Abstract B57: Comprehensive molecular characterization of acquired resistance to anti-EGFR monoclonal antibodies (MoAbs) in patients with metastatic colorectal cancer (mCRC)

2015 ◽  
Author(s):  
Filippo Pietrantonio ◽  
Rosa Berenato ◽  
Federica Perrone ◽  
Annunziata Gloghini ◽  
Elena Tamborini ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Monoclonal Antibodies ◽  
Metastatic Colorectal Cancer ◽  
Molecular Characterization ◽  
Acquired Resistance

scholarly journals Molecular Characterization of Circulating Tumor Cells in Human Metastatic Colorectal Cancer

PLoS ONE ◽  
2012 ◽  
Vol 7 (7) ◽  
pp. e40476 ◽  
Author(s):  
Jorge Barbazán ◽  
Lorena Alonso-Alconada ◽  
Laura Muinelo-Romay ◽  
María Vieito ◽  
Alicia Abalo ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Metastatic Colorectal Cancer ◽  
Tumor Cells ◽  
Molecular Characterization ◽  
Circulating Tumor Cells

Heterogeneity of Acquired Resistance to Anti-EGFR Monoclonal Antibodies in Patients with Metastatic Colorectal Cancer

2016 ◽  
Vol 23 (10) ◽  
pp. 2414-2422 ◽  
Author(s):  
Filippo Pietrantonio ◽  
Claudio Vernieri ◽  
Giulia Siravegna ◽  
Alessia Mennitto ◽  
Rosa Berenato ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Monoclonal Antibodies ◽  
Metastatic Colorectal Cancer ◽  
Acquired Resistance

scholarly journals Germline Profiling and Molecular Characterization of Early Onset Metastatic Colorectal Cancer

2020 ◽  
Vol 10 ◽  
Author(s):  
Ting Xu ◽  
Yinjie Zhang ◽  
Jing Zhang ◽  
Changsong Qi ◽  
Dan Liu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Metastatic Colorectal Cancer ◽  
Molecular Characterization ◽  
Early Onset

A Critical Review of Second-generation anti-EGFR Monoclonal Antibodies in Metastatic Colorectal Cancer

2020 ◽  
Vol 21 ◽  
Author(s):  
Daniel Sur ◽  
Andrei Havasi ◽  
Alecsandra Gorzo ◽  
Claudia Burz
Keyword(s):  
Colorectal Cancer ◽  
Drug Resistance ◽  
Clinical Trials ◽  
Monoclonal Antibodies ◽  
Metastatic Colorectal Cancer ◽  
Second Generation ◽  
Current Data ◽  
Braf Mutations ◽  
Durable Response ◽  
Ongoing Research

Background: Anti-EGFR monoclonal antibodies (mAbs) have become a relevant solution for the treatment of patients with metastatic colorectal cancer. Current anti-EGFR monoclonal antibodies face a series of problems, including resistance and non-durable response, and RAS and BRAF mutations serve as exclusion criteria for treatment with anti-EGFR mAbs. Advances in molecular tumor profiling and information on subsequent pathways responsible for disease progression and drug resistance helped develop a new generation of anti-EGFR mAbs. These second-generation mAbs have been developed to overcome existing resistance mechanisms and to limit common side effects. For the moment, existing literature suggests that these novel anti-EGFR mAbs are far from finding their way to clinical practice soon. Objective: In this review, we summarize and evaluate current data regarding ongoing research and completed clinical trials for different second-generation anti-EGFR monoclonal antibodies. Conclusion: Anti-EGFR mAbs exhibit efficacy in advanced colorectal cancer, but second-generation mAbs failed to prove their benefit in the treatment of metastatic colorectal cancer. Understanding the biological basis of primary and acquired drug resistance could allow scientists to design better clinical trials and develop improved second-generation mAbs.

scholarly journals Lessons to Learn for Adequate Targeted Therapy Development in Metastatic Colorectal Cancer Patients

2021 ◽  
Vol 22 (9) ◽  
pp. 5019
Author(s):  
Helena Oliveres ◽  
David Pesántez ◽  
Joan Maurel
Keyword(s):  
Colorectal Cancer ◽  
Metastatic Colorectal Cancer ◽  
Cancer Patients ◽  
Tyrosine Kinases ◽  
Epithelial To Mesenchymal Transition ◽  
Acquired Resistance ◽  
Post Translational Modification ◽  
Mesenchymal Transition ◽  
Igf1r Signaling ◽  
Colorectal Cancer Patients

Insulin-like growth factor 1 receptor (IGF1R) is a receptor tyrosine kinase that regulates cell growth and proliferation. Upregulation of the IGF1R pathway constitutes a common paradigm shared with other receptor tyrosine kinases such as EGFR, HER2, and MET in different cancer types, including colon cancer. The main IGF1R signaling pathways are PI3K-AKT and MAPK-MEK. However, different processes, such as post-translational modification (SUMOylation), epithelial-to-mesenchymal transition (EMT), and microenvironment complexity, can also contribute to intrinsic and acquired resistance. Here, we discuss new strategies for adequate drug development in metastatic colorectal cancer patients.

scholarly journals Molecular characterization of a virulence-associated epitope on the lipopolysaccharide ofLegionella pneumophilaserogroup 1

1995 ◽  
Vol 115 (1) ◽  
pp. 71-78 ◽  
Author(s):  
J. H. Helbig ◽  
P. C. Lück ◽  
Y. A. Knirel ◽  
W. Witzleb ◽  
U. Zähringer
Keyword(s):  
Monoclonal Antibodies ◽  
Molecular Characterization ◽  
Legionella Pneumophila ◽  
Reactivity Pattern ◽  
Virulence Marker ◽  
Nonulosonic Acid ◽  
Acetyl Group

SummaryFor identification of lipopolysaccharide (LPS)-associated epitopes ofLegionella pneumophilaserogroup 1, LPS of strain Philadelphia 1 was investigated using monoclonal antibodies (MAbs). The O-specific chain of LPS is a homopolymer of 5-acetamidino-7-acetamido-8-O-acetyl-3,5,7,9-tetradeoxy-D-glycero-L-galacto-nonulosonic acid. At least four immunoaccessible epitopes were recognized by different MAbs on the intact LPS. AfterO-deacetylation of LPS, the reactivity of one of the MAbs (MAb 3/1) was lost, indicating thus that the corresponding epitope is associated with the 8-O-acetyl group. Since the reactivity pattern of the MAb 3/1 is identical with those of the MAb 2 which was considered as a virulence marker for serogroup 1, this epitope may be involved in mediating virulence inL. pneumophila. Four MAbs specific to strains of serogroup 1 other than the monoclonal subtype Philadelphia recognized epitopes on theO-deacetylated LPS of strain Philadelphia 1 and, therefore, the virulence-associated epitope blocks recognition of the immunodeterminants that are accessible on the intact LPS of the strains lacking this epitope.

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