<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Petrick JL</submitter><funding>Intramural NIH HHS</funding><funding>NIDDK NIH HHS</funding><funding>NHLBI NIH HHS</funding><funding>NCI NIH HHS</funding><pagination>1156-62</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4704448</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>8(12)</volume><pubmed_abstract>Chronic inflammation plays a pivotal role in the pathogenesis of hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC), the two most common types of liver cancer. A number of prior experimental studies have suggested that nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin and ibuprofen, may potentially protect against liver cancer. However, no observational study has examined the association between aspirin duration and dose or other over-the-counter non-aspirin NSAIDs, such as ibuprofen, and liver cancer incidence. Furthermore, the association between NSAID use and risk of ICC is unclear. As part of the Liver Cancer Pooling Project, we harmonized data on 1,084,133 individuals (HCC = 679, ICC = 225) from 10 U.S.-based prospective cohort studies. Cox proport</pubmed_abstract><journal>Cancer prevention research (Philadelphia, Pa.)</journal><pubmed_title>NSAID Use and Risk of Hepatocellular Carcinoma and Intrahepatic Cholangiocarcinoma: The Liver Cancer Pooling Project.</pubmed_title><pmcid>PMC4704448</pmcid><funding_grant_id>DK098311</funding_grant_id><funding_grant_id>UM1 CA182934</funding_grant_id><funding_grant_id>CA87969</funding_grant_id><funding_grant_id>UM1 CA182913</funding_grant_id><funding_grant_id>R01 HL043851</funding_grant_id><funding_grant_id>K24 DK098311</funding_grant_id><funding_grant_id>P01 CA087969</funding_grant_id><funding_grant_id>CA047988</funding_grant_id><funding_grant_id>CA186107</funding_grant_id><funding_grant_id>CA167552</funding_grant_id><funding_grant_id>Z01 CP010158-07</funding_grant_id><funding_grant_id>UM1 CA167552</funding_grant_id><funding_grant_id>HL080467</funding_grant_id><funding_grant_id>HL099355</funding_grant_id><funding_grant_id>RC1 HL099355</funding_grant_id><funding_grant_id>P30 CA060553</funding_grant_id><funding_grant_id>UM1 CA164974</funding_grant_id><funding_grant_id>R01 HL080467</funding_grant_id><funding_grant_id>R01 CA047988</funding_grant_id><funding_grant_id>UM1 CA186107</funding_grant_id><pubmed_authors>Schairer C</pubmed_authors><pubmed_authors>Sesso HD</pubmed_authors><pubmed_authors>Wactawski-Wende J</pubmed_authors><pubmed_authors>McGlynn KA</pubmed_authors><pubmed_authors>King LY</pubmed_authors><pubmed_authors>Hollenbeck AR</pubmed_authors><pubmed_authors>Palmer JR</pubmed_authors><pubmed_authors>Beane-Freeman LE</pubmed_authors><pubmed_authors>Chong DQ</pubmed_authors><pubmed_authors>Petrick JL</pubmed_authors><pubmed_authors>Jacobs EJ</pubmed_authors><pubmed_authors>Freedman ND</pubmed_authors><pubmed_authors>Rosenberg L</pubmed_authors><pubmed_authors>Zeleniuch-Jacquotte A</pubmed_authors><pubmed_authors>Graubard BI</pubmed_authors><pubmed_authors>Chan AT</pubmed_authors><pubmed_authors>Chen J</pubmed_authors><pubmed_authors>Buring JE</pubmed_authors><pubmed_authors>Linet MS</pubmed_authors><pubmed_authors>Purdue MP</pubmed_authors><pubmed_authors>Sahasrabuddhe VV</pubmed_authors><pubmed_authors>Alavanja MC</pubmed_authors><pubmed_authors>Giovannucci E</pubmed_authors><pubmed_authors>Hou L</pubmed_authors><pubmed_authors>Lee IM</pubmed_authors><pubmed_authors>Campbell PT</pubmed_authors><pubmed_authors>Sigurdson AJ</pubmed_authors><pubmed_authors>Fuchs CS</pubmed_authors><pubmed_authors>Koshiol J</pubmed_authors><pubmed_authors>Gaziano JM</pubmed_authors></additional><is_claimable>false</is_claimable><name>NSAID Use and Risk of Hepatocellular Carcinoma and Intrahepatic Cholangiocarcinoma: The Liver Cancer Pooling Project.</name><description>Chronic inflammation plays a pivotal role in the pathogenesis of hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC), the two most common types of liver cancer. A number of prior experimental studies have suggested that nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin and ibuprofen, may potentially protect against liver cancer. However, no observational study has examined the association between aspirin duration and dose or other over-the-counter non-aspirin NSAIDs, such as ibuprofen, and liver cancer incidence. Furthermore, the association between NSAID use and risk of ICC is unclear. As part of the Liver Cancer Pooling Project, we harmonized data on 1,084,133 individuals (HCC = 679, ICC = 225) from 10 U.S.-based prospective cohort studies. Cox proport</description><dates><release>2015-01-01T00:00:00Z</release><publication>2015 Dec</publication><modification>2025-04-22T07:15:05.496Z</modification><creation>2019-03-27T02:06:28Z</creation></dates><accession>S-EPMC4704448</accession><cross_references><pubmed>26391917</pubmed><doi>10.1158/1940-6207.CAPR-15-0126</doi><doi>10.1158/1940-6207.capr-15-0126</doi></cross_references></HashMap>