Establishment of internal-image anti-idiotype monoclonal antibodies to a human antibody to lung cancer

1997 ◽  
Vol 44 (2) ◽  
pp. 83-87 ◽  
Author(s):  
Hiroaki Saito ◽  
Masaru Taniguchi ◽  
Toshio Fukasawa ◽  
Yutaka Yamaguchi ◽  
T. Fujisawa
Keyword(s):  
Lung Cancer ◽  
Monoclonal Antibodies ◽  
Human Antibody ◽  
Internal Image

Internal Image-Bearing Anti-ldiotypic Monoclonal Antibodies

Tumor Biology ◽  
1995 ◽  
Vol 16 (1) ◽  
pp. 48-55 ◽  
Author(s):  
Y. Hinoda ◽  
M. Tsujisaki ◽  
K. Imai ◽  
A. Yachi
Keyword(s):  
Monoclonal Antibodies ◽  
Internal Image

Anti-EGFR and antiangiogenic monoclonal antibodies in metastatic non-small-cell lung cancer

2016 ◽  
Vol 16 (6) ◽  
pp. 747-758 ◽  
Author(s):  
Tania Losanno ◽  
Antonio Rossi ◽  
Paolo Maione ◽  
Alba Napolitano ◽  
Cesare Gridelli
Keyword(s):  
Lung Cancer ◽  
Monoclonal Antibodies ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung

KRAS Mutation: Should We Test for It, and Does It Matter?

2013 ◽  
Vol 31 (8) ◽  
pp. 1112-1121 ◽  
Author(s):  
Patrick J. Roberts ◽  
Thomas E. Stinchcombe
Keyword(s):  
Lung Cancer ◽  
Monoclonal Antibodies ◽  
Predictive Value ◽  
Clinical Utility ◽  
Mutational Analysis ◽  
Small Cell ◽  
Small Cell Lung ◽  
Kras Mutations ◽  
Mutational Status ◽  
Egfr Tki

Lung cancer is the leading cause of cancer mortality in the United States and worldwide. Previously, lung cancer was simplistically divided into non–small-cell lung cancer (NSCLC) and small-cell lung cancer. However, in the last decade, we have gone from a simplistic binary system of classifying lung cancer to defining NSCLC on the basis of molecular subsets. KRAS mutations represent the most common molecular change in NSCLC. The presence of KRAS mutation has been shown to be associated with a poor prognosis in NSCLC, but this is of little clinical utility. More important is determining the clinical utility of KRAS mutational analysis for predicting benefit of chemotherapy, epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), anti-EGFR monoclonal antibodies, or other novel therapeutics. Current data does not support the routine use of KRAS mutational analysis for predicting chemotherapy benefit. Additionally, there was significant interest in using KRAS status to select patients for EGFR TKI and anti-EGFR monoclonal antibodies. However, the EGFR mutational status has demonstrated significant predictive value in the selection of patients for EGFR TKI therapy and is now the preferred test. An association between KRAS mutational status and benefit of anti-EGFR monoclonal antibodies has not been demonstrated in NSCLC. Here we review, in the context of NSCLC, the underlying biology of KRAS mutations, the predictive value of KRAS mutations for therapeutic intervention, and the integration of KRAS mutational testing into our current clinical paradigms.

scholarly journals Potent Neutralization of Hendra and Nipah Viruses by Human Monoclonal Antibodies

2006 ◽  
Vol 80 (2) ◽  
pp. 891-899 ◽  
Author(s):  
Zhongyu Zhu ◽  
Antony S. Dimitrov ◽  
Katharine N. Bossart ◽  
Gary Crameri ◽  
Kimberly A. Bishop ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
Cell Fusion ◽  
Hendra Virus ◽  
Soluble Form ◽  
Enzyme Linked Immunosorbent Assay ◽  
Human Antibody ◽  
Emerging Viruses ◽  
Human Monoclonal Antibodies ◽  
Initial Attempt ◽  
Fusion Event

ABSTRACT Hendra virus (HeV) and Nipah virus (NiV) are closely related emerging viruses comprising the Henipavirus genus of the Paramyxovirinae. Each has a broad species tropism and can cause disease with high mortality in both animal and human hosts. These viruses infect cells by a pH-independent membrane fusion event mediated by their attachment (G) and fusion (F) envelope glycoproteins (Envs). Seven Fabs, m101 to -7, were selected for their significant binding to a soluble form of Hendra G (sG) which was used as the antigen for panning of a large naïve human antibody library. The selected Fabs inhibited, to various degrees, cell fusion mediated by the HeV or NiV Envs and virus infection. The conversion of the most potent neutralizer of infectious HeV, Fab m101, to immunoglobulin G1 (IgG1) significantly increased its cell fusion inhibitory activity: the 50% inhibitory concentration was decreased more than 10-fold to approximately 1 μg/ml. The IgG1 m101 was also exceptionally potent in neutralizing infectious HeV; complete (100%) neutralization was achieved with 12.5 μg/ml, and 98% neutralization required only 1.6 μg/ml. The inhibition of fusion and infection correlated with binding of the Fabs to full-length G as measured by immunoprecipitation and less with binding to sG as measured by enzyme-linked immunosorbent assay and Biacore. m101 and m102 competed with the ephrin-B2, which we recently identified as a functional receptor for both HeV and NiV, indicating a possible mechanism of neutralization by these antibodies. The m101, m102, and m103 antibodies competed with each other, suggesting that they bind to overlapping epitopes which are distinct from the epitopes of m106 and m107. In an initial attempt to localize the epitopes of m101 and m102, we measured their binding to a panel of 11 G alanine-scanning mutants and identified two mutants, P185A and Q191 K192A, which significantly decreased binding to m101 and one, G183, which decreased binding of m102 to G. These results suggest that m101 to -7 are specific for HeV or NiV or both and exhibit various neutralizing activities; they are the first human monoclonal antibodies identified against these viruses and could be used for treatment, prophylaxis, and diagnosis and as research reagents and could aid in the development of vaccines.

scholarly journals Targeted Therapies for Pancreatic Cancer

Cancers ◽  
2018 ◽  
Vol 10 (2) ◽  
pp. 36 ◽  
Author(s):  
Idoroenyi Amanam ◽  
Vincent Chung
Keyword(s):  
Lung Cancer ◽  
Pancreatic Cancer ◽  
Overall Survival ◽  
Monoclonal Antibodies ◽  
Small Molecule ◽  
Targeted Therapies ◽  
Median Overall Survival ◽  
The Third ◽  
One Year ◽  
Targeted Approach

Pancreatic cancer is the third leading cause of cancer related death and by 2030, it will be second only to lung cancer. We have seen tremendous advances in therapies for lung cancer as well as other solid tumors using a molecular targeted approach but our progress in treating pancreatic cancer has been incremental with median overall survival remaining less than one year. There is an urgent need for improved therapies with better efficacy and less toxicity. Small molecule inhibitors, monoclonal antibodies and immune modulatory therapies have been used. Here we review the progress that we have made with these targeted therapies.

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