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Colorectal Cancer

Overview of attention for book
Cover of 'Colorectal Cancer'

Table of Contents

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    Book Overview
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    Chapter 1 Cell Line Models of Molecular Subtypes of Colorectal Cancer
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    Chapter 2 Dissecting Oncogenic RTK Pathways in Colorectal Cancer Initiation and Progression
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    Chapter 3 Identification of Response Elements on Promoters Using Site-Directed Mutagenesis and Chromatin Immunoprecipitation
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    Chapter 4 Identification and Functional Analysis of Gene Regulatory Sequences Interacting with Colorectal Tumor Suppressors
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    Chapter 5 Methods for In Vivo Functional Studies of Chromatin-Modifying Enzymes in Early Steps of Colon Carcinogenesis
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    Chapter 6 The Colorectal Cancer Microenvironment: Strategies for Studying the Role of Cancer-Associated Fibroblasts
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    Chapter 7 Methods for Assessing Apoptosis and Anoikis in Normal Intestine/Colon and Colorectal Cancer
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    Chapter 8 Molecular Analysis of the Microbiome in Colorectal Cancer
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    Chapter 9 Proteomics Analysis of Colorectal Cancer Cells
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    Chapter 10 Autophagic Flux Assessment in Colorectal Cancer Cells
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    Chapter 11 Classification of Colorectal Cancer in Molecular Subtypes by Immunohistochemistry
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    Chapter 12 Stool DNA Integrity Method for Colorectal Cancer Detection
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    Chapter 13 RT-qPCR for Fecal Mature MicroRNA Quantification and Validation
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    Chapter 14 A Stool Multitarget mRNA Assay for the Detection of Colorectal Neoplasms
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    Chapter 15 Colorectal Cancer Detection Using Targeted LC-MS Metabolic Profiling
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    Chapter 16 Proteomic Profiling for Colorectal Cancer Biomarker Discovery
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    Chapter 17 Tumor-Derived Microparticles to Monitor Colorectal Cancer Evolution
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    Chapter 18 Molecular Testing for the Treatment of Advanced Colorectal Cancer: An Overview
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    Chapter 19 Testing Cell-Based Immunotherapy for Colorectal Cancer
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    Chapter 20 Patient-Derived Xenograft Models of Colorectal Cancer: Procedures for Engraftment and Propagation
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    Chapter 21 Use of Organoids to Characterize Signaling Pathways in Cancer Initiation
  23. Altmetric Badge
    Chapter 22 Identification of Novel Molecules Targeting Cancer Stem Cells
Attention for Chapter 2: Dissecting Oncogenic RTK Pathways in Colorectal Cancer Initiation and Progression
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Chapter title
Dissecting Oncogenic RTK Pathways in Colorectal Cancer Initiation and Progression
Chapter number 2
Book title
Colorectal Cancer
Published in
Methods in molecular biology, January 2018
DOI 10.1007/978-1-4939-7765-9_2
Pubmed ID
Book ISBNs
978-1-4939-7764-2, 978-1-4939-7765-9
Authors

Stephen McManus, Walid Chababi, Dominique Arsenault, Claire M. Dubois, Caroline Saucier

Abstract

Colorectal cancer (CRC) is a progressive disorder associated with an accumulation of multiple heterogeneous genetic alterations in intestinal epithelial cells (IEC). However, when these cells undergo neoplastic transformation and become cancerous and metastatic, they invariably acquire hallmarks conferring them the ability to hyperproliferate, escape growth-inhibitory and death-inducing cues, and promote angiogenesis as well as epithelial-to-mesenchymal transformation (EMT), fostering their invasive dissemination from primary tumor into distant tissues. Compelling clinical and experimental evidence suggest that aberrant engagement of cell surface growth factor receptor tyrosine kinase (RTK) signaling, like that of the hepatocyte growth factor (HGF)/MET receptor, underlies CRC metastatic progression by promoting these cancer hallmarks. To date, though, the use of RTK-targeting agents has been viewed as a promising approach for the treatment of metastatic CRC, clinical success has been modest.Our vision is that the prospect of designing RTK-based, improved and innovative CRC therapies and prognostic markers likely rests on a comprehensive understanding of the biological processes and underlying regulatory molecular mechanisms by which deregulation of RTK signaling governs IEC's neoplastic transformation and their transition from noninvasive to metastatic and malignant cells. Herein, we describe our scheme for defining the full scope of oncogenic MET-driven cancer biological processes, in cellulo and in vivo, as well as the individual contribution of MET-binding effectors in a nontransformed IEC model, the IEC-6 cell line.

Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 15 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 15 100%

Demographic breakdown

Readers by professional status Count As %
Student > Master 5 33%
Student > Postgraduate 2 13%
Unspecified 1 7%
Student > Ph. D. Student 1 7%
Unknown 6 40%
Readers by discipline Count As %
Medicine and Dentistry 3 20%
Biochemistry, Genetics and Molecular Biology 3 20%
Unspecified 1 7%
Immunology and Microbiology 1 7%
Agricultural and Biological Sciences 1 7%
Other 0 0%
Unknown 6 40%