Meet Inspiring Speakers and Experts at our 3000+ Global Conference Series Events with over 1000+ Conferences, 1000+ Symposiums
and 1000+ Workshops on Medical, Pharma, Engineering, Science, Technology and Business.

Explore and learn more about Conference Series : World's leading Event Organizer

Back

Hajime Orita

Shizuoka Hospital-Juntendo University, Japan

Title: Serum fatty acid synthase as a marker of digestive neoplasia

Biography

Biography: Hajime Orita

Abstract

The aim of this study is to evaluate FAS as a marker of digestive cancer to measure FAS serum levels in patients with digestive cancer and explore each digestive cancer metabolic features.

Cancer metabolism is a futuristic strategy point for diagnosis and management. Lipid metabolism in particular is a vast uncharted territory for targeting tumor control. It is well known that many cancer cells up-regulate of fatty acid synthesis. Cancer cells require fatty acid for building blocks of new organelles and cells. Fatty acid synthase (FAS) is the enzyme responsible for fatty acid biosynthesis. It is over-expressed in many human cancers, reported to be correlated with cancer growth, contributes to poor prognosis and inhibition of FAS results in decreased cell proliferation, and loss of cell viability.

Previously we have reported high expression not only in tissue, but also in serum in patients with digestive cancers. Although FAS is found to be over-expressed in many solid tumors, its role in digestive cancer has not been extensively evaluated. We have reported that it seems to be up-regulated during the early stages of tumorigenesis.

In Digestive neoplasm, Upper GI (esophageal and gastric) and colorectal ones have different characteristics due to carcinogenesis. Upper GI neoplasm results from the continuous inflammation from Helicobacter pylori and various other factors. Therefore colorectal one arises from adenoma carcinoma sequences. Our results show a different tendency for each other. Compare between premalignant status and malignancy, by using serum and tumor FAS level we can approach the mechanism of reprogramming the regulation of metabolic pathways.