scholarly journals Biomarker analysis of fucosylated kininogen through depletion of lectin reactive heterophilic antibodies in hepatocellular carcinoma

2018 ◽  
Vol 462 ◽  
pp. 59-64 ◽  
Author(s):  
Mengjun Wang ◽  
Jiabin Shen ◽  
Harmin Herrera ◽  
Amit Singal ◽  
Charles Swindell ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Heterophilic Antibodies ◽  
Biomarker Analysis

scholarly journals OSlihc: An Online Prognostic Biomarker Analysis Tool for Hepatocellular Carcinoma

2020 ◽  
Vol 11 ◽  
Author(s):  
Yang An ◽  
Qiang Wang ◽  
Guosen Zhang ◽  
Fengjie Sun ◽  
Lu Zhang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Prognostic Biomarker ◽  
Analysis Tool ◽  
Biomarker Analysis

Comprehensive multiplatform biomarker analysis of 313 hepatocellular carcinoma to identify potential therapeutic options.

2015 ◽  
Vol 33 (3_suppl) ◽  
pp. 283-283
Author(s):  
Ghassan K. Abou-Alfa ◽  
John Thomas Miura ◽  
T. Clark Gamblin ◽  
Joanne Xiu ◽  
Sherri Z. Millis ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Kinase Inhibitors ◽  
Therapeutic Option ◽  
Alkylating Agents ◽  
Treatment Options ◽  
Treatment Strategies ◽  
Molecular Heterogeneity ◽  
Biomarker Analysis ◽  
Pi3 Kinase Pathway ◽  
Kinase Pathway

283 Background: Effective treatment strategies for hepatocellular carcinoma (HCC) remain limited. Identification of additional therapies remains paramount as currently available agents have resulted in marginal improvements in overall survival. Methods: 313 HCC sampleswere evaluated using a multiplatform profiling service (Caris Life Sciences, Phoenix, AZ), including gene sequencing (Sanger, NGS [N=79]), protein expression (IHC) and gene amplification (ISH). Results: Biomarker changes of interest are shown. See Table. TP53 was mutated in 28%, CTNNB1 in 23%, and BRCA2 in 20%; other gene mutation rates were < 5%.TP53-mutated tumors show significantly higher TOPO2A (89% vs. 39%, p<0.0001), TS (70% vs. 32%, p=0.0067) and RRM1 expression (40% vs. 12%, p=0.017), implying high rates of proliferation and DNA synthesis. CTNNB1-mutated tumors showed significantly higher SPARC (67% vs. 21%, p=0.0013) and AR expression (53% vs. 22%, p=0.025). Primary HCC (N=209) exhibited significantly higher PD-1 (89% vs. 33%, p=0.01) and TS expression (35% vs. 13%, p<0.0001) than metastatic (N=105). Patient history/outcomes relative to biomarker status are being evaluated. Conclusions: These data suggest potential therapeutic targets, such as tyrosine kinase inhibitors, anti-PD1 agents, or PI3 kinase pathway inhibitors. Although no evidence shows that cytotoxics are effective in patients with HCC, irinotecan, alkylating agents, fluoropyrimidines, anthracyclines, nab-paclitaxel, gemcitabine, or taxanes may be therapeutically relevant. The protein changes associated with CTNNB1-mutated tumors suggest potential benefit of targeting WNT pathway in combination with nab-paclitaxel or anti-androgens. Immuno-modulatory agents may be a therapeutic option in primary HCC, based on the higher levels of PD-1. Multiplatform tumor profiling reveals molecular heterogeneity HCC, similar overall to previous reports, and identifies different potential treatment options for molecular subtypes. [Table: see text]

Mixed Hepatocellular Carcinoma, Neuroendocrine Carcinoma of the Liver

2016 ◽  
Vol 82 (11) ◽  
pp. 1121-1125 ◽  
Author(s):  
Erin Baker ◽  
Carl Jacobs ◽  
John Martinie ◽  
David A. Iannitti ◽  
Dionisios Vrochides ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Neuroendocrine Carcinoma ◽  
Gene Mutations ◽  
Lateral Lobe ◽  
Cell Types ◽  
High Grade ◽  
Large Tumor ◽  
Pathologic Features ◽  
Platinum Based Chemotherapy ◽  
Biomarker Analysis

We present the case of a 76-year-old male found to have a large tumor involving the left lateral lobe of the liver, presumed to be hepatocellular carcinoma (HCC). After resection, pathologic features demonstrated both high-grade HCC and high-grade neuroendocrine carcinoma (NEC). Areas of NEC stained strongly for synaptophysin, which was not present in HCC component. The HCC component stained strongly for Hep-Par 1, which was not present in the NEC component. The patient underwent genetic analysis for biomarkers common to both tumor cell types. Both tumor components contained gene mutations in CTNNB1 gene (S33F located in exon 3). They also shared mutations in PD-1, PGP, and SMO. Mixed HCC/NEC tumors have been rarely reported in the literature with generally poor outcomes. This patient has been referred for adjuvant platinum-based chemotherapy; genetic biomarker analysis may provide some insight to guide targeted chemotherapy.

Phase II Study of Sorafenib in Patients With Advanced Hepatocellular Carcinoma

2006 ◽  
Vol 24 (26) ◽  
pp. 4293-4300 ◽  
Author(s):  
Ghassan K. Abou-Alfa ◽  
Lawrence Schwartz ◽  
Sergio Ricci ◽  
Dino Amadori ◽  
Armando Santoro ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Phase Ii ◽  
Anticancer Agents ◽  
Phase Ii Study ◽  
Expression Patterns ◽  
Single Agent ◽  
Advanced Hepatocellular Carcinoma ◽  
Multikinase Inhibitor ◽  
Minor Response ◽  
Biomarker Analysis

Purpose This phase II study of sorafenib, an oral multikinase inhibitor that targets Raf kinase and receptor tyrosine kinases, assessed efficacy, toxicity, pharmacokinetics, and biomarkers in advanced hepatocellular carcinoma (HCC) patients. Methods Patients with inoperable HCC, no prior systemic treatment, and Child–Pugh (CP) A or B, received continuous, oral sorafenib 400 mg bid in 4-week cycles. Tumor response was assessed every two cycles using modified WHO criteria. Sorafenib pharmacokinetics were measured in plasma samples. Biomarker analysis included phosphorylated extracellular signal regulated kinase (pERK) in pretreatment biopsies (immunohistochemistry) and blood-cell RNA expression patterns in selected patients. Results Of 137 patients treated (male, 71%; median age, 69 years), 72% had CP A, and 28% had CP B. On the basis of independent assessment, three (2.2%) patients achieved a partial response, eight (5.8%) had a minor response, and 46 (33.6%) had stable disease for at least 16 weeks. Investigator-assessed median time to progression (TTP) was 4.2 months, and median overall survival was 9.2 months. Grade 3/4 drug-related toxicities included fatigue (9.5%), diarrhea (8.0%), and hand–foot skin reaction (5.1%). There were no significant pharmacokinetic differences between CP A and B patients. Pretreatment tumor pERK levels correlated with TTP. A panel of 18 expressed genes was identified that distinguished “nonprogressors” from “progressors” with an estimated 100% accuracy. Conclusion Although single-agent sorafenib has modest efficacy in HCC, the manageable toxicity and mechanisms of action support a role for combination regimens with other anticancer agents.

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