CD44 Expression Is a Prognostic Factor in Patients with Intrahepatic
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Prediction of Distant Metastasis by Using Reverse Transcriptase Polymerase Chain Reaction for Epithelial and Variant CD44 Mrna I
ORIGINAL ARTICLE Prediction of Distant Metastasis by Using Reverse Transcriptase–Polymerase Chain Reaction for Epithelial and Variant CD44 mRNA in the Peripheral Blood of Patients With Colorectal Cancer Shozo Yokoyama, MD; Hiroki Yamaue, MD Background: Reverse transcriptase–polymerase chain Main Outcome Measure: The clinical significance of reaction (RT-PCR) has been used to identify small num- RT-PCR for epithelial and variant CD44 mRNA in pe- bers of tumor cells. Molecular detection is thought to pro- ripheral blood. vide useful information for the clinical management of postoperative adjuvant therapy regimens. Results: During 3 years of follow-up, 2 patients whose peripheral blood had carcinoembryonic antigen and Objective: To use RT-PCR to identify messenger RNA CD44 variant mRNA also had distant metastases (lung (mRNA) coding for carcinoembryonic antigen, epithelial or spleen). Expression of epithelial and variant CD44 and variant CD44, and matrix metalloproteinase 7 in the mRNA in peripheral blood was more highly correlated portal venous and peripheral blood of patients with colo- with the clinical cancer stage than with expression rectal carcinoma to predict live or distant metastasis. of carcinoembryonic antigen and matrix metallopro- teinase 7. Design: Prospective consecutive series. Conclusions: Molecular detection of epithelial and Setting: University hospital. variant CD44 mRNA in the peripheral blood may help determine distant metastases in patients with colorectal Patients and Methods: Portal venous and peripheral carcinoma. Molecular detection in the peripheral blood blood samples were obtained from 22 patients with colo- at surgical treatment suggests that systemic hemato- rectal cancer during surgical manipulation. Using comple- genic tumor cell dissemination is an early event of dis- mentary DNA primers specific for carcinoembryonic tant metastasis. -
Stem Cells and Cancer
Stem Cells and Cancer Cancer Education Project Stem Cells and Cancer Overview: This series of activities is designed to introduce students to the theory that some cancers arise from cancer stem cells. This theory provides a possible explanation for why cancers reoccur after cancer treatment. It also provides insights that may lead to new types of chemotherapy drugs. • Part 1: Stem Cells and Cancer PowerPoint (40 minutes) Students view a PowerPoint presentation that introduces stem cell biology and shows ways that cancer stem cell research might lead to more effective cancer therapy treatments. Students answer questions as they view the PowerPoint. Then they create a cartoon strip to illustrate their understanding of cancer stem cells. • Part 2: The Bad Seed: Rare stem cells appear to drive cancers (20 minutes) Students read a brief article that introduces stem cell biology and explains how cancer stem cell research might lead to more effective cancer therapy treatments. Students answer questions based on this article. This activity may be done in class or for homework. • Part 3: Plant Derivative Attacks the Roots of Leukemia (20 minutes) Students read a brief article on the development of a potential chemotherapy agent that specifically targets cancer stem cells. Students answer questions based on this article. This activity may be done in class or for homework. • Part 4: Clinical Trials: Parthocet (40 minutes) Students answer questions about the design of a large-scale, randomized, double-blind clinical trial to determine if Parthocet (a fictitious chemotherapy drug) is safe and effective. Life Sciences Learning Center – Cancer Education Project 1 Copyright © 2007, University of Rochester May be copied for classroom use Stem Cells and Cancer Teacher Instructions - Part 1 Stem Cells and Cancer PowerPoint Presentation Students view a PowerPoint presentation that introduces stem cell biology and shows ways that cancer stem cell research might lead to more effective cancer therapy treatments. -
CD44 Predicts Early Recurrence in Pancreatic Cancer Patients Undergoing Radical Surgery
in vivo 32 : 1533-1540 (2018) doi:10.21873/invivo.11411 CD44 Predicts Early Recurrence in Pancreatic Cancer Patients Undergoing Radical Surgery CHIH-PO HSU 1* , LI-YU LEE 2* , JUN-TE HSU 1, YU-PAO HSU 1, YU-TUNG WU 1, SHANG-YU WANG 1, CHUN-NAN YEH 1, TSE-CHING CHEN 2 and TSANN-LONG HWANG 1 1Department of General Surgery, Chang Gung Memorial Hospital at Linkou, Chang Gung University College of Medicine, Taoyuan, Taiwan, R.O.C.; 2Department of Pathology, Chang Gung Memorial Hospital at Linkou, Chang Gung University College of Medicine, Taoyuan, Taiwan, R.O.C. Abstract. Background/Aim: Pancreatic ductal adeno- predicted ER. Conclusion: High CA19-9 levels, CD44 H- carcinoma (PDAC) is one of the most aggressive types of scores and poor differentiation are independent predictors digestive cancer. Recurrence within one year after surgery is for ER in PDAC patients undergoing radical resection. inevitable in most PDAC patients. Recently, cluster of Therefore, the determination of CD44 expression might help differentiation 44 (CD44) has been shown to be associated in identifying patients at a high risk of ER for more with tumor initiation, metastasis and prognosis. This study aggressive treatment after radical surgery. aimed to explore the correlation of CD44 expression with clinicopathological factors and the role of CD44 in Pancreatic ductal adenocarcinoma (PDAC) is the fourth most predicting early recurrence (ER) in PDAC patients after common cause of cancer-related death worldwide, with an radical surgery. Materials and Methods: PDAC patients who 8% 5-year survival rate for all stages of disease (1). underwent radical resection between January 1999 and Although various treatment modalities are available, only March 2015 were enrolled in this study. -
Supplementary Table 1: Adhesion Genes Data Set
Supplementary Table 1: Adhesion genes data set PROBE Entrez Gene ID Celera Gene ID Gene_Symbol Gene_Name 160832 1 hCG201364.3 A1BG alpha-1-B glycoprotein 223658 1 hCG201364.3 A1BG alpha-1-B glycoprotein 212988 102 hCG40040.3 ADAM10 ADAM metallopeptidase domain 10 133411 4185 hCG28232.2 ADAM11 ADAM metallopeptidase domain 11 110695 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 195222 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 165344 8751 hCG20021.3 ADAM15 ADAM metallopeptidase domain 15 (metargidin) 189065 6868 null ADAM17 ADAM metallopeptidase domain 17 (tumor necrosis factor, alpha, converting enzyme) 108119 8728 hCG15398.4 ADAM19 ADAM metallopeptidase domain 19 (meltrin beta) 117763 8748 hCG20675.3 ADAM20 ADAM metallopeptidase domain 20 126448 8747 hCG1785634.2 ADAM21 ADAM metallopeptidase domain 21 208981 8747 hCG1785634.2|hCG2042897 ADAM21 ADAM metallopeptidase domain 21 180903 53616 hCG17212.4 ADAM22 ADAM metallopeptidase domain 22 177272 8745 hCG1811623.1 ADAM23 ADAM metallopeptidase domain 23 102384 10863 hCG1818505.1 ADAM28 ADAM metallopeptidase domain 28 119968 11086 hCG1786734.2 ADAM29 ADAM metallopeptidase domain 29 205542 11085 hCG1997196.1 ADAM30 ADAM metallopeptidase domain 30 148417 80332 hCG39255.4 ADAM33 ADAM metallopeptidase domain 33 140492 8756 hCG1789002.2 ADAM7 ADAM metallopeptidase domain 7 122603 101 hCG1816947.1 ADAM8 ADAM metallopeptidase domain 8 183965 8754 hCG1996391 ADAM9 ADAM metallopeptidase domain 9 (meltrin gamma) 129974 27299 hCG15447.3 ADAMDEC1 ADAM-like, -
The Role of the Carcinoembryonic Antigen Receptor in Colorectal Cancer Progression
gra nte tive f I O o l n a c o n r l o u g o y J Bajenova et al., J Integr Oncol 2017, 6:2 Journal of Integrative Oncology DOI: 10.4172/2329-6771.1000192 ISSN: 2329-6771 Research Article Open Access The Role of the Carcinoembryonic Antigen Receptor in Colorectal Cancer Progression Olga Bajenova1,2, Elena Tolkunova3, Sergey Koshkin3, Sergey Malov1, Peter Thomas4, Alexey Tomilin3 and Stephen O’Brien1 1Theodosius Dobzhansky Center for Genome Bioinformatics at St. Petersburg State University, St. Petersburg, Russia 2Department of Genetics and Biotechnology, St. Petersburg State University, St. Petersburg, Russia 3Institute of Cytology, Russian Academy of Sciences, St. Petersburg, Russia 4Department of Surgery, Creighton University, Omaha, USA *Corresponding author: Olga Bajenova, Theodosius Dobzhansky Center for Genome Bioinformatics at St. Petersburg State University, 41-43 Sredniy Prospekt, St Petersburg, Russia, Tel: +7-812-363-6103; E-mail: [email protected] Received Date: March 25, 2017; Accepted Date: April 18, 2017; Published Date: April 28, 2017 Copyright: © 2017 Bajenova O, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Clinical and experimental data suggest that carcinoembryonic antigen (CEA, CD66e, CEACAM-5) plays a key role in the formation of hepatic metastasis from colorectal and other types of epithelial cancers. The molecular events involved in CEA-induced metastasis have yet to be defined. Our group first cloned the gene (CEAR) for CEA- binding protein from the surface of fixed liver macrophages, (Kupffer cells). -
Cancer Stem Cells and Nucleolin As Drivers of Carcinogenesis
pharmaceuticals Review Cancer Stem Cells and Nucleolin as Drivers of Carcinogenesis Laura Sofia Carvalho 1,Nélio Gonçalves 1 , Nuno André Fonseca 1,2 and João Nuno Moreira 1,3,* 1 CNC—Center for Neurosciences and Cell Biology, Center for Innovative Biomedicine and Biotechnology (CIBB), Faculty of Medicine (Polo 1), University of Coimbra, Rua Larga, 3004-504 Coimbra, Portugal; laurasofi[email protected] (L.S.C.); [email protected] (N.G.); [email protected] (N.A.F.) 2 TREAT U, SA—Parque Industrial de Taveiro, Lote 44, 3045-508 Coimbra, Portugal 3 UC—University of Coimbra, CIBB, Faculty of Pharmacy (FFUC), Pólo das Ciências da Saúde, Azinhaga de Santa Comba, 3000-548 Coimbra, Portugal * Correspondence: [email protected]; Tel.: +351-239-820-190 Abstract: Cancer, one of the most mortal diseases worldwide, is characterized by the gain of specific features and cellular heterogeneity. Clonal evolution is an established theory to explain heterogeneity, but the discovery of cancer stem cells expanded the concept to include the hierarchical growth and plasticity of cancer cells. The activation of epithelial-to-mesenchymal transition and its molecular players are widely correlated with the presence of cancer stem cells in tumors. Moreover, the acquisition of certain oncological features may be partially attributed to alterations in the levels, location or function of nucleolin, a multifunctional protein involved in several cellular processes. This review aims at integrating the established hallmarks of cancer with the plasticity of cancer cells as an emerging hallmark; responsible for tumor heterogeneity; therapy resistance and relapse. The discussion will contextualize the involvement of nucleolin in the establishment of cancer hallmarks and its application as a marker protein for targeted anticancer therapies Keywords: tumor heterogeneity; drug resistance; cancer stem cells; nucleolin; targeted therapies; epithelial-to-mesenchymal transition Citation: Carvalho, L.S.; Gonçalves, N.; Fonseca, N.A.; Moreira, J.N. -
Soluble Carcinoembryonic Antigen Activates Endothelial Cells and Tumor Angiogenesis
Published OnlineFirst October 11, 2013; DOI: 10.1158/0008-5472.CAN-13-0123 Cancer Microenvironment and Immunology Research Soluble Carcinoembryonic Antigen Activates Endothelial Cells and Tumor Angiogenesis Kira H. Bramswig1, Marina Poettler1, Matthias Unseld1, Friedrich Wrba2, Pavel Uhrin3, Wolfgang Zimmermann4, Christoph C. Zielinski1, and Gerald W. Prager1 Abstract Carcinoembryonic antigen (CEA, CD66e, CEACAM-5) is a cell-surface–bound glycoprotein overexpressed and released by many solid tumors that has an autocrine function in cancer cell survival and differentiation. Soluble CEA released by tumors is present in the circulation of patients with cancer, where it is used as a marker for cancer progression, but whether this form of CEA exerts any effects in the tumor microenvironment is unknown. Here, we present evidence that soluble CEA is sufficient to induce proangiogenic endothelial cell behaviors, including adhesion, spreading, proliferation, and migration in vitro and tumor microvascularization in vivo. CEA-induced activation of endothelial cells was dependent on integrin b-3 signals that activate the focal- adhesion kinase and c-Src kinase and their downstream MAP–ERK kinase/extracellular signal regulated kinase and phosphoinositide 3-kinase/Akt effector pathways. Notably, while interference with VEGF signaling had no effect on CEA-induced endothelial cell activation, downregulation with the CEA receptor in endothelial cells attenuated CEA-induced signaling and tumor angiogenesis. Corroborating these results clinically, we found -
Cancer from the Perspective of Stem Cells and Misappropriated Tissue Regeneration Mechanisms
Leukemia (2018) 32:2519–2526 https://doi.org/10.1038/s41375-018-0294-7 REVIEW ARTICLE Corrected: Correction Stem cell biology Cancer from the perspective of stem cells and misappropriated tissue regeneration mechanisms 1,2 1 1 1,2 1 Mariusz Z. Ratajczak ● Kamila Bujko ● Aaron Mack ● Magda Kucia ● Janina Ratajczak Received: 8 September 2018 / Accepted: 17 September 2018 / Published online: 30 October 2018 © The Author(s) 2018. This article is published with open access Abstract Tumorigenesis can be considered as pathologically misappropriated tissue regeneration. In this review we will address some unresolved issues that support this concept. First, we will address the issue of the identity of cancer-initiating cells and the presence of cancer stem cells in growing tumors. We will also ask are there rare and distinct populations of cancer stem cells in established tumor cell lines, or are all of the cells cancer stem cells? Second, the most important clinical problem with cancer is its metastasis, and here a challenging question arises: by employing radio-chemotherapy for tumor treatment, do we unintentionally create a prometastatic microenvironment in collateral organs? Specifically, many factors upregulated in response to radio-chemotherapy-induced injury may attract highly migratory cancer cells that survived initial treatment. 1234567890();,: 1234567890();,: Third, what is the contribution of normal circulating stem cells to the growing malignancy? Do circulating normal stem cells recognize a tumor as a hypoxia-damaged tissue that needs -
Role of Liver ICAM‑1 in Metastasis (Review)
ONCOLOGY LETTERS 14: 3883-3892, 2017 Role of liver ICAM‑1 in metastasis (Review) AITOR BENEDICTO, IRENE ROMAYOR and BEATRIZ ARTETA Department of Cell Biology and Histology, School of Medicine and Nursing, University of The Basque Country, UPV/EHU, Leioa, E-48940 Vizcaya, Spain Received January 17, 2017; Accepted July 7, 2017 DOI: 10.3892/ol.2017.6700 Abstract. Intercellular adhesion molecule (ICAM)-1, is a frequently diagnosed cancer types and is the fourth leading transmembrane glycoprotein of the immunoglobulin (Ig)-like cause of cancer-related death (1). The spreading of cells from superfamily, consisting of five extracellular Ig‑like domains, a the primary lesion to a secondary organ and the subsequent transmembrane domain and a short cytoplasmic tail. ICAM-1 is development of distant metastases is a key factor that limits expressed in various cell types, including endothelial cells and patient survival rate. This remains one of the most complex leukocytes, and is involved in several physiological processes. issues faced in medicine (2). Furthermore, it has additionally been reported to be expressed The liver is the main target organ for metastatic CRC in various cancer cells, including melanoma, colorectal cancer cells and the second most commonly invaded organ, after and lymphoma. The majority of studies to date have focused the lymph nodes (3). In fact, 15-25% of CRC patients present on the expression of the ICAM‑1 on the surface of tumor cells, with synchronous hepatic metastases at the time of diagnosis, without research into ICAM‑1 expression at sites of metastasis. and a further 30% will later develop liver metastasis (4,5). -
The Immunomodulatory CEA Cell Adhesion Molecule 6 (CEACAM6/Cd66c) Is a Candidate Receptor for the Influenza a Virus
bioRxiv preprint doi: https://doi.org/10.1101/104026; this version posted January 30, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 1 The immunomodulatory CEA cell adhesion molecule 6 (CEACAM6/CD66c) is a 2 candidate receptor for the influenza A virus 3 Shah Kamranur Rahmana *, Mairaj Ahmed Ansarib, Pratibha Gaurc, Imtiyaz Ahmada, 4 Chandrani Chakravartya,d, Dileep Kumar Vermaa, Sanjay Chhibbere, Naila Nehalf, 5 Shanmugaapriya Sellathanbyd, Dagmar Wirthc, Gulam Warisb and Sunil K. Lala,g # 6 7 Virology Group, International Centre for Genetic Engineering & Biotechnology, New Delhi, 8 Indiaa. 9 Department of Microbiology and Immunology, H. M. Bligh Cancer Research Laboratories, 10 Rosalind Franklin University of Medicine and Science, Chicago Medical School, North 11 Chicago, Illinois, USAb. 12 Helmholtz Centre for Infection Research, Braunschweig, Germanyc. 13 Department of Biomedical Science, Bharathidasan University, Trichy, Indiad. 14 Microbiology Department, Panjab University, Chandigarh, Indiae. 15 Career Institute of Medical & Dental Sciences and Hospital, Lucknow, Indiaf. 16 School of Science, Monash University, Selangor DE, Malaysiag. 17 18 Running Head: Protein receptor for Influenza A Virus 19 20 # Corresponding author: Professor of Microbiology, School of Science, Monash University, 21 47500 Bandar Sunway, Selangor DE, Malaysia. 22 Email: [email protected]; Telephone: (+603) 551 59606 23 24 * Current address: Department of Pathogen Molecular Biology, London School of Hygiene & 25 Tropical Medicine, Keppel Street, London WC1E 7HT, United Kingdom. 26 1 bioRxiv preprint doi: https://doi.org/10.1101/104026; this version posted January 30, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. -
Receptor for Mouse Hepatitis Virus Is a Member of the Carcinoembryonic Antigen Family of Glycoproteins
Proc. Natl. Acad. Sci. USA Vol. 88, pp. 5533-5536, July 1991 Medical Sciences Receptor for mouse hepatitis virus is a member of the carcinoembryonic antigen family of glycoproteins (coronavirus/immunoglobulin superfamily/host resistance to virus/virus tissue tropism/virus receptor) RICHARD K. WILLIAMS, GUI-SEN JIANG, AND KATHRYN V. HOLMES* Department of Pathology, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814 Communicated by Dorothy M. Horstmann, April 1, 1991 (receivedfor review February 28, 1991) ABSTRACT The receptor for mouse hepatitis virus binds neither MHV-A59 virus nor anti-receptor mAb CC1, (MHV), a murine coronavirus, is a 110- to 120-kDa glycopro- we postulated that it has a mutation affecting the domain of tein on intestinal brush border membranes and hepatocyte the glycoprotein that normally would bind MHV and mAb membranes. The N-terminal 25-amino acid sequence of immu- CC1 (4). In this communication we demonstrate that the noaffinity-purified MHV receptor was identical to the pre- MHV receptor glycoprotein of BALB/c and Swiss Webster dicted mature N termini of two mouse genes related to human mice and its SJL/J homolog are members of the carcinoem- carcinoembryonic antigen (CEA) and was strongly homologous bryonic antigen (CEA) family of glycoproteins in the immu- to the N termini of members of the CEA family in humans and noglobulin superfamily. rats. Polyclonal antibodies to human CEA recognized the immunoaffinity-purified MHV receptor and the MHV receptor in liver membranes and intestinal brush border membranes MATERIALS AND METHODS from MHV-susceptible mouse strains. In membranes from Tissue Preparations and Tissue-Binding Assay. -
Canalicular Immunostaining of Aminopeptidase N (CD13) As a Diagnostic Marker for Hepatocellular Carcinoma Cro¨Cken, J Licht, a Roessner, S Carl-Mcgrath
1069 J Clin Pathol: first published as 10.1136/jcp.2005.026328 on 27 September 2005. Downloaded from ORIGINAL ARTICLE Canalicular immunostaining of aminopeptidase N (CD13) as a diagnostic marker for hepatocellular carcinoma CRo¨cken, J Licht, A Roessner, S Carl-McGrath ............................................................................................................................... J Clin Pathol 2005;58:1069–1075. doi: 10.1136/jcp.2005.026328 Background: Aminopeptidase N (CD13) is expressed in normal and neoplastic liver tissue, where it exhibits a characteristic canalicular pattern (CD13can), similar to that seen for CD10 and when antibodies crossreact with biliary glycoprotein I (p-CEA). Aim: To compare the putative diagnostic use of CD13can in differentiating between hepatocellular (HCC) See end of article for authors’ affiliations and non-hepatocellular carcinomas metastatic to the liver (non-HCC). ....................... Methods: Aretrospectivestudycomparing53HCCspecimenswith32non-HCCspecimens. Immunostaining was performed with HepPar1 and antibodies directed against CD10, CD13, p-CEA, Correspondence to: Professor C Ro¨cken, and a fetoprotein (AFP). Department of Pathology, Results: In the HCC group, a canalicular staining pattern was found for CD13, p-CEA, and CD10 in 51, Otto-von-Guericke- 43, and 33 specimens, respectively. HepPar1 was positive in 29 and AFP in 17 HCC specimens. In the University, Leipziger Str. non-HCC group, canalicular immunostaining for CD10 and p-CEA was confined to non-neoplastic liver 44, D-39120 Magdeburg, Germany; christoph. tissue. One poorly differentiated cholangiocarcinoma showed apical expression of CD13, resembling to [email protected] some extent CD13can. Sensitivity and specificity were 96.2% and 97.0%, respectively, for CD13can, 81.1% magdeburg.de and 100% for p-CEAcan, 62.3% and 100%, for CD10can, 54.7% and 99.9% for HepPar1, and 32.1% and 100% for AFP.