Research Papers:

Molecular characteristics of hepatocellular carcinomas from different age groups

Celina Ang _, Anthony Shields, Joanne Xiu, Zoran Gatalica, Sandeep Reddy, Mohamed E. Salem, Carol Farhangfar, Jimmy Hwang, Igor Astsaturov and John L. Marshall

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Oncotarget. 2017; 8:101591-101598. https://doi.org/10.18632/oncotarget.21353

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Celina Ang1, Anthony Shields2, Joanne Xiu3, Zoran Gatalica4, Sandeep Reddy3, Mohamed E. Salem5, Carol Farhangfar6, Jimmy Hwang7, Igor Astsaturov3,7 and John L. Marshall5

1Department of Medicine, Hematology/Oncology, Icahn School of Medicine at Mount Sinai, New York, NY, USA

2Department of Oncology, Molecular Imaging & Diagnostics Program, Karmanos Cancer Center, Wayne State University, Detroit, MI, USA

3Department of Medical Affairs, Caris Life Sciences, Phoenix, AZ, USA

4Department of Pathology, Caris Life Sciences, Phoenix, AZ, USA

5Hematology/Oncology, Lombardi Comprehensive Cancer Center, Georgetown, University, Washington, DC, USA

6Levine Cancer Institute, Carolinas Healthcare System, Charlotte, NC, USA

7Department of Hematology/Oncology, Fox Chase Cancer Center, Philadelphia, PA, USA

Correspondence to:

Celina Ang, email: [email protected]

Keywords: hepatocellular carcinoma; age differences; multiplatform profiling; pathogenic mutations

Received: July 03, 2017     Accepted: August 31, 2017     Published: September 27, 2017


While most patients in Western countries who are diagnosed with HCC are in their 50s and 60s, HCCs diagnosed at extremes of the age spectrum (i.e., < 40 years and ≥ 75 years) are less common and have been linked with distinct geographic locations and etiologies. Using multiplatform profiling, we identified differences in genetic alterations and protein expression in different age groups within a large cohort of HCC patients (N = 421). Young adult HCC patients (18-39 years’ old) were more likely to be female, living in the West and Midwestern United States, and showed decreased androgen receptor, drug resistance and pro-angiogenic protein expression compared to older patients. TP53 mutations were the most frequent alteration in young adults (19%), whereas CTNNB1 mutations occurred in 30-33% of patients ≥ 40 years’ old. The overall frequency of pathogenic and presumed pathogenic mutations was observed to increase significantly with advancing age. To our knowledge, these data represent one of the only studies to analyze age-specific molecular profiles in HCC, and provide a basis for further exploration and validation of these findings with respect to their clinical and therapeutic implications.

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