{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,29]],"date-time":"2026-06-29T14:26:18Z","timestamp":1782743178139,"version":"3.54.5"},"reference-count":84,"publisher":"MDPI AG","issue":"9","license":[{"start":{"date-parts":[[2025,8,28]],"date-time":"2025-08-28T00:00:00Z","timestamp":1756339200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["CIMB"],"abstract":"<jats:p>Acute lymphoblastic leukemia (ALL) is the most common childhood cancer, with pediatric ALL having a ~90 percent cure rate, while the adult cure rate is considerably lower. B-cell acute lymphoblastic leukemia (B-ALL) is the most common subtype of ALL and is generally treated through a variety of chemotherapy drugs that can cause undesired side effects, adverse events, or other complications. Consequently, there is a need for improved understanding of the shared gene expression profiles and underlying molecular mechanisms shared among various B-ALL subtypes. In this study, 259 publicly available RNA-sequencing samples were evaluated and retrieved from the NCBI Gene Expression Omnibus (GEO) database and then pre-processed using a robust computational workflow. Differential gene expression, pathway enrichment, marker prediction, and drug repurposing analyses were then performed to facilitate a better mechanistic understanding of disease. We found both previously identified as well as novel differentially expressed genes. Specifically, we observed upregulation in the HIST2H2AA3, EPHA7, and MPR1 genes; while downregulation was observed for the IGHA1, ANGPTL1, and CHAD genes. We identified multiple pathways, including \u201cIntegrins in Angiogenesis\u201d, to be significantly affected in B-ALL. We then used these significant pathways to predict and rank 306 existing therapeutic targets that could potentially be repurposed for B-ALL, including three that have not been evaluated in human clinical trials. Using a tree-based classification algorithm, we also predicted ADAM28 as a possible mechanistic marker. The results of this study have potential implications for patients who have been diagnosed with B-ALL by providing improved mechanistic understanding and information on possible diagnostics and repurposed therapeutics for B-ALL.<\/jats:p>","DOI":"10.3390\/cimb47090699","type":"journal-article","created":{"date-parts":[[2025,8,28]],"date-time":"2025-08-28T15:03:14Z","timestamp":1756393394000},"page":"699","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Histone-, Receptor-, and Integrin-Related Gene Products and ADAM28 as Relevant to B-Cell Acute Lymphoblastic Leukemia (B-ALL)"],"prefix":"10.3390","volume":"47","author":[{"given":"Makayla R. K.","family":"Wilkins","sequence":"first","affiliation":[{"name":"Department of Microbiology and Molecular Biology, Brigham Young University, Provo, UT 84062, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7930-8160","authenticated-orcid":false,"given":"Brett E.","family":"Pickett","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Molecular Biology, Brigham Young University, Provo, UT 84062, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2025,8,28]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","unstructured":"Inaba, H., and Pui, C.H. (2021). Advances in the Diagnosis and Treatment of Pediatric Acute Lymphoblastic Leukemia. J. Clin. 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