<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Fiadjoe HK</submitter><funding>NIAID NIH HHS</funding><funding>NCI NIH HHS</funding><funding>National Institutes of Health</funding><funding>NIH HHS</funding><pagination>2179</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12662978</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>16(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Histidine (His) ammonia Lyase (HAL) is a key rate-limiting enzyme that catalyzes the first reaction in the metabolism of histidine. Deficiencies in HAL lead to histidinemia, characterized by elevated levels of His in the blood and other body fluids. The level of HAL in these fluids is known to impact the sensitivity of cancer cells to certain chemotherapeutics by regulating His. However, the molecular role and impacts of HAL in the progression of hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA) are unknown at present. Thus, we investigated the expression of HAL in HCC and CCA tumors.&lt;h4>Method&lt;/h4>The Cancer Genome Atlas (TCGA) database, quantitative real-time PCR (qRT-PCR), and immunoblot analysis were utilized to examine the expression of HAL in HCC and CCA </pubmed_abstract><journal>Discover oncology</journal><pubmed_title>Histidine ammonia lyase expression characteristics in primary liver cancer: hepatocellular carcinoma and cholangiocarcinoma.</pubmed_title><pmcid>PMC12662978</pmcid><funding_grant_id>R21 CA283524</funding_grant_id><funding_grant_id>CA283524</funding_grant_id><funding_grant_id>R21 AI179337</funding_grant_id><funding_grant_id>AI179337</funding_grant_id><pubmed_authors>Chaudhary P</pubmed_authors><pubmed_authors>Jones HP</pubmed_authors><pubmed_authors>Park IW</pubmed_authors><pubmed_authors>Fiadjoe HK</pubmed_authors><pubmed_authors>Hoteit T</pubmed_authors></additional><is_claimable>false</is_claimable><name>Histidine ammonia lyase expression characteristics in primary liver cancer: hepatocellular carcinoma and cholangiocarcinoma.</name><description>&lt;h4>Background&lt;/h4>Histidine (His) ammonia Lyase (HAL) is a key rate-limiting enzyme that catalyzes the first reaction in the metabolism of histidine. Deficiencies in HAL lead to histidinemia, characterized by elevated levels of His in the blood and other body fluids. The level of HAL in these fluids is known to impact the sensitivity of cancer cells to certain chemotherapeutics by regulating His. However, the molecular role and impacts of HAL in the progression of hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA) are unknown at present. Thus, we investigated the expression of HAL in HCC and CCA tumors.&lt;h4>Method&lt;/h4>The Cancer Genome Atlas (TCGA) database, quantitative real-time PCR (qRT-PCR), and immunoblot analysis were utilized to examine the expression of HAL in HCC and CCA </description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Nov</publication><modification>2026-06-07T04:39:45.072Z</modification><creation>2026-06-07T03:07:48.577Z</creation></dates><accession>S-EPMC12662978</accession><cross_references><pubmed>41313389</pubmed><doi>10.1007/s12672-025-04043-4</doi></cross_references></HashMap>