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Jon E. Peterson

Researcher at Bristol-Myers Squibb

Publications -  15
Citations -  707

Jon E. Peterson is an academic researcher from Bristol-Myers Squibb. The author has contributed to research in topics: Cancer & Lipid A. The author has an hindex of 9, co-authored 15 publications receiving 660 citations.

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VEGF, PF4 and PDGF are elevated in platelets of colorectal cancer patients

TL;DR: Platelets sequester angiogenesis regulatory proteins which suggests an avenue for developing biomarkers to monitor disease and Multivariable logistic regression analysis indicated that PDGF, PF4 and VEGF were independent predictors of colorectal carcinoma and as a set provided statistically significant discrimination.
Journal Article

Platelet-associated PF-4 as a biomarker of early tumor growth. Commentary

TL;DR: Evidence is presented that changes in platelet-associated platelet factor-4 (PF-4) detect malignant growth across a spectrum of human cancers in mice and concludes that platelets-associated PF-4, but not its plasma counterpart, may represent a potential biomarker of early tumor presence.
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Influence of fine structure of lipid A on Limulus amebocyte lysate clotting and toxic activities.

TL;DR: The LAL test is not a valid measure of all parameters of toxicity of a lipid A or lipid A-like compound and can yield false-positive results, but these findings are not in conflict with the widespread use of the LAL assay for pyrogens in the pharmaceutical industry.
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Lipid A and Immunotherapy

TL;DR: Comparison of chromatographic fractions reveals that components of toxic and nontoxic lipid A can be paired according to structure, andStructural analogs of monophosphoryl lipid A, which differ in degree of O-acylation and type and distribution of fatty acids, have comparable antitumor activity.
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Detection of Hepatitis C Core Antigen in the Antibody Negative ‘Window’ Phase of Hepatitis C Infection

TL;DR: Results indicate that HCV core antigen can be identified by routine serological ELISA in specimens from the early antibody–negative phase of HCV infection.