{"doi":"10.1053/j.gastro.2019.12.030","title":"Recent Decline in Hepatocellular Carcinoma Rates in the United States","abstract":"In the United States, hepatocellular carcinoma (HCC), a highly lethal cancer with limited treatment options, is primarily caused by chronic infection with hepatitis B virus (HBV) or hepatitis C virus (HCV), nonalcoholic steatohepatitis (NASH), and excessive alcohol consumption.1Islami F. et al.CA Cancer J Clin. 2017; 67: 273-289Crossref PubMed Scopus (161) Google Scholar HCC development generally requires decades-long exposure to 1 or more risk factors. HCC rates in the United States have increased over several decades.1Islami F. et al.CA Cancer J Clin. 2017; 67: 273-289Crossref PubMed Scopus (161) Google Scholar This trend was largely attributed an HCV epidemic during the 1960s–1980s and an increase in obesity-associated NASH. Based on data from 18 Surveillance, Epidemiology, and End Results (SEER) cancer registries during 2000 through 2012, HCC rates were projected to increase approximately 2.8%/y through 2030 if observed trends continued into the future.2Petrick J.L. et al.J Clin Oncol. 2016; 34: 1787-1794Crossref PubMed Scopus (307) Google Scholar However, a recent analysis of 13 SEER registries suggested that HCC rates plateaued during 2010–2015.3Rich N.E. et al.Clin Gastroenterol Hepatol. 2020; 18: 242-248Abstract Full Text Full Text PDF PubMed Scopus (47) Google Scholar Here, we use data from 21 SEER registries to provide updated HCC rates through 2016. HCC incidence data were obtained from SEER-21, population-based cancer registries covering 37% of the US population. Cases were identified using International Classification of Diseases for Oncology, 3rd edition, codes (site: C22.0; histology: 8170-8175). Incidence rates were age-standardized to the 2000 US population and estimated overall and by sex, age group, and race/ethnicity. Annual percent changes (APCs) were estimated using Joinpoint (National Cancer Institute, Bethesda, MD) regression, which identifies statistically significant inflection points in rate trajectories.4Kim H.J. et al.Stat Med. 2000; 19: 335-351Crossref PubMed Scopus (3799) Google Scholar Rate ratios (RRs) comparing 2015 and 2016 were estimated. We also estimated delay-adjusted rates of all liver/intrahepatic bile duct cancers (HCC-specific estimates are unavailable) to assess the potential impact of delayed reporting.5Midthune D.N. et al.J Am Stat Assoc. 2005; 100: 61-70Crossref Scopus (47) Google Scholar During 2000–2016, 119,078 HCC cases occurred in SEER-21 registries (rate, 5.84/100,000). In 2016, rates were higher in men (10.6/100,000) than women (2.83/100,000), increased with age (20–34-year-olds, 0.23/100,000; ≥65-year-olds, 27.6/100,000), and were highest among American Indian/Alaska Native (14.5/100,000) and Hispanic (9.74/100,000) individuals. Overall, HCC rates increased 5.64%/y (P < .001) during 2000–2007, increased 2.68%/y (P < .001) during 2007–2013, and then plateaued starting in 2013 (APC, –1.44%/y; P = .12) (Figure 1 and Supplementary Table 1). Rates plateaued among men and women beginning in 2012 and 2013, respectively. For ≥65-year-olds, rates increased during the entire time period (APC, 2.69%/y; P < .001). In contrast, inflections and significant decreases occurred among 35–49-year-olds starting in 2006 (APC, –4.93%/y; P < .001) and among 50–64-year-olds in 2014 (APC, –6.64%/y; P = .04). After years of strong increases, HCC rates plateaued among white individuals beginning in 2013 (APC, –0.91%/y; P = .45) and among black individuals in 2009 (APC, 0.27%/y; P = .65). Among Hispanic individuals, HCC incidence decreased nonsignificantly (–6.55%/y; P = .08) beginning in 2014. Among Asian/Pacific Islander (API) individuals, starting in 2007, HCC rates decreased –2.72%/y (P < .001). In contrast, for American Indian/Alaska Native individuals, HCC rates increased 4.60%/y (P < .001) across the time period. Comparing rates in 2016 to those in 2015, we observed a significant decrease in HCC incidence overall (RR, 0.96; P = .007) (Supplementary Table 1). Statistically significant (P < .05)","journal":"Gastroenterology","year":2020,"id":62219,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":52,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9576,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2020-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":24060,"name":"Thomas R. OʼBrien","orcid":"0000-0003-0003-6065","position":1,"is_corresponding":false},{"id":281460,"name":"Meredith S. Shiels","orcid":"0000-0001-8390-6091","position":0,"is_corresponding":true}],"reference_count":9,"raw_metadata":null,"created_at":"2026-07-18T21:10:11.612909Z","pmid":"31962125","pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}