# Glycopathology of HCC: identification of the source cells of serum fucosylation

> **NIH NIH U01** · MEDICAL UNIVERSITY OF SOUTH CAROLINA · 2021 · $413,676

## Abstract

Abstract:
In the Annual Report to the Nation on the Status of Cancer, mortality from Hepatocellular
carcinoma (HCC) increased at an annual rate of 2.8% in men and 2.2% in women,
making it the cancer with the greatest increase in mortality in the United States (USA)
over the last 10 years. The occurrence of liver cancer is predicted to continue rising in
the USA and will exceed 50,000 cases by 2021. The majority of HCC arises in the
background of liver fibrosis and cirrhosis, usually associated with chronic viral infection
(hepatitis B and hepatitis C virus) or nonalcoholic fatty liver disease/nonalcoholic
steatohepatitis (NAFLD/NASH) associated with obesity.
 Our laboratory has shown alterations in both core and outer-arm fucosylation in
HCC. These glycan modifications have promise as biomarkers of cancer and are actively
being commercialized by a number of groups (including us). We have a developed a
diagnostic panel that is comprised of clinical data along with one additional novel
biomarker, fucosylated kininogen, that dramatically improves upon the detection of HCC,
and in particular, the identification of those with early stage HCC.
 In an effort to identify the source of fucosylated serum glycoprotein, we have
developed a novel method for tissue-based glycan analysis. In an analysis of 145 HCC
tissue and 112 adjacent control or cirrhotic tissue control samples, we have identified two
major changes in the N-linked glycan family that are associated with HCC. The first
change observed was increased levels of fucosylation, a modification also often
observed in serum of patients with HCC. However, ~50% of the tissue samples
analyzed had no increase in fucose. Often these tumors without increased fucosylation
had increases in tetra-antennary glycan. We hypothesize that the genetic heterogeneity
of the tumor might have an impact upon the glycan heterogeneity in the tissue and
serum. Consequently, the glycans may not only be used as biomarkers for the early
detection of cancer but offer information into the specific genetics of the cancer. In this
application, we will link the glycomic changes observed in both tissue and serum with the
underlying genetic changes. As we will have matching tissue and serum, we will be able
to determine if our current biomarker panel is capable of identifying fucose negative
HCC. Lastly, we will utilize several proteomic and glycomic methods to identify
biomarkers for cancer without increased levels of fucosylation.

## Key facts

- **NIH application ID:** 10112197
- **Project number:** 5U01CA226052-03
- **Recipient organization:** MEDICAL UNIVERSITY OF SOUTH CAROLINA
- **Principal Investigator:** RICHARD R. DRAKE
- **Activity code:** U01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $413,676
- **Award type:** 5
- **Project period:** 2019-03-14 → 2024-02-29

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10112197

## Citation

> US National Institutes of Health, RePORTER application 10112197, Glycopathology of HCC: identification of the source cells of serum fucosylation (5U01CA226052-03). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10112197. Licensed CC0.

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