995 Jun;48(6):539-44 [7665697.001]
  • [Cites] Eur J Cancer. 1996 Jan;32A(1):141-5 [8695222.001]
  • [Cites] Immunol Today. 1997 Feb;18(2):89-95 [9057360.001]
  • [Cites] Br J Cancer. 1997;76(7):836-44 [9328140.001]
  • [Cites] Int J Cancer. 1997 Dec 19;74(6):582-7 [9421352.001]
  • [Cites] Am J Pathol. 1999 Mar;154(3):745-54 [10079252.001]
  • [Cites] Clin Cancer Res. 2005 Jan 1;11(1):67-72 [15671529.001]
  • [Cites] Clin Cancer Res. 2005 Jan 15;11(2 Pt 1):498-504 [15701833.001]
  • [Cites] Cancer Immunol Immunother. 2006 Aug;55(8):891-9 [16187081.001]
  • [Cites] Cancer Res. 2006 Sep 15;66(18):9281-9 [16982773.001]
  • [Cites] J Gastrointest Surg. 1997 Jul-Aug;1(4):316-23 [9834364.001]
  • [Cites] Cancer Sci. 2006 Dec;97(12):1374-80 [16995877.001]
  • [Cites] J Urol. 2007 Apr;177(4):1269-72; discussion 1272 [17382705.001]
  • [Cites] Tissue Antigens. 2007 Apr;69 Suppl 1:264-8 [17445216.001]
  • [Cites] Cancer Sci. 2007 Sep;98(9):1424-30 [17645781.001]
  • [Cites] J Clin Oncol. 2007 Sep 10;25(26):4110-7 [17827461.001]
  • [Cites] Cancer Immunol Immunother. 2008 Feb;57(2):197-206 [17622526.001]
  • [Cites] Cancer Immunol Immunother. 2008 May;57(5):601-9 [17874100.001]
  • [Cites] J Surg Oncol. 2008 Apr 1;97(5):451-5 [18247377.001]
  • [Cites] Cancer Sci. 2008 Jul;99(7):1448-54 [18452554.001]
  • [Cites] Cancer Immunol Immunother. 2008 Nov;57(11):1719-26 [18408926.001]
  • [Cites] Cancer Immunol Immunother. 2008 Dec;57(12):1903-10 [18317754.001]
  • [Cites] Adv Immunol. 2000;74:181-273 [10605607.001]
  • [Cites] J Exp Med. 2001 Sep 17;194(6):833-46 [11560998.001]
  • [Cites] Carcinogenesis. 2001 Oct;22(10):1615-23 [11577000.001]
  • [Cites] Surgery. 2003 May;133(5):486-94 [12773976.001]
  • [Cites] J Clin Oncol. 2003 Dec 15;21(24):4592-6 [14673047.001]
  • [Cites] Ann Surg. 1994 Sep;220(3):364-72; discussion 372-3 [8092902.001]
  • (PMID = 18841157.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Histocompatibility Antigens Class I
  • [Other-IDs] NLM/ PMC2579690
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86. Karamitopoulou E, Cioccari L, Jakob S, Vallan C, Schaffner T, Zimmermann A, Brunner T: Active caspase 3 and DNA fragmentation as markers for apoptotic cell death in primary and metastatic liver tumours. Pathology; 2007 Dec;39(6):558-64
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  • [Title] Active caspase 3 and DNA fragmentation as markers for apoptotic cell death in primary and metastatic liver tumours.
  • AIMS: The induction of tumour cell death by apoptosis is a major goal of cancer therapy and the in situ detection of apoptosis in tumour tissue has become an important diagnostic parameter.
  • Different apoptosis detection methods assess distinct biochemical processes in the dying cell.
  • The aim of this study was to compare the immunohistochemical detection of active caspase 3 and single-stranded DNA in primary and metastatic liver tumours as markers of apoptotic cell death.
  • METHODS: We studied detection of active caspase 3 and single-stranded DNA in 20 primary hepatocellular carcinomas (HCC) and 20 liver metastases from colorectal carcinomas (CRC) using immunohistochemistry on paraffin sections.
  • CONCLUSION: The sensitivity of apoptosis detection using immunohistochemistry for active caspase 3 and single-stranded DNA may be tumour cell type dependent.
  • [MeSH-major] Apoptosis. Carcinoma, Hepatocellular / enzymology. Carcinoma, Hepatocellular / genetics. Caspase 3 / metabolism. Colorectal Neoplasms / enzymology. DNA Fragmentation. Liver Neoplasms / enzymology. Liver Neoplasms / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor. Cell Line, Tumor. DNA, Neoplasm. DNA, Single-Stranded. Female. Humans. Immunoenzyme Techniques. Male. Middle Aged


87. Di Benedetto F, Di Sandro S, De Ruvo N, Montalti R, Ballarin R, Guerrini GP, Spaggiari M, Guaraldi G, Gerunda G: First report on a series of HIV patients undergoing rapamycin monotherapy after liver transplantation. Transplantation; 2010 Mar 27;89(6):733-8
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  • [Title] First report on a series of HIV patients undergoing rapamycin monotherapy after liver transplantation.
  • We present the preliminary results of a prospective nonrandomized trial concerning the first HIV patient series receiving RAPA monotherapy after liver transplantation (LT).
  • METHODS: Since June 2003, 14 HIV patients have received cadaveric donor LT due to end-stage liver disease (ESLD) associated or not associated with hepatocellular carcinoma, scored by the model for ESLD system.
  • Patients were assessed using the following criteria for HIV characterization: CD4 T-cell count more than 100/mL and HIV-RNA levels less than 50 copies/mL.
  • Primary immunosuppression was based on calcineurin inhibitors (CI), whereas switch to RAPA monotherapy occurred in cases of CI complications or Kaposi's sarcoma.
  • All patients were affected by ESLD, which was associated with hepatocellular carcinoma in seven patients.
  • [MeSH-major] Anti-HIV Agents / therapeutic use. HIV Infections / drug therapy. HIV-1 / drug effects. Hepatitis B / surgery. Hepatitis C / surgery. Immunosuppressive Agents / therapeutic use. Liver Transplantation. Sirolimus / therapeutic use
  • [MeSH-minor] Adult. Antiretroviral Therapy, Highly Active. CD4 Lymphocyte Count. Female. Graft Rejection / etiology. Graft Rejection / prevention & control. Graft Survival. Hepacivirus / genetics. Hepatitis B virus / genetics. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Prospective Studies. RNA, Viral / blood. Time Factors. Treatment Outcome. Viral Load


88. Huang JH, Wu PH, Gu YK, Zhang FJ, Li CX, Gao F, Zhang L, Fan WJ, Li CJ: [Study on primary hepatocellular carcinoma associated with hypersplenism treated by partial splenic embolization combined with hepatic arterial chemoembolization]. Ai Zheng; 2006 Aug;25(8):1003-6
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  • [Title] [Study on primary hepatocellular carcinoma associated with hypersplenism treated by partial splenic embolization combined with hepatic arterial chemoembolization].
  • BACKGROUND & OBJECTIVE: 70-90% of patients of primary hepatocellular carcinoma (PHC) are associated with liver cirrhosis, portal hypertension and hypersplenism.
  • The treatment of PHC is usually hampered by low or slow recovery of blood cell counts.
  • RESULTS: Satisfactory effects were achieved in PSE combined with TACE group in terms of correction of blood cell counts compared with cases treated with TACE alone.
  • CONCLUSION: PSE associated with TACE is safe and effective for the treatment of patients with PHC associated with liver cirrhosis, portal hypertension and hypersplenism.
  • [MeSH-major] Carcinoma, Hepatocellular / therapy. Chemoembolization, Therapeutic. Hypersplenism / therapy. Liver Neoplasms / therapy
  • [MeSH-minor] Adult. Blood Cell Count. Embolization, Therapeutic / methods. Female. Hepatic Artery. Humans. Iodized Oil. Male. Splenic Artery

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  • (PMID = 16965683.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 8001-40-9 / Iodized Oil
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89. Morimoto O, Nagano H, Miyamoto A, Fujiwara Y, Kondo M, Yamamoto T, Ota H, Nakamura M, Wada H, Damdinsuren B, Marubashi S, Dono K, Umeshita K, Nakamori S, Sakon M, Monden M: Association between recurrence of hepatocellular carcinoma and alpha-fetoprotein messenger RNA levels in peripheral blood. Surg Today; 2005;35(12):1033-41
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  • [Title] Association between recurrence of hepatocellular carcinoma and alpha-fetoprotein messenger RNA levels in peripheral blood.
  • PURPOSE: Intra- and extrahepatic recurrence is common, even after curative resection for hepatocellular carcinoma (HCC), suggesting preoperative or intraoperative tumor cell dissemination.
  • Reverse transcription - polymerase chain reaction (RT-PCR) for alpha-fetoprotein (AFP) is used to detect circulating liver cancer cells.
  • The detection of AFP mRNA was significantly correlated with extrahepatic metastasis after primary surgery, and a shorter disease-free survival time (P = 0.0245 each).
  • [MeSH-major] Carcinoma, Hepatocellular / blood. Liver Neoplasms / blood. Neoplasm Recurrence, Local / blood. RNA, Messenger / blood. alpha-Fetoproteins / metabolism
  • [MeSH-minor] Adult. Aged. Bone Marrow / metabolism. Case-Control Studies. Chi-Square Distribution. Female. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Neoplasm Metastasis. Polymerase Chain Reaction. Prognosis. Prospective Studies. Statistics, Nonparametric

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  • [Cites] Hepatology. 1993 Jul;18(1):47-53 [7686879.001]
  • [Cites] Lancet. 1996 Mar 9;347(9002):649-53 [8596379.001]
  • [Cites] Ann Surg. 1995 Oct;222(4):415-23; discussion 423-5 [7574923.001]
  • [Cites] Hepatology. 1994 Dec;20(6):1418-25 [7527002.001]
  • [Cites] Arch Surg. 2000 Dec;135(12):1456-9 [11115352.001]
  • [Cites] Int J Oncol. 2001 Mar;18(3):527-32 [11179482.001]
  • [Cites] Arch Surg. 2000 Feb;135(2):213-8 [10668884.001]
  • [Cites] Dig Dis Sci. 2000 Jul;45(7):1376-82 [10961717.001]
  • [Cites] J Clin Oncol. 1991 Oct;9(10):1749-56 [1919627.001]
  • [Cites] Clin Cancer Res. 1999 Dec;5(12):4021-7 [10632334.001]
  • [Cites] Hepatology. 1990 Oct;12 (4 Pt 1):680-7 [1698703.001]
  • [Cites] Hepatology. 1994 Apr;19(4):889-94 [8138262.001]
  • [Cites] Gastroenterology. 1995 Mar;108(3):768-75 [7875479.001]
  • [Cites] Cancer Metastasis Rev. 1989 Aug;8(2):98-101 [2673568.001]
  • [Cites] Hepatogastroenterology. 1999 Jan-Feb;46(25):381-6 [10228826.001]
  • [Cites] Hepatogastroenterology. 1996 Jul-Aug;43(10):919-25 [8884314.001]
  • [Cites] Hepatology. 2002 Apr;35(4):853-60 [11915031.001]
  • [Cites] Cancer. 1994 Nov 15;74(10):2772-80 [7954236.001]
  • [Cites] Am J Gastroenterol. 2004 Aug;99(8):1503-9 [15307868.001]
  • [Cites] Lancet. 1992 Sep 19;340(8821):685-9 [1381801.001]
  • [Cites] Ann Surg. 1997 Jul;226(1):43-50 [9242336.001]
  • [Cites] Am J Surg Pathol. 1989 Dec;13(12):1064-7 [2556944.001]
  • [Cites] World J Gastroenterol. 2002 Oct;8(5):818-21 [12378622.001]
  • [Cites] Br J Cancer. 1997;76(5):628-33 [9303362.001]
  • [Cites] J Gastroenterol Hepatol. 2001 Apr;16(4):445-51 [11354284.001]
  • [Cites] Br J Cancer. 1997;75(6):928-33 [9062418.001]
  • [Cites] Arch Surg. 2002 Jan;137(1):94-9 [11772225.001]
  • [Cites] Life Sci. 1998;62(21):1973-84 [9619847.001]
  • [Cites] Hepatogastroenterology. 1995 Sep-Oct;42(5):469-72 [8751199.001]
  • [Cites] Cancer. 1992 Nov 1;70(9):2263-7 [1327495.001]
  • [Cites] Surgery. 2002 Jan;131(1):34-43 [11812961.001]
  • [Cites] Biochem Biophys Res Commun. 2000 Dec 20;279(2):500-4 [11118315.001]
  • [Cites] Langenbecks Arch Surg. 2001 Mar;386(2):118-23 [11374044.001]
  • [Cites] J Clin Oncol. 1992 Oct;10(10):1534-9 [1403032.001]
  • [Cites] Cancer. 1995 May 1;75(9):2214-9 [7536120.001]
  • [Cites] Cancer Res. 1992 Mar 15;52(6):1504-9 [1347253.001]
  • (PMID = 16341483.001).
  • [ISSN] 0941-1291
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / alpha-Fetoproteins
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90. Cioppa T, Marrelli D, Neri A, Caruso S, Pedrazzani C, Malagnino V, Pinto E, Roviello F: A case of small-cell gastric carcinoma with an adenocarcinoma component and hepatic metastases: treatment with systemic and intra-hepatic chemotherapy. Eur J Cancer Care (Engl); 2007 Sep;16(5):453-7
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  • [Title] A case of small-cell gastric carcinoma with an adenocarcinoma component and hepatic metastases: treatment with systemic and intra-hepatic chemotherapy.
  • Primary small-cell carcinoma (SmCC) of the stomach is a rare neoplasm with a poor prognosis and unclear histogenesis: to date, only 50 cases, including ours, have been reported in the literature.
  • In this paper, the authors present a clinical case and the surgical treatment of an adult with a SmCC of the stomach associated with gastric adenocarcinoma.
  • After laparotomy, a large neoplasm with locoregional extension and multiple liver metastases were found.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Small Cell / secondary. Kidney Neoplasms / secondary. Stomach Neoplasms / pathology

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  • (PMID = 17760934.001).
  • [ISSN] 0961-5423
  • [Journal-full-title] European journal of cancer care
  • [ISO-abbreviation] Eur J Cancer Care (Engl)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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91. Kianmanesh R, O'toole D, Sauvanet A, Ruszniewski P, Belghiti J: [Surgical treatment of gastric, enteric, and pancreatic endocrine tumors Part 1. Treatment of primary endocrine tumors]. J Chir (Paris); 2005 May-Jun;142(3):132-49
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  • [Title] [Surgical treatment of gastric, enteric, and pancreatic endocrine tumors Part 1. Treatment of primary endocrine tumors].
  • The surgical goals are to: 1. prolong survival by resecting the primary tumor and any nodal or hepatic metastases, 2. control the symptoms related to hormonal secretion, 3. prevent or treat local complications.
  • They are usually malignant and of advanced stage at diagnosis presenting as a palpable or obstructing mass or as liver metastases.
  • But the eventual development of liver metastases which are the most common cause of mortality still argues for an aggressive surgical approach in the early stages of the disease.
  • [MeSH-major] Carcinoid Tumor / surgery. Carcinoma, Islet Cell / surgery. Carcinoma, Neuroendocrine / surgery. Insulinoma / surgery. Intestinal Neoplasms / surgery. Multiple Endocrine Neoplasia Type 1 / surgery. Pancreatic Neoplasms / surgery. Stomach Neoplasms / surgery. Zollinger-Ellison Syndrome / surgery
  • [MeSH-minor] Adult. Gastrinoma / diagnosis. Gastrinoma / surgery. Glucagonoma / diagnosis. Glucagonoma / surgery. Humans. Liver Neoplasms / secondary. Lymphatic Metastasis. Malignant Carcinoid Syndrome / diagnosis. Malignant Carcinoid Syndrome / surgery. Multicenter Studies as Topic. Pancreatectomy. Postoperative Care. Postoperative Complications. Prognosis. Somatostatinoma / diagnosis. Somatostatinoma / surgery. Vipoma / diagnosis. Vipoma / surgery

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  • (PMID = 16142076.001).
  • [ISSN] 0021-7697
  • [Journal-full-title] Journal de chirurgie
  • [ISO-abbreviation] J Chir (Paris)
  • [Language] fre
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 236
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92. Iwamoto A, Ikeguchi M, Matsumoto S, Hukumoto Y, Inoue M, Ozaki T, Ataka M, Tanida T, Endo K, Katano K, Hirooka Y: Tumor cyclooxygenase-2 gene suppresses local immune responses in patients with hepatocellular carcinoma. Tumori; 2006 Mar-Apr;92(2):130-3
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  • [Title] Tumor cyclooxygenase-2 gene suppresses local immune responses in patients with hepatocellular carcinoma.
  • AIMS AND BACKGROUND: In several neoplastic diseases including hepatocellular carcinoma (HCC) immunosuppression is correlated with disease stage, progression and outcome.
  • The present study analyzed the correlation between local immune responses and COX-2 gene expression levels in patients with primary HCCs.
  • The COX-2 gene expression levels were quantified by real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and compared with the CD8+ T cell densities detected by immunohistochemistry.
  • The CD8+ T cell density in COX-2-expressing tumors (6.1 cells/high-power field (HPF), x200 magnification) was suppressed compared with that in non-COX-2-expressing tumors (13.6 cells/HPF, P = 0.009).
  • CONCLUSIONS: Elevation of the tumor COX-2 level is correlated with the suppression of local immune responses in HCCs, suggesting that COX-2 plays a role in early tumor recurrence in the residual liver in patients after HCC resection.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Carcinoma, Hepatocellular / immunology. Cyclooxygenase 2 / metabolism. Liver Neoplasms / immunology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. CD8-Positive T-Lymphocytes / immunology. Disease-Free Survival. Female. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16724692.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 1.14.99.1 / Cyclooxygenase 2
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93. Nagao Y, Sata M: High incidence of multiple primary carcinomas in HCV-infected patients with oral squamous cell carcinoma. Med Sci Monit; 2009 Sep;15(9):CR453-9
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  • [Title] High incidence of multiple primary carcinomas in HCV-infected patients with oral squamous cell carcinoma.
  • We investigated the association among oral squamous cell carcinoma (OSCC), multiple primary cancers (MPCs), insulin resistance and HCV infection.
  • MATERIAL/METHODS: Upper gastrointestinal tract examination and determination of the presence of HCV infection were routinely done for 60 primary OSCC patients.
  • In HCV-infected cases, 10 MPCs with patients, hepatocellular carcinoma (HCC) was the most common outcome (5 cases), whereas gastric cancer was the most common outcome (6 cases) in non-HCV-infected 11 MPCs.
  • CONCLUSIONS: HCV infection was strongly associated with the occurrence of MPCs as well as primary OSCC.
  • In patients with HCV infection, it is important to clinically examine organs other than the liver.
  • [MeSH-major] Carcinoma, Squamous Cell. Hepacivirus / metabolism. Hepatitis C. Mouth Neoplasms. Neoplasms, Multiple Primary / etiology. Neoplasms, Multiple Primary / virology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Insulin Resistance. Male. Middle Aged. Multivariate Analysis. Retrospective Studies. Risk Factors


94. Kannangai R, Sahin F, Torbenson MS: EGFR is phosphorylated at Ty845 in hepatocellular carcinoma. Mod Pathol; 2006 Nov;19(11):1456-61
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  • [Title] EGFR is phosphorylated at Ty845 in hepatocellular carcinoma.
  • Epidermal growth factor receptor (EGFR) is overexpressed in a significant proportion of hepatocellular carcinomas.
  • Recent studies of EGFR inhibitors to treat hepatocellular carcinoma have been encouraging and better understanding of EGFR signaling may lead to more effective strategies for inhibiting this key pathway.
  • Cell line and animal studies have shown that MAPK and STAT-3 are important mediators of the EGFR signal in liver cells.
  • However, little is known about EGFR phosphorylation and subsequent signaling in primary hepatocellular carcinoma.
  • We investigated the site of EGFR phosphorylation by Western blot in 18 hepatocellular carcinomas.
  • Fourteen of 18 hepatocellular carcinomas had detectable EGFR by Western blotting and 13 of 14 showed phosphorylation at tyrosine 845.
  • These findings were further explored by examination of EGFR expression and signaling pathway activation in tissue arrays comprised of 73 hepatocellular carcinomas using antibodies that recognize phosphorylated (or activated) proteins.
  • We conclude that EGFR is phosphorylated at tyrosine 845 in most hepatocellular carcinomas and that EGFR expression by immunohistochemistry does not correlate well with STAT-3, STAT-5, MAPK, or AKT immunostaining.
  • [MeSH-major] Carcinoma, Hepatocellular / chemistry. Liver Neoplasms / chemistry. Receptor, Epidermal Growth Factor / analysis. Tyrosine / analysis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Blotting, Western. Cell Line, Tumor. Cell Proliferation. Child. Female. Humans. Immunohistochemistry. Male. Middle Aged. Mitogen-Activated Protein Kinase 1 / analysis. Mitogen-Activated Protein Kinase 3 / analysis. Phosphorylation. Proto-Oncogene Proteins c-akt / analysis. STAT3 Transcription Factor / analysis. STAT5 Transcription Factor / analysis. Signal Transduction. Tissue Array Analysis

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  • (PMID = 16936701.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / STAT5 Transcription Factor; 42HK56048U / Tyrosine; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
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95. Sternberg CN, Davis ID, Mardiak J, Szczylik C, Lee E, Wagstaff J, Barrios CH, Salman P, Gladkov OA, Kavina A, Zarbá JJ, Chen M, McCann L, Pandite L, Roychowdhury DF, Hawkins RE: Pazopanib in locally advanced or metastatic renal cell carcinoma: results of a randomized phase III trial. J Clin Oncol; 2010 Feb 20;28(6):1061-8
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  • [Title] Pazopanib in locally advanced or metastatic renal cell carcinoma: results of a randomized phase III trial.
  • This randomized, double-blind, placebo-controlled phase III study evaluated efficacy and safety of pazopanib monotherapy in treatment-naive and cytokine-pretreated patients with advanced renal cell carcinoma (RCC).
  • PATIENTS AND METHODS Adult patients with measurable, locally advanced, and/or metastatic RCC were randomly assigned 2:1 to receive oral pazopanib or placebo.
  • The primary end point was progression-free survival (PFS).
  • [MeSH-major] Bone Neoplasms / drug therapy. Carcinoma, Renal Cell / drug therapy. Kidney Neoplasms / drug therapy. Liver Neoplasms / drug therapy. Lung Neoplasms / drug therapy. Pyrimidines / therapeutic use. Sulfonamides / therapeutic use
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Double-Blind Method. Female. Humans. International Agencies. Male. Middle Aged. Neoplasm Staging. Placebos. Prognosis. Survival Rate. Treatment Outcome. Young Adult


96. Kang MH, Kim SN, Kim NK, Park YI, Kim YW, Ryu KW, Lee JH, Lee JS, Park SR: Clinical outcomes and prognostic factors of metastatic gastric carcinoma patients who experience gastrointestinal perforation during palliative chemotherapy. Ann Surg Oncol; 2010 Dec;17(12):3163-72
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  • [Title] Clinical outcomes and prognostic factors of metastatic gastric carcinoma patients who experience gastrointestinal perforation during palliative chemotherapy.
  • BACKGROUND: We conducted the current study to investigate the clinical outcomes of metastatic gastric carcinoma (MGC) patients who experienced gastrointestinal (GI) perforation during palliative chemotherapy and to examine the prognostic factors associated with survival after perforation.
  • Patients with perforation at the primary gastric site were more likely to have ulcerative gastric cancer lesion (90.5 vs. 40.0%, P = 0.034) or gastric tumor bleeding (28.6 vs. 0%, P = 0.298), and less likely to have Bormann type IV (14.3 vs. 60.0%, P = 0.062), than patients with perforation at nongastric sites.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Carcinoma, Signet Ring Cell / drug therapy. Intestinal Perforation / chemically induced. Liver Neoplasms / drug therapy. Peritoneal Neoplasms / drug therapy. Stomach Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Female. Humans. Male. Medical Records. Middle Aged. Neoplasm Staging. Palliative Care. Survival Rate. Treatment Outcome

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  • (PMID = 20585878.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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97. Otegbayo JA, Yakubu A, Akere A, Igetei R, Aje AO: Quality of life among primary liver cell carcinoma patients in Ibadan, Nigeria. Afr J Med Med Sci; 2005 Mar;34(1):51-4
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  • [Title] Quality of life among primary liver cell carcinoma patients in Ibadan, Nigeria.
  • A descriptive prospective study was conducted to evaluate the quality of life of patients with primary liver cell carcinoma at the University College Hospital, Ibadan, Nigeria.
  • [MeSH-major] Carcinoma / psychology. Liver Neoplasms / psychology. Quality of Life. Sickness Impact Profile
  • [MeSH-minor] Adult. Aged. Female. Hospitals, University. Humans. Male. Middle Aged. Nigeria. Patient Satisfaction. Prognosis. Prospective Studies. Surveys and Questionnaires

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  • (PMID = 15971554.001).
  • [ISSN] 0309-3913
  • [Journal-full-title] African journal of medicine and medical sciences
  • [ISO-abbreviation] Afr J Med Med Sci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Nigeria
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98. Shi M, Qian S, Chen WW, Zhang H, Zhang B, Tang ZR, Zhang Z, Wang FS: Hepatitis B virus (HBV) antigen-pulsed monocyte-derived dendritic cells from HBV-associated hepatocellular carcinoma patients significantly enhance specific T cell responses in vitro. Clin Exp Immunol; 2007 Feb;147(2):277-86
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  • [Title] Hepatitis B virus (HBV) antigen-pulsed monocyte-derived dendritic cells from HBV-associated hepatocellular carcinoma patients significantly enhance specific T cell responses in vitro.
  • To investigate whether hepatitis B virus (HBV) antigen-pulsed monocyte-derived dendritic cells (MoDC) could mount a T cell response in hepatocellular carcinoma (HCC) patients associated with chronic HBV infection, peripheral blood mononuclear cells (PBMCs) from 36 HBV-associated HCC patients were induced into MoDC and pulsed with hepatitis B core antigen (HBcAg) and hepatitis B surface antigen (HBsAg), alone and in combination.
  • MoDC pulsed with HBcAg or HBsAg + HBcAg also had the strongest ability to stimulate autologous T cell proliferation and intracellular interferon (IFN)-gamma production.
  • HBcAg- or HBsAg + HBcAg-pulsed MoDC could also induce HBV core peptide-specific CD8(+) T cell proliferation determined by tetramer staining.
  • In addition, the antigen-pulsed MoDC were found to have a stronger capacity to produce IL-12 and induce T cell response in vitro for patients with higher alanine transaminase (ALT) levels than those with lower ALT levels, indicating that antigen pulse could substantially reverse the impaired function of MoDC in primary HCC patients with active chronic hepatitis B.
  • In conclusion, HBV antigen-pulsed MoDC from HCC patients with chronic hepatitis B could induce HBV-specific T cell response in vitro.
  • [MeSH-major] Carcinoma, Hepatocellular / immunology. Dendritic Cells / immunology. Hepatitis B Antigens / immunology. Hepatitis B, Chronic / immunology. Liver Neoplasms / immunology
  • [MeSH-minor] Adult. Aged. Alanine Transaminase / blood. CD8-Positive T-Lymphocytes / immunology. Cell Differentiation / immunology. Cell Proliferation. Cells, Cultured. Female. Humans. Immunophenotyping. Interferon-gamma / biosynthesis. Lymphocyte Activation / immunology. Male. Middle Aged. Monocytes / immunology. T-Lymphocytes / immunology. Viral Load

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  • [Cites] Nat Med. 2000 Mar;6(3):332-6 [10700237.001]
  • [Cites] J Immunol. 2006 May 1;176(9):5644-51 [16622034.001]
  • [Cites] J Gastroenterol Hepatol. 2000 Apr;15(4):431-6 [10824889.001]
  • [Cites] Annu Rev Immunol. 2001;19:65-91 [11244031.001]
  • [Cites] J Immunol. 2006 Jul 1;177(1):739-47 [16785573.001]
  • [Cites] Nat Immunol. 2000 Sep;1(3):199-205 [10973276.001]
  • [Cites] Blood. 2001 May 15;97(10):3171-6 [11342445.001]
  • [Cites] Immunology. 2001 May;103(1):90-7 [11380696.001]
  • [Cites] Cancer Res. 2001 Sep 1;61(17):6451-8 [11522640.001]
  • [Cites] Cancer. 2002 Jan 15;94(2):406-14 [11900226.001]
  • [Cites] World J Gastroenterol. 2001 Aug;7(4):537-41 [11819824.001]
  • [Cites] J Exp Med. 2002 May 6;195(9):1089-101 [11994415.001]
  • [Cites] J Virol. 2002 Sep;76(17):8609-20 [12163580.001]
  • [Cites] Cancer Immunol Immunother. 2002 Dec;51(11-12):637-44 [12439609.001]
  • [Cites] Int J Mol Med. 2003 Feb;11(2):169-74 [12525872.001]
  • [Cites] Hepatology. 2003 Jul;38(1):4-13 [12829979.001]
  • [Cites] Immunology. 2003 Aug;109(4):487-95 [12871214.001]
  • [Cites] Clin Exp Immunol. 2004 Mar;135(3):462-6 [15008979.001]
  • [Cites] N Engl J Med. 2004 Mar 11;350(11):1118-29 [15014185.001]
  • [Cites] World J Gastroenterol. 2004 Apr 15;10(8):1146-51 [15069715.001]
  • [Cites] N Engl J Med. 2004 Apr 1;350(14):1461-3 [15070799.001]
  • [Cites] Curr Drug Targets Infect Disord. 2004 Jun;4(2):93-101 [15180457.001]
  • [Cites] Int J Mol Med. 2004 Aug;14(2):295-9 [15254781.001]
  • [Cites] J Gen Virol. 2004 Oct;85(Pt 10):2829-36 [15448344.001]
  • [Cites] Res Virol. 1993 Jan-Feb;144(1):75-80 [8446782.001]
  • [Cites] J Clin Invest. 1997 Jun 15;99(12):3025-33 [9185527.001]
  • [Cites] J Hepatol. 1997 Jul;27(1):170-5 [9252092.001]
  • [Cites] J Immunol. 1997 Aug 15;159(4):2001-8 [9257867.001]
  • [Cites] Eur J Immunol. 1997 Dec;27(12):3135-42 [9464798.001]
  • [Cites] Nat Med. 1998 Mar;4(3):328-32 [9500607.001]
  • [Cites] J Immunol. 1998 Nov 1;161(9):4520-9 [9794377.001]
  • [Cites] J Hepatol. 1999 May;30(5):755-64 [10365798.001]
  • [Cites] J Hepatol. 1999 Aug;31(2):323-31 [10453947.001]
  • [Cites] Virology. 1999 Sep 1;261(2):165-72 [10497102.001]
  • [Cites] J Urol. 2004 Dec;172(6 Pt 2):2532-8 [15538202.001]
  • [Cites] J Clin Immunol. 2004 Nov;24(6):637-46 [15622448.001]
  • [Cites] J Gastroenterol Hepatol. 2005 Feb;20(2):234-42 [15683426.001]
  • [Cites] World J Gastroenterol. 2005 Mar 28;11(12):1806-8 [15793869.001]
  • [Cites] Zhonghua Yi Xue Za Zhi. 2005 Jan 26;85(4):248-52 [15854486.001]
  • [Cites] J Cancer Res Clin Oncol. 2005 Jul;131(7):429-38 [15818505.001]
  • [Cites] Am J Pathol. 2000 Apr;156(4):1117-32 [10751335.001]
  • (PMID = 17223969.001).
  • [ISSN] 0009-9104
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hepatitis B Antigens; 82115-62-6 / Interferon-gamma; EC 2.6.1.2 / Alanine Transaminase
  • [Other-IDs] NLM/ PMC1810470
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99. Peng N, Li L, Cai X, Tan S, Wu T: Liver stem/progenitor cells in the canals of Hering: cellular origin of hepatocellular carcinoma with bile duct tumor thrombi? Stem Cell Rev; 2010 Dec;6(4):579-84
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  • [Title] Liver stem/progenitor cells in the canals of Hering: cellular origin of hepatocellular carcinoma with bile duct tumor thrombi?
  • It is generally believed that the invasion of hepatocellular carcinoma (HCC) into the biliary tree ultimately leads to the formation of bile duct tumor thrombi (BDTT).
  • However, recent studies revealed that primary tumor might be small, even undetectable, and there was no histopathologic evidence of direct tumor invasion into bile duct wall in some patients.
  • During the last decade, efforts on stem cell biology may shed light on the pathogenesis of BDTT.
  • (1) the canals of Hering (CoH) are the most likely origin of liver stem/progenitor cells (LSPCs) in adult livers;.
  • (2) similar signalling pathways may regulate self-renewal in LSPCs and liver cancer cells, and a substantial proportion of liver tumors may often originate from the transformation of LSPCs; and (3) liver cancer contains rare cells with stem cell-like properties, which could derive from malignant transformation of LSPCs.
  • Herein, we propose that HCC with BDTT, especially with small or undetectable primary lesion and/or no histopathologic evidence for bile duct invasion, might arise from LSPCs residing in the CoH and, possibly, some primary lesions are formed firstly within the intrahepatic biliary tree.
  • When "tumor thrombi" extends mainly along bile duct, there might be "BDTT" alone; when it invades into surrounding parenchyma, there might often be small "primary tumor" with "BDTT".
  • If this holds true, the putative type may be a particular subset of HCC, and most importantly it would facilitate our understanding of stem-cell origin of HCC.
  • [MeSH-major] Bile Duct Neoplasms / pathology. Bile Ducts, Intrahepatic / pathology. Carcinoma, Hepatocellular / pathology. Liver / pathology. Liver Neoplasms / pathology. Neoplastic Stem Cells / pathology

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  • [ErratumIn] Stem Cell Rev. 2011 Nov;7(4):1046
  • [Cites] Med Chir Dig. 1975;4(5-6):267-70 [173942.001]
  • [Cites] Int J Clin Pract. 2008 Aug;62(8):1212-8 [18479363.001]
  • [Cites] World J Gastroenterol. 2004 May 15;10 (10 ):1397-401 [15133842.001]
  • [Cites] Gastroenterology. 2007 Jun;132(7):2542-56 [17570225.001]
  • [Cites] Cancer Res. 2008 Mar 1;68(5):1451-61 [18316609.001]
  • [Cites] Langenbecks Arch Surg. 2009 Nov;394(6):1033-9 [19421771.001]
  • [Cites] Cancer Res. 2007 Nov 15;67(22):10831-9 [18006828.001]
  • [Cites] Surgery. 2001 Jun;129(6):692-8 [11391367.001]
  • [Cites] Cancer Sci. 2004 Jul;95(7):592-5 [15245596.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2006 May;290(5):G859-70 [16322088.001]
  • [Cites] J Clin Invest. 2006 Jan;116(1):249-60 [16395407.001]
  • [Cites] Gut. 2010 Feb;59(2):247-57 [19880964.001]
  • [Cites] Liver Int. 2009 Aug;29(7):955-65 [19490415.001]
  • [Cites] Surgery. 2000 Nov;128(5):779-83 [11056440.001]
  • [Cites] Histopathology. 2008 Jan;52(2):224-32 [18184271.001]
  • [Cites] World J Gastroenterol. 2005 Jul 7;11(25):3966-9 [15991304.001]
  • [Cites] Hepatology. 2008 Jan;47(1):288-95 [17929301.001]
  • [Cites] Dis Markers. 2008;24(4-5):223-9 [18525116.001]
  • [Cites] Hepatology. 2006 Jul;44(1):240-51 [16799977.001]
  • [Cites] J Hepatol. 2010 Jan;52(1):117-29 [19913937.001]
  • [Cites] Arch Med Res. 2007 Aug;38(6):612-20 [17613352.001]
  • [Cites] J Pathol. 1997 Mar;181(3):330-7 [9155721.001]
  • [Cites] World J Surg. 2004 May;28(5):471-5 [15085398.001]
  • [Cites] Gastroenterology. 2007 Sep;133(3):937-50 [17673212.001]
  • [Cites] Carcinogenesis. 2002 Mar;23(3):435-45 [11895858.001]
  • [Cites] Int J Gastrointest Cancer. 2006;37(1):27-34 [17290078.001]
  • [Cites] Gastroenterology. 2009 Mar;136(3):1012-24 [19150350.001]
  • [Cites] J Hepatol. 2000 Jul;33(1):76-84 [10905589.001]
  • [Cites] Dig Liver Dis. 2009 Jul;41(7):455-62 [19403350.001]
  • [Cites] Hepatology. 2010 Apr;51(4):1401-9 [20054870.001]
  • [Cites] Eur J Gastroenterol Hepatol. 2009 Nov;21(11):1320-1 [19826380.001]
  • [Cites] Gastroenterology. 2007 Nov;133(5):1579-91 [17983805.001]
  • [Cites] Hepatogastroenterology. 1994 Aug;41(4):349-54 [7959570.001]
  • [Cites] Histopathology. 1996 Apr;28(4):291-9 [8732337.001]
  • [Cites] J Hepatobiliary Pancreat Surg. 2007;14(2):204-9 [17384916.001]
  • [Cites] Cancer. 1982 May 15;49(10):2144-7 [6280834.001]
  • [Cites] Am J Surg Pathol. 2001 Nov;25(11):1388-96 [11684955.001]
  • [Cites] Br J Cancer. 2009 Jun 2;100(11):1765-70 [19436294.001]
  • [Cites] Cancer Res. 2006 May 1;66(9):4553-7 [16651403.001]
  • [Cites] Intern Med. 2006;45(5):229-33 [16595985.001]
  • [Cites] Hum Pathol. 2009 Sep;40(9):1304-11 [19386347.001]
  • [Cites] Nature. 2001 Nov 1;414(6859):105-11 [11689955.001]
  • [Cites] Hepatol Res. 2005 May;32(1):52-7 [15888382.001]
  • [Cites] Hepatology. 2001 Mar;33(3):738-50 [11230756.001]
  • [Cites] Hepatology. 1999 Dec;30(6):1425-33 [10573521.001]
  • [Cites] Eur J Radiol. 2010 Oct;76(1):103-9 [19501994.001]
  • [Cites] Hepatology. 1992 Dec;16(6):1327-33 [1280243.001]
  • [Cites] Hepatology. 2009 Sep;50(3):992-3 [19714715.001]
  • [Cites] J Cancer Res Clin Oncol. 2008 May;134(5):535-41 [17917742.001]
  • [Cites] J Cancer Res Clin Oncol. 2009 Aug;135(8):1073-80 [19294418.001]
  • [Cites] Nat Med. 2006 Apr;12(4):410-6 [16532004.001]
  • [Cites] Hepatology. 2009 May;49(5):1655-63 [19309719.001]
  • [Cites] Ann N Y Acad Sci. 2009 Feb;1155:206-21 [19250206.001]
  • [Cites] Environ Health Perspect. 1993 Dec;101 Suppl 5:15-26 [7516873.001]
  • [Cites] Stem Cells. 2006 Aug;24(8):1852-8 [16627685.001]
  • [Cites] J Gastroenterol. 2002 Jan;37(1):55-8 [11824802.001]
  • [Cites] Eur J Cancer. 2010 Apr;46(6):1056-61 [20202823.001]
  • [Cites] J Clin Oncol. 2008 Jun 10;26(17):2800-5 [18539957.001]
  • [Cites] Cancer Res. 2008 Jun 1;68(11):4287-95 [18519688.001]
  • (PMID = 20809255.001).
  • [ISSN] 1558-6804
  • [Journal-full-title] Stem cell reviews
  • [ISO-abbreviation] Stem Cell Rev
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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100. Koeberle D, Montemurro M, Samaras P, Majno P, Simcock M, Limacher A, Lerch S, Kovàcs K, Inauen R, Hess V, Saletti P, Borner M, Roth A, Bodoky G: Continuous Sunitinib treatment in patients with advanced hepatocellular carcinoma: a Swiss Group for Clinical Cancer Research (SAKK) and Swiss Association for the Study of the Liver (SASL) multicenter phase II trial (SAKK 77/06). Oncologist; 2010;15(3):285-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Continuous Sunitinib treatment in patients with advanced hepatocellular carcinoma: a Swiss Group for Clinical Cancer Research (SAKK) and Swiss Association for the Study of the Liver (SASL) multicenter phase II trial (SAKK 77/06).
  • The objective of this trial was to demonstrate antitumor activity of continuous SU treatment in patients with hepatocellular carcinoma (HCC).
  • PATIENTS AND METHODS: Key eligibility criteria included unresectable or metastatic HCC, no prior systemic anticancer treatment, measurable disease, and Child-Pugh class A or mild Child-Pugh class B liver dysfunction.
  • The primary endpoint was progression-free survival at 12 weeks (PFS12).
  • CONCLUSION: Continuous SU treatment with 37.5 mg daily is feasible and has moderate activity in patients with advanced HCC and mild to moderately impaired liver dysfunction.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Hepatocellular / drug therapy. Indoles / therapeutic use. Liver Neoplasms / drug therapy. Pyrroles / therapeutic use
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease-Free Survival. Female. Humans. Male. Middle Aged. Treatment Outcome

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  • [Cites] J Natl Cancer Inst. 2000 Feb 2;92(3):205-16 [10655437.001]
  • [Cites] J Clin Oncol. 2009 Sep 1;27(25):4068-75 [19652072.001]
  • [Cites] Cancer Res. 2001 Oct 15;61(20):7669-74 [11606410.001]
  • [Cites] Int J Cancer. 2001 Oct 15;94(2):290-6 [11668511.001]
  • [Cites] Lancet Oncol. 2001 Sep;2(9):533-43 [11905707.001]
  • [Cites] Clin Biochem. 2003 Nov;36(8):585-90 [14636871.001]
  • [Cites] Liver Transpl. 2004 Feb;10(2 Suppl 1):S115-20 [14762851.001]
  • [Cites] Br J Surg. 1973 Aug;60(8):646-9 [4541913.001]
  • [Cites] Control Clin Trials. 1989 Mar;10(1):1-10 [2702835.001]
  • [Cites] N Engl J Med. 1999 Mar 11;340(10):745-50 [10072408.001]
  • [Cites] Clin Cancer Res. 2004 Dec 15;10(24):8421-5 [15623621.001]
  • [Cites] J Clin Oncol. 2006 Jan 1;24(1):25-35 [16314617.001]
  • [Cites] J Clin Oncol. 2006 Sep 10;24(26):4293-300 [16908937.001]
  • [Cites] J Clin Oncol. 2007 Mar 1;25(7):884-96 [17327610.001]
  • [Cites] J Clin Oncol. 2007 May 1;25(13):1753-9 [17470865.001]
  • [Cites] N Engl J Med. 2007 May 31;356(22):2330-1 [17538098.001]
  • [Cites] World J Gastroenterol. 2008 Jan 7;14(1):1-14 [18176955.001]
  • [Cites] J Natl Cancer Inst. 2008 May 21;100(10):698-711 [18477802.001]
  • [Cites] J Clin Oncol. 2008 Jun 20;26(18):2992-8 [18565886.001]
  • [Cites] N Engl J Med. 2008 Jul 24;359(4):378-90 [18650514.001]
  • [Cites] Hepatology. 2008 Oct;48(4):1312-27 [18821591.001]
  • [Cites] Lancet Oncol. 2009 Jan;10(1):25-34 [19095497.001]
  • [Cites] J Clin Oncol. 2009 Jan 20;27(3):446-52 [19064965.001]
  • [Cites] Cancer Cell. 2009 Mar 3;15(3):232-9 [19249681.001]
  • [Cites] J Clin Oncol. 2009 Jun 20;27(18):3027-35 [19470923.001]
  • [Cites] Eur J Cancer. 2009 Jul;45(11):1959-68 [19282169.001]
  • [Cites] Oncologist. 2009 Jul;14(7):717-25 [19581525.001]
  • [Cites] Lancet Oncol. 2009 Aug;10(8):794-800 [19586800.001]
  • [Cites] J Hepatol. 2001 Sep;35(3):421-30 [11592607.001]
  • (PMID = 20203173.001).
  • [ISSN] 1549-490X
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00699374
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Indoles; 0 / Pyrroles; V99T50803M / sunitinib
  • [Other-IDs] NLM/ PMC3227954
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